Rapid Review·Cardiovascular

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PATHOLOGY

T2High yield

Cardiomyopathies & Myocarditis

FA P314-315, 320

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concentric hypertrophy, the pressure-overload pattern.
eccentric hypertrophy, the volume-overload pattern with a dilated, thin-walled chamber.
"Titin is thin, myosin is more": titin gives dilated, myosin gives hypertrophic.
the most common, about 90% of cases. Often idiopathic or familial, from a TTN mutation shortening titin.
drugs (alcohol, cocaine, doxorubicin), infection (coxsackie B, Chagas, so ask where the patient has lived), ischemia (CAD), systemic disease (hemochromatosis, sarcoidosis, thyrotoxicosis, wet beriberi), and peripartum cardiomyopathy, during or shortly after pregnancy. In Chagas the usual cause of death is sudden cardiac death from ventricular arrhythmia.
heart failure, S3, systolic regurgitant murmur, dilated heart on echo (large LV cavity, low EF, normal or thin wall), balloon appearance on CXR. Systolic dysfunction with eccentric hypertrophy.
where balanced enlargement physiologically supports a higher stroke volume.
sodium restriction, ACE inhibitors or ARBs, beta-blockers, sacubitril/valsartan, diuretics, spironolactone, ICD, transplant.
the second most common cardiomyopathy, and the most common cause of sudden cardiac death in athletes and teenagers. 60 to 70% familial, autosomal dominant, from sarcomeric mutations in beta-myosin heavy chain or myosin-binding protein C. Also from chronic hypertension and Friedreich ataxia.
syncope during exercise, and a risk of sudden death in young athletes from ventricular arrhythmia.
S4, systolic murmur, sometimes mitral regurgitation from impaired mitral closure. Diastolic dysfunction with concentric hypertrophy, often septal; on echo a small LV cavity with a normal EF and a thick wall. Histology shows myofibrillar disarray and fibrosis.
the subset where the LV outflow tract is obstructed by asymmetric septal hypertrophy plus systolic anterior motion of the mitral valve, with a bifid carotid pulse.
the aim is to keep the LV full (high preload, low heart rate, low contractility). Beta-blockers or a nondihydropyridine calcium channel blocker (verapamil) lengthen diastolic filling and raise end-systolic volume; mavacamten if refractory; stop high-intensity athletics; ICD if high risk. AVOID anything that lowers preload (diuretics, vasodilators), because a smaller ventricle worsens the obstruction.
  • Postradiation fibrosis
  • Löffler endocarditis, from hypereosinophilic syndrome with eosinophilic myocardial infiltrates
  • Endocardial fibroelastosis, thick fibroelastic endocardium in young children
  • Amyloidosis
  • Sarcoidosis
  • Hemochromatosis
diastolic dysfunction from reduced compliance; echo shows a normal cavity, a normal or thick wall, and a preserved EF. The giveaway is a low-voltage ECG despite a thick myocardium, classically in amyloidosis.
the cardiac changes of athletic training, which differ by the kind of training.
inflammation of the myocardium, and a major cause of sudden cardiac death in adults under 40.
dyspnea, chest pain, fever, arrhythmias. Persistent tachycardia out of proportion to the fever is characteristic. A young patient who develops heart failure after a viral prodrome (fever, congestion, myalgias) has viral myocarditis until proven otherwise.
sudden death, arrhythmias, heart block, dilated cardiomyopathy, heart failure, mural thrombus with systemic emboli.

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Sarcomere geometry and the ventricular cross-section it produces. Top: the normal sarcomere with Z disks, I band, A band and H zone, beside a normal ventricular wall. Middle: sarcomeres added in parallel thicken the wall inward, giving concentric hypertrophy (the pressure-overload pattern of hypertrophic cardiomyopathy and hypertension). Bottom: sarcomeres added in series lengthen the fibre, giving eccentric hypertrophy with a dilated chamber and thin wall (the volume-overload pattern of dilated cardiomyopathy).

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Endomyocardial fibrosis with prominent eosinophilic infiltrate is associated with which type of endocarditis?

(...) endocarditis

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