A 62-year-old woman with HFrEF and rate-controlled atrial fibrillation is prescribed verapamil for rate control. Over the following weeks her dyspnea worsens and echocardiography shows a drop in ejection fraction. The most likely explanation is:

• A Verapamil-induced fluid retention via aldosterone activation
• B Verapamil's pronounced negative inotropic effect from cardiac calcium channel blockade ✓
• C Reflex sympathetic activation raising myocardial oxygen demand
• D Verapamil-induced bradycardia reducing cardiac output despite preserved contractility

Explanation

Non-dihydropyridine calcium channel blockers such as verapamil and diltiazem depress sinoatrial and atrioventricular nodal function and also exert significant negative inotropy by blocking L-type calcium channels in working ventricular myocytes. In HFrEF this depresses contractility and can precipitate overt worsening of failure, so these drugs are avoided in reduced ejection fraction. Dihydropyridines like amlodipine spare the myocardium and produce reflex tachycardia instead, which is the opposite hemodynamic pattern.

Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th ed.

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Written and medically reviewed by the StethoPrep medical team.