Cardio-Oncology — Cardiology Guide

START

CV
Emergencies

ICI Myocarditis hold ICI IV methylprednisolone 1 g/d × 3 d then taper after objective response. Urgent specialist escalation for deterioration or inadequate response. Adjunctive immunosuppression is individualized. 25–50% mortality in fulminant cases. Permanent discontinuation.

Anthracycline acute HF Acute symptomatic HF → hold, urgent assessment + phenotype-directed GDMT. Anthracycline restart is an MDT decision after recovery. Consider dexrazoxane / liposomal options.

Hypertensive crisis VEGF/TKI: SBP ≥180 or DBP ≥110 → hold, assess end-organ injury. IV therapy for hypertensive emergency. Reassess restart below 160/100, subject to product-label restrictions.

QTc ≥500 ms / Torsades hold the agent. For torsades: IV magnesium and urgent rhythm care. Correct K⁺/Mg²⁺ and stop QT drugs. Pace if pause-dependent. Permanently d/c after Torsades (esp. ribociclib).

5-FU / Capecitabine ACS stop exposure, ECG/troponin + ACS evaluation. Nitrates/CCB for vasospasm. Exclude obstructive CAD. Rechallenge only after MDT review, prophylaxis, and a monitored plan.

01

Baseline CV risk assessment

Before cancer therapy

HFA-ICOS pre-treatment workup

History prior HF / CAD / valve · cumulative anthracycline · chest RT · smoking · DM · HTN · CKD · pregnancy / late effects of childhood Ca.
Exam + vitals BP both arms · HR · weight · JVP · edema · murmur.
ECG if pre-existing CVD / CV risk, or the planned therapy is associated with arrhythmia or high CV-toxicity risk.
LV imaging for drugs associated with LV dysfunction: TTE + GLS if available. CMR if echo quality is poor. MUGA if TTE is unavailable or infeasible.
Biomarkers consider baseline hs-troponin · BNP for HIGH / V·HIGH risk rather than as a universal bundle.
Labs lipids + A1c within 6 mo for systemic therapy. CBC · BMP · Mg / K · TSH according to regimen and comorbidity.

Stratify before cycle 1 Combine the therapy-specific HFA-ICOS proforma with patient factors to assign LOW MED HIGH V·HIGH. The tier informs monitoring, HIGH / V·HIGH referral, and multidisciplinary risk–benefit review. It is not itself a drug-hold rule.

Primary prevention candidates

No routine prophylactic CV drug bundle Evidence does not support starting an ACEi/ARB, β-blocker, statin, or SGLT2i solely for primary CTR-CVT prevention. Treat standard CV indications. A specialist may select neurohormonal therapy or a statin in HIGH / V·HIGH risk.
Anthracycline mitigation in HIGH-risk patients needing further therapy, consider dexrazoxane or a liposomal formulation, particularly near/above cumulative doxorubicin 250 mg/m² or with pre-existing cardiomyopathy.
Lifestyle + risk factors exercise · smoking cessation · healthy diet · weight. CPS targets: A1c <7 · BP <130/80 · LDL <70. Individualize during active therapy.

02

Surveillance principles

Echo · biomarkers · ECG cadence

Echo / GLS cadence

Anthracycline baseline LV imaging when dysfunction risk is present. Follow the drug/risk schedule. At 12 mo post-Tx, echo if early-stage/curative intent and cumulative doxorubicin ≥ 250 mg/m² or equivalent.
HER2 baseline LV imaging + drug-specific on-Tx surveillance. Echo at 12 mo post-Tx.
VEGF / TKI baseline · q3–6 mo if CV risk factors.
BRAF/MEK baseline · 1 mo · then q3 mo.
Survivorship after adult-onset cancer therapy: annual symptoms + CV risk-factor review. Re-stratify at 5 y. Childhood-cancer survivors follow their separate exposure-based pathway.
Long-term echo MODERATE risk: q5y may be considered (IIb-C). HIGH / V·HIGH: years 1, 3, 5, then q5y (IIa-C). Evidence is limited.

Biomarkers

hs-Tn / ECG ICI: baseline and early-cycle surveillance per risk pathway. New symptoms, troponin rise or conduction change → urgent clinical assessment, then targeted TTE/CMR. Do not wait for imaging if unstable.
BNP echo cadence + at any new dyspnea / volume change.
Trend > absolute — the patient is their own control only while modality, acquisition, loading, rhythm, vendor/software, and analysis remain comparable. Exclude technically invalid trend points.

ECG / electrolytes

Pre-dose for any QT-prolonger. Review interacting drugs.
Ribociclib ECG before therapy and ~day 14 of cycle 1, then as indicated. Start only if QTcF <450 ms. Correct electrolytes.
Vandetanib / arsenic follow distinct label ECG and electrolyte schedules. Increase monitoring if unstable.

03

Therapy-specific decision rules

When to hold · who to call

EF drop trigger (asymptomatic CTRCD)

Confirm LVEF/GLS and symptoms. Asymptomatic EF 40–49%: interrupt anthracycline. Selected HER2 therapy may continue with ACEi/ARB + BB and close monitoring. Follow the exact agent label and MDT plan.

Symptomatic HF (any cause)

New HF symptoms → hold diurese, GDMT (ARNI/ACE/ARB + BB + MRA + SGLT2 as tolerated). CV consult. Echo + biomarkers. Rule out ischemia.

QTc thresholds

Use QTcF: 480–500 ms → correct causes + closer monitoring. ≥500 ms → hold. Δ >60 ms alone below 500 is not an automatic hold. Stricter agent-label rules apply, including ribociclib and arsenic.

Hypertension (any agent)

Treat elevated BP. ≥160/100 generally needs ACEi/ARB + DHP-CCB. ≥180 systolic or ≥110 diastolic → hold culprit therapy pending control. Emergency = end-organ injury. Product labels may require earlier holds.

When to call cardio-onc

New CVD · LVEF <53% and/or relative GLS drop >15% · new arrhythmia · uncontrolled CV risk factors · important DDI concern. These CPS examples prompt evaluation/referral, not an automatic cancer-therapy hold.

B

Biomarker thresholds at a glance

Assay · context · serial change

hs-Troponinng/L

≥ 99th percentile ULN + symptoms → CMR + cardiac consult. Interpret assay variation, renal disease, ischemia and myositis. During ICI therapy, a new rise requires urgent myocarditis assessment, not an automatic diagnosis.

BNPpg/mL

BNP > 35 (NT-proBNP > 125 equiv.) abnormal in non-acute setting. Rising trend → echo. Consider diuresis if volume-overloaded.

LVEF% by 3D / GLS

New EF <40%: severe asymptomatic CTRCD. EF 40–49%: moderate if fall ≥10 points, or a smaller fall plus new GLS/biomarker abnormality. EF ≥50%: mild only with new GLS/biomarker abnormality.

GLS% relative Δ

Subclinical injury signal: Δ > 15% relative drop from baseline. Confirm comparability and refer/evaluate. This signal alone is not an automatic hold criterion.

R

Baseline risk domains — not a scoring substitute

Use the therapy-specific proforma

Cardiac history

HF · CAD · MI · valvular · AF · prior cardiotoxic Tx

Imaging

EF < 50% · GLS reduced · ↑ LV mass · diastolic dysfn

Biomarkers

↑ hs-Tn · ↑ BNP at baseline

Demographics

Age ≥ 65 · pediatric · pregnancy · ethnicity (S Asian, AA)

CV risk factors

HTN · DM · CKD · obesity · smoking · dyslipidemia · OSA

Prior exposure

Anthracycline > 250 mg/m² · chest RT · prior HER2 / VEGF

START

L

How to score — count point-bearing rows, apply ceiling factors

Six point-based tools · ADT uses ASCVD risk

LOWNo risk factors or a single Medium point. 0–1 med pts

MEDIUM2–4 Medium points. No High / Very-High factor. 2–4 med pts

HIGH≥5 Medium pts or any High-tier factor. ≥5 med · or any HIGH

V·HIGHAny Very-High factor (HF / cardiomyopathy etc). any VERY HIGH

A

Risk tier → pre-treatment action

Each drug card carries its own HFA-ICOS mini-score

LOW

Proceed with routine class-based surveillance (echo / Tn per card).

MEDIUM

Closer monitoring. manage CV risk factors. Consider cardiology referral.

HIGH

Discuss risk / benefit. Refer to cardio-onc. Consider baseline Tn / BNP. Do not auto-start prophylactic CV drugs solely from the tier.

V·HIGH

MDT on alternative regimen / ↓ cum-dose / liposomal / dexrazoxane. Optimize established CVD. Specialist-selected prevention may be reasonable.

G

CTCAE / ASTCT grade criteria — what the grades actually mean

Versioned reference · use the trial-specified CTCAE edition

Toxicity	Grade 1	Grade 2	Grade 3	Grade 4
HypertensionCTCAE v5	SBP 120–139 or DBP 80–89	SBP 140–159 / DBP 90–99. Symptomatic. Monotherapy indicated	SBP ≥160 / DBP ≥100. >1 agent or more intensive Tx	Life-threatening — malignant HTN, crisis, neuro deficit. Urgent IV Tx
Heart failureCTCAE v5 · LVSD is a separate term	Asymptomatic. Abnormal imaging / biomarker only	Symptoms with moderate activity / exertion	Symptoms at rest / minimal exertion. Intervention indicated	Life-threatening. Urgent Tx — inotropes / mechanical support
MyocarditisCTCAE v5	Not defined	Symptoms on moderate exertion	Symptoms at rest/minimal activity, intervention needed	Life-threatening, urgent support needed
Pericardial effusionCTCAE v5	Not defined	Asymptomatic small-to-moderate effusion	Physiologic consequences	Life-threatening, urgent intervention
QTc prolongationCTCAE v5	450–480 ms	481–500 ms	≥501 ms or Δ >60 ms from baseline	Torsades / polymorphic VT / signs of serious arrhythmia
Atrial fibrillationCTCAE v5	Asymptomatic. No intervention	Non-urgent medical intervention	Symptomatic, urgent Tx (rate/rhythm control, cardioversion)	Life-threatening. Hemodynamic compromise. Urgent intervention
Cytokine release (CRS)ASTCT 2019	Fever ≥38°C. no hypotension / hypoxia	↓BP not needing pressors and/or hypoxia on low-flow O₂ ≤6 L/min	↓BP needing 1 pressor (±vasopressin) and/or O₂ >6 L/min / mask	↓BP needing multiple pressors excluding vasopressin and/or positive-pressure ventilation
Peripheral sensory neuropathyCTCAE v5	Asymptomatic. Loss of DTRs / paresthesia	Moderate. Limiting instrumental ADL	Severe. Limiting self-care ADL	Life-threatening. Urgent intervention
ProteinuriaCTCAE v5	1+. <1.0 g/24h	2+. 1.0–3.4 g/24h	≥3.5 g/24h (nephrotic-range)	—
DiarrheaCTCAE v5	<4 stools/day over baseline	4–6 stools/day over baseline	≥7/day. Incontinence. Hospitalization	Life-threatening. Urgent intervention

How to read the cards that follow Each drug class is one block: agents (US brand + generic) · use / benefit · CV & non-cardiac toxicity · its HFA-ICOS mini-score (or a note where no proforma exists) · surveillance · and a granular, grade-tiered management plan with doses and hold / resume / rechallenge thresholds. CRS uses ASTCT. Grade by the worse hypotension/hypoxia domain. Fever need not persist after antipyretic or anti-cytokine therapy. A troponin rise alone is not a CTCAE v5 myocarditis grade. The 2026 ASTCT consensus retains the CRS framework with clarifications. ICANS assessment for developmental limitations or abnormal baseline cognition follows that updated consensus.

W

Worked example — patient → HFA-ICOS tier → action

New to cardio-onc? This is the workflow every card supports

1 · The patient

68 F · HER2+ breast Ca · h/o HTN · prior doxorubicin 240 mg/m² · baseline EF 53%, GLS −16% (borderline). Now starting trastuzumab.

→

2 · Count points

Age 68 2 + HTN 1 + EF 53% 2 = 5 medium points → HIGH already. Remote anthracycline adds 2, or current sequential anthracycline adds 1. Borderline GLS is not a separate High-tier factor.

→

3 · Tier

HIGH

→

4 · Action

Refer cardio-onc · baseline echo+GLS. Consider hs-Tn/BNP · optimize standard CV indications. Discuss rather than automatically start prophylactic ACEi/BB · follow the trastuzumab surveillance plan.

DRUGS

CLASS MAP

Anthracyclines

Dose-dependent · cumulative · partly reversible

AnthracyclinesDNA topo-II inhibition · ROS / iron-mediated injury

CLASS

AgentsDoxorubicin (Adriamycin) · liposomal doxorubicin (Doxil) · Daunorubicin (Cerubidine) · Epirubicin (Ellence) · Idarubicin (Idamycin) · Mitoxantrone (Novantrone) · Valrubicin (Valstar).

UseBreast · HL / NHL · AML / ALL · sarcoma · gastric. Curative-intent backbone.Benefit≈ 33% ↓ breast-Ca mortality. > 80% cure in Hodgkin (ABVD). Core of AML 7+3 & pediatric ALL — often irreplaceable.

CV toxicity

HFrEF / CTRCD: cumulative-dose injury with variable recovery. Historical doxorubicin trials estimated CHF in 5% at 400 and 26% at 550 mg/m². These are cohort estimates, not individual thresholds.
Cumulative exposure increases risk. ≥250 mg/m² doxorubicin flags higher surveillance risk. There is no universally safe dose or absolute 550 mg/m² prohibition.
A new GLS decline or troponin rise may precede LVEF decline. Neither appears in every case, and alternative causes must be assessed.
Acute arrhythmia / myopericarditis during infusion (rare).

Non-cardiac toxicity

Myelosuppression — neutropenia dose-limiting. Febrile neutropenia.
Vesicant — extravasation necrosis. Mucositis · alopecia · N/V.
Secondary leukemia (t-AML / MDS). Benign red urine.

HFA-ICOS · Anthracyclinepre-Tx

V·HIGHHF / cardiomyopathy

HIGHSevere valvular dz · MI / prior PCI / CABG · Stable angina · LVEF <50% · Prior anthracycline · Prior L-chest / mediastinal RT · Age ≥80

MEDLVEF 50–54%² · Age 65–79² · ↑ baseline Tn¹ · ↑ baseline BNP¹ · HTN¹ · DM¹ · CKD¹ · Prior non-anthra chemo¹ · Smoking¹ · Obesity¹

≥1 V·HIGH → V·High · any HIGH or ≥5 MED-pts → High · 2–4 → Med · 0–1 → Low

Cum. dose ≥250 mg/m² doxorubicin (≥600 epirubicin) independently ↑ risk.

Surveillance

Baseline CV Hx · BP · ECG if CVD/risk or arrhythmia risk · echo + GLS. Consider hs-Tn/BNP if HIGH / V·HIGH.
Echo + GLS on-Tx per drug/risk. 12 mo post if early-stage/curative and cumulative doxorubicin ≥250 mg/m². Longer intervals by risk.
hs-Tn each cycle if high-risk — trend > absolute.

Management — granular

PREHFA-ICOS High / V-High → cardio-onc/MDT review. Optimize standard CV indications. Do not automatically start ACEi/ARB, BB, statin, or SGLT2i solely for CTR-CVT prophylaxis. Specialist-selected neurohormonal/statin therapy may be considered.

MILDΔ GLS >15% rel. or new ↑Tn with EF ≥50% → validate the trend + cardio-onc review. Consider ACEi/ARB + BB as appropriate. do not automatically hold chemo.

CTRCDModerate/severe asymptomatic CTRCD or symptomatic HF → interrupt anthracycline and assess urgently. Treat the HF phenotype, confirm the trajectory and agree on reassessment with the MDT.

PROTDexrazoxane: labeled cardioprotection in women with metastatic breast cancer continuing doxorubicin after 300 mg/m². Broader high-risk use may be off-label. Ratio 10:1. Reduce 50% if CrCl <40. Verify product/timing.

RESUMERechallenge after recovery only by MDT risk–benefit review. Optimize HF therapy, exposure mitigation, and monitoring. No universal EF/4-week restart rule.

FactoidDexrazoxane and liposomal formulations can reduce anthracycline cardiac injury. Cumulative exposure and baseline susceptibility still matter.

CLASS MAP

VEGF axis · ICI · CAR-T · alkylators · mTOR

Recognize myocarditis · HTN · arrhythmia early

VEGF Inhibitors (TKI)Multi-kinase · VEGFR signaling blockade

CLASS

AgentsSunitinib (Sutent) · Sorafenib (Nexavar) · Pazopanib (Votrient) · Axitinib (Inlyta) · Cabozantinib (Cabometyx) · Lenvatinib (Lenvima) · Regorafenib (Stivarga) · Vandetanib (Caprelsa).

UseRCC · HCC · differentiated & medullary thyroid · GIST · sarcoma · CRC (rego).BenefitDoubles PFS in RCC / HCC. Lenvatinib PFS benefit in RAI-refractory thyroid.

CV toxicity

HTN 30–40% all-grade (G3 ≈10–15%: SBP ≥160 / DBP ≥100, needs >1 agent).
LV dysfunction 5–8% — often reversible off-drug.
QT prolongation (vandetanib, sunitinib). Arterial & venous thrombo-embolism.

Non-cardiac toxicity

Proteinuria · nephrotic syndrome · TMA.
Hand-foot skin reaction · stomatitis · diarrhea.
Hypothyroidism · fatigue · hepatotoxicity · impaired wound healing.

HFA-ICOS · VEGF inhibitorspre-Tx

V·HIGHHF / cardiomyopathy · Arterial vascular dz (IHD·PCI·CABG·angina·TIA/stroke·PVD)

HIGHVenous thrombosis (DVT/PE) · LVEF <50% · QTc ≥480 ms · Hypertension · Age ≥75 · Prior anthracycline

MEDLVEF 50–54%² · QTc 450–<480 (M)/460–<480 (F)² · Arrhythmia² · ↑Tn¹ · ↑BNP¹ · Age 65–74¹ · DM¹ · Hyperlipidemia¹ · CKD¹ · Proteinuria¹ · Prior L-chest RT¹ · Smoking¹ · Obesity¹

≥1 V·HIGH → V·High · any HIGH or ≥5 MED-pts → High · 2–4 → Med · 0–1 → Low

HTN is the commonest VEGF AE — counts HIGH here.

Surveillance

BP each visit. Home BP daily during the first cycle, after dose increases, then every 2–3 weeks. Reassess antihypertensives when VEGF therapy stops.
Baseline + periodic ECG (QTc) if QT-risk drug / DDI.
Echo if symptoms. TFTs q cycle. UPCR periodically.

Management — granular

HTNSBP 140–159 / DBP 90–99 → treat with ACEi/ARB or DHP-CCB as appropriate. Generally continue VEGF with monitoring.

G3 HTNSBP ≥160 / DBP ≥100 → intensify to ACEi/ARB + DHP-CCB. Review the label. Hold at ≥180 systolic / ≥110 diastolic or for uncontrolled severe HTN.

G4 HTNAcute end-organ injury → admit and titrated IV therapy. Restart or permanent cessation follows the agent label. Do not use an oral-agent-count rule.

LVSDEF ↓ ≥10 pt to <50% → hold + GDMT (ACE/ARB + BB ± SGLT2i). Echo 2–4 wk.

QTcQTcF ≥500 ms → hold, correct electrolytes/DDIs. Restart by label. Δ >60 ms alone below 500 warrants review, not automatic interruption.

MONTreat thyroid dysfunction. Monitor proteinuria. Proteinuria hold thresholds are agent-specific. Evaluate nephrotic syndrome or renal injury.

FactoidVEGF-pathway hypertension can occur early. Treat BP to preserve therapy when feasible. Hypertension is not a validated individual tumor-response test. Severe or uncontrolled BP can require interruption.

Anti-VEGF mAbsLigand / receptor binding anti-angiogenics

CLASS

AgentsBevacizumab (Avastin) · Ramucirumab (Cyramza) · Ziv-aflibercept (Zaltrap).

UseCRC · NSCLC · RCC · cervical · ovarian · gastric · HCC · glioblastoma.BenefitAdds PFS (and OS in some) when combined with chemotherapy backbones.

CV toxicity

Severe HTN ≈8% G3 — dose-related.
Arterial thrombo-embolism (MI / stroke) ≈3–4%. VTE.
CHF (esp. prior anthracycline / chest RT). Rare PRES.

Non-cardiac toxicity

Proteinuria · nephrotic syndrome.
GI perforation · fistula · impaired wound healing.
Hemorrhage — pulmonary, GI, CNS. Infusion reactions.

HFA-ICOS · VEGF inhibitorspre-Tx

V·HIGHHF / cardiomyopathy · Arterial vascular dz (IHD·PCI·CABG·angina·TIA/stroke·PVD)

HIGHVenous thrombosis (DVT/PE) · LVEF <50% · QTc ≥480 ms · Hypertension · Age ≥75 · Prior anthracycline

MEDLVEF 50–54%² · Arrhythmia² · ↑Tn¹ · ↑BNP¹ · Age 65–74¹ · DM¹ · Hyperlipidemia¹ · CKD¹ · Proteinuria¹ · Prior L-chest RT¹ · Smoking¹ · Obesity¹

≥1 V·HIGH → V·High · any HIGH or ≥5 MED-pts → High · 2–4 → Med · 0–1 → Low

Summary only. The complete VEGF proforma also includes QTc 450–<480 (M) / 460–<480 (F) as 2 medium points. Monitoring remains drug-specific.

Surveillance

BP every cycle. Home log if elevated.
Monitor urine protein per label. For bevacizumab, dipstick ≥2+ prompts 24-hour quantification. Hold at ≥2 g/24 h and discontinue for nephrotic syndrome.
Perioperative holds are agent-specific. Bevacizumab: ≥28 days before elective surgery and ≥28 days after major surgery, with adequate healing.

Management — granular

G3 HTNBevacizumab: hold severe HTN uncontrolled with medical therapy. Resume after control. Stop permanently for hypertensive crisis/encephalopathy.

ATEArterial thrombo-embolism (MI/stroke) → permanently discontinue. Manage event per ACS / stroke pathway.

VTETreat VTE with an appropriate anticoagulant. Stop bevacizumab for grade 4 VTE. Other continuation decisions require oncology review.

BLEEDG3–4 hemorrhage or GI perforation/fistula → discontinue. Surgical / IR management.

SURGBevacizumab: hold ≥28 d before elective surgery and ≥28 d after major surgery, until healed. Other agents differ.

FactoidAnti-VEGF agents are not interchangeable. Bevacizumab and ramucirumab both carry arterial-event warnings. Ramucirumab requires permanent discontinuation after an arterial thromboembolic event.

DRUGS

Immune Checkpoint InhibitorsPD-1 / PD-L1 / CTLA-4 blockade

CLASS

AgentsPembrolizumab (Keytruda) · Nivolumab (Opdivo) · Cemiplimab (Libtayo) · Atezolizumab (Tecentriq) · Durvalumab (Imfinzi) · Ipilimumab (Yervoy) · Tremelimumab (Imjudo).

UseMelanoma · NSCLC · RCC · urothelial · H&N · MSI-high · adjuvant & metastatic.BenefitDurable responses. Melanoma 5-y OS > 50% with combo. Practice-changing.

CV toxicity

ICI myocarditis is uncommon but can be fatal. A multicenter registry reported prevalence 1.14% and median onset 34 days (IQR 21–75). Late presentations occur. Normal LVEF does not exclude severe disease.
Pericarditis · arrhythmia / high-grade AV block · Takotsubo.
Overlap myositis / myasthenia (bulbar / respiratory weakness). Late accelerated atherosclerosis.

Non-cardiac toxicity

Multisystem irAEs — colitis · hepatitis · pneumonitis · dermatitis.
Endocrinopathy — thyroiditis · hypophysitis · adrenal insufficiency · T1DM.
Combo CTLA-4 + PD-1 → higher irAE rate & severity.

No HFA-ICOS proformaNo formal HFA-ICOS proforma for ICI. Use general baseline CV risk assessment (P.1) + baseline troponin/ECG. A new troponin rise requires urgent evaluation for myocarditis and competing causes.

Surveillance

Baseline ECG + hs-Tn + CK ± BNP before cycle 1.
Repeat hs-Tn / ECG with first 1–3 cycles (highest-risk window).
Low threshold for echo / cardiac MRI on any new symptom.

Management — granular

SUSPAny troponin rise + symptom → hold ICI admit, telemetry, echo + CMR. CK / aldolase for myositis overlap.

TREATIV methylprednisolone 500–1000 mg/day ×3–5 d when myocarditis is likely. Follow clinical/Tn response and an individualized oral taper.

REFRACTDeterioration or inadequate response by 48–72 h → urgent specialist review for additional immunosuppression and circulatory/respiratory support. No automatic multidrug regimen.

ARRHYHigh-grade AV block or VT → urgent rhythm support and continuous monitoring. Monitoring duration follows electrical/hemodynamic stability and the specialist plan, not troponin normalization alone.

RECHALPermanently discontinue after confirmed grade ≥2 myocarditis. Treat concurrent irAEs with organ-specific steroids.

FactoidA rising troponin with normal early LVEF is the warning sign — treat on suspicion with pulse steroids. Don't await biopsy. Abatacept is emerging for steroid-refractory disease.

CAR-T & CellularCRS-mediated cardiovascular collapse

CLASS

AgentsTisagenlecleucel (Kymriah) · Axicabtagene ciloleucel (Yescarta) · Lisocabtagene maraleucel (Breyanzi) · Brexucabtagene autoleucel (Tecartus) · Idecabtagene vicleucel (Abecma) · Ciltacabtagene autoleucel (Carvykti).

UseR/R B-ALL · LBCL · follicular & mantle-cell lymphoma · multiple myeloma.BenefitDurable remission in chemo-refractory disease. LBCL CR ≈40%.

CV toxicity

CRS can cause distributive shock, arrhythmia and LV dysfunction. In Alvi et al. (137 adults), 17 patients (12%) had CV events, all with grade ≥2 CRS.
Arrhythmia (AF / VT). Demand ischemia. Rare stress cardiomyopathy.
Higher CV-event rate with CRS grade ≥2 & pre-existing CVD. Capillary leak.

Non-cardiac toxicity

CRS fever / hypoxia. ICANS — immune-effector-cell–associated neurotoxicity syndrome (encephalopathy · aphasia · seizures).
Prolonged cytopenias. Hypogammaglobulinemia → infection.
HLH / MAS. Tumor-lysis syndrome.

No HFA-ICOS proformaNo HFA-ICOS proforma. Pre-treat per general CV risk (P.1). ASTCT CRS grade (not CTCAE) drives cardiac risk — see grading reference.

Surveillance

Baseline echo + ECG + troponin / BNP before infusion.
Continuous telemetry & daily troponin during CRS.
Echo for hypotension unresponsive to fluids / tocilizumab.

Management — granular

G1 CRSFever ≥38°C, no hypotension/hypoxia → supportive. Antipyretics. Rule out infection. Telemetry.

G2 CRSGrade 2 CRS: cellular-therapy pathway, cautious fluid and oxygen support. Tocilizumab in patients ≥30 kg: 8 mg/kg IV, maximum 800 mg. Repeat no sooner than 8 h, maximum four doses, if indicated.

G3 CRSGrade 3 CRS: ICU, vasopressor/oxygen support and product-specific tocilizumab/steroid treatment. Assess LV function and avoid indiscriminate fluid loading.

G4 CRSGrade 4 CRS: multiple pressors excluding vasopressin and/or positive-pressure ventilation. ICU and cellular-therapy team direct corticosteroids and organ support.

ARRHYAF/VT during CRS → ACLS. GDMT if persistent LV dysfunction after recovery.

FactoidIn the Alvi cohort, each 12-h delay to tocilizumab was associated with 1.7-fold higher CV-event risk. This observational association supports prompt CRS recognition, not a causal dosing deadline.

High-dose AlkylatorsDNA cross-linkers · SCT conditioning

CLASS

AgentsCyclophosphamide (Cytoxan) · Ifosfamide (Ifex) · Melphalan (Alkeran / Evomela) · Bendamustine (Treanda / Bendeka) · Busulfan (Busulfex / Myleran) · Carmustine (BiCNU) · Dacarbazine (DTIC-Dome).

UseLymphoma · leukemia · myeloma · breast · ovarian · sarcoma · SCT conditioning.BenefitBackbone of curative combination & transplant-conditioning regimens.

CV toxicity

High-dose cyclophosphamide can cause acute hemorrhagic myocarditis and HF. Risk depends on dose and conditioning regimen. Do not apply one incidence or threshold to all alkylators.
Pericarditis · arrhythmia (AF) · rare tamponade.
Risk ↑ with prior anthracycline / chest RT. Usually within 1–3 wk.

Non-cardiac toxicity

Myelosuppression · hemorrhagic cystitis (cyclo / ifos — give mesna).
SIADH. Ifosfamide encephalopathy & Fanconi.
Pulmonary fibrosis (busulfan, carmustine). VOD/SOS (busulfan).

No HFA-ICOS proformaNo HFA-ICOS proforma. Use general CV risk (P.1). Pre-conditioning echo mandatory after prior cardiotoxic therapy.

Surveillance

Baseline CV Hx + BP + ECG. echo before high-dose / conditioning.
Telemetry + daily weights during conditioning admission.
Troponin / BNP if symptoms or known CVD.

Management — granular

MYOCARAcute myocarditis / HF → discontinue (rarely resumable). Supportive HF care + diuresis. Telemetry.

PERICPericarditis / effusion → NSAID/colchicine if no thrombocytopenia. Echo for tamponade → drainage.

CYSTPrevent hemorrhagic cystitis with regimen-specific mesna and hydration. Balance fluid against cardiac and renal reserve. New hematuria needs evaluation, not automatic fluid escalation.

METABCorrect Na⁺ for SIADH. methylene blue for ifosfamide encephalopathy.

FactoidCyclophosphamide injury may occur within days of high-dose exposure. Current dose, prior treatment and baseline cardiac reserve all matter.

DRUGS

mTOR InhibitorsEverolimus / temsirolimus (± VEGF)

CLASS

AgentsEverolimus (Afinitor) · Temsirolimus (Torisel) — often combined with VEGF TKIs / bevacizumab.

UseRCC · neuroendocrine tumors · HR+ breast (everolimus + exemestane) · TSC.BenefitAdds PFS in RCC / NET. Everolimus + exemestane doubles PFS in HR+ mBC.

CV toxicity

HTN · myocardial ischemia · CHF · QT prolongation (VEGF combination).
Arterial thromboembolism.
Dyslipidemia-driven atherosclerosis. Additive with VEGF agents.

Non-cardiac toxicity

Stomatitis / mucositis. Non-infectious pneumonitis.
Hyperglycemia · hyperlipidemia.
Immunosuppression → infection. Proteinuria.

No HFA-ICOS proformaNo HFA-ICOS proforma. Metabolic (lipids, glucose, BP) toxicity dominates — manage per Primary Prevention card (P.14).

Surveillance

Baseline ECG / BP / lipids / glucose.
Home BP q3 mo × 1 y, then q6 mo. Fasting lipids & glucose periodically.
Chest imaging for pneumonitis.

Management — granular

HTNTreat HTN with an interaction-aware agent. Avoid concomitant ACE inhibitors with everolimus because angioedema risk is increased. Review CYP3A4/P-gp interactions.

LIPIDStatin for mTOR dyslipidemia (rosuva / prava — review CYP and transporter interactions). Tight glucose control.

PNEUMGrade ≥2 pneumonitis → hold mTOR + steroids. Dose-reduce for stomatitis.

RENALProteinuria, hematuria or AKI → renal assessment. Treat arterial events and venous thrombosis by their distinct pathways and bleeding risk.

FactoidThe dominant CV liability is metabolic — dyslipidemia (up to ~75%) and new hyperglycemia — not direct myocardial injury. Manage with statin + glycemic control, rarely cessation.

CLASS MAP

HER2 · BRAF/MEK · BCR-ABL · CDK4/6 · PI · BTK

Baseline + symptom-driven surveillance

HER2 mAbs / ADCsErbB2 receptor & payload conjugates

CLASS

AgentsTrastuzumab (Herceptin) · Pertuzumab (Perjeta) · T-DM1 / trastuzumab emtansine (Kadcyla) · T-DXd / trastuzumab deruxtecan (Enhertu) · Margetuximab (Margenza) · Tucatinib (Tukysa) · Neratinib (Nerlynx) · Lapatinib (Tykerb).

UseHER2+ breast (adjuvant & metastatic) · HER2+ gastric / GEJ · HER2-low.BenefitAdjuvant trastuzumab ↓ recurrence ≈50%. T-DXd transformed HER2+/HER2-low mBC.

CV toxicity

HER2-related LV dysfunction often improves with interruption/HF therapy but recovery is not assured. Risk varies by agent, trial definition and prior anthracycline exposure.
Symptomatic HF <1–4%. Mostly recovers off-drug.
Risk ↑ with concurrent / sequential anthracycline & left chest RT.

Non-cardiac toxicity

Infusion reactions. T-DXd ILD / pneumonitis — can be fatal. Monitor.
Diarrhea (pertuzumab, neratinib, tucatinib).
Thrombocytopenia / hepatotoxicity (T-DM1).

HFA-ICOS · HER2 therapypre-Tx

V·HIGHHF / cardiomyopathy · Prior trastuzumab cardiotoxicity

HIGHMI / CABG · Stable angina · Severe valvular dz · LVEF <50% · Age ≥80

MEDLVEF 50–54%² · Arrhythmia² · ↑Tn² · ↑BNP² · Age 65–79² · Prior (remote) anthracycline² · Prior L-chest/mediastinal RT² · Anthracycline before HER2¹ · HTN¹ · DM¹ · CKD¹ · Smoking¹ · Obesity¹

≥1 V·HIGH → V·High · any HIGH or ≥5 MED-pts → High · 2–4 → Med · 0–1 → Low

HIGH if anthracycline + trastuzumab given concurrently.

Surveillance

Baseline echo. Consider hs-Tn/BNP at HIGH / V·HIGH risk.
Echo per drug/risk during therapy and at 12 mo post-Tx.
Chest imaging for new dyspnea / cough (ILD).

Management — granular

MODERATEAsymptomatic EF 40–49%: ESC supports continuing selected HER2 therapy with ACEi/ARB + BB and frequent monitoring. Reconcile the specific product label.

HOLDAsymptomatic EF <40% or moderate/severe symptomatic CTRCD → hold, HF treatment + MDT. Mild symptoms require individualized discussion.

RESUMEESC: consider restart when asymptomatic and EF ≥40% (ideally ≥50%), with HF therapy and close surveillance. Agent-label criteria may differ.

ILDT-DXd: hold + steroids for any-grade ILD. Permanently d/c for grade ≥2 pneumonitis.

SEQSequence (not concurrent) with anthracycline where possible. If HFA-ICOS HIGH / V·HIGH, refer and consider specialist-selected cardioprotection rather than automatic prophylaxis.

FactoidRecovery is possible, not guaranteed. The historical type I/type II split is too rigid. For T-DXd, evaluate new respiratory symptoms for ILD as well as HF.

BRAF / MEK InhibitorsMAPK-pathway combination therapy

CLASS

AgentsDabrafenib (Tafinlar) + Trametinib (Mekinist) · Vemurafenib (Zelboraf) + Cobimetinib (Cotellic) · Encorafenib (Braftovi) + Binimetinib (Mektovi).

UseBRAF V600E/K melanoma · NSCLC · anaplastic thyroid · CRC (with anti-EGFR).BenefitCombo OS ≈ 25 vs 18 mo in melanoma. Rapid disease control.

CV toxicity

QT prolongation. LV dysfunction ≈5% (MEK-driven) — usually reversible.
Hypertension. Reduced LVEF more common with the combination.
Venous thromboembolism. Pyrexia syndrome → hypotension.

Non-cardiac toxicity

Pyrexia (dab + tram). Fatigue · chills.
Cutaneous SCC / keratoacanthoma / new melanoma (BRAF mono).
MEK retinopathy / RVO. Hepatotoxicity.

HFA-ICOS · RAF-MEK inhibitorspre-Tx

V·HIGHHF / cardiomyopathy

HIGHMI / CABG · Stable angina · Severe valvular dz · Prior anthracycline

MEDLVEF 50–54%² · HTN² · ↑Tn² · ↑BNP² · Prior L-chest/mediastinal RT² · Arrhythmia¹ · Age ≥65¹ · DM¹ · CKD¹ · Smoking¹ · Obesity¹

≥1 V·HIGH → V·High · any HIGH or ≥5 MED-pts → High · 2–4 → Med · 0–1 → Low

QT-prolonging MEK combos — keep K⁺ ≥4.0, Mg²⁺ ≥2.0.

Surveillance

Baseline ECG + echo + BP.
Echo + ECG at 1 mo, then q3 mo.
Monitor electrolytes. Dermatology & ophthalmology review.

Management — granular

LVSDTrametinib: asymptomatic LVEF fall ≥10 points below the lower limit of normal → withhold up to 4 weeks. Restart at lower dose only after recovery. Apply separate dabrafenib rules.

QTcQTcF ≥500 ms → hold culprit QT drug, correct K⁺/Mg²⁺ and DDIs. Delta alone below 500 is not a generic hold. Follow the product label.

RESUMERestart BRAF/MEK therapy only after agent-specific recovery criteria and MDT review. The MEK and BRAF labels have different hold/dose rules.

HTNTreat per CTCAE grade (ACEi/ARB ± CCB). Anticoagulate VTE.

PYREXPyrexia syndrome → interrupt dab/tram ± steroids. Fluids for hypotension. Excise cutaneous SCC.

FactoidMEK-associated LV decline may recover. Recovery and restart are agent-specific. Trametinib requires permanent cessation for symptomatic cardiomyopathy or persistent non-recovery by label criteria.

DRUGS

BCR-ABL TKIsCML / Ph+ ALL kinase inhibition

CLASS

AgentsImatinib (Gleevec) · Dasatinib (Sprycel) · Nilotinib (Tasigna) · Bosutinib (Bosulif) · Ponatinib (Iclusig) · Asciminib (Scemblix).

UseChronic-phase & advanced CML. Ph+ ALL. GIST (imatinib).BenefitCML 10-y survival > 80% — near-normal life expectancy.

CV toxicity

Ponatinib arterial occlusive events up to 30% (dose-related) · HTN.
Nilotinib PAD · QT prolongation · dysglycemia.
Dasatinib pulmonary arterial hypertension · pleural effusion. Imatinib CV-favorable.

Non-cardiac toxicity

Fluid retention / periorbital edema (imatinib).
Pleural effusion (dasatinib). Cytopenias.
Hepatotoxicity. Pancreatitis (nilotinib / ponatinib).

HFA-ICOS · BCR-ABL TKIspre-Tx

V·HIGHArterial vascular dz (IHD·PCI·CABG·angina·TIA/stroke·PVD) · Arterial thrombosis on prior TKI

HIGHHF / LV systolic dysfunction · Prior BCR-ABL TKI LVSD · Abnormal ABPI ≤0.9 · Pulmonary HTN (PASP ≥35) · LVEF <50% · QTc ≥480 ms · CVD 10-yr risk >20% · Age ≥75 · Smoking

MEDVTE² · Arrhythmia² · QTc 450–<480 (M)/460–<480 (F)² · Age 65–74² · HTN² · DM¹ · Hyperlipidemia¹ · Age ≥60¹ · CKD¹ · FHx thrombophilia¹ · Obesity¹

≥1 V·HIGH → V·High · any HIGH or ≥5 MED-pts → High · 2–4 → Med · 0–1 → Low

Apply the highest applicable age band once. Ponatinib/nilotinib require particular attention to arterial risk.

Surveillance

Baseline ASCVD risk · BP · lipids · glucose · ECG.
BP / lipids / glucose q3–6 mo (esp. ponatinib, nilotinib).
Echo + BNP if dyspnea (dasatinib PAH). ECG for QT on nilotinib.

Management — granular

PREOptimize CV risk factors. statin (rosuvastatin 5–10 mg) + ASA where indicated. Choose lowest-CV-risk TKI for high-risk patients.

ATENew ACS, limb ischemia or stroke → urgent vascular care and oncology review. Hold/stop or change the TKI according to toxicity, resistance mutation, cancer status and label. No automatic substitute fits every CML patient.

PAHSuspected dasatinib PAH → PH assessment and RHC. Echo pressure alone is not diagnostic. Permanently stop dasatinib for RHC-confirmed PAH. Select an alternative.

QTcNilotinib QTc >480 ms → hold and correct causes. Follow formulation-specific restart criteria and ECG after dose changes.

MONQuarterly BP / lipids / glucose. ABPI if claudication. Echo if dyspnea.

FactoidSignature vessels: ponatinib→arterial occlusion, nilotinib→PAD, dasatinib→PAH. imatinib is CV-favorable.

CDK 4/6 InhibitorsCell-cycle arrest at G1/S

CLASS

AgentsPalbociclib (Ibrance) · Ribociclib (Kisqali) · Abemaciclib (Verzenio) · Trilaciclib (Cosela).

UseHR+ / HER2− metastatic & high-risk early breast Ca. Trilaciclib myeloprotection (SCLC).Benefit+ PFS ≈ 8–12 mo vs endocrine alone. Ribociclib OS advantage (MONALEESA).

CV toxicity

Ribociclib dose-dependent QT prolongation ≈3%.
Rare AF. VTE (abemaciclib).
No meaningful LV dysfunction signal. QT additive with other QT drugs.

Non-cardiac toxicity

Neutropenia (palbo / ribo) — dose-limiting.
Diarrhea (abemaciclib). Fatigue · nausea.
Hepatotoxicity (ribociclib). Rare ILD.

No HFA-ICOS proformaNo HFA-ICOS proforma. QT risk is the cardiac issue — baseline + serial ECG for ribociclib. General CV risk otherwise.

Surveillance

Ribociclib: ECG before treatment, approximately day 14 of cycle 1, then as indicated. Start only with QTcF <450 ms. Check electrolytes at baseline and cycle starts for the first six cycles.
Avoid co-administered QT-prolongers. Keep K⁺ ≥ 4.0.
CBC per protocol. LFTs (ribociclib).

Management — granular

QTc G2Ribociclib QTcF >480 ms → interrupt until ≤480. Correct K⁺/Mg²⁺ and DDIs. Restart dose differs by early versus advanced breast-cancer label.

QTc G3Ribociclib QTcF >500 ms → interrupt, restart at lower dose when ≤480. discontinue if >500 recurs.

TdPRibociclib QTcF >500 or Δ >60 with serious arrhythmia/syncope → permanently discontinue. Urgent rhythm care.

VTEAbemaciclib VTE → anticoagulate. Manage neutropenia / diarrhea by dose modification.

FactoidMonitoring is drug-specific, not class-wide: ribociclib → QT (serial ECG), abemaciclib → VTE. palbociclib has no consistent CV signal.

AntimetabolitesCoronary vasospasm with fluoropyrimidines

CLASS

Agents5-Fluorouracil / 5-FU (Adrucil) · Capecitabine (Xeloda) · Cytarabine (Cytosar-U) · Gemcitabine (Gemzar) · Methotrexate (Trexall) · Azacitidine (Vidaza) · Decitabine (Dacogen).

UseColorectal · breast · pancreas · gastric · head & neck · AML / MDS · ALL.BenefitBackbone of FOLFOX / FOLFIRI & adjuvant CRC. AML CR ≈ 70% with cytarabine.

CV toxicity

Coronary vasospasm / ACS 1–10% on 5-FU / capecitabine.
Usually no fixed obstruction. Chest pain during infusion.
Arrhythmia · rare Takotsubo · sudden death. Risk ↑ with continuous infusion, high dose & CAD.

Non-cardiac toxicity

Myelosuppression. Mucositis · diarrhea.
Hand-foot syndrome (capecitabine).
DPD deficiency toxicity — severe / fatal. MTX nephro-/hepatotoxicity.

No HFA-ICOS proformaNo HFA-ICOS proforma. Use general CV risk (P.1). CAD & prior vasospasm are the key flags before fluoropyrimidine.

Surveillance

Baseline CV history and ECG. In symptomatic CVD, assess LV function. CAD screening is considered selectively in high-risk patients, not as an automatic stress test for every prior CAD diagnosis.
Telemetry for high-risk infusions. ECG with chest pain.
Test for DPYD variants before systemic fluorouracil or capecitabine unless immediate treatment is necessary. Avoid in complete DPD deficiency. A negative test does not eliminate toxicity risk.

Management — granular

EVENTVasospasm / chest pain → stop infusion sublingual/IV nitrates + diltiazem or amlodipine. ACS pathway + troponin. With LV dysfn / ↑Tn → admit + coronary angio.

RECHALAvoid rechallenge if confirmed. If essential, prefer bolus over infusion + dose-reduce, or switch to raltitrexed/S-1.

PROPHYEssential rechallenge requires MDT agreement, exclusion of severe CAD, long-acting nitrate/CCB prophylaxis and monitored re-exposure. Drug choice and dose are individualized. There is no universal prophylactic infusion schedule.

DPDFor overdose or early severe/life-threatening fluoropyrimidine toxicity, obtain urgent oncology/toxicology input for uridine triacetate within 96 h of the end of exposure. Later efficacy is unestablished.

FactoidFluoropyrimidine chest pain can reflect vasospasm, ACS or other injury. A clean angiogram is not guaranteed. Stop exposure and assess urgently. Rechallenge evidence comes mainly from selected series.

DRUGS

Hormonal — ProstateADT · AR-axis inhibition

CLASS

AgentsLeuprolide (Lupron / Eligard) · Goserelin (Zoladex) · Degarelix (Firmagon) · Relugolix (Orgovyx) · Abiraterone (Zytiga) · Enzalutamide (Xtandi) · Apalutamide (Erleada) · Darolutamide (Nubeqa).

UseAdvanced / high-risk & metastatic prostate cancer. With AR inhibitor in mCRPC / mHSPC.BenefitADT + AR inhibitor ↑ OS ≈30% in metastatic disease.

CV toxicity

Metabolic syndrome · accelerated CAD · MACE.
Abiraterone — fluid retention · HTN · hypokalemia.
GnRH-antagonist CV benefit is suggestive, not settled. HERO favored relugolix, while the adjudicated PRONOUNCE trial stopped early and was inconclusive.

Non-cardiac toxicity

Osteoporosis / fracture. Hot flashes. Sexual dysfunction.
Insulin resistance · weight gain · sarcopenia.
Enzalutamide seizure / falls. Darolutamide best CNS profile.

No HFA-ICOS proformaNo HFA-ICOS proforma. Treat as ASCVD primary/secondary prevention — see Primary Prevention card (P.14).

Surveillance

Baseline ASCVD · BP · lipids · A1c · DEXA.
BP / lipids / glucose q3–6 mo.
ECG if QT risk. Bone-density monitoring on long-term ADT.

Management — granular

PREAggressive risk-factor control + statin per 2026 lipid goals. Lifestyle. prefer GnRH antagonist (relugolix) if established CVD.

EVENTAfter a CV event, stabilize the event and jointly reassess ADT choice. A GnRH antagonist may be considered, but switching is not a proven universal secondary-prevention strategy.

ABIRAAbiraterone → monitor K⁺, BP, LFTs. Correct hypokalemia. Hold for severe HTN / HF.

BONEAssess fracture risk and bone density during ADT. Use antiresorptive treatment when osteoporosis, fracture risk or an oncologic indication warrants it. Ensure adequate calcium/vitamin D, renal and dental review.

METABA1c + fasting glucose q3–6 mo. New-onset DM on ADT → metformin first-line. Target A1c < 7%. Exercise ≥ 150 min/wk.

QTcAR inhibitors (enzalutamide, apalutamide) — ECG if QT-prolonging co-meds. Correct lytes. Darolutamide has best safety profile.

FactoidTwo trials answer different questions. HERO reported fewer unadjudicated MACE with relugolix. PRONOUNCE compared degarelix with leuprolide in established ASCVD but was underpowered after early termination.

Proteasome Inhibitors26S proteasome blockade (± IMiDs)

CLASS

AgentsCarfilzomib (Kyprolis) · Bortezomib (Velcade) · Ixazomib (Ninlaro) — often with IMiDs lenalidomide (Revlimid) / pomalidomide (Pomalyst).

UseMultiple myeloma (relapsed / refractory & frontline). Mantle-cell lymphoma.BenefitDeep responses & PFS gains. Carfilzomib superior PFS vs bortezomib (ENDEAVOR).

CV toxicity

Carfilzomib — HF / ↓ EF ~5–11%. bortezomib lower · HTN · ischemia · dyspnea.
Risk highest early cycles. Greater with prior CVD / fluid loading. PAH.
IMiDs → VTE. Ixazomib lowest CV risk.

Non-cardiac toxicity

Peripheral neuropathy (bortezomib, esp. IV) — dose-limiting.
Thrombocytopenia. Diarrhea.
Herpes-zoster reactivation — acyclovir prophylaxis.

HFA-ICOS · Multiple-myeloma therapypre-Tx

V·HIGHHF / cardiomyopathy · Prior PI cardiotoxicity · VTE (DVT/PE) · Cardiac amyloidosis · Arterial vascular dz

HIGHPrior IMiD CV toxicity · LVEF <50% · ↑ baseline BNP · Age ≥75 · Prior anthracycline

MEDLVEF 50–54%² · Arrhythmia² · ↑Tn² · LV hypertrophy¹ · Age 65–74¹ · HTN¹ · DM¹ · Hyperlipidemia¹ · CKD¹ · FHx thrombophilia¹ · Prior thoracic-spine RT¹ · Dexamethasone >160 mg/mo¹ · Smoking¹ · Obesity¹

≥1 V·HIGH → V·High · any HIGH or ≥5 MED-pts → High · 2–4 → Med · 0–1 → Low

Screen for AL amyloidosis at very-high risk (CMR ± biopsy).

Surveillance

Cardio-onc eval + BNP before carfilzomib.
Home BP monitoring + BNP q cycle. Echo if symptoms.
Careful IV-fluid management on carfilzomib days.

Management — granular

PRECarfilzomib: BNP + echo baseline. VTE prophylaxis with IMiDs (ASA if low risk, LMWH/DOAC if high).

HFNew HF symptoms → urgent clinical assessment, TTE and volume/BP review. BNP elevation alone is not an automatic hold. Withhold carfilzomib for grade 3–4 cardiac toxicity until recovery.

RESUMEAfter recovery, consider a one-level lower carfilzomib dose only after individualized benefit–risk review. EF recovery alone does not establish safe rechallenge.

NEUROBortezomib neuropathy → switch IV → subcut, weekly dosing, or dose-reduce. Acyclovir prophylaxis.

HTNCarfilzomib HTN — treat per CTCAE grade. avoid excessive pre-hydration (worsens fluid overload + BP). ACEi/ARB first-line.

VTEIMiD thromboprophylaxis: use a validated myeloma VTE assessment and current hematology guidance, balancing platelets, bleeding, renal function and interactions. Avoid a crude factor-count rule.

FactoidCarfilzomib (irreversible) causes far more HF/HTN than bortezomib, peaking early — often reversible if caught fast.

BTK InhibitorsBruton tyrosine-kinase blockade

CLASS

AgentsIbrutinib (Imbruvica) · Acalabrutinib (Calquence) · Zanubrutinib (Brukinsa) · Pirtobrutinib (Jaypirca).

UseCLL / SLL · mantle-cell & marginal-zone lymphoma · Waldenström · chronic GVHD.BenefitTransformed CLL therapy — durable, chemo-free remissions.

CV toxicity

Atrial fibrillation up to 10% (ibrutinib > 2nd-gen).
Hypertension. Ventricular arrhythmia & rare sudden death. HF reported with ibrutinib (higher than 2nd-gen).
2nd-gen (acala / zanu) — lower AF / HTN / HF risk.

Non-cardiac toxicity

Bleeding / bruising (platelet dysfunction) — caution with anticoagulants.
Infection risk. Diarrhea. Arthralgia.
Cytopenias.

No HFA-ICOS proformaNo HFA-ICOS proforma. AF & HTN are the key signals — baseline ECG + BP, then symptom-driven.

Surveillance

Baseline ECG / BP. Pulse checks for AF each visit.
Home BP monitoring during initiation and dose changes, then regularly throughout BTK therapy. Review BP and pulse at clinical visits.
Symptomatic palpitations → Holter / ECG.

Management — granular

AFNew AF → assess stability and triggers. β-blocker rate control is often preferred. Avoid verapamil/diltiazem when CYP3A4 interactions or LV dysfunction make them unsuitable. Individualize anticoagulation and bleeding review.

ACAvoid warfarin + ibrutinib. Prefer DOAC (apixaban) — screen CYP3A4 DDIs. Hold around procedures for bleeding risk.

SWITCHPersistent CHF / refractory arrhythmia → hold, switch to acalabrutinib / zanubrutinib (lower CV risk).

HTNTreat HTN per CTCAE grade (ACEi/ARB first-line). G4 / VT → urgent cardiology.

BLEEDHold ibrutinib 3–7 d before procedures (platelet dysfunction). Caution with dual antiplatelet + DOAC. Avoid warfarin.

SCDIbrutinib ventricular arrhythmia / sudden death — ECG if palpitations / syncope. Low threshold for Holter. 2nd-gen preferred if VT risk.

FactoidAF is lower, not absent with acalabrutinib. ELEVATE-RR reported AF/flutter in 9.4% versus 16.0% with ibrutinib in previously treated CLL.

DRUGS

CLASS MAP

EGFR · ALK · microtubule · topo · platinum · hormonal

Baseline + symptom-driven monitoring

EGFR TKIsEGFR tyrosine-kinase blockade

CLASS

AgentsErlotinib (Tarceva) · Gefitinib (Iressa) · Afatinib (Gilotrif) · Osimertinib (Tagrisso) · Dacomitinib (Vizimpro).

UseEGFR-mutant NSCLC (1st-line & adjuvant). Erlotinib + gemcitabine in pancreas.BenefitOsimertinib median OS ≈ 38.6 mo in EGFR+ NSCLC. Adjuvant DFS benefit.

CV toxicity

Osimertinib — uncommon ↓ EF / HF. QTc prolongation.
Rare cardiomyopathy reversible on hold.
Low overall CV burden.

Non-cardiac toxicity

Acneiform rash · paronychia · pruritus.
Diarrhea. Stomatitis.
ILD / pneumonitis — uncommon but serious. Hepatotoxicity.

No HFA-ICOS proformaNo HFA-ICOS proforma. Baseline ECG (osimertinib QTc). Otherwise general CV risk.

Surveillance

Baseline ECG. Repeat if QT risk / DDIs.
Echo if osimertinib + cardiac risk / symptoms.
Monitor for new dyspnea / cough (ILD).

Management — granular

QTcOsimertinib QTc >500 on ≥2 ECGs → hold. Restart 40 mg at QTc <481 or baseline if baseline ≥481, per label.

LVSDOsimertinib: assess LV decline with cardiology. permanently discontinue for symptomatic CHF per label. HF therapy as indicated.

ILDHold + steroids for pneumonitis (can be fatal).

DERMTopical / oral antibiotics for rash. Loperamide for diarrhea.

AFOsimertinib new AF → rate control. Anticoagulate per CHA₂DS₂-VASc. Continue drug unless hemodynamically unstable.

DDIReview CYP3A4 interactions (osimertinib substrate). Avoid strong inducers. QT-additive drugs → serial ECG.

FactoidOsimertinib can cause QT prolongation and cardiomyopathy. Symptomatic CHF requires permanent discontinuation under the US label, even if LVEF later improves.

ALK / ROS1 TKIsFusion-driven NSCLC

CLASS

AgentsCrizotinib (Xalkori) · Ceritinib (Zykadia) · Alectinib (Alecensa) · Brigatinib (Alunbrig) · Lorlatinib (Lorbrena) · Entrectinib (Rozlytrek).

UseALK+ or ROS1+ NSCLC (1st-line & later, CNS-active agents).BenefitAlectinib PFS > 34 mo. Durable CNS control.

CV toxicity

Bradycardia (crizotinib, ceritinib). QT prolongation.
Edema. Rare HF.
Lorlatinib hyperlipidemia → accelerated atherosclerosis. HTN / edema.
Crizotinib QTc prolongation (~5%). Risk ↑ with concomitant CYP3A4 inhibitors or hypokalemia.

Non-cardiac toxicity

Visual disturbance (crizotinib). GI upset.
Hepatotoxicity. ILD / pneumonitis.
Lorlatinib CNS / mood effects.

No HFA-ICOS proformaNo HFA-ICOS proforma. Lorlatinib dyslipidemia is the main CV issue — manage per Primary Prevention card (P.14).

Surveillance

Baseline ECG + HR. lipids on lorlatinib (then periodically).
Monitor HR for bradycardia. ECG for QT.
LFTs per protocol. Assess edema / weight.

Management — granular

BRADYSymptomatic bradycardia (HR <50) → review DDIs (BB, non-DHP CCB), dose-reduce / hold.

LIPIDStatin for lorlatinib dyslipidemia (start early). Treat HTN per grade.

QTcQTc ≥501 ms → hold. Correct K⁺/Mg²⁺.

ILDHold + steroids for pneumonitis / G3 hepatotoxicity.

EDEMAFluid retention (crizotinib, lorlatinib) → diuretics PRN. distinguish from HF with echo / BNP if significant.

CNSLorlatinib CNS effects (cognition, mood, speech, seizures) require separate assessment and severity-based dose modification. Lipid severity is not a validated proxy for CNS toxicity.

FactoidLorlatinib causes severe dyslipidemia (cholesterol ~82%, triglycerides ~61%) — usually needs a interaction-reviewed statin (rosuva/pitava) within weeks of starting.

Microtubule AgentsTaxanes · vinca alkaloids · epothilones

CLASS

AgentsPaclitaxel (Taxol) · nab-paclitaxel (Abraxane) · Docetaxel (Taxotere) · Cabazitaxel (Jevtana) · Vincristine (Oncovin) · Vinblastine (Velban) · Vinorelbine (Navelbine) · Eribulin (Halaven).

UseBreast · NSCLC · ovarian · prostate · lymphoma · sarcoma.BenefitCore of curative & palliative regimens across many tumor types.

CV toxicity

Bradyarrhythmia / heart block (paclitaxel infusion).
Hypersensitivity-related hypotension (taxanes).
Rare ischemia. Fluid retention (docetaxel). Low cardiomyopathy risk.

Non-cardiac toxicity

Peripheral neuropathy (sensory) — dose-limiting.
Neutropenia. Alopecia · mucositis.
Hypersensitivity (taxanes — premedicate). Vinca vesicant + ileus.

No HFA-ICOS proformaNo HFA-ICOS proforma. Infusion conduction events + neuropathy are the issues — telemetry for first taxane if CAD.

Surveillance

Cardiac monitoring during 1st taxane infusion (telemetry if CAD).
Neuro exam each cycle (neuropathy grading).
Premedicate taxanes (steroid + antihistamine + H2).

Management — granular

HSRInfusion reaction → stop infusion and assess severity. Suspected anaphylaxis needs immediate emergency treatment. Severe paclitaxel hypersensitivity must not undergo routine rechallenge.

BLOCKSymptomatic heart block → cardiology, hold paclitaxel. Asymptomatic G1 brady → observe.

NEURODose-reduce / delay for G2 neuropathy (limiting instrumental ADL). Hold for G3 (limiting self-care).

VINCABowel regimen for vinca. never give vinca intrathecally (fatal).

FLUIDDocetaxel fluid retention — dexamethasone premedication 8 mg BID × 3 d starting day before. Diurese if symptomatic edema / effusions.

PREMEDSolvent-based paclitaxel requires formulation-specific premedication. Albumin-bound paclitaxel differs. Severe previous reactions require specialist planning, not simply slower infusion.

FactoidPaclitaxel bradycardia (up to ~29%) and 1°-AV block are usually benign — reassure. Reserve telemetry for pre-existing conduction disease. Nab-paclitaxel has lower HSR risk (no Cremophor) but similar neuropathy. No steroid premed needed.

DRUGS

Topoisomerase InhibitorsTopoisomerase I / II

CLASS

AgentsIrinotecan (Camptosar) · Topotecan (Hycamtin) · Etoposide (Vepesid / Toposar) · Teniposide (Vumon).

UseColorectal (irino) · small-cell & ovarian (topo) · testicular / lung / lymphoma (etoposide).BenefitBackbone of SCLC (EP) & curative testicular (BEP) regimens.

CV toxicity

Generally low direct cardiotoxicity.
Etoposide — rare infusion hypotension / vasospasm / MI. Rate-dependent.
Irinotecan cholinergic syndrome → transient bradycardia · diaphoresis · cramping (early, within min).
Topotecan — occasional hypotension. Irinotecan diarrhea → electrolyte depletion (Mg/K) → QT risk.

Non-cardiac toxicity

Myelosuppression.
Irinotecan diarrhea — early cholinergic + delayed.
Etoposide secondary AML (11q23). Hypersensitivity.

No HFA-ICOS proformaNo HFA-ICOS proforma. Symptom-driven cardiac review. Main events are infusion-related.

Surveillance

Baseline CBC. Symptom-driven cardiac review.
Slow etoposide infusion. Monitor BP for hypotension.
UGT1A1 status to guide irinotecan dosing.

Management — granular

HYPOEtoposide hypotension → slow / stop infusion. IV fluids. Resume at half rate. Infuse over ≥ 30–60 min.

CHOLIrinotecan early cholinergic symptoms: atropine 0.25–1 mg IV/SC if appropriate. Delayed diarrhea needs the oncology rescue plan, fluid/electrolyte review and prompt escalation for fever, neutropenia or dehydration.

MI/VASPEtoposide rare vasospasm / MI → ACS pathway. Troponin + ECG. Nitrates if vasospasm. D/c if confirmed event.

LYTESIrinotecan diarrhea → Mg / K depletion → QT risk. Replete aggressively. ECG if QTc-prolonging co-therapy.

MYELOGrowth factors / dose-modify for neutropenia. UGT1A1 *28/*28 → reduce irinotecan dose (severe tox). Supportive care for HSR.

FactoidInfuse etoposide over ≥30–60 min to prevent rate-related hypotension. Mitoxantrone — a topo-II agent — is itself directly cardiotoxic (anthracycline-like).

Platinum AgentsDNA cross-linking agents

CLASS

AgentsCisplatin (Platinol) · Carboplatin (Paraplatin) · Oxaliplatin (Eloxatin).

UseTesticular · ovarian · lung · bladder · colorectal · head & neck.BenefitCurative in testicular (> 90%) & many GU / GI cancers.

CV toxicity

Late vascular toxicity — MI, stroke, Raynaud in survivors (cisplatin). CV risk peaks 10–20 yr post-Tx.
VTE risk elevated (cisplatin > carboplatin). HTN.
Cisplatin endothelial injury → premature atherosclerosis · metabolic syndrome in testicular Ca survivors.
QT risk via Mg²⁺ / K⁺ wasting (cisplatin nephrotoxicity). Hypomagnesemia can persist months.

Non-cardiac toxicity

Nephrotoxicity & Mg / K wasting (cisplatin) — hydrate.
Ototoxicity. Peripheral neuropathy. Highly emetogenic.
Oxaliplatin cold dysesthesia · laryngopharyngeal spasm.

No HFA-ICOS proformaNo HFA-ICOS proforma. The cardiac story is late survivorship vascular risk — lifelong ASCVD prevention (P.14).

Surveillance

Baseline + periodic renal function & electrolytes (Mg, K).
Aggressive hydration ± Mg repletion (cisplatin).
Long-term CV risk-factor surveillance in survivors.

Management — granular

HYDRACisplatin hydration and magnesium replacement depend on dose, regimen, renal function and cardiac reserve. Monitor electrolytes and weight. Avoid a fixed fluid volume in patients with HF.

LYTEReplete Mg / K aggressively — cisplatin Mg wasting can persist months. ECG if QTc concern. Oral Mg supplement long-term.

VTEAnticoagulate VTE (LMWH or DOAC). Cisplatin-based regimens may warrant thromboprophylaxis in high-risk inpatients.

RAYNDCisplatin Raynaud's — nifedipine XL 30 mg or amlodipine. Avoid cold. May persist years. Circulating Pt detectable > 20 yr.

SURVSurvivorship: annual lipids / BP / glucose / BMI. Statin per ASCVD risk. Testicular Ca survivors — metabolic syndrome screening lifelong.

SWITCHSwitch to carboplatin (AUC-dosed) if cisplatin nephro- / neuro- / ototoxicity-limited. Lower vascular risk profile.

FactoidCisplatin drives late vascular disease — accelerated atherosclerosis, Raynaud's, thrombosis years on. Circulating platinum is detectable 20 years later. Risk is biphasic.

Hormonal — BreastSERM · aromatase inhibitor · SERD

CLASS

AgentsTamoxifen (Nolvadex / Soltamox) · Anastrozole (Arimidex) · Letrozole (Femara) · Exemestane (Aromasin) · Fulvestrant (Faslodex).

UseHR+ breast cancer — adjuvant (5–10 y) & metastatic endocrine therapy.BenefitAdjuvant endocrine therapy ↓ recurrence & mortality over 10 y.

CV toxicity

Tamoxifen — VTE (DVT / PE ~2–7%). Mild LDL-lowering (partial estrogen agonist).
Aromatase inhibitors — dyslipidemia · HTN · modest ↑ ischemic events. endothelial dysfunction (loss of estrogen).
No significant LV dysfunction. Net CV risk modest but cumulative over 5–10 yr therapy.
AI-exposed patients show ↑ arterial stiffness. Tamoxifen VTE risk highest in first 2 yr & with obesity/immobility.

Non-cardiac toxicity

Tamoxifen — endometrial cancer · hot flashes · cataract.
AIs — arthralgia · osteoporosis / fracture.
Vasomotor symptoms · vaginal dryness · mood.

No HFA-ICOS proformaNo HFA-ICOS proforma. AIs cause dyslipidemia/HTN. Tamoxifen is prothrombotic — manage risk factors (P.14).

Surveillance

Baseline lipids / BP. Periodic on AIs.
DEXA bone density on aromatase inhibitors.
VTE vigilance on tamoxifen. Gynecologic review for bleeding.

Management — granular

VTETamoxifen VTE → hold + anticoagulate (DOAC or LMWH). Switch to AI if postmenopausal. Avoid tamoxifen + HRT.

LIPIDAI dyslipidemia → statin per ASCVD risk. Lipid panel at baseline + q6–12 mo. BP target < 130/80.

BONEDEXA at AI start + q2 yr. Bisphosphonate or denosumab if T-score ≤ −2.0. Ca 1200 mg + vit-D 800–1000 IU.

MSKAI arthralgia (~50%) — exercise · NSAID / acetaminophen. Consider switch AI or to tamoxifen if limiting adherence.

ENDOTamoxifen: annual gynecologic review. Report abnormal bleeding → endometrial biopsy. Risk ↑ after > 5 yr.

CVRUse the current ASCVD prevention framework, comorbidities and life expectancy to guide statins. The endocrine agent alone does not determine one universal threshold.

FactoidToxicity flips by agent: tamoxifen → VTE (prothrombotic SERM, also mildly lipid-lowering). aromatase inhibitors → worse lipids and a modest rise in ischemic events.

DRUGS

CLASS MAP

Thoracic radiotherapy & miscellaneous biologics

Late effects — surveillance is the game

Thoracic RadiotherapyExternal-beam photon / proton

CLASS

IndicationsBreast (left) · Hodgkin lymphoma (mantle) · lung · esophageal · thymic.

UseDefinitive, adjuvant & palliative thoracic / mediastinal irradiation.BenefitImproves local control. Cures ≈ 50% limited-stage HL — late CV cost decades later.

CV toxicity

Coronary artery disease — premature, ostial / proximal LAD.
Valvular disease (AS / AR / MR) — calcific, fibrotic.
Constrictive pericarditis. Restrictive cardiomyopathy. Conduction disease.
HF at 25 yr (HL, no anthracycline): 0–15 Gy 4.4%, 16–20 Gy 6.2%, ≥21 Gy 13.3%.

Non-cardiac toxicity

Radiation pneumonitis / pulmonary fibrosis.
Esophagitis / stricture. hypothyroidism (neck fields).
Secondary malignancy (breast, lung, sarcoma).

No HFA-ICOS proformaNo HFA-ICOS proforma. Surveillance is the entire game — risk persists decades. Calcium-score at 10 y.

Surveillance

Consider CAD screening from 5 years after high-risk cardiac radiation exposure, using functional imaging or CCTA according to the clinical question.
Post-RT echo follows exposure, baseline risk and time since therapy. High-risk survivors commonly need 5-yearly reassessment after early follow-up, with prompt imaging for symptoms.
Annual CV review and risk-factor management. Mean-heart/substructure dose and co-exposure inform risk. Radiation dose alone is not an automatic statin prescription.

Management — granular

PREVOptimize BP, lipids, diabetes and tobacco exposure. Prescribe statins for standard CV indications and individual risk, not a universal radiation-dose cutoff.

CAD/VHDTreat CAD/valve disease through a Heart Team. Prior RT increases surgical complexity, but transcatheter versus surgical treatment depends on anatomy, cancer status, durability and procedural risk.

PERICConstrictive pericarditis → pericardiectomy. Restrictive CM → HF care.

MDTMultidisciplinary survivorship clinic. Thyroid function for neck fields.

CASCORECoronary Ca²⁺ score 5–10 yr post-RT. If elevated → CCTA or stress. Repeat q5 yr. HL survivors especially high-yield.

DIBHLeft-breast / mediastinal RT → deep-inspiration breath-hold or prone positioning to ↓ mean heart dose. Proton beam if available.

FactoidDarby et al. found a relative 7.4% increase in major coronary events per Gy mean-heart dose in a historical breast-cancer cohort. Absolute risk depends on baseline risk and modern exposure.

Misc Cytotoxics / BiologicsNiche but high-impact

CLASS

AgentsBleomycin (Blenoxane) · Mitomycin-C (Mutamycin) · Arsenic trioxide (Trisenox) · Tretinoin / ATRA (Vesanoid) · Pegaspargase (Oncaspar) · Aldesleukin / IL-2 (Proleukin) · Interferon alfa-2b (Intron A).

UseHodgkin · testicular · anal · APL · melanoma / RCC · ALL.BenefitCurative in niche disease — APL with ATRA + arsenic ≈ 90% cure.

CV toxicity

Arsenic trioxide → QT prolongation / Torsades.
IL-2 → capillary-leak, hypotension, arrhythmia.
L-asparaginase → VTE (incl. cerebral sinus thrombosis). ATRA → differentiation syndrome.

Non-cardiac toxicity

Bleomycin pulmonary fibrosis (dose / O₂-sensitive).
ATRA / arsenic differentiation syndrome.
Asparaginase pancreatitis. IL-2 multi-organ. IFN flu-like / depression.

No HFA-ICOS proformaNo HFA-ICOS proforma. Agent-specific — arsenic QT & IL-2 capillary leak need ICU-level vigilance.

Surveillance

Arsenic → label ECG/electrolyte surveillance. More frequent testing for instability.
IL-2 → ICU monitoring. CVP / pressors prepared.
Bleomycin → PFTs / DLCO. Limit cumulative dose.

Management — granular

QTcArsenic: QTc Framingham >450 ms (M) / >460 ms (F) → hold + correct causes. Reduced-dose restart after normalization, per label.

DIFFSuspected differentiation syndrome: dexamethasone 10 mg IV every 12 h and hemodynamic monitoring. Hold ATRA/arsenic for severe disease according to the agent label.

LEAKIL-2 capillary leak → stop drug. Fluids / pressors. ICU.

VTEAnticoagulate asparaginase VTE. Supportive care.

BLEOBleomycin: document lifetime units, lung symptoms, kidney function, and prior injury. Individualize peri-op oxygen to adequate oxygenation. Avoid a rigid FiO₂ ceiling.

LYTESArsenic: maintain K⁺ >4 mEq/L, Mg >1.8 mg/dL. ECG at least weekly, more often if unstable. Follow label QT hold/restart steps.

FactoidDistinct mechanisms: arsenic→QT/torsades (electrolyte-driven), IL-2→capillary-leak shock (~50%), asparaginase→thrombosis via antithrombin depletion (watch for CVST).

CLASS MAP

Less prominent direct myocardial toxicity

Review indirect and agent-specific risks

Lower direct myocardial burdenLow CV concern · confirm no indirect mechanism

CLASS

ScopeLittle or no direct myocardial, vascular, or arrhythmic toxicity documented. No HFA-ICOS proforma applies.

Low documented CV toxicity

Antimetabolites — pemetrexed · fludarabine · cladribine · pentostatin · mercaptopurine · hydroxyurea.
PARP inhibitors — olaparib · talazoparib · rucaparib (niraparib excepted: HTN).
Hedgehog — vismodegib · sonidegib. NTRK — larotrectinib.
Anti-CD20 / CD38 mAbs — rituximab · obinutuzumab · daratumumab · isatuximab.
Non-HER2 ADCs — brentuximab · enfortumab · sacituzumab · polatuzumab.
Anti-EGFR mAbs — cetuximab · panitumumab.

No proforma · low concernLow documented risk is not zero. Use general CV risk (P.1) only if comorbid CVD or symptoms. Some labels require specific cardiac or electrolyte surveillance.

Still on your radar (indirect)

Infusion reactions — rituximab · daratumumab · cetuximab (rate-related hypotension / arrhythmia).
Hypomagnesemia — cetuximab / panitumumab → QT / arrhythmia. Replete Mg.
Anemia → demand ischemia with marrow-suppressive agents.
Metabolic — bexarotene hypertriglyceridemia · PI3K-inhibitor hyperglycemia.

Approach — granular

BASEBaseline testing is risk- and agent-specific. Cetuximab carries a cardiopulmonary-arrest warning in selected head-and-neck regimens. Do not classify it as cardiovascularly neutral.

LYTECetuximab: monitor Mg, K and Ca weekly during treatment and for at least 8 weeks after. Correct deficits and assess rhythm risk.

INFUSPremedicate and rate-control first infusions (rituximab / daratumumab). Stop for reaction.

NEWERTreat "no documented toxicity" cautiously for newer agents with short follow-up. Reassess if signals emerge.

NIRAPNiraparib: BP/HR weekly ×2 mo, then monthly ×1 y. CBC weekly ×1 mo, then monthly ×11 mo. Follow label thereafter.

ANEMIAAnemia management depends on symptoms, bleeding, ACS, and cancer intent. Use the relevant transfusion pathway. ESAs have restricted noncurative chemotherapy-associated indications.

FactoidAlmost no oncology drug has a truly zero cardiac signal — "no documented cardiotoxicity" usually means low incidence or short follow-up, not proven safety.

ALGOS

E

EF-gated initiation — anthracyclines & HER2 inhibitors

Baseline risk informs an agent-specific MDT plan

Baseline EF< 40%

Anthracyclines / HER2 inhibitors usually NOT recommended. Evaluate on case-by-case basis with cardio-onc. If chemo is essential, treat HF first (full GDMT) and reassess EF before any exposure.

Baseline EF40 – 55%

Refer/evaluate and plan with the cancer team. Treat established HF/LV dysfunction for its standard indication. Do not automatically hold therapy or start a prophylactic multidrug bundle solely from this screening band.

Baseline EF> 55%

Use therapy/risk-specific surveillance and treat standard CV indications. At HIGH / V·HIGH risk, specialist-selected neurohormonal or statin prevention may be considered. There is no routine prophylactic bundle.

GLS: calculate the relative decline from baseline

1 · Use absolute magnitudes|−20| = 20 and |−16| = 16

2 · Divide the loss by baseline(20 − 16) ÷ 20 × 100 = 20% relative decline

3 · Interpret with LVEF and symptomsWith LVEF ≥50% and no HF symptoms, a new relative GLS decline >15% meets the imaging criterion for mild asymptomatic CTRCD.

Illustrative values. A 4-point change is a 20% relative decline here. Check image quality, tracking, loading conditions and the same analysis method before attributing the change to therapy. A single low GLS without a baseline cannot establish a relative decline.

M

Management of CTRCD — EF-stratified branch

Symptoms + drug class + LVEF/GLS trajectory

A

LVEF 40–49%

Asymptomatic mod. CTRCD (EF 40–49%)

Differentiate interrupt anthracyclines for moderate CTRCD. Selected HER2 therapy may continue under ESC guidance, with label/MDT reconciliation.
Workup rule out CAD · hyperthyroidism · anemia.
Consider ACEi/ARB and an evidence-based β-blocker as tolerated, with therapy-specific management and comorbidity review.
Follow Clinical review and TTE/biomarkers at a frequency matched to the therapy, severity and trajectory. Use frequent surveillance if HER2 therapy continues.
Symptomatic on therapy → discuss discontinuation of the involved cancer treatment.

B

LVEF < 40%

Severe asymptomatic CTRCD or HFrEF

Hold the involved cancer treatment per protocol.
Initiate full GDMT ACE/ARB or ARNi · BB · MRA · SGLT2i.
Reassess clinical status and LV function during HF optimization. Agree on the cancer-therapy hold/restart plan and monitoring interval with the MDT.
NYHA I (recovered) discuss resumption of cancer Tx if EF improves (reversibility or partial).
NYHA II–IV (persistent) discuss discontinuation. Bridge with optimized GDMT.

G

GDMT drug-titration — initiation & target doses (ACC/AHA/HFSA)

Same pillars as chronic HFrEF

Class	Agent	Initiation	Target	Notes
ARNI / ACE / ARB	Sacubitril/Valsartan	24/26 mg BID	97/103 mg BID	Preferred when tolerated
	Losartan (ARB)	25 mg daily	150 mg daily	Evidence-based ARB
	Valsartan (ARB)	40 mg BID	160 mg BID	ARB alt
	Lisinopril (ACEi)	2.5 mg daily	40 mg daily	ACEi option if ARNI unsuitable
β-blocker	Carvedilol	3.125 mg BID	25 mg BID	Evidence-based HFrEF option
β-blocker	Metoprolol succinate	12.5 mg daily	200 mg daily	—
MRA	Spironolactone	12.5–25 mg daily	25–50 mg daily	K⁺ & Cr at 1 wk
MRA	Eplerenone	25 mg daily	50 mg daily	If gynecomastia on spiro
Hydralazine + Nitrate	Hydralazine	25 mg TID	100 mg TID	NYHA III–IV self-reported AA
Hydralazine + Nitrate	Isosorbide dinitrate	20 mg TID	40 mg TID	ISMN is not the studied substitute
SGLT2i	Empagliflozin · Dapagliflozin	10 mg daily	10 mg daily	Drug-specific renal / peri-op gates

Start the four HFrEF pillars early as tolerated. Do not wait for one drug to reach target. MRA eligibility requires eGFR >30 and K⁺ <5.0 mmol/L, with early and ongoing laboratory monitoring. Stop the MRA if K⁺ cannot be maintained <5.5. Apply SGLT2 inhibitor renal, acute-illness, fasting and surgical precautions. Add hydralazine/isosorbide dinitrate for eligible patients with persistent NYHA III–IV HFrEF despite optimal therapy.

Early abnormalities require a comparable baseline. Confirm LVEF, GLS, biomarkers, loading and symptoms. A new abnormality prompts assessment and a therapy-specific plan. It does not automatically justify the same hold or cardioprotective regimen for every drug. Suspected ICI myocarditis follows the urgent pathway in chapters 12–13.

ICI

Highest
Risk

Window Dual ICI raises risk. Myocarditis often appears early (median 34 days in the initial registry), but a later presentation remains possible.

Patient risk factors Pre-existing CVD · prior autoimmune dz · prior chest RT · advanced age · DM / obesity · co-administered cardiotoxic Tx.

Suspect when New troponin rise · new arrhythmia / AV block · unexplained dyspnea or fatigue · ptosis or proximal weakness (overlap MG/myositis).

Stat workup hs-Tn · BNP · CK · ECG · TTE immediately. Prompt CMR if stable. EMB when needed for diagnostic uncertainty. Do not delay urgent treatment for either test.

3M

Triple-M overlap screen — myocarditis · myositis · myasthenia gravis

Treat the syndrome, not just the heart

M1

Myocarditis

Inflammatory myocardial injury

Dx troponin + & imaging / EMB evidence ± conduction or hemodynamic compromise.
CMR Lake Louise (T2 edema + T1 / LGE), native T1 + T2 mapping. May be falsely negative early.
EMB diagnostic uncertainty or fulminant. Histo: lymphocytic infiltrate + necrosis.
Do not be reassured by preserved LVEF when troponin or conduction abnormalities are evolving.

M2

Myositis

Skeletal-muscle inflammation

Dx proximal weakness or myalgia + CK > ULN (often > 5×) ± MRI muscle edema.
Supportive aldolase · AST/ALT (muscle source) · myoglobin.
Serologies ANA · myositis panel — anti-Jo-1 · anti-PM-Scl · anti-Mi-2 · anti-HMGCR.
If unclear EMG or muscle biopsy.

M3

Myasthenia gravis

NMJ block — bulbar / respiratory

Dx fluctuating / fatigable weakness (ocular, bulbar, limb, resp).
Studies anti-AChR / anti-MuSK antibodies and neurology-directed RNS or SFEMG. Negative antibodies do not exclude ICI-associated MG.
Bedside assess ocular, bulbar, cough and respiratory strength. Obtain serial NIF / FVC with urgent neurology review.
Red flags ptosis · diplopia · dysphagia · weak cough.

Why the overlap matters

ICI can produce concurrent myocardial and skeletal-muscle inflammation and neuromuscular-junction dysfunction. Shared T-cell reactivity is a proposed mechanism, not a complete explanation for every case. Screen all three domains because respiratory or conduction failure may develop despite preserved LVEF.

Rx

Hold ICI, establish severity and treat promptly

1 · Stabilize and investigate

Hold ICI and admit suspected myocarditis for continuous ECG monitoring. Use CICU for shock, serious arrhythmia, high-grade block or respiratory compromise. Normal LVEF or an early negative CMR does not exclude myocarditis.

2 · Start corticosteroids

When myocarditis is considered likely, ESC recommends IV methylprednisolone 500–1000 mg daily for 3–5 days. Do not delay treatment for CMR or biopsy in an unstable patient. Assess troponin, rhythm, ventricular function and symptoms together.

3 · Escalate with specialists

Persistent injury or instability prompts additional immunosuppression. Abatacept/ruxolitinib experience is observational and does not establish one regimen for everyone. Severe MG overlap may require early IVIG/PLEX and airway support. See chapter 13 for response and taper principles.

Published endomyocardial biopsy with H&E and Masson trichrome panels, followed by CD3, CD4, CD8, CD20, CD68 and CD138 immunostains. Lymphocytes infiltrate the myocardium, with more CD8-positive than CD4-positive T cells in this case. — **What to see.** A: lymphocytic infiltration on H&E. B: stromal fibrosis on Masson trichrome. C: immunostains characterize the infiltrate, including CD3-positive and CD8-positive T cells.
**What the image cannot establish.** This is one reported case after pembrolizumab and recent SARS-CoV-2 infection. The authors could not fully exclude viral contribution. Histology supports myocarditis, while drug causation requires the clinical context.
Figure 4, © 2023 Nishiyama et al., *Frontiers in Immunology*. Original source · CC BY 4.0. Reproduced without alteration.

M

Mechanical support · pacing · airway — bridges, not destinations

Resuscitation and goals of care proceed together

Bridges

Shock

Activate the shock/MCS team. Select temporary support from hemodynamics, ventricular involvement, oxygenation, reversibility and cancer prognosis. LV unloading during VA-ECMO is individualized.

Pacing

High-grade AV block / symptomatic bradycardia → urgent pacing/EP support. Temporary support may allow recovery. permanent pacing timing is individualized, without a fixed 28-day wait.

Vent · 20/30/40

Urgent airway assessment for bulbar weakness, weak cough, fatigue or deteriorating mechanics. FVC <20 mL/kg, NIF weaker than −30 or MEP <40 cm H₂O are warning signs, not standalone intubation rules. Do not wait for hypercapnia.

SCD prev

EP-guided risk assessment. Consider temporary protection selectively. Sustained VT/VF, scar, ventricular recovery and prognosis guide ICD decisions. Completion of immunosuppression is not a universal prerequisite.

Transplant

MCS as bridge to recovery. Heart-transplant eligibility after malignancy depends on tumor type, stage, recurrence risk, and oncology assessment. no universal 3- or 5-year wait.

ICI

R

Response criteria — when to advance, hold, or step back up

Anchored to troponin trajectory

Adequate response @ 72 h

Troponin ↓ > 50% from peak + rhythm / LV stable. If not met → Step 2.

Begin taper

Sustained trop trending normal · BNP stable · LVEF stable / recovered · no arrhythmias · FVC stable.

Pause / re-intensify

Rising Tn/BNP, recurrent symptoms, or falling FVC/LVEF → urgently assess relapse and other causes. Specialist-guided treatment.

Do not rechallenge

Generally avoid after severe myocarditis. Exceptions need MDT review of recovery and cancer benefit.

⏱

Monitoring intensity — match the trajectory

Serial cardiac and respiratory reassessment

Parameter	Inpatient	Outpatient
hs-Tn / CK	Serial troponin to establish trend. CK if myositis. Use the same assay and interpret persistent elevation in context.	Early follow-up during taper, with frequency set by response and relapse risk.
BNP	When clinical course or congestion makes the result useful.	As indicated by symptoms, volume and treatment response.
ECG / telemetry	Continuous.	Weekly early → space as stable.
Echo + GLS	At diagnosis and with clinical change. Repeat before discharge or major treatment decisions as indicated.	Repeat to document recovery or investigate symptoms. Individualize the interval.
CMR (if feasible)	Prompt CMR when feasible. A normal early study does not exclude ICI myocarditis.	Follow-up CMR when it will change care. Imaging alone does not determine ICD eligibility.
FVC · NIF/MIP · MEP	q 4–6h if overlap sx / evolving. Daily if stable on IS.	As clinically indicated.

↓

Taper schedule — begin after sustained improvement

Response-guided, individualized taper

Phase	Prednisone	Other agents
After response	After IV pulse and objective improvement: prednisone/prednisolone 1 mg/kg/day, max 80 mg/day (ESC).	Individualize with oncology/neurology for myositis or MG overlap.
Each reduction	Follow symptoms, ECG/conduction, LV function, troponin, and respiratory strength. Taper more slowly at low doses.	Monitor adrenal suppression and infection risk. The calendar alone does not determine treatment.
Relapse / persistent injury	Pause taper, assess other causes, and discuss escalation with specialists.	MMF, abatacept, ruxolitinib, IVIG, or PLEX selection and withdrawal require an expert plan.

PX

Prophylaxis & supportive care on prolonged IS

Layer per regimen

PJP

PJPTMP-SMX is commonly used when prednisone ≥20 mg/day is expected for ≥4 weeks or combined immunosuppression creates comparable risk. Check renal function, potassium and counts. Alternatives require individual selection, including G6PD testing before dapsone.

HSV / VZV / CMV

HSV / VZV / CMVUse oncology/infectious-disease risk assessment based on serostatus, agents and immune deficit. Pulse steroids alone do not mandate valacyclovir or valganciclovir. CMV prophylaxis or pre-emptive monitoring is regimen-specific.

Fungal

FungalAntifungal prophylaxis is reserved for defined high-risk settings, including expected profound, prolonged neutropenia. MCS alone is not an indication. Review azole interactions and QT effects.

GI

GIAssess ulcer and bleeding risk. Acid suppression is selective, especially with prior ulcer or concurrent antithrombotics, rather than an automatic consequence of steroids.

Bone

Calcium 1000–1200 mg + Vit D 800 IU daily on long-term GCs. Formal bone-health eval if prolonged or pre-existing fracture risk.

Vaccines

No live vaccines on IS. Update inactivated (influenza, pneumococcal, HBV, COVID, recombinant zoster) before / after the IS window.

VTE prophylaxis

VTE preventionAssess thrombosis, bleeding, platelet count and existing therapeutic anticoagulation. Coordinate device anticoagulation with the MCS team rather than adding duplicate prophylaxis.

Goals-of-care

Early palliative-care involvement when oncologic prognosis informs MCS / Tx eligibility. Frame MCS as bridge to recovery, not destination.

Rx

Why these drugs — mechanism · onset · watch-fors

Anchors clinical reasoning

Agent

Methylpred

Broad genomic + non-genomic suppression of all leukocyte lineages — fastest available anti-inflammatory.

Onset/t½ hours · 2–3 h · effect 24–36 h

WatchHyperglycemia · HTN · infection · GI bleed · psych · myopathy.

MMF

Inhibits IMPDH → blocks de novo purine synthesis. B/T-lymphocyte-selective. Prevents clonal expansion.

Onset/t½ days–wk · ~17 h (MPA)

WatchCytopenia · GI · opportunistic infection · hold ANC < 1.3.

Abatacept

CTLA-4–Ig blocks CD80/86–CD28 T-cell co-stimulation. Its use in ICI myocarditis is off label and does not literally reverse every ICI target.

Onset/t½ Response timing in ICI myocarditis is not established. Dosing is specialist-led

WatchLatent TB / HBV reactivation · infusion reaction · screen at baseline.

Ruxolitinib

JAK 1/2 inhibitor — dampens IFN-γ / IL-6 signaling driving cytotoxic T-cell effector function.

Onset/t½ hours · ~3 h · PO BID

WatchCytopenia · HSV/VZV reactivation · cytokine rebound on abrupt stop.

IVIG

FcRn saturation, complement modulation, autoantibody neutralization — antibody-mediated MG / antisynthetase overlap.

Onset/t½ days · ~3 wk

WatchRenal injury, volume load, thrombosis, hemolysis and infusion reactions. Review prior immunoglobulin reactions and product-specific precautions.

References ESC 2022 and ASCO/ESMO irAE guidance inform care. Salem 2023's abatacept/ruxolitinib strategy is observational. It does not establish a universal regimen. Use specialist guidance for infection prevention, respiratory support, and pacing.

PREVENT

2026
Guideline

Goals are backLDL-C targets return (not just % reduction). PREVENT-ASCVD replaces Pooled-Cohort risk. Measure Lp(a) once in adulthood.

Lower for longerEarlier therapy, even in younger adults. 10- & 30-yr risk. CAC, apoB & Lp(a) sharpen who to treat.

Cancer patientsContinue lipid-lowering therapy through cancer treatment unless contraindicated. Defer in pregnancy / lactation.

1

Estimate risk — PREVENT-ASCVD (age 30–79, no ASCVD, LDL 70–189)

10- & 30-year risk

LOW < 3%

Lifestyle (Life's Essential 8). No routine LLT.

BORDERLINE 3–<5%

LLT reasonable after clinician–patient discussion + risk enhancers.

INTERMEDIATE 5–<10%

LLT recommended. CAC may refine. Moderate-intensity statin.

HIGH ≥ 10%

Statin (often high-intensity). Treat to goal below.

2

Treatment goals — LDL-C & non-HDL-C

Lower LDL = lower risk

Borderline / Intermediate

3–<10% · primary prevention

< 100 mg/dL

non-HDL-C < 130. Any CAC → favor statin to this goal.

High

PREVENT-ASCVD ≥10%. Diabetes / CKD have separate risk-based pathways.

< 70 mg/dL

non-HDL-C < 100. High-intensity statin first-line.

Very-High ASCVD

established ASCVD · secondary prev.

< 55 mg/dL

non-HDL-C < 85. Statin + ezetimibe ± PCSK9.

Severe ↑LDL / FH

LDL ≥190 or familial hyperchol.

↓ ≥50%

Goal <100 mg/dL if no added risk. <70 with FH, added risk or CAC. <55 with ASCVD. Add nonstatin therapy as needed.

3

Lipid-lowering therapy — statin first, then add on to goal

Statin remains the foundation

Step	Agent & dose	LDL ↓	Use when
High-intensity	Atorvastatin (Lipitor) 40–80 mg · Rosuvastatin (Crestor) 20–40 mg	≥50%	ASCVD · LDL ≥190 · high / very-high risk · diabetes 40–75 + risk.
Moderate	Rosuvastatin 5–10 · Atorvastatin 10–20 · Pravastatin (Pravachol) 40–80 · Pitavastatin (Livalo) 1–4 · simvastatin 20–40	30–49%	Intermediate risk · statin-associated symptoms on high-intensity.
+ Ezetimibe	Ezetimibe (Zetia) 10 mg PO daily	+18–25%	1st add-on when not at goal on max-tolerated statin.
+ Bempedoic	Bempedoic acid (Nexletol) 180 mg PO daily	+17–18%	Statin-intolerant or needs more. Oral ACL inhibitor.
+ PCSK9 mAb	Evolocumab (Repatha) 140 mg q2wk · Alirocumab (Praluent) 75–150 mg q2wk SC	+50–60%	Very-high ASCVD or FH not at <55. Large gap to goal.

Rx

Risk enhancers & advanced testing

Sharpen the borderline patient

Lp(a) measure once in adulthood (universal). Lifestyle won't change it — ↑ Lp(a) raises risk independent of LDL.
apoB residual-risk marker when CKM syndrome · T2DM · high TG · known CVD already at LDL/non-HDL goal.
CAC scan men ≥40 / women ≥45 at borderline–intermediate — any CAC → statin, goal <100. Higher score → lower target.
Enhancers FHx premature ASCVD · LDL ≥160 · metabolic syndrome · CKD · chronic inflammation · S-Asian ethnicity · preeclampsia / early menopause · ABI <0.9.
Diabetes age 40–75 without ASCVD: at least moderate-intensity statin, usually LDL-C <100. Multiple risk factors can justify a lower goal. Apply separate CKD/HIV recommendations and individualize outside these ages.
Triglycerides address secondary causes and use statins for ASCVD risk. Icosapent ethyl requires eligible risk and TG criteria. Persistent TG ≥500, especially ≥1000 mg/dL, prompts a pancreatitis-prevention plan.

CO

Cardio-oncology specifics

Treat through cancer · mind DDIs

Continue LLT through active cancer treatment unless contraindicated — do not reflexively stop statins (2026 guideline).
Pro-atherogenic Rx VEGF/TKI · nilotinib / ponatinib · ADT · everolimus (mTOR) · lorlatinib · mediastinal RT · ICI (accelerated atherosclerosis) — lower the threshold to start a statin.
CTRCD prevention specialist-selected statin therapy may be considered at HIGH / V·HIGH toxicity risk. Radiation dose alone is not a universal statin indication.
Drug interactions prefer rosuvastatin · pravastatin · pitavastatin (minimal CYP3A4). avoid simvastatin / lovastatin with strong CYP3A4 inhibitors & many oral TKIs.
Defer most LLT during conception, pregnancy & lactation.

One-line plan Run PREVENT-ASCVD → set the LDL goal → start max-tolerated interaction-reviewed statin → add ezetimibe ± PCSK9 to hit goal → check Lp(a) once → reassess interactions and tolerance during cancer therapy.

4

Statin intolerance (SAMS) — keep patients on therapy

True intolerance is uncommon

1 · Confirm

Check CK · TSH · vitamin-D. Exclude hypothyroidism & CYP3A4 DDIs (azoles · TKIs). Most "intolerance" is not true myositis.

2 · Rechallenge

Stop 2–4 wk → rechallenge same or lower dose, symptom-guided. Try ≥ 2–3 statins before declaring intolerance.

3 · Switch

Rosuvastatin alternate-day or pravastatin / pitavastatin. Fewer CYP3A interactions does not mean interaction-free. Check transporters, renal function and dose limits.

4 · Non-statin

Still off goal / truly intolerant → ezetimibe → bempedoic acid → PCSK9 mAb to reach target.

5

Monitoring & follow-up

Adherence > titration

Lipid panel

Recheck 4–12 wk after start / dose change, then q3–12 mo. Confirm ≥ 50% LDL drop on high-intensity.

Liver

Baseline ALT. Routine repeat testing not required unless symptoms.

Muscle (CK)

Check only if symptomatic. CK ≥ 10× ULN or rhabdomyolysis → stop now.

Glucose

Small ↑ new-onset DM risk — do not stop the statin. Manage glycemia, benefit outweighs.

22%fewer events / 1 mmol/L LDL ↓

Why it pays off — in oncologyStandard ASCVD prevention remains valuable during cancer care. CTT found about 22% relative reduction in major vascular events per 1 mmol/L LDL-C reduction across trial follow-up. This is not a 22% annual reduction or a proven CTRCD-prevention effect.

PREVENT

2025
Guideline

Diagnose & targetHTN at ≥130/80. General treatment goal <130/80, individualized for tolerability, orthostasis, frailty and goals of care.

Risk-based with PREVENTPREVENT replaces pooled-cohort risk. Stage 1 → drug if ASCVD · DM · CKD or 10-yr risk ≥7.5%.

Cancer patientsContinue BP therapy through treatment. VEGF / TKI HTN is the commonest cardio-onc HTN — treat and continue.

1

BP categories — same thresholds as 2017

Diagnose ≥ 130/80 · confirm out-of-office

NORMAL

<120 and <80. Reassess yearly.

ELEVATED

120–129 and <80. Lifestyle.

STAGE 1

130–139 or 80–89. Risk-based Rx.

STAGE 2

≥140 or ≥90. Two-drug Rx.

2

When to treat & target — lower for most

Target < 130/80

Elevated

120–129 / <80

Lifestyle

No drug unless it progresses. Reassess 3–6 mo.

Stage 1 · lower risk

PREVENT < 7.5%

< 130/80

Lifestyle 3–6 mo, then drug if still ≥130/80.

Stage 1 · higher risk

ASCVD · DM · CKD · ≥7.5%

< 130/80

Start drug now + lifestyle.

Stage 2

≥140 / ≥90

< 130/80

Start 2 agents, ideally single-pill combination.

3

Drug therapy — race-neutral first-line

Thiazide · ACEi/ARB · DHP-CCB

Step	Agents	Use when
1st-line	Thiazide-like chlorthalidone 12.5–25 / indapamide 1.25–2.5 · ACEi lisinopril / ARB losartan (example option) · DHP-CCB amlodipine 5–10	Most adults — any of the four classes. Not ACEi + ARB together.
Start 2	Two classes, ideally a single-pill combination (e.g. ARB + amlodipine)	Stage 2, or BP ≥20/10 above goal.
+ MRA	Spironolactone 25–50 · eplerenone	Resistant HTN (4th agent). Screen primary aldosteronism first.
+ Other	β-blocker · hydralazine · others	Compelling indication (CAD · HF · arrhythmia) or still uncontrolled.
Cardio-onc	Avoid non-DHP CCB (verapamil / diltiazem) with CYP3A4-metabolized oral TKIs	Use DHP-CCB (amlodipine) + ACEi/ARB instead.

Lx

Lifestyle — foundational

For every BP category

Sodium <2300 mg/day, ideal <1500 (cut ≥1000/day). Potassium-based salt substitute — not in CKD or K-sparing drugs.
Diet DASH-style — more fruit / vegetables / whole grains.
Weight loss if overweight. GLP-1 / weight management where appropriate.
Activity 90–150 min/wk aerobic + resistance.
Alcohol ≤2/day (men) · ≤1/day (women). Stress management.

CO

Cardio-oncology specifics

Treat through cancer · mind DDIs

VEGF / TKI HTN monitor home BP daily in the first cycle and after dose increases, then every 2–3 weeks. The goal and treatment plan depend on prognosis, tolerability and the exact agent.
First-line ACEi/ARB ± DHP-CCB (amlodipine). Avoid non-DHP CCB with CYP3A4 TKIs.
Abiraterone mineralocorticoid HTN + hypokalemia — prefer eplerenone (spironolactone has anti-androgen / AR-agonist concern in prostate Ca).
Also drug-induced ibrutinib / BTK (independently ↑ CV events) · mTOR · steroids · calcineurin inhibitors · EPO agents.
Severe HTN if SBP ≥180 or DBP ≥110 mmHg, hold the causative cancer therapy while urgently assessing and treating BP. Acute organ injury is an emergency. Resume only after control and oncology review.

4

Secondary HTN — when to work up & how

Resistant · onset <30 · abrupt · unprovoked ↓K⁺ · incidentaloma · crisis

Primary aldosteronism

Screen aldosterone-to-renin ratio (↑aldo + suppressed renin). Correct K⁺, don't salt-restrict, stop MRA 4–6 wk first. Confirm saline / Na-load, then subtype CT + AVS. Screen resistant HTN or suggestive features. Screening may also be considered in stage 2 HTN.

Renovascular

Renal duplex · CTA / MRA. Clues: bruit, flash pulmonary edema, Cr ↑ >30% on ACEi/ARB, young woman (FMD).

Pheo / paraganglioma

Plasma-free or 24-h urine metanephrines. Clues: episodic HTN, headache, palpitations, sweats.

Cushing · endocrine

1-mg overnight dexamethasone / late-night salivary cortisol. Also TSH, Ca / PTH.

Renal · OSA

Cr / UA / renal US. STOP-BANG → sleep study. Cheap — do early in every work-up.

5

Monitoring & follow-up

Recheck · home BP · electrolytes

Recheck

About 1 month after start/change, and monthly until controlled. Space follow-up once stable.

Home BP

VEGF: daily in cycle 1 and after dose increases, then every 2–3 weeks. Increase checks if BP rises.

Labs

BMP (K⁺ / Cr) at baseline and 1–2 wk after ACEi/ARB/MRA start.

Don't stop

Continue indicated BP treatment. Severe HTN or acute organ injury may require holding the causative cancer drug.

6

Home BP — how, when & time of day

Validated cuff · average ≥ 130/80 = HTN

Device

Validated automated upper-arm cuff, correct size. Not wrist / finger / smartwatch.

Prepare

Empty bladder. 5 min seated rest, back supported, feet flat, arm at heart level. No caffeine / smoke / exercise ×30 min. Don't talk.

When · time of day

Morning (before meds & breakfast) + evening (before bed). 2 readings 1 min apart each.

How long

7 days (min 3) before each visit. discard day 1, average the rest.

Interpret

Average ≥ 130/80 = HTN (office 130 ↔ home 130. Office 140 ↔ home 135/85).

20%fewer CV events / 10 mmHg SBP ↓

Why it pays off — in oncologyTreat hypertension for its established cardiovascular benefits. Choose a tolerable goal, check interacting drugs and monitor for hypotension when a VEGF inhibitor stops. Do not extrapolate a fixed trial risk reduction to every patient with active cancer.

PROTO

T

Hematopoietic stem-cell transplant — cardiac workup

High-dose conditioning · amyloid screen

Before conditioning

Before conditioningHistory and exam, ECG, BP and baseline cardiac imaging. Review prior cardiotoxic exposures and conditioning regimen. Biomarkers and additional testing depend on risk and planned serial use.

During admission

Telemetry + daily weights through conditioning. Watch cyclophosphamide / melphalan hemorrhagic myocarditis / HF (1–3 wk). Strict fluid balance. Correct K⁺ / Mg²⁺.

Post-transplant

After transplantRisk-based follow-up. High-risk survivors need early reassessment and a long-term plan. New dyspnea, edema, chest pain or arrhythmia warrants prompt testing.

Amyloid screen

Suspected AL amyloidosisSerum free light chains plus serum and urine immunofixation, cardiac imaging and hematology review. CMR characterizes involvement but cannot type amyloid. Tissue confirmation/typing may be needed.

Echo & biomarker standardsUse measured LVEF, preferably 3-D when feasible, and comparable GLS acquisition. Use ultrasound enhancement when endocardial definition is inadequate. CMR adjudicates uncertain imaging. BNP or NT-proBNP is acceptable. Keep assay and modality consistent.

D

Common drug–drug interactions to be aware of

Screen before co-prescribing

Interaction	Why it matters	What to do
Strong CYP3A4 inhibitor + oral TKI / CDK4-6 / AR inhibitor	Strong CYP3A inhibitors can raise exposure to ibrutinib, ribociclib and many TKIs. The effect is drug-specific. Abiraterone does not share this simple rule.	Avoid strong inhibitors. If unavoidable, dose-reduce per label. ECG + electrolytes. Choose an interaction-sparing antimicrobial.
Non-DHP CCB (verapamil / diltiazem) + VEGF-TKI / mTOR	CYP3A4 inhibition ↑ anticancer-drug exposure.	Treat HTN with a DHP-CCB (amlodipine). ACEi/ARB first-line.
Simvastatin / lovastatin + CYP3A4 inhibitor / TKI	↑ statin levels → myopathy / rhabdomyolysis.	Consider pravastatin, rosuvastatin or pitavastatin after a full interaction check. Transporter interactions still matter, including darolutamide–rosuvastatin.
Warfarin + ibrutinib / capecitabine / TKI	Ibrutinib platelet dysfunction → bleeding. Capecitabine markedly ↑ INR.	Prefer a DOAC with ibrutinib (screen CYP3A4). If warfarin + capecitabine, check INR q3–5 d.
QT-additive stacking	Ribociclib · vandetanib · arsenic · nilotinib + ondansetron / azoles / fluoroquinolone / methadone → Torsades.	Minimize stacking. Baseline + serial ECG. Keep K⁺ ≥ 4.0 · Mg²⁺ ≥ 2.0.
DOAC + enzalutamide / apalutamide (strong inducers)	Enzalutamide and apalutamide have different transporter effects. Strong CYP induction may reduce apixaban/rivaroxaban exposure. Apalutamide also induces P-gp.	Review CYP3A and P-gp effects for the exact combination. Dabigatran/edoxaban are not automatically safe substitutes. Consider LMWH or another anticoagulant with oncology/pharmacy input.
Anthracycline + trastuzumab (concurrent)	Additive cardiotoxicity → higher CTRCD risk.	Sequence when oncologically appropriate. Follow drug-specific echo surveillance. At HIGH / V·HIGH risk, use cardio-onc review for any specialist-selected prevention.

S

Cancer-survivor evaluation

Annual review · risk-based echo

2026 IC-OS/MASCC minimum-care layer for adults treated for adult-onset cancer: after cancer therapy, review symptoms and CV risk factors annually and re-stratify CTR-CVT risk at 5 years. Obtain a 12-month echo after HER2-targeted therapy or, for early-stage cancer treated with curative intent, cumulative doxorubicin ≥250 mg/m² (or equivalent). In asymptomatic survivors, q5y echo may be considered for MODERATE risk (IIb-C). HIGH / V·HIGH risk: years 1, 3, and 5, then q5y (IIa-C). Imaging-frequency evidence is limited. Childhood-cancer survivors follow their separate exposure-based pathway, and new symptoms trigger referral at any time.

Exposure	Asymptomatic	Symptomatic (chest pain · dyspnea · palpitations · syncope · fatigue)
Anthracycline	Annual symptoms + CV risk factors. Echo at 12 mo if early-stage/curative intent and cumulative doxorubicin ≥250 mg/m². Thereafter use post-Tx risk tier.	Above + metabolic stress test. CMR ± stress. Consider rest/exercise RHC. Ziopatch / Holter. CTA-Heartflow (intermediate) or coronary angio (high suspicion).
Chest RT > 1 y	Annual symptom/risk review. Tailor echo and CAD screening to heart dose, field, elapsed time and risk. Do not wait for year 10 if symptoms develop.	Above + CMR ± stress. BNP / lipids / TSH. CTA-Heartflow or coronary angio (per CAD suspicion). Metabolic stress. Rest/exercise RHC. Ziopatch / Holter.
HER2 / trastuzumab	Annual symptoms + CV risk factors. echo at 12 mo post-Tx, then symptoms and post-Tx risk tier guide longer surveillance.	Above + BNP. Repeat echo. CMR if persistent LV dysfunction. resume / continue GDMT if EF not fully recovered.
ADT / hormonal	ASCVD risk. BP · lipids · A1c · weight q6–12 mo. DEXA. Lifestyle + statin by risk.	Above + stress test / CTA per CAD suspicion. Optimize metabolic syndrome. Cardiology if MACE.

Why lifelong: in 5-year childhood-cancer survivors the 30-year cumulative incidence of symptomatic cardiac events (CHF the most common) reached 7.3% after anthracyclines and 12.6% (~1 in 8) after anthracyclines + chest RT — risk climbs exponentially with cumulative dose, so surveillance never fully stops.

Nursing monitoring protocol

VEGF / TKI · BPHome BP daily in cycle 1 and after dose increases, then every 2–3 weeks. Escalate severe BP or symptoms promptly.

Anthracycline / HER2 Ask weight, dyspnea, edema, orthopnea each cycle. Echo per schedule. Call if new HF symptoms.

ICI · myocarditisUse the agreed risk-based ECG/troponin plan. New symptoms, ECG changes or troponin rise require urgent assessment.

QT agents Pre-dose ECG + K⁺ / Mg²⁺. Keep K⁺ ≥4.0, Mg²⁺ ≥2.0. Call if QTc ≥500 or the agent-specific threshold is reached, or for syncope.

WORKUP

Same symptoms, shifted differential Cancer patients present like everyone else—but therapy reshapes the odds. For every workup ask: which target/pathway, which agent and combinations, what cumulative exposure, and how long since the last cycle? Class effects predict the common toxicity. Agent pharmacology, prior radiation, and host reserve explain the exception. Pair the evaluation with the drug-class card and HFA-ICOS tier. Keep a low threshold for ECG + troponin + echo.

E

Symptom-based work-ups

Think culprit drug first

SYN

Syncope

Rule out arrhythmic & structural

First pass 12-lead ECG (QTc · conduction · ischemia) · orthostatic vitals · glucose · Hgb · electrolytes.
Reflex / orthostatic volume depletion (vomiting · diarrhea · poor intake) · autonomic neuropathy (vinca · platinum) → rehydrate, med review.
Arrhythmic — red flags exertional · supine · no prodrome · FHx SCD → admit + telemetry. QT drugs (ribociclib · vandetanib · arsenic). Anthracycline / RT conduction disease.
Structural severe AS (RT valve) · HCM / amyloid (myeloma) · large PE → echo.
Escalate echo → ambulatory monitor (Ziopatch / Holter). implantable loop if recurrent unexplained.

SOB

Dyspnea / shortness of breath

Cardiac vs pulmonary vs anemia

First pass SpO₂ · BNP · troponin · ECG · CBC · echo + GLS.
HF / CTRCD anthracycline · HER2 · VEGF · carfilzomib → echo + BNP. Treat as CTRCD card.
Pericardial effusion / tamponade (RT · dasatinib · ICI · cyclophosphamide) → echo.
Vascular PE / VTE (cancer-hypercoagulable · IMiDs · asparaginase) → CTA-PE. PAH (dasatinib) → echo PASP.
Pulmonary suspected pneumonitis/ILD → CT chest and urgent oncology/pulmonary review. Exclude infection and PE. Holding therapy and corticosteroids depend on the agent and grade. T-DXd ILD has specific permanent-stop rules.

PALP

Palpitations

Capture the rhythm

First pass 12-lead ECG during symptoms · K⁺ / Mg²⁺ · TSH · echo.
Atrial fibrillation ibrutinib · alkylators / SCT · ICI · melphalan → rate control (BB. Non-DHP CCB mind DDIs). Use CHA₂DS₂-VASc as an input, then add active cancer, thrombocytopenia/coagulopathy, intracranial disease, interactions, procedures, prognosis, and goals. Cancer neither erases the score nor lets it decide alone. Avoid warfarin with ibrutinib.
Sinus tach / SVT anemia · thyroiditis (TKI / ICI) · pain · hypovolemia · steroids → treat cause. Check TSH.
Ventricular / QT QT-prolonging drugs → ECG + electrolytes. PVC / NSVT after anthracycline / RT → echo + monitor.
Capture Ziopatch / Holter. Event monitor if infrequent.

CP

Chest pain

Vasospasm · ischemia · pericardial

First pass 12-lead ECG + troponin (vs baseline) · telemetry if active.
Vasospasm / ACS 5-FU / capecitabine during or soon after infusion → stop infusion, nitrates + CCB. ICI myocarditis if troponin ↑ → emergency (P.12).
Fixed CAD mediastinal RT (premature, ostial) · cisplatin / VEGF (accelerated atherosclerosis) → stress imaging / CTA.
Pericardial RT · cyclophosphamide · ICI · anthracycline → diffuse ST, echo for effusion / tamponade.
Non-cardiac PE (pleuritic) · RT esophagitis · musculoskeletal.

EDEMA

Edema / volume / weight gain

HF vs drug vs renal vs venous

First pass weight trend · JVP · BNP · echo + GLS · BMP / albumin.
HF / CTRCD anthracycline · HER2 · VEGF · carfilzomib → echo + BNP, GDMT.
Drug fluid retention docetaxel · imatinib (periorbital) · abiraterone (mineralocorticoid) · steroids.
Renal VEGF proteinuria / nephrotic → UPCR. Cisplatin nephrotoxicity.
Venous unilateral → DVT duplex. Lymphedema (post-op / RT). SVC / IVC obstruction (tumor).

FATIGUE

Fatigue / reduced tolerance

Don't miss early CTRCD

First pass H&P · CBC · TSH · BMP · BNP · echo + GLS. Functional capacity (METs / DASI).
Early HF / CTRCD subclinical EF / GLS decline (anthracycline · HER2 · VEGF) → echo + GLS, biomarkers.
Anemia investigate severity and cause. Transfusion and ESA decisions depend on symptoms, treatment intent and oncology guidance. ESAs carry thrombotic risk.
Endocrine hypothyroidism (TKI / ICI / neck RT) · adrenal insufficiency / hypophysitis (ICI) → TSH, AM cortisol.
Other deconditioning · cachexia → cardiac rehab after ruling out the above.

When to escalate now Syncope with exertion or documented arrhythmia · new HF with hypotension · suspected tamponade · sustained VT or QTc ≥ 500 ms · massive PE → admit, telemetry, urgent cardiology. Suspected ICI myocarditis at any presentation → treat as emergency (P.12).

WORKUP

Cancer patients come to surgery often Resection · access · biopsy — carrying cardiotoxic exposure, hypercoagulability & deconditioning. Co-manage with oncology · anesthesia · surgery, and don't reflexively stop cardiac meds. For every case ask: which drug, what cumulative dose, how long since the last cycle?

1

Who to refer & what to assess

RCRI · METs / DASI · biomarkers

REFER

Refer to cardio-onc if

Higher peri-op CV risk

Exposure active / recent cardiotoxic Tx · prior CTRCD · mediastinal RT · HFA-ICOS high / V-high.
Functional poor capacity (< 4 METs) · new dyspnea / angina / edema.
Surgery intermediate / high-risk or major oncologic resection.
Rhythm / device AF · prior arrhythmia · CIED interrogation if pacemaker / ICD.

ASSESS

Pre-op assessment

Function · cardiac · heme

Risk scores RCRI · METs / DASI · surgery-specific risk.
Cardiac ECG and biomarkers according to surgical/patient risk. Echo for new symptoms, suspected ventricular dysfunction or significant valve disease. Do not order echo or stress testing solely because cancer is present.
Heme platelets · anticoagulation status. Cancer hypercoagulability & bleeding risk.
Volume / lytes correct anemia · K⁺ / Mg²⁺ · hydration (cisplatin).

2

Agent-specific peri-op management

Hold windows · wound healing · bleeding

Agent / class	Peri-op action
VEGF / anti-VEGF (bevacizumab · TKIs)	Use agent-specific holds. Bevacizumab: ≥28 d before elective surgery. ≥28 d after major surgery and until healed. TKIs have different windows.
BTK inhibitors (ibrutinib)	Hold ~3–7 d peri-op — platelet dysfunction / bleeding.
Anticoagulant — cancer VTE (DOAC / LMWH)	Time interruption and restart to drug, renal function, procedure, and hemostasis. do not routinely bridge DOACs. Recent VTE needs specialist planning.
Antiplatelet / post-PCI DAPT	Continue aspirin if bleeding allows. delay elective surgery per stent-timing rules.
Anthracycline / cardiotoxic chemo	Don't schedule major surgery at nadir. Coordinate cycle timing & marrow recovery.
ICI	Generally continue. Keep myocarditis vigilance peri-op (troponin if symptoms).
Tamoxifen / hormonal	VTE risk — consider holding for high-VTE-risk surgery. Weigh recurrence.

3

Optimize · timing · post-op

Don't stop secondary prevention

OPT

Optimize & time

Before the OR

Individualize continue indicated statin/β-blocker. Manage ASA and RAAS drugs by surgery/HF risk. Hold SGLT2i 3–4 d before elective surgery.
Do not stop chronic β-blocker / clonidine abruptly (rebound).
Timing coordinate with oncology — surgery vs chemo nadir. Allow marrow recovery. VEGF washout.
Prehab exercise / cardiac rehab when time allows. Correct anemia.

POST

Post-op

MINS · VTE · rhythm

MINS troponin surveillance (0 / 24 / 48 h) in high-risk — injury is often silent.
VTE high — pharmacologic prophylaxis unless contraindicated. extended after major cancer surgery.
Rhythm watch post-op AF (esp. thoracic). Telemetry in high-risk.
Resume GDMT early. Restart anticoagulation & cancer therapy per recovery / wound healing.

Defer or escalate Active ischemia · decompensated HF · severe symptomatic valve disease · uncontrolled arrhythmia · BP ≥ 180/110 → optimize first, defer elective surgery. Suspected ICI myocarditis → emergency (P.12). Emergent surgery → proceed with invasive monitoring & cardiology co-management.

4

Extended VTE prophylaxis — cancer surgery is different

major abdominal / pelvic oncologic surgery

WHO

Candidates for extended prophylaxis

Beyond the standard 7–10 d

Major abdominal / pelvic oncologic surgery with limited mobility, high BMI, or advanced stage.
High Caprini score (≥7) — most cancer resections qualify.
Prior VTE or active chemo-related hypercoagulability.
Duration consider up to 4 weeks after high-risk major abdominal/pelvic cancer surgery, with bleeding and mobility reassessed.

HOW

Agents & practical points

Balance bleeding vs thrombosis

LMWH enoxaparin 40 mg SC daily × 4 wk — best evidence base.
Oral options apixaban or rivaroxaban may be offered to selected patients after initial LMWH/UFH. ASCO rates this a weak recommendation. PROLAPS II tested rivaroxaban against placebo after the first postoperative week, not non-inferiority to LMWH.
Bleeding check hold if active bleed / drain output high. Resume once surgical hemostasis stable.
Selection review bleeding, renal function, drug interactions, absorption and adherence. Do not generalize trial safety to every resection.

5

Peri-op risk scores — quick reference

RCRI · DASI · METs · surgery risk

Tool	Components	Interpretation
RCRI	High-risk surgery · IHD · HF · CVA/TIA · DM on insulin · Cr >2 mg/dL	Use a validated perioperative calculator with its stated endpoint and population. The same RCRI score does not imply one universal event probability.
DASI	12-item Sx questionnaire → estimated METs (walk 2 blocks, climb stairs, run, etc.)	DASI ≤34 or <4 METs signals poor capacity. Stress testing only in selected elevated-risk cases where it changes management
Functional	Can walk 4 mph? Climb 2 flights? Heavy housework?	≥4 METs = adequate capacity → proceed without testing if no active cardiac condition
Surgery risk	Low: endoscopy, cataract. Intermediate: abdominal, ortho, H&N. High: aortic, major vascular	Cancer resection = usually intermediate or high. Combine with RCRI + function

Cancer therapy may reduce functional capacity through fatigue, anemia and deconditioning. Evaluate reversible causes and use prehabilitation when feasible. Treat anemia by cause and clinical context, without a universal Hb 10 g/dL intervention threshold.

REF

H

Hold / Stop & Resume criteria — by therapy class

Check the exact label · no universal restart threshold

Therapy class	When to HOLD / STOP	Immediate management	When to RESUME (or switch)	Tests before resumption	Post-resumption surveillance
AnthracyclinesDox · Epi · Idarubicin	Interrupt for moderate/severe asymptomatic CTRCD or clinically important HF. Isolated Tn/GLS change needs assessment.	HF therapy. Exclude other causes. Assess dexrazoxane/liposomal options.	MDT after recovery and benefit-risk review. No universal EF/4-week rule.	TTE/GLS, Tn/NP. Lifetime exposure.	Close monitoring, often each 1–2 cycles after restart. Risk-based survivorship.
HER2 therapiesTrastuzumab · ADCs	Interrupt for EF <40% or moderate/severe symptomatic CTRCD. Reconcile exact label.	HF therapy and MDT. Asymptomatic EF 40–49% may continue with protection/monitoring.	ESC: asymptomatic, EF ≥40% (ideally ≥50%). Individual labels differ.	TTE/GLS, Tn/NP.	TTE/biomarkers every 2 cycles initially after restart, then risk-based.
VEGF / multi-TKIsSunitinib · Lenvatinib	Severe/uncontrolled HTN, important CTRCD, vascular toxicity or QT per label.	≥180 systolic or ≥110 diastolic: hold. Treat BP and evaluate organ injury.	BP <160/100 after severe HTN per ESC, plus stricter product recovery rules.	BP log. Renal/electrolytes. ECG/TTE by phenotype.	Home BP and agent/risk-specific ECG, renal, and LV surveillance.
Anti-VEGF mAbBevacizumab	Hold severe HTN uncontrolled medically. Discontinue crisis/encephalopathy, severe ATE or grade 4 VTE.	Treat BP/event. Evaluate bleeding, renal injury, proteinuria.	HTN: once medically controlled. No restart after label-defined permanent-stop toxicity.	BP. Urine protein/renal function. Wound status.	BP at least every 2–3 weeks. Serial urine protein assessment. Follow exact label hold thresholds.
BCR-ABL TKIsNilotinib · Ponatinib	New ischemic limb/neurologic/coronary symptoms: urgent assessment and label-based hold.	Treat vascular event. Antithrombotics by indication and bleeding risk.	MDT weighs alternative TKI. No universal ABI-normalization restart rule.	Vascular assessment, ECG, lipids/BP.	Agent- and event-specific vascular follow-up.
Dasatinib (PAH)CML	Suspected PAH: interrupt/evaluate. RHC confirms hemodynamic phenotype.	PH specialist assessment. Manage RV failure and PAH as indicated.	Permanently discontinue if PAH confirmed. Choose alternate cancer therapy.	Echo, BNP, RHC as indicated.	Follow PH/RV recovery. Do not rechallenge based only on improvement.
Immune checkpointPembro · Nivo · Ipi	Suspected myocarditis: hold immediately and urgently assess.	Prompt steroids when likely/unstable. Monitored care. Specialist adjuncts if refractory.	Usually discontinue confirmed disease. Any rechallenge is exceptional MDT judgment.	Clinical/rhythm, Tn, TTE ± CMR. Assess neuromuscular overlap.	Individual plan through taper and after recovery.
CAR-T (CRS)Axi-cel · Tisa-cel	CRS is managed after cell infusion. It is not a reversible oral-drug hold.	Grade-based cellular-therapy pathway. Tocilizumab/steroids as indicated. Support perfusion.	Future cancer therapy only after recovery and cellular-therapy team review.	Hemodynamics, oxygenation, rhythm. TTE/biomarkers as indicated.	Product pathway and follow-up of residual injury.
CDK4/6Ribociclib	QTcF >480 ms: interrupt. Recurrent >500 ms or serious QT-associated arrhythmia requires permanent discontinuation per label.	Correct electrolytes/DDIs. Serious arrhythmia requires emergency care.	≤480 ms. Same/lower dose by cancer setting and event history in label.	ECG. K/Mg. Interaction list.	ECG at baseline, ~day 14 C1, and as clinically indicated.
ALK / ROS1 TKIsCrizo · Alectinib	Symptomatic bradycardia or significant QT prolongation: apply specific label.	Hold if indicated. Assess nodal drugs, conduction and reversible causes.	Symptoms resolve and agent-specific HR/QT recovery criteria are met.	ECG, pulse, electrolytes.	Agent-specific ECG/pulse monitoring.
EGFR TKIOsimertinib	QTc >500 ms on ≥2 ECGs. Permanently stop life-threatening QT arrhythmia or symptomatic CHF.	Hold, correct electrolytes/DDIs. Urgent rhythm/HF care as indicated.	QTc <481 or baseline if baseline ≥481. Resume 40 mg per label.	ECG, electrolytes. LV assessment by risk/symptoms.	ECG/electrolytes in at-risk patients. LV surveillance as indicated.
Fluoropyrimidines5-FU · Capecitabine	Chest pain/ACS, ischemic ECG or other acute CV toxicity: stop exposure.	ECG/Tn, ACS evaluation. Nitrates/CCB for vasospasm.	Alternative regimen preferred when feasible. Essential rechallenge needs MDT prophylaxis/monitoring.	Exclude severe CAD. Assess ischemia and LV function.	Monitored re-exposure according to the agreed protocol.
High-dose alkylatorsSCT conditioning	Acute HF/instability or suspected myocardial injury: urgent transplant-team evaluation.	Support circulation. Phenotype-directed HF/arrhythmia care. No automatic steroid rule.	Alternative or further therapy after MDT recovery assessment.	TTE/biomarkers. Renal, fluid, infection assessment.	Transplant and cardiac follow-up matched to injury.
PlatinumCis · Carbo · Oxali	Acute vascular event, severe renal/electrolyte or hemodynamic toxicity.	ACS/vascular care. Correct electrolytes and manage volume.	Oncology/MDT decision by event, kidney function, alternatives and recovery.	Renal/electrolytes. CV tests driven by event.	Renal/electrolytes during therapy. Long-term vascular risk.
BRAF / MEKDab + Tram	LV decline, symptoms or QT toxicity by the individual agent label.	Hold responsible agent(s) as indicated. HF therapy and correction of causes.	Recovery, dose, and permanent-stop thresholds differ by drug.	TTE, ECG, electrolytes as indicated.	Label-directed LV/BP and QT monitoring.
BTK inhibitorsIbrutinib	Serious arrhythmia, uncontrolled severe HTN, or bleeding: assess label hold criteria.	Rate/rhythm care. Individual anticoagulation/DDI/platelet review.	MDT may restart, reduce or switch after control. AF alone is not an automatic permanent stop.	ECG, BP. Thrombotic/bleeding risk.	Pulse/BP and bleeding assessment each visit.
Proteasome inhibitorsCarfilzomib	Significant HF or CV toxicity: hold per label. BNP rise alone needs context.	Assess congestion, BP, renal function and other causes. Treat HF.	Consider lower-dose restart after recovery and MDT benefit-risk assessment.	TTE/NP as indicated. BP and volume.	BP/volume and risk-directed cardiac testing.
Hormonal — prostateAbiraterone · ADT	Severe HTN, hypokalemia, fluid retention or HF: assess and hold as indicated.	Correct K/BP/volume. Verify steroid pairing and interactions.	Label and oncology plan after control. ADT selection individualized.	K, BP, liver tests and volume status.	Abiraterone: BP/K/fluid retention at least monthly.
mTOR inhibitorsEverolimus	Significant pneumonitis, infection, metabolic or vascular toxicity per label.	Identify cause. Drug hold/steroids depend on severity and diagnosis.	Recovery and dose-modification rules are product-specific.	Pulmonary evaluation, BP, lipids/glucose, renal and counts.	Periodic metabolic/organ surveillance by label and risk.

EVIDENCE

E

Recommendation class is not a patient risk score

ESC 2022 · interpretation

IRecommended. Expected benefit supports the action in the stated population.

IIaShould be considered. Evidence or opinion favors usefulness.

IIbMay be considered. Usefulness is less well established.

IIINot recommended. No benefit or potential harm in the specified setting.

Evidence levelA: multiple randomized trials/meta-analyses. B: a randomized trial or large non-randomized studies. C: consensus, small studies or registries. A strong recommendation can rest on limited trial data. Neither risk-factor stacking nor clinician confidence changes the published class.

1

Identify which kind of statement you are reading

Source	What it answers	How to apply it
Regulatory label	Approved indication, formulation, dose modifications, monitoring and permanent-stop criteria.	Check the exact agent and cancer setting. A class summary cannot replace a product label.
Society guideline	A recommendation for a defined clinical population.	Retain its year, population, class and evidence level. Read exceptions and contraindications.
Clinical practice statement	Consensus implementation where evidence is evolving.	Distinguish a proposed minimum-care approach from a trial-proven optimum.
Randomized trial	A comparison in enrolled patients using specified outcomes.	Check absolute risk, endpoint and follow-up. LVEF preservation does not establish a survival benefit.
Observational study	Association, feasibility or a safety signal.	Consider confounding, selection and surveillance bias. Association is not proof that intervention changes outcomes.
Example schedule	One way a program may operationalize monitoring.	Adapt to actual drug, risk, symptoms and available care. It is not a universal mandate.

2

Three decisions where the distinction changes care

HER2 therapy

Selected asymptomatic patients with LVEF 40–49% may continue under a cardio-oncology plan. This does not erase the different hold/resume rules for trastuzumab, T-DM1 and T-DXd.

ICI myocarditis

Urgent treatment follows clinical suspicion and severity. Abatacept/ruxolitinib experience is promising but largely observational. It is not a fixed rescue regimen for every patient.

Primary prevention

Treat established CV indications. Selective high-risk prevention is different from routinely prescribing a multi-drug cardioprotective bundle to every patient.

Primary sourcesESC cardio-oncology 2022, HFA-ICOS baseline assessment 2020, IC-OS/MASCC 2026 and current product labels. The drug cards and hold/resume matrix preserve the clinical context for their use.

EVIDENCE

II

Selective care requires a reason and a reassessment plan

Guideline options · individualized decisions

Class II does not become Class I by accumulation. Multiple risks may strengthen the case for an intervention, but do not change its published recommendation class. Document the expected benefit, competing harms and patient preference.

Decision	Reason to consider	Guardrail
ACEi/ARB, beta-blocker or statin before exposure	ESC 2022 offers selective prevention in high/very-high toxicity risk.	Not a routine bundle. Standard hypertension, ASCVD and HF indications remain separate. Review hypotension, renal function and interactions.
Dexrazoxane / liposomal anthracycline	Necessary anthracycline treatment with substantial cardiac vulnerability.	Match cancer efficacy, cumulative exposure and regulatory indication. A single 250 mg/m² threshold does not define every eligible or ineligible patient.
New isolated GLS or troponin change	A reproducible signal may precede LVEF decline.	Check loading, rhythm, assay, image quality and other causes. Do not use an invented absolute GLS cutoff or automatically stop cancer treatment.
CMR / biopsy	Uncertain ventricular function, tissue disease or unresolved suspected myocarditis.	Ask what diagnostic uncertainty the test resolves. Do not delay urgent treatment in an unstable patient.
After radiation	Exposure-informed surveillance and conventional CV prevention.	Use field, mean-heart/substructure dose, time and symptoms. No universal radiation dose mandates statin, aspirin or coronary CT.
ADT choice	Cardiovascular history can inform agonist versus antagonist discussion.	Trial populations and endpoints differ. Do not promise a cardiovascular advantage for every patient.
SGLT2 inhibitor	Established HF, diabetes or CKD indication.	Do not label primary CTRCD prophylaxis an ESC 2022 Class II recommendation. Evaluate the current indication and safety.
Rehabilitation / exercise	Functional limitation, deconditioning and eligible cardiac disease.	Prescribe to symptoms and safety. Cancer exposure alone does not establish payer eligibility for cardiac rehabilitation.

?

Before ordering, answer four questions

1 · What problem is being prevented?

Distinguish HF, an imaging change, a vascular event and treatment interruption. Benefits for one endpoint do not prove benefits for the others.

2 · Does this patient resemble the evidence?

Check age, cancer stage, drug, cumulative dose, baseline function and prior therapy. A lymphoma statin trial is not a universal cancer prevention protocol.

3 · What can the intervention harm?

Assess BP, renal function, electrolytes, thrombocytopenia, interactions and treatment burden. Avoid aspirin solely for TKI exposure without an established indication or a specific specialist plan.

4 · How will the plan be reassessed?

Name the symptom, laboratory or imaging trigger, the clinician responsible and the timing. New toxicity changes the risk assessment.

Keep the treatment goal explicitPreserve effective cancer care while managing cardiovascular risk. A palliative treatment goal does not automatically exclude useful cardiovascular therapy, and curative intent does not make every optional intervention mandatory.

PEARLS

Reframe
the field

BidirectionalCancer therapy → CV disease, and CV disease → cancer (shared biology & risk factors). Not "reverse" — bidirectional.

Beyond a low EFCardiotoxicity is much broader than HFrEF — HFpEF, vascular, metabolic, arrhythmic, pulmonary-vascular.

Permissive cardiotoxicityThe immediate threat is the cancer — don't reflexively stop life-saving therapy for mild LV dysfunction.

1

Bidirectional cardio-oncology

shared biology, not one-way

→

Therapy → CV disease

the classic axis

Direct toxicity anthracyclines, HER2, VEGF, ICI, RT — across the CV spectrum.
Aging survivors >18 M US survivors. Metastatic disease is now chronic → years of cumulative exposure.

←

CV disease → cancer

reverse axis

Association CV disease and cancer share exposures and biological pathways. Observed associations do not establish that one disease directly causes the other in an individual patient.
HF and cancer cohort estimates vary with age, smoking, comorbidity and surveillance. Interpret relative risk alongside the population and absolute incidence.
Mechanism inflammation · clonal hematopoiesis · neurohormonal activation · shared risk factors.

2

Cardiotoxicity is broader than a low EF

phenotype by drug

HFpEF

HFpEFTreatment-related HF can occur with preserved EF. Symptomatic CTRCD includes a confirmed HF syndrome. Investigate filling pressure, valves, pericardium and alternative causes.

Vascular

accelerated atherosclerosis (RT, TKI), vasospasm / ACS (5-FU, capecitabine), PAD.

Metabolic

ADT → ↑ fat mass, diabetes, HTN, metabolic syndrome, fatigue.

Hypertension

VEGF / VEGF-TKI — on-target, within the first week (~↑10 mm Hg).

Arrhythmia

BTK inhibitors → AF and VT. QT prolongation with several agents.

PH · valve · pericardium

dasatinib → PAH. Radiation → valve, pericardial & conduction disease.

3

Anthracyclines & permissive cardiotoxicity

dose · mechanism · don't stop reflexively

A

Anthracyclines

still in wide use

Dose-dependent risk rises sharply > 250 mg/m², but there is no truly safe dose.
Mechanism topoisomerase-2β, ROS, iron handling, titin → systolic and diastolic (HFpEF) injury.
Prognosis cardiotoxicity can complicate cancer care. An association with worse survival does not prove that prevention restores a fixed amount of survival.

↔

Permissive cardiotoxicity

HER2 & beyond

HER2 EF decline common (3–33%, highest after anthracycline), usually reversible.
Don't reflexively stop life-saving therapy for mild LV dysfunction → start neurohormonal Rx, monitor closely, continue cancer therapy.
Small prospective studies SAFE-HEaRt: 27/30 evaluable patients completed planned HER2 therapy. SCHOLAR: 18/20 completed trastuzumab, but 2/20 developed clinically important HF. Both used specialist follow-up and HF therapy.

4

Why the field matters

a growing, aging, exposed population

Survivors

Cancer survivors may live for decades after treatment. Exposure history and competing risks shape long-term CV care.

Competing mortality

CV disease is a leading cause of non-cancer death in survivors.

Metastatic = chronic

prolonged survival on serial cardiotoxic regimens → cumulative risk.

Risk varies

by cancer & therapy — AF with targeted agents, IHD in lung cancer, HF with anthracyclines.

Association is not treatment effectAAML0531 linked cardiotoxicity with worse pediatric AML outcomes. It did not randomize cardioprotection or show that avoiding cardiotoxicity recovers a 20% survival benefit.

5

Clonal hematopoiesis — the biological bridge

CHIP / CCUS · shared biology · emerging target

CH

What it is

somatic mutations in blood

CHIP somatic mutations (DNMT3A, TET2, ASXL1, TP53, JAK2) in hematopoietic cells at VAF ≥2% without cytopenias or hematologic malignancy.
Prevalence 10–20% of adults >70 y. Rises with age, smoking, prior chemo / RT.
CV link CHIP is associated with vascular risk, with important variation by gene and clone size. These associations do not yet define a routine cardio-oncology screening or treatment pathway.

CO

Cardio-onc relevance

why it matters here

Cancer Tx → CHIP cytotoxic chemo (alkylators, platinums) and RT select for pre-existing clones (esp. TP53, PPM1D) — cancer treatment accelerates CHIP.
Progression risk depends on mutation, clone size, cytopenias and other features. Avoid applying a single annual transformation rate to every clone.
Double hit CHIP patients who receive anthracyclines may face compounded CV + hematologic risk — an emerging reason to integrate hematology and cardiology surveillance.

6

Key terminology — precision in language

what the terms actually mean

CTRCD

CTRCDSymptomatic: a confirmed HF syndrome. Asymptomatic: severe LVEF <40%, moderate LVEF 40–49% with the specified EF/GLS/biomarker changes, or mild LVEF ≥50% with new relative GLS reduction >15% and/or biomarker rise. Use the complete severity definition.

Reversibility

RecoveryDescribe symptoms, LVEF, GLS and biomarkers over time. EF normalization does not guarantee complete myocardial recovery. Avoid an unsupported universal 5-point/12-month irreversibility rule.

Cardioprotection

Primary = before exposure. CV drugs are not a routine bundle, though specialist-selected neurohormonal/statin therapy may be considered at HIGH / V·HIGH risk. Secondary follows detected injury.

PEARLS

1

Radiation heart disease

no threshold dose

Gy

The dose-response

Darby, NEJM 2013

+7.4% / Gy major coronary events per Gy mean heart dose, no threshold. Begins <5 yr, persists >20 yr.
Modern era mean heart dose is far lower (~1–2 Gy vs ~4.9 historically)—but historical mantle-field risk does not transport directly to modern conformal therapy.
Read the plan record field and era, mean-heart dose, and relevant substructure dose. Late disease follows beam geometry and tissue dose—not a generic “chest radiation” label. LV dose informs HF risk and pulmonary-vein dose may inform AF risk.

Rx

What it causes

screen + modify risk

Spectrum CAD, HFpEF, valve disease, pericardial disease, conduction disease.
Manage control conventional risk factors. Statins follow ASCVD/risk indications. Select CAD screening by exposure and clinical risk, rather than treating all prior radiation identically.
Late, additive often a "second hit" decades later — keep it on the survivorship problem list.

2

Monitoring — what actually predicts

change > baseline

Anthracycline echo

baseline. At 12 mo post-Tx if early-stage/curative intent and cumulative doxorubicin ≥250 mg/m². Then risk-based (limited evidence).

GLS

the change (not baseline) predicts subsequent EF decline. Clinical actionability still evolving.

Biomarkers

not a universal baseline bundle. Consider hs-Tn/BNP at HIGH / V·HIGH risk, then interpret trends in clinical context.

CMR

EF adjudication (gold standard), ICI myocarditis dx, post-RT fibrosis / tissue characterization.

Serial imaging is a measurement contract. Keep modality, acquisition, loading, rhythm, vendor/software, and analysis constant. Prefer 3-D EF when feasible, and ask whether change exceeds repeatability. GLS change is prognostic, but SUCCOUR did not prove that every GLS-guided strategy improves outcomes.
“Late toxicity” is usually a second hit. Anthracycline EF decline is often detectable early. Later presentations commonly acquire a trigger such as HTN, AF, or coronary disease.

3

Prevention — risk-guided, then go hard on risk factors

intensive RF modification is the lever

Cp

Cardioprotection

not one-size-fits-all

Not routine ACEi/ARB, β-blocker, statin, or SGLT2i solely for primary CTR-CVT prophylaxis. Treat standard CV indications. Specialist-selected neurohormonal/statin therapy may be considered at HIGH / V·HIGH risk.
Enalapril Cardinale 2006: LVEF decline 43% control vs 0% enalapril (P <0.001) in troponin-positive patients after high-dose chemotherapy (114 randomized).
HER2 cardioprot. Guglin 2019: in the anthracycline-pretreated subgroup, cardiotoxicity-free survival longer on carvedilol (P = 0.009) and lisinopril (P = 0.015) vs placebo (overall cohort NS).
STOP-CA lymphoma patients: LVEF decline ≥10 points to <55% at 12 months occurred in 13/150 (9%) on atorvastatin and 33/150 (22%) on placebo. HF events did not differ significantly. Generalizability is limited.
PRADA II sacubitril/valsartan did not significantly improve the primary LVEF endpoint in early breast cancer. Secondary imaging/biomarker signals require separate interpretation.

RF

Intensive risk-factor control

the biggest win

Blood pressure use evidence-based treatment with individual tolerability. Do not assume general-population intensive-BP trial results apply unchanged during active cancer.
VEGF-TKI HTN rises in the first week → treat & continue the drug.
Opportunistic CAC use calcium on oncology CT to inform ASCVD discussion and treatment. Integrate burden, age, competing illness and patient preference.

4

Drug-specific prevention

tailor to the agent

ADT (prostate)

metabolic syndrome — treat BP, lipids, glucose. Statin. CV risk burden is high & undertreated.

VEGF / TKI

VEGF / TKIHome BP daily in cycle 1 and after dose increases, then every 2–3 weeks. Severe HTN needs a treatment hold and coordinated care.

Anthracycline

baseline echo. Minimize cumulative dose. Use cardio-onc review for any specialist-selected prevention at HIGH / V·HIGH risk—no routine CV-drug bundle.

Fluoropyrimidine

5-FU / capecitabine → coronary vasospasm / ACS — counsel, recognize, treat.

5

Equity & the cardiologist's role

don't write the patient off

Disparities assess medication cost, transport, access to BP devices and reliable follow-up. Do not attribute one fixed proportion of racial disparities to a single pathway without a specific study and population.
Environment air pollution (PM2.5, ozone) associates with systolic dysfunction. Neighborhood walkability with lower HTN / diabetes / obesity.
The role a cancer diagnosis is not a reason to under-treat CV disease — manage it intensively so the patient can complete the life-saving cancer therapy & avoid an interrupting CV event.

6

Exercise & cardiac rehabilitation in cancer

underused, evidence-based, safe

Rx

Why exercise matters

during & after treatment

Exercise improves fitness, function and fatigue in selected cancer populations. Prevention of clinical anthracycline HF remains unproven.
Mortality physical activity is associated with better survival in observational studies. Magnitude varies by cancer and study design. Do not promise a universal mortality reduction.
Function combats cancer-related fatigue (the #1 patient complaint), deconditioning, sarcopenia from ADT / steroids.
Mental health reduces depression & anxiety. Improves QoL scores across cancer types.

How

Prescribing exercise

structured & supervised

Goal 150 min/wk moderate-intensity aerobic + 2 d/wk resistance training (ACS / ACSM guideline).
Rehabilitation refer to oncology exercise or cardiac rehabilitation when clinically appropriate. Standard cardiac diagnoses and payer rules determine covered cardiac rehabilitation.
Prehab 2–4 wk structured exercise before major surgery ↓ LOS & complications.
Safety exercise is safe during chemo/RT with appropriate screening. avoid high-intensity if active myocarditis, unstable arrhythmia, or symptomatic HF.

Shared treatment goalSupport effective cancer treatment through timely CV care. The oncologic consequence of a hold depends on regimen, setting, duration and alternatives. Some treatment interruptions are necessary to prevent serious harm.

REF

D

Disease-group cardio-onc workup matrix

Expanded reference · cross-ref P.3–10 drug cards

How to use this pageMatch the disease group to the actual agents, dose, stage and treatment intent. These prompts do not replace current labels or the individualized surveillance plan. New symptoms take priority over a routine interval.

Disease	Cardiotoxic regimens	CV signals	Assessment prompts	Clinical pearls	Escalate to cardio-onc
BreastHER2+ · HR+ · TNBC	AC-T (doxo + cyclo → taxane) Trastuzumab ± pertuzumab × 1 yr T-DM1 / T-DXd (ADC) Ribociclib / palbociclib (CDK4/6) Tamoxifen · AI. Left chest RT	CTRCD risk rises with prior anthracycline exposure. The magnitude depends on regimen and host risk. QTc ↑ (ribociclib) VTE (tamoxifen) Late CAD / valve (RT)	Echo + GLS q3 mo on HER2 Rx Troponin/NP surveillance by anthracycline risk and treatment plan ECG d1 + d14 with ribociclib (QTc) BNP if dyspnea / edema Baseline ASCVD risk + lipids if RT planned	Anthra → HER2 is sequential insult: GLS often drops before EF Trastuzumab cardiotoxicity is usually reversible — don't abandon too early Left breast RT + IMN fields = highest cardiac dose CDK4/6: ribociclib QTc >> palbociclib / abema	GLS ↓ > 15% relative on HER2 EF ↓ ≥ 10 pt or < 50% Tn rise post-anthracycline Ribociclib: QTcF >480 ms or symptoms, using label rules
GI / PancreaticCRC · Gastric · HCC	5-FU / capecitabine (FOLFOX, FOLFIRI, CapeOx) Bevacizumab. Ramucirumab Oxaliplatin. Irinotecan Regorafenib (TKI). Lenvatinib (HCC)	Coronary vasospasm (5-FU — can mimic STEMI) HTN (anti-VEGF) ATE (bevacizumab) HF (regorafenib / lenvatinib)	CAD evaluation for symptoms or selected high-risk patients BP every cycle on anti-VEGF Chest-pain action plan for fluoropyrimidines. Antianginal prophylaxis is individualized. Bevacizumab: serial urine protein. Dipstick ≥2+ prompts quantitative assessment. Echo baseline if HCC TKI	Fluoropyrimidine ischemia may coexist with obstructive CAD. Evaluate ACS rather than presuming a normal angiogram. After toxicity, discuss alternatives or monitored rechallenge with oncology/cardiology. No single substitute fits every cancer or country. Capecitabine can also cause ischemia/vasospasm. Risks are not identical across schedules.	Chest pain / ST Δ on 5-FU SBP ≥ 180 on anti-VEGF ATE event New proteinuria ≥ 2+
GUProstate · RCC · Testicular	ADT (GnRH ± AR inhibitors: enza, apa, daro, abi) VEGF-TKIs (cabo, suni, lenva — RCC) ICI (pembro, nivo). Platinum (testicular) mTOR (everolimus)	Metabolic syndrome (ADT — ↑ weight, lipids, A1c) HTN (TKI / abi) MACE ↑ (ADT long-term) LV dysfunction (TKI). hypoK⁺ (abi)	ASCVD risk calc at ADT initiation BP / lipids / A1c q3–6 mo Echo if HFA-ICOS ≥ high or TKI start Vascular exam and symptom-directed testing for the actual GU regimen K⁺ monitoring (abiraterone)	ADT accelerates atherosclerosis — treat lipids + BP aggressively GnRH antagonists (degarelix, relugolix) may have lower MACE vs agonists Lifelong vascular risk review after cisplatin. Use standard risk-based prevention.	New MACE event on ADT BP uncontrolled on 3 agents EF drop on VEGF-TKI Metabolic syndrome worsening
Thoracic / H&NNSCLC · SCLC · H&N SCC	ICI (pembro, nivo, atezo, durva) Platinum doublets (carbo-pem, cis-gem) Osimertinib (EGFR). Alectinib / lorlatinib (ALK) Chest RT (definitive or concurrent)	ICI myocarditis — highest risk with combo ICI QTc ↑ (osimertinib, crizotinib) Bradycardia (crizotinib, lorlatinib) Late CAD / valve / pericardial (RT)	Baseline ECG + hs-Tn before ICI ICI ECG/troponin monitoring by risk and the agreed schedule ECG for QTc on EGFR TKIs HR monitoring on ALK TKIs Long-term CAD screening post-RT	ICI myocarditis: median onset 30 d — most cases in first 3 cycles Combo ICI (nivo + ipi) = highest myocarditis risk Osimertinib: HF signal in FLAURA — monitor if pre-existing CV disease Concurrent CRT: pericarditis may mimic progression	Any Tn rise on ICI New HF sx on TKI QTcF ≥500, symptoms, or stricter drug-label threshold. Delta alone prompts review Symptomatic brady
GynecologicOvarian · Cervical · Endometrial	Carboplatin + paclitaxel ± bevacizumab PARP maintenance (olaparib, niraparib) Pegylated liposomal doxorubicin (2L) Topotecan. Gemcitabine	HTN (bevacizumab, niraparib) ATE / VTE (bevacizumab) Bradycardia (paclitaxel) Low direct myocardial burden	BP each cycle on bevacizumab / niraparib UPCR if proteinuria (bevacizumab) Baseline echo if prior anthracycline ECG if QT-relevant co-meds	Bevacizumab HTN is the main signal — treat and continue Niraparib: monitor BP and pulse at least weekly for 2 months, monthly for the first year, then periodically. Liposomal doxorubicin has lower CTRCD risk than conventional	SBP ≥ 180 on bevacizumab ATE event New proteinuria ≥ 2+ EF drop if prior anthracycline
Mal HemLeukemia · Lymphoma · Myeloma	R-CHOP (anthra + cyclo). BEAM conditioning BCR-ABL TKIs (nilo, pona, dasa) CAR-T (axi-cel, liso-cel, cilta-cel) Arsenic + ATRA (APL). carfilzomib (MM) Ibrutinib / acalabrutinib (BTK)	HFrEF (anthracycline, carfilzomib) ATE / PAD (nilotinib, ponatinib) CRS hypotension (CAR-T) QTc ↑ (arsenic). PAH (dasatinib) AF (ibrutinib). VTE	Anthracycline echo/biomarkers by cumulative exposure, baseline risk and symptoms Vascular assessment during nilotinib/ponatinib. Test further for symptoms or abnormal findings. Arsenic: label ECG/electrolyte schedule. Intensify if unstable CAR-T monitoring follows the current product and cellular-therapy pathway BP + BNP each cycle on carfilzomib	Anthracycline dysfunction is dose-related and may recover, especially with early treatment. Ponatinib can cause arterial events at any dose. Symptoms and vascular risk guide evaluation. Treat CAR-T CRS by grade and product pathway. CV instability may require intensive support. Ibrutinib AF: switch to 2nd-gen BTK (acala, zanu) when possible	EF ↓ at any dose checkpoint ABI ↓ > 0.15 or new claudication CRS with Tn ↑ or hypotension Arsenic: QTc Framingham >450 ms (M) / >460 ms (F). Hold per label New AF on BTK
Melanoma / SarcomaICI-heavy · anthracycline	ICI: nivo + ipi (combo). Pembrolizumab (mono) BRAF + MEK (dabrafenib + trametinib) Anthracycline (sarcoma — doxorubicin) High-dose IL-2 (melanoma)	Myocarditis (combo ICI) EF ↓ + QTc ↑ (BRAF/MEK) HFrEF (anthracycline — sarcoma) Capillary leak (IL-2)	ECG + Tn baseline for all ICI ICI ECG/troponin monitoring by risk and the agreed schedule Echo at 1 mo on BRAF/MEK Echo + cum-dose tracking (sarcoma anthra) ICU monitoring for HD IL-2	Combination ICI increases myocarditis risk relative to single-agent therapy. Avoid absolute cross-regimen rankings. BRAF/MEK dysfunction may improve. Hold the responsible agent(s) according to their separate labels. Sarcoma anthracycline doses can reach very high cumulative levels	Any Tn rise on combo ICI BRAF/MEK: symptoms or label-defined EF decline, including the lower limit of normal Approaching doxo 400 mg/m²
Neuro-OncGBM · CNS mets	Temozolomide + RT Bevacizumab Lomustine (CCNU)	HTN (bevacizumab) ATE / proteinuria (bevacizumab) Rare LV dysfunction	BP each cycle Baseline echo on bevacizumab UPCR if proteinuria develops	Generally lower CV burden than other disease groups Bevacizumab in neuro-onc: HTN management is main cardio-onc role	Refractory HTN on bev Proteinuria ≥ 2+
Benign Hem / Sickle CellSCD · Thalassemia	Hydroxyurea Chronic transfusion (iron overload) Hydroxyurea and hematology-directed transfusion or disease-modifying treatment. Voxelotor was withdrawn in 2024. Iron chelation (deferasirox, deferoxamine)	Iron-overload cardiomyopathy Pulmonary HTN (SCD) Diastolic HF Stroke risk (SCD)	SCD: diagnostic echo for symptoms/signs. Routine screening echo is not advised in asymptomatic patients. Iron assessment depends on transfusion burden and disease. Cardiac T2* is selected for suspected cardiac iron. BNP. Ferritin q3 mo TCD for stroke screening (peds)	*T2 < 20 ms = iron overload. < 10 ms = severe → intensify chelation SCD: isolated TRJV 2.5–2.9 m/s does not automatically require RHC. Integrate symptoms, repeat echo, NT-proBNP and exercise capacity with PH expertise. Chelation can reverse** iron cardiomyopathy if caught before EF drops	T2* < 10 ms Elevated TRJV with symptoms or other evidence of PH New HF symptoms EF decline on echo

Baseline assessmentBefore potentially cardiotoxic therapy, document CV history and conventional risk factors. Use a validated therapy-specific HFA-ICOS proforma where applicable. The disease label alone does not determine risk or surveillance.

Rx

R

Representative cancer therapies — identify the CV exposure

For the cardiologist — what your patient is receiving

Why this page existsUse these examples to recognize cardiovascular exposures, not to select an oncology regimen. Stage, biomarkers, prior therapy, approvals and treatment intent determine sequencing. This table is not exhaustive and does not rank current first-line options.

Cancer	Common treatment examples	Other settings / later therapies	Key CV-toxic agents (→ drug card page)
SOLID TUMORS
Breast, HER2+	AC-T → trastuzumab ± pertuzumab × 1 yr TCHP (docetaxel, carbo, trastu, pertu)	T-DXd (trastuzumab deruxtecan) T-DM1. Tucatinib + cape + trastu Lapatinib + capecitabine	CV Doxorubicin → P.3 (CTRCD) CV Trastuzumab → P.5 (LV dysfxn) CV Cyclophosphamide → P.4
Breast, HR+/HER2−	AI or tamoxifen + CDK4/6 (ribociclib, palbociclib, abemaciclib) ± LHRH agonist (premenopausal)	Fulvestrant + CDK4/6 or alpelisib Capecitabine. Eribulin T-DXd (if HER2-low)	CV Ribociclib → P.6 (QTc ↑) LO Tamoxifen (VTE) CV Capecitabine → P.6 (vasospasm)
Breast, TNBC	Pembrolizumab + carbo + paclitaxel → AC Early TNBC pembrolizumab eligibility is not restricted to PD-L1-positive disease. Metastatic eligibility is different.	Sacituzumab govitecan Capecitabine. Gemcitabine + carbo	CV Pembrolizumab → P.4 (myocarditis) CV Doxorubicin → P.3
Gynecologic / Ovarian	Carboplatin + paclitaxel ± bevacizumab PARP maintenance (olaparib, niraparib) for BRCA / HRD	Pegylated liposomal doxorubicin Gemcitabine. Topotecan. Bevacizumab	CV Bevacizumab → P.3 (HTN, ATE) LO Niraparib (HTN, tachycardia) LO Liposomal doxorubicin → P.3 (low CTRCD)
Colorectal	FOLFOX or FOLFIRI ± bevacizumab FOLFOX ± cetuximab / panitumumab (RAS WT) Pembro if MSI-H/dMMR	Switch backbone ± anti-VEGF Regorafenib. TAS-102 (trifluridine) ± ICI if MSI-H	CV 5-FU → P.6 (vasospasm) CV Bevacizumab → P.3 (HTN, ATE) CV Regorafenib → P.3 (HTN, HF)
Pancreatic	FOLFIRINOX (5-FU, leucovorin, irinotecan, oxaliplatin) Gem + nab-paclitaxel	After gemcitabine: liposomal irinotecan + 5-FU/leucovorin. NALIRIFOX adds oxaliplatin and is a first-line metastatic option. Gem mono. Olaparib maint (BRCA+)	CV 5-FU → P.6 (vasospasm) LO Oxaliplatin (rare vasospasm)
Gastric / Esoph	FOLFOX or CapeOx ± nivolumab (or pembro) Trastuzumab + chemo (HER2+)	Paclitaxel ± ramucirumab TAS-102. T-DXd (HER2+)	CV 5-FU / Cape → P.6 CV Trastuzumab → P.5 CV Ramucirumab → P.3 (HTN)
RCC	Pembro + lenvatinib (or axitinib) Nivo + cabozantinib Nivo + ipilimumab	Cabozantinib mono. Lenva + everolimus Sunitinib. Pazopanib. Axitinib	CV VEGF-TKIs → P.3 (HTN, HF) CV Nivo + ipi → P.4 (myocarditis) LO Everolimus (HTN, lipids)
ProstateSeparate mCSPC from mCRPC	mCSPC: ADT with a stage-appropriate androgen-pathway inhibitor. mCRPC options depend on prior exposure and biomarkers. Darolutamide + ADT, with or without docetaxel, belongs to the mCSPC setting.	Docetaxel. Cabazitaxel Radium-223. Olaparib (BRCA+) Lu-PSMA-617	CV ADT → P.7 (metabolic, MACE) CV Abiraterone → P.7 (HTN, hypoK⁺) LO Enzalutamide (HTN)
NSCLC	Pembrolizumab ± carbo-pemetrexed Osimertinib (EGFR+). alectinib / lorlatinib (ALK+) Durvalumab post-CRT (stage III)	Docetaxel ± ramucirumab ICI if not in 1L. amivantamab (EGFR exon 20)	CV ICI → P.4 (myocarditis) CV Osimertinib → P.8 (QTc, HF) CV Crizotinib → P.8 (QTc, brady)
SCLC	Carbo + etoposide + atezolizumab (or durvalumab)	Topotecan. Lurbinectedin	CV ICI → P.4 (myocarditis) LO Etoposide (rare)
Head & Neck	Pembrolizumab ± platin + 5-FU Cetuximab + platin + 5-FU (EXTREME)	Nivolumab. Cetuximab mono. Methotrexate	CV ICI → P.4. 5-FU → P.6 CV Cisplatin → P.9 (vascular)
Melanoma	Nivo + ipi (combo ICI). Pembrolizumab Dabrafenib + trametinib (BRAF V600+)	Switch ICI backbone. Encorafenib + binimetinib High-dose IL-2	CV Nivo + ipi → P.4 (myocarditis — highest risk) CV BRAF + MEK → P.5 (EF↓, QTc) CV IL-2 → P.10 (capillary leak)
HEMATOLOGIC MALIGNANCIES
DLBCL	R-CHOP (rituximab + cyclo + doxo + vincristine + pred) Pola-R-CHP (polatuzumab vedotin)	Salvage chemo (R-ICE, R-DHAP) → auto-SCT CAR-T (axi-cel, liso-cel, tisa-cel)	CV Doxorubicin → P.3 (CTRCD) CV Cyclophosphamide → P.4 CV CAR-T → P.4 (CRS)
CML	Imatinib. Dasatinib. nilotinib. Bosutinib	Ponatinib. Asciminib Allo-SCT (blast crisis)	CV Nilotinib → P.6 (ATE, PAD) CV Ponatinib → P.6 (ATE — highest risk) CV Dasatinib → P.6 (PAH, effusion)
Mult Myeloma	VRd (bortezomib + lenalidomide + dex) DaraVRd (+ daratumumab)	Carfilzomib + dex. Pomalidomide BCMA-targeted: teclistamab. cilta-cel (CAR-T)	CV Carfilzomib → P.7 (HF, HTN) CV CAR-T → P.4 (CRS) LO Lenalidomide (VTE)
AML / APL	AML: 7+3 (daunorubicin + cytarabine). Or venetoclax + aza APL: ATRA + arsenic trioxide	Gilteritinib (FLT3+). Enasidenib (IDH2+) Allo-SCT	CV Daunorubicin → P.3 (CTRCD) CV Arsenic → P.10 (label-specific QT/ECG rules) CV SCT conditioning → P.4
CLL / SLL	Ibrutinib or acalabrutinib ± obinutuzumab Venetoclax + obinutuzumab	Switch BTK or to venetoclax-based Zanubrutinib. pirtobrutinib	CV Ibrutinib → P.7 (AF, HTN, HF) LO Acalabrutinib (AF lower)
Hodgkin	ABVD (doxo, bleo, vinblastine, dacarbazine) BV + AVD (brentuximab vedotin)	Pembrolizumab. Nivolumab Relapsed Hodgkin: salvage strategies, auto-SCT, PD-1 therapy or trials. CAR-T is not routine approved Hodgkin therapy.	CV Doxorubicin → P.3 CV Mediastinal RT → P.10 (late CAD/valve) CV ICI / CAR-T → P.4
SPECIAL POPULATIONS
Sarcoma	Doxorubicin ± ifosfamide Gem + docetaxel (leiomyo, UPS)	Trabectedin. pazopanib Eribulin (liposarcoma)	CV Doxorubicin → P.3 (high cumulative doses) CV Pazopanib → P.3 (HTN, QTc)
Testicular	BEP (bleomycin, etoposide, cisplatin)	TIP. VeIP. High-dose carbo → auto-SCT	CV Cisplatin → P.9 (lifelong ASCVD ↑) LO Bleomycin (pulm, Raynaud)

Page numbers after each agent (→ P.3, P.5, etc.) point to the drug-class card with full toxicity profile, HFA-ICOS scoring, and management. CV = significant cardiotoxicity. LO = lower risk but monitor.

Rx

A

Common regimen acronyms — what your patient is actually getting

Shorthand decoded · CV = cardiotoxic

Why this page exists When a patient's chart says "on R-CHOP" or "completed KEYNOTE-522," a cardiologist needs to know which drugs are inside that acronym — and which ones are cardiotoxic. The bolded letter in each component maps to the acronym. Cross-reference with P.3–10 drug cards for management.

Regimen	Components (generic)	Used in	CV-toxic agent(s)
R-CHOP	Rituximab · Cyclophosphamide · Hydroxydaunorubicin (CV doxorubicin) · Oncovin (vincristine) · Prednisone	DLBCL · NHL	CV Doxorubicin → P.3
ddAC-T	Dose-dense CV Adriamycin (doxorubicin) + Cyclophosphamide q2wk → Taxane (paclitaxel q2wk)	Breast (neo/adj)	CV Doxorubicin → P.3
KEYNOTE-522	CV Pembrolizumab + carboplatin/paclitaxel, then anthracycline + cyclophosphamide, followed by adjuvant pembrolizumab after surgery. Original trial AC/EC was every 3 weeks. Dose-dense variants are modified regimens.	TNBC (neoadj)	CV Pembro → P.4. Doxo → P.3
FOLFOX	CV Fluorouracil (5-FU) + Leucovorin (FOL) + Oxaliplatin	CRC · Gastric	CV 5-FU → P.6 (vasospasm)
FOLFIRI	CV Fluorouracil + Leucovorin + Irinotecan	CRC, in several treatment settings	CV 5-FU → P.6
FOLFIRINOX	CV 5-FU + leucovorin + irinotecan + oxaliplatin	Pancreatic	CV 5-FU → P.6
CapeOx	CV Capecitabine (oral 5-FU) + Oxaliplatin	CRC · Gastric	CV Capecitabine → P.6
BEP	Bleomycin + Etoposide + cisPlatin	Testicular (curative)	CV Cisplatin → P.9
ABVD	CV Adriamycin (doxorubicin) + Bleomycin + Vinblastine + Dacarbazine	Hodgkin lymphoma	CV Doxorubicin → P.3
TCHP	Taxotere (docetaxel) + Carboplatin + CV Herceptin (trastuzumab) + Perjeta (pertuzumab)	Breast, HER2+	CV Trastuzumab → P.5
VRd	Velcade (bortezomib) + Revlimid (lenalidomide) + dexamethasone	Mult myeloma (1L)	LO Lenalidomide (VTE)
KRd	CV Kyprolis (carfilzomib) + Revlimid + dexamethasone	Multiple myeloma, selected treatment settings	CV Carfilzomib → P.7
R-ICE	Rituximab + Ifosfamide + Carboplatin + Etoposide	DLBCL salvage → SCT	CV Ifosfamide → P.4
BEAM	BCNU (carmustine) + Etoposide + Ara-C (cytarabine) + Melphalan	Auto-SCT conditioning	CV High-dose alkylators → P.4
7+3	Cytarabine × 7 d + daunorubicin × 3 d	AML induction	CV Daunorubicin → P.3

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