Loperamide Toxicity Revealing Apical Hypertrophic Cardiomyopathy

Abstract

Loperamide, a μ-opioid receptor agonist, can cause cardiotoxicity by inhibiting the potassium ion channel and slowing cardiomyocyte repolarization. This, in turn, can lead to frequent early afterdepolarizations, the most common mechanism of drug-induced long QT syndrome and torsades de pointes. Apical hypertrophic cardiomyopathy (AHCM) is a nonobstructive hypertrophic cardiomyopathy rarely associated with malignant arrhythmias. We present a case of loperamide-induced malignant ventricular arrhythmia revealing underlying AHCM in a 25-year-old woman with a history of sudden cardiac arrest (SCA) and opioid use. It is important to evaluate for structural heart disease in all patients presenting with SCA, regardless of presumed etiology such as drug-induced cardiotoxicity, to prevent missed opportunities for adequate treatment. Furthermore, the diagnosis of AHCM in SCA warrants further genetic evaluation for variances with a predilection for malignant arrhythmias.

Keywords: apical hypertrophic cardiomyopathy; loperamide; structural heart disease; sudden cardiac arrest; ventricular tachycardia.

Figure 1.

A 12-lead electrocardiogram showing giant, inverted T waves (> 10 mm) in V4-V6 and QT interval prolongation (QTc = 506 ms)

Figure 2.

Cardiac magnetic resonance imaging demonstrating localized apical hypertrophy and the “ace of spades” sign at end-diastole (arrow). Maximum left ventricular (LV) wall thickness is 19 mm in the anteroseptal segment. Focal late gadolinium enhancement is seen in the apical, septal, and basolateral walls with total scar burden involving 6% of LV mass.

Figure 3.

A 12-lead electrocardiogram showed a corrected QT interval measuring 463 ms and the same inverted T-waves in the anterolateral leads.