Key result
Increased verapamil linked to cardiogenic shock and a ~33% LVEF drop in obstructive HCM.
Why the study?
Verapamil is commonly used to treat symptomatic hypertrophic cardiomyopathy, but its potential for adverse effects needs to be recognized.
Does verapamil toxicity cause haemodynamic compromise in patients with obstructive hypertrophic cardiomyopathy?
Case Report (n=1)
No
Does verapamil toxicity cause haemodynamic compromise in patients with obstructive hypertrophic cardiomyopathy?
Verapamil toxicity in patients with obstructive hypertrophic cardiomyopathy can cause cardiogenic shock and acute decline in LV systolic function, highlighting the need for careful dosage monitoring.
Verapamil escalation may precipitate cardiogenic shock in obstructive HCM; this case leaves open questions of risk magnitude and generalizability.
Background Hypertrophic cardiomyopathy (HCM) is an inherited condition characterized by left ventricular (LV) hypertrophy unexplained by increased afterload, often with concomitant outflow tract obstruction. Verapamil is commonly used to treat symptomatic patients. However, its potential for adverse effects should be recognized. Case summary This report provides a case of cardiogenic shock in HCM, where a patient presented with chief complaint of fatigue and shortness of breath with an acute decline in LV systolic function on echocardiogram. His symptoms were attributed to verapamil toxicity following a recent increase in dosage. He achieved rapid symptom relief after holding his home medications, in addition to conservative management. Discussion This case report aims to elucidate the potential for multiple adverse effects involved with verapamil use in patients with obstructive HCM.
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Gau et al. (2024) conducted a case report in Obstructive hypertrophic cardiomyopathy (n=1). Verapamil was evaluated on Cardiogenic shock and decline in left ventricular systolic function. In a 34-year-old man with obstructive hypertrophic cardiomyopathy, an increased dose of verapamil led to cardiogenic shock and an acute decline in left ventricular ejection fraction from 68% to 35%.
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