1 · Cine: bright blood outlines the myocardium; use a loop to assess contraction, not this still image.

2 · T2-weighted: a brighter myocardial region raises the question of edema; confirm location, source quality and complementary findings.

3 · Conventional LGE: the subendocardial bright band is a synthetic injury example; bright blood can make its inner edge difficult to see.

4 · Blood-nulled LGE: darker blood makes the scar–cavity border more conspicuous. The exact blood/myocardial appearance varies with technique.

1 · Magnitude + phase: locate the vessel on magnitude images, track its contour each frame, and check phase direction, VENC, aliasing and offsets. Black versus white has no universal direction.

2 · Velocity to flow: sum velocity × pixel area across the lumen. Integrate flow rate over time to obtain volume.

3 · Use the right denominator: direct semilunar regurgitant fraction = reverse / forward × 100%. Indirect MR fraction = (LV stroke volume − aortic forward volume) / LV stroke volume × 100%.

4 · Reconcile: compare flow with ventricular volumes and the clinical question. An attractive curve does not validate the acquisition.

1. Top left and top right: Use both long-axis planes to prescribe the short-axis stack across the ventricles.

2. Bottom, slices 1–9: Scroll from base to apex and confirm complete LV and RV coverage.

3. Bottom, static frames: These are still frames from cine slices. Ventricular function and wall motion require the full cardiac cycle.

1. Native T1 row: T1 can rise with edema or amyloid and fall with iron or Fabry disease; interpret the pattern with the rest of the study.

2. ECV row: An expanded extracellular volume is a tissue signal, not a disease-specific diagnosis.

3. T2 and T2* rows: T2 increases with edema; iron shortens T2*. The sequences answer different questions.

4. Whole figure: Colors are display choices. Judge quantitative values against the scanner, sequence, field strength, and laboratory reference range.

1. a: The inferior defect is subendocardial, more than one pixel wide, and follows a coronary territory.

2. b: The very thin, dark rim is an artifact example. The source notes onset before myocardial contrast arrival; confirm timing in the full series.

3. c: Red and green contours bound myocardium; the blue blood-pool ROI samples the input signal.

1. Inferolateral and lateral wall: The brighter myocardial signal is the abnormal finding described in this acute myocarditis example.

2. Whole image: STIR is a qualitative T2-weighted image, not a quantitative T2 map in milliseconds.

3. Myocardial borders: Confirm that high signal is within myocardium and review for motion, coil, and slow-flow artifact before calling edema.

1. Left: The etched appearance of normal myocardium signals a too-short inversion time; the inferior LGE is underestimated.

2. Right: Repeating with a longer inversion time reveals a larger inferior LGE zone.

3. Both panels: This is a technical acquisition comparison, not interval scar progression. These are magnitude images, not PSIR.

1. a–b: Normal myocardium retains signal longer; the illustrated fitted T2* is 33.3 ms.

2. c: The iron-overloaded myocardium loses signal rapidly as TE increases.

3. d–e: Late echoes near the noise floor can bias the decay fit. Truncation changes the illustrated estimate from 9.1 to 6.7 ms.

4. Quantitative interpretation: Use a validated myocardial ROI and fitting method. Common <20 ms and <10 ms clinical thresholds apply to validated 1.5 T methods.

1. Top, magnitude frames: Use anatomy to place and track the vessel contour through the cardiac cycle.

2. Top, phase frames: Phase carries velocity information. Bright/dark direction depends on the acquisition convention and must be checked.

3. Bottom: Integrating the flow curves gives pulmonary and systemic flow; Qp exceeds Qs in this illustrated VSD with left-to-right shunting.

1. Top versus bottom, T1 mapping: The conventional map is distorted near the device; wideband imaging reduces the artifact in the corresponding map.

2. Top versus bottom, perfusion and LGE: Device-related signal changes can resemble a perfusion defect or scar. Compare the corresponding wideband images.

3. Right: The chest radiograph shows the subcutaneous ICD responsible for the adjacent field disturbance.

1. A–D — Cine SSFP: First describe the concentric wall thickening and papillary muscles. These panels show morphology, not a dedicated scar acquisition.

2. E and H — Dashed arrows: Locate bright inferolateral midwall LGE. Its position within the wall is the key feature.

3. F–H — Arrowheads: Additional midwall enhancement shows that Fabry involvement need not be confined to one basal segment.

1. A — Postcontrast T1 map: This is a postcontrast map, not native T1. Interpret only with its acquisition and contrast context.

2. B — Intramural bright signal: Identify the intense intramural LGE described by the authors; LGE characterizes myocardial injury.

3. C — Focal FDG uptake: PET adds metabolic information. Its interpretation requires appropriate myocardial suppression and clinical context.

1. 1-a versus 2-a — Both lack obvious LGE: The second row is an amyloidosis example despite no visible LGE; a negative LGE image does not exclude diffuse involvement.

2. 3-a and 4-a — Patchy versus global enhancement: Describe the LGE distribution before assigning an etiology.

3. Rows 2–4, columns c and d — Native T1 and ECV summaries: The authors report increased native T1 and ECV. Use local reference ranges; these printed values are not portable diagnostic thresholds.

1. a — Cine SSFP: Describe ventricular morphology and the pleural effusion. Functional interpretation uses the entire cine, not one frame.

2. b and c — T2-STIR and LGE: Look for corresponding inferior-wall subepicardial high signal. Edema and nonischemic injury are separate observations.

3. d–f — Native T1, postcontrast T1, and ECV: Compare like locations. ECV combines myocardial and blood T1 before/after contrast with hematocrit; a bright map alone is not a diagnosis.

1. Initial Presentation, LGE column — Red arrows: Locate the initial enhancement at the marked levels; then compare the same slice positions at follow-up.

2. Follow-up, basal row — Red arrowheads: Persistent basal LGE coexists with lower, blue-coded T2 in the corresponding region.

3. T2 Map and Fraction >80 ms columns — Different displays of one measurement: The >80-ms overlay was specific to this study and sequence; it is not a universal clinical threshold.

1. c and f — T2 and T1 maps: Locate the abnormal region and compare the same myocardial location across the other sequences; both are measured in milliseconds, with different display ranges.

2. e — LGE: The dark core within the bright infarct was interpreted by the authors as most likely microvascular obstruction; compare its location with STIR (d).

3. a versus b — Fat suppression differs: The two bright-blood edema preparations do not make fat and fluid look identical. The sequence label is part of the interpretation.

1. Leftmost panel — Long arrow: Bright cavity blood competes with the subendocardial infarct signal, making the border less conspicuous.

2. Second through fourth panels — Long arrows: Increasing blood suppression separates the bright subendocardial lesion from the darker cavity.

3. Leftmost panel, short arrow — Septal blood-pool border: The source identifies Gibbs ringing that is not present on the dark-blood images; avoid calling this narrow border artifact scar.

1. Left panel — Three arrows: Inspect the apparently bright lateral subendocardial region; adjacent cavity/trabecular blood can mimic enhancement.

2. Right panel — Corresponding lateral border: With blood suppressed, the proposed lesion is no longer convincing. The authors identify the original signal as blood in trabeculae.

1. B and C — Arrows: The apical mass is visible on cine and dark-blood images; morphology establishes its location.

2. D — Solid and dashed arrows: Standard LGE shows the thrombus and adjacent anteroseptal myocardial scar as separate findings.

3. E — Arrow; TI 600 ms in this study: The thrombus is homogeneously dark against enhancing tissue on the long-TI acquisition. The applicable TI depends on the protocol.