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Q1: Definition, causes and pathophysiology (3 min)
- Define myocarditis and inflammatory cardiomyopathy. How are they related (WHO/ISFC 1995)?
- Name the commonest viral cause and the receptor it uses to enter the cardiomyocyte.
- Walk me through the three-phase model of viral myocarditis. What cleaves dystrophin, and why does the ECG/troponin mimic MI?
Expected. Myocarditis = inflammatory disease of myocardium confirmed by histological (Dallas), immunological and immunohistochemical criteria; inflammatory cardiomyopathy = myocarditis with ventricular dysfunction. Commonest viral cause: coxsackievirus B3 (uses the CAR coxsackievirus-adenovirus receptor with DAF co-receptor). Three phases: (1) acute injury — viral entry via CAR, replication, proteases 2A and 3C cleave dystrophin, myocyte necrosis and troponin leak; (2) immune — innate (NK, macrophages, IFN via TLR3/TLR4, NLRP3 inflammasome) then adaptive (CD8+ T cells, anti-cardiac myosin autoantibodies by molecular mimicry); (3) chronic — viral persistence and adverse remodelling to dilated cardiomyopathy in 5–10%.
Q2: Diagnosis and investigations (3 min)
- A young adult has chest pain, raised troponin, ST changes and normal coronaries. How do you make the diagnosis?
- Reproduce the Lake Louise Criteria (2009 original and 2018 update).
- When is endomyocardial biopsy indicated, and what does the Dallas criteria report?
Expected. Syndromic diagnosis after excluding obstructive CAD (coronary angiography); confirm with cardiac MRI using Lake Louise Criteria. 2009: 2 of 3 (regional wall motion, T2 oedema ≥ 1.8 ratio or T2 ≥ 59 ms, non-ischaemic LGE — mid-wall/subepicardial, inferolateral). 2018: at least one T2-based AND one T1-based criterion (T1/T2 mapping ≥ 2 SD above normal, increased ECV, or non-ischaemic LGE). EMB indicated when it changes management — fulminant/rapidly progressive HF, sustained VT or high-grade AV block (suspect giant cell), refractory shock for MCS/transplant, suspected eosinophilic/drug. Dallas: active (infiltrate + necrosis) vs borderline (infiltrate only).
Q3: Management and subtypes (3 min)
- Outline the management of a typical case of lymphocytic viral myocarditis. Which drug class must you NOT use, and why?
- When IS immunosuppression indicated? Name the regimen for giant cell myocarditis and the trial that informs the lymphocytic decision.
- What is the fulminant paradox?
Expected. Supportive heart-failure therapy (ACEi/ARNI, beta-blocker once stable, MRA, loop diuretic), telemetry, no competitive sport for 3–6 months. Avoid NSAIDs — they worsen inflammation and outcomes in myocarditis. Immunosuppression only for giant cell, eosinophilic/hypersensitivity and sarcoid myocarditis; giant cell: cyclosporine + corticosteroids (transforms survival from median 11 months to several years). The Myocarditis Treatment Trial (Mason 1995) showed no benefit of immunosuppression in lymphocytic myocarditis. Fulminant paradox (McCarthy NEJM 2000): fulminant myocarditis has BETTER long-term transplant-free survival than non-fulminant (93% vs 45% at 11 years) if supported through the acute phase.
Q4: Return-to-play and pitfalls (2 min)
- An athlete has recovered from myocarditis. What are the return-to-play criteria?
- Name three classic pitfalls in managing myocarditis.
Expected. Return-to-play after 3–6 months requires all five: (1) asymptomatic, (2) normal biomarkers (troponin, BNP), (3) normal/stable ECG with no new arrhythmia on Holter, (4) normal biventricular systolic function on echo/CMR, (5) no significant arrhythmia on exercise and ambulatory monitoring. Pitfalls: giving NSAIDs; missing giant cell myocarditis by not biopsying fulminant/arrhythmic presentations; failing to restrict activity for 3–6 months; giving immunosuppression to typical lymphocytic myocarditis; not stopping clozapine in eosinophilic myocarditis.