Cardiac MRI — structured viva

Stem

Practice viva. The examiner hands you a CMR report and asks what each sequence shows, how you read an LGE pattern, how CMR helps in suspected amyloid, where stress CMR and viability testing stand, and how you scan a patient with a pacemaker.^{[1][2][3][4][9]}

Branch A — The sequences

Examiner: What should a routine cardiomyopathy CMR include, and what does each part show?^[1]

Strong answer:

• ESC 2023: initial evaluation should routinely include cine imaging sequences, T2-weighted sequences, pre- and post-contrast T1 mapping, and LGE; T2* mapping should be employed when haemochromatosis is suspected.^[1]
• ESC 2025: myocardial oedema and changes due to inflammation lead to increased tissue water content that can be detected as increased signal on T2-weighted imaging and/or T2 mapping; increased tissue free water also leads to increased signal in T1 mapping and ECV quantification; myocyte necrosis and fibrosis can result in non-ischaemic patterns of LGE.^[2]
• ESC 2026 HF: CMR is considered the gold standard for assessing LV volumes and mass, and parametric mapping (T1, T2, T2*, LGE and ECV) enables classification of cardiomyopathies and of cardiac amyloid.^[3]

Follow-up: Which rows tell you to scan a cardiomyopathy patient?^[1]

• ESC 2023 Recommendation Table 5: contrast-enhanced CMR is recommended at initial evaluation (Class I, Level B) and should be considered during follow-up to monitor progression and aid risk stratification and management (Class IIa, Level C).^[1]
• ESC 2026 HF (specialised investigations in patients with established HF; investigations for underlying aetiology in HFpEF or HFrEF): contrast-enhanced CMR is recommended in patients with suspected cardiomyopathy, or where the underlying aetiology of HF is uncertain if further characterisation is likely to add value to patient care (Class I, Level C).^[3]

Branch B — Reading LGE

Examiner: The report says mid-wall LGE. How do you reason from the pattern?^[2]

Strong answer:

• First, coronary or not: ESC 2024 says LGE can reveal a typical pattern of scarred myocardium after MI, while ESC 2025 says non-ischaemic patterns (e.g. mid-wall, subepicardial, patchy) do not typically follow a coronary artery distribution.^[4][2]
• Then the phenotype: ESC 2023 says LGE is present in 65% of patients with HCM (range 33–84%), typically in a patchy mid-wall pattern in areas of hypertrophy and at the anterior and posterior RV insertion points; in DCM, the LGE distribution may point towards specific aetiologies (e.g. subepicardial in post-myocarditis forms, patchy in sarcoidosis, extensive inferolateral in dystrophinopathies, septal mid-wall in LMNA carriers, and ring-like in DSP and FLNC-truncating variant carriers).^[1]
• ESC 2023 cautions that CMR rarely distinguishes the causes of HCM by magnetic properties alone; the distribution and severity of interstitial expansion can, in context, suggest specific diagnoses.^[1]

Follow-up: The patient is a 19-year-old athlete with hypertrophy and no LGE. Does that exclude HCM?^[1]

• No. ESC 2023 says the absence of fibrosis may help separate HCM from physiological adaptation in athletes, but LGE may be absent in people with HCM, particularly young people and those with mild disease.^[1]
• AHA/ACC 2024: for LVH with suspicion of alternative diagnoses, including infiltrative or storage disease as well as athlete's heart, CMR imaging is useful (COR 1, LOE B-NR).^[7]

Branch C — Amyloid

Examiner: Which CMR findings make you think of amyloid, and does CMR settle the diagnosis?^[3]

Strong answer:

• ESC 2026 HF Table 20 CMR red flags, each for both TTR and AL: global subendocardial or transmural LGE, elevated native T1 values, increased extracellular volume and abnormal gadolinium kinetics; its footnote says CMR can be diagnostic for cardiac amyloidosis.^[3]
• ESC 2026 HF says invasive criteria apply to all forms, whereas non-invasive criteria are accepted only for ATTR; among investigations for underlying aetiology in patients with HFpEF or HFrEF, it recommends initial diagnostic testing with serum and urine immunofixation, a serum free light chain assay and DPD/PYP/HMDP bone scintigraphy in patients with HF and a suspicion of cardiac amyloidosis (Class I, Level B).^[3]
• ESC 2023 non-invasive route: typical echocardiographic/CMR findings plus grade 2 or 3 radiotracer uptake on scintigraphy and exclusion of a clonal dyscrasia.^[1]

Branch D — Ischaemia and viability

Examiner: When do you use stress CMR in suspected CCS, and what result is high risk?^[4]

Strong answer:

• ESC 2024, for CMR if available and supported by local expertise: in suspected CCS with moderate or high (>15%–85%) pre-test likelihood of obstructive CAD, stress CMR perfusion imaging is recommended to diagnose and quantify ischaemia and/or scar and estimate the risk of MACE (Class I, Level B).^[4]
• ESC 2024 Recommendation Table 14 (Class I, Level B): high risk on stress CMR is ≥2 of 16 segments with stress perfusion defects or ≥3 dobutamine-induced dysfunctional segments; in high-risk individuals, regardless of symptoms, ICA with FFR/iFR when appropriate is recommended (Class I, Level A).^[4]
• AHA/ACC 2021 chest pain: for intermediate-high risk patients with stable chest pain and no known CAD, stress imaging (stress echocardiography, PET/SPECT MPI or CMR) is effective for diagnosis of myocardial ischaemia and for estimating risk of MACE (COR 1, LOE B-R).^[13]
• Once CCD is established, AHA/ACC 2023: in CCD with a change in symptoms or functional capacity persisting despite GDMT, stress PET/SPECT MPI, CMR or stress echocardiography is recommended to detect the presence and extent of myocardial ischaemia, estimate risk of MACE and guide therapeutic decision-making (COR 1, LOE B-NR).^[8]

Follow-up: Will a viability CMR tell you whether PCI helps a patient with an EF of 30%?^[3]

• ESC 2026 HF says evidence supporting viability testing to identify suitable patients for revascularisation is lacking.^[3]
• In the prespecified REVIVED-BCIS2 viability analysis (JAMA Cardiol 2023; prespecified secondary analysis of a prospective open-label randomised trial; 610 patients with LVEF ≤35%, extensive CAD and evidence of viability in at least 4 myocardial segments that were dysfunctional at rest; blinded core-laboratory CMR and dobutamine stress echo; median follow-up 3.4 years), there was no interaction between the extent of viable or nonviable myocardium and the effect of PCI on the primary outcome (the composite of all-cause death or hospitalisation for HF) or any secondary outcome, though the extent of nonviable myocardium, but not of viable myocardium, was associated with event-free survival.^[11]

Branch E — Safety

Examiner: The patient has a pacemaker and an eGFR of 45 mL/min/1.73 m². How do you proceed?^[9][1]

Strong answer:

• Check the whole system: ESC 2021 says the entire CIED system (generator and leads from the same manufacturer) determines MRI conditionality.^[9]
• ESC 2021 pacing rows: in patients with MRI-conditional pacemaker systems (an MRI-conditional generator and lead(s) from the same manufacturer), MRIs can be performed safely following the manufacturer's instructions (Class I, Level A); in patients with non-MRI-conditional pacemaker systems, MRI should be considered if no alternative imaging mode is available and if no epicardial, abandoned or damaged leads or lead adaptors/extenders are present (Class IIa, Level B); in pacemaker patients with abandoned transvenous leads, MRI may be considered if no alternative imaging modality is available (Class IIb, Level C).^[9]
• ESC 2025 myocarditis and pericarditis, in its CMR section: programming of the device before and after the scan is warranted in all cases, as well as patient monitoring.^[2]
• Kidney: ESC 2023 says gadolinium-based contrast agents can be safely administered with an eGFR >30 mL/min/1.73 m², which covers an eGFR of 45, and that nephrogenic systemic fibrosis is virtually unreported with newer linear or macrocyclic agents.^[1]
• For patients with severe renal impairment, ESC 2023 says non-contrast CMR modalities and mapping procedures are particularly valuable when assessing Anderson–Fabry disease and cardiac amyloidosis.^[1]