Heart failure, cardiomyopathy and pericardial disease
Heart Failure and Cardiomyopathy
Core concepts
Heart failure is a syndrome, not a single ejection fraction. HFrEF benefits from four medication pillars: ARNI, ACE inhibitor, or ARB; an evidence-based beta blocker; an MRA; and an SGLT2 inhibitor, plus diuretics for congestion. HFmrEF and HFpEF require treatment of congestion and comorbidities, and SGLT2 inhibitors have benefit across the spectrum. Identify reversible causes such as ischemia, tachycardia, thyroid disease, alcohol, toxins, infiltrative disease, and valvular disease. Cardiomyopathy classification includes dilated, hypertrophic, restrictive, arrhythmogenic, and peripartum forms. Cardiac amyloidosis is suggested by discordant wall thickness, low voltage, carpal tunnel syndrome, and elevated troponin with preserved EF.
Question traps
Do not equate diastolic dysfunction on echocardiography with clinical HFpEF. Natriuretic peptides are aides, not rules: obesity lowers them, while AF, renal failure, and age raise them. Initiating or increasing beta blockade requires clinical stabilization and assessment of perfusion, congestion, blood pressure and contraindications. Do not turn the presence of congestion into an automatic rule to stop every established beta blocker. Device questions hinge on EF, QRS duration and morphology, NYHA class, and duration of optimal medical therapy. Do not miss infiltrative disease before prescribing vasodilators.
Worked example / rule of thumb
A 62-year-old with EF 30%, NYHA II symptoms, LBBB with QRS 155 ms, and three months of optimized GDMT is a CRT candidate. If QRS is 130 to 149 ms, benefit is less certain. Rule: optimize four pillars, confirm persistent symptoms, then consider devices.
Pericardial and Myocardial Disease
Core concepts
Pericardial disease includes acute pericarditis, pericardial effusion, tamponade, and constrictive pericarditis. Myocardial disease includes myocarditis, stress cardiomyopathy, infiltrative disease, sarcoidosis, and toxin-related injury. Acute pericarditis is diagnosed by two of four criteria: chest pain, friction rub, diffuse ST elevation or PR depression, and new effusion. Tamponade physiology includes hypotension, elevated JVP, pulsus paradoxus, and echocardiographic right-heart collapse. Constrictive pericarditis causes right-heart failure, a pericardial knock, and septal bounce.
Question traps
Do not label diffuse ST elevation as STEMI without considering pericarditis; reciprocal ST depression is uncommon in pericarditis. Pulsus paradoxus is not specific. Myocarditis can mimic MI with troponin release and normal coronaries. Stress cardiomyopathy often follows physical or emotional stress and has regional wall-motion abnormalities beyond a single coronary territory. Avoid NSAIDs in myocarditis with significant LV dysfunction.
Worked example / rule of thumb
A young patient with pleuritic chest pain, diffuse ST elevation, and PR depression is treated for acute pericarditis with NSAIDs and colchicine after risk stratification. Rule: diffuse ST elevation plus PR depression favors pericarditis; focal ST elevation with reciprocal changes favors ischemia.