Hypertrophic Obstructive Cardiomyopathy
A 27-year-old man has exertional dyspnea and two episodes of near syncope while playing football. A harsh systolic murmur at the left sternal border increases with Valsalva. Echocardiography shows asymmetric septal hypertrophy of 19 mm, systolic anterior motion of the mitral valve, and a resting left ventricular outflow gradient of 60 mm Hg. What is the most appropriate initial therapy?
- A.Nifedipine
- B.Furosemide
- C.Digoxin
- D.MetoprololCorrect
Explanation
A non-vasodilating beta blocker such as metoprolol, bisoprolol, or atenolol is first line for symptomatic hypertrophic obstructive cardiomyopathy. The obstruction is dynamic: a hypertrophied septum narrows the outflow tract, and rapid ejection drags the anterior mitral leaflet into the tract through the Venturi effect, producing systolic anterior motion, a late peaking systolic murmur, and mitral regurgitation. The gradient worsens with anything that reduces preload or afterload or increases contractility, which is why the murmur intensifies with Valsalva and standing and softens with squatting and handgrip. Beta blockers help by slowing the heart rate, prolonging diastolic filling, increasing ventricular volume, and reducing contractility, all of which widen the outflow tract. Verapamil is the alternative when beta blockers are not tolerated, and disopyramide is added for persistent symptoms; myectomy or alcohol septal ablation is reserved for refractory symptoms with gradients of 50 mm Hg or more, and cardiac myosin inhibitors such as mavacamten are a newer option. Vasodilators including nifedipine, dihydropyridines generally, nitrates, and ACE inhibitors reduce afterload and increase the gradient, so they are contraindicated. Diuretics reduce preload and can precipitate syncope, and are used only cautiously for congestion. Digoxin increases contractility and worsens obstruction. Competitive sport restriction, family screening, and risk stratification for an implantable defibrillator, using septal thickness of 30 mm or more, unexplained syncope, family history of sudden death, and non-sustained ventricular tachycardia, are essential parts of care.
Why each option
- A.
- Nifedipine is a dihydropyridine vasodilator; reducing afterload increases the outflow gradient and can cause hemodynamic collapse in obstructive disease.
- B.
- Diuretics lower preload and reduce ventricular cavity size, which worsens obstruction and may precipitate syncope. They are used only cautiously for congestion.
- C.
- Digoxin is a positive inotrope; increasing contractility accentuates systolic anterior motion and the outflow gradient.
- D.
- Correct. Non-vasodilating beta blockers slow the heart rate, improve diastolic filling, and reduce contractility, relieving dynamic outflow obstruction.
Reference: AHA/ACC Guideline for the Management of Hypertrophic Cardiomyopathy, 2024
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