HCM is inherited in an autosomal dominant fashion, resulting from mutation in genes encoding
for myocardial contractile proteins of the cardiac sarcomere. Cardiac myosin-binding protein C
and cardiac beta-myosin heavy chain are most commonly affected, accounting for
approximately 40% and 30% of identifiable mutations, respectively. Affected patients often have
a recognizable family history of HCM but not always because sporadic mutations can occur
Mechanical prosthetic aortic valve can present with prosthetic valve dysfunction (PVD),
which most commonly occurs in the following forms:
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Paravalvular leak (regurgitation around the valve): more commonly with mechanical
(rather than bioprosthetic) valves and results from dehiscence of the valve from the aortic
or mitral annulus, often due to annular degeneration or underlying infective endocarditis.
Transvalvular regurgitation (regurgitation through the valve): more commonly affects
bioprosthetic (rather than mechanical) valves and can result from cusp degeneration or
occasionally valvular thrombus that impairs valve closure. Patients are often initially
asymptomatic but can develop severe heart failure; those with significant regurgitation
generally have a poor prognosis.
Diagnosis of exclusion
Ventricular aneurysm
Pulsus paradoxus can be seen in COPD and asthma
Nitrates cause vasodilation decreasing systemic vascular resistance
Coronary stent thrombosis is a serious complication of coronary stent placement that can occur
acutely (within 24 hours) or subacutely (within 30 days) or be delayed up to a year or more. The
risk is greatest prior to reendothelialization because exposed stent material is thrombogenic
Sarcoidosis cardiac manifestations
Aspirin is a common trigger for bronchoconstriction in patients with asthma, especially those
with concurrent chronic rhinitis and nasal polyps. Nonselective beta blockers (eg,
propranolol, nadolol, sotalol, timolol) act on β1 and β2 receptors and often trigger
bronchoconstriction in patients with underlying asthma. Cardioselective beta blockers (eg,
metoprolol, atenolol, bisoprolol, nebivolol) act predominantly on β1 receptors and are generally
considered safe in patients with mild-to-moderate asthma. However, all beta blockers can trigger
bronchoconstriction, especially when administered in large doses.
This medication-triggered bronchoconstriction can lead to a cough. In addition, ACE inhibitors
(eg, lisinopril) can cause dry cough through increased levels of circulating bradykinin and
resultant bronchial irritation. Onset of the cough can occur soon after ACE inhibitor initiation
(as is likely the case in this patient) or can be delayed (eg, months); it is not affected by
underlying asthma.