Key result
Oral verapamil suppresses refractory short-coupled VF triggered by PVCs following acute MI.
Why the study?
Short-coupled ventricular fibrillation is traditionally characterized as an idiopathic syndrome in structurally normal hearts, but its emergence during subacute remodeling following acute myocardial infarction is rare.
Case Report (n=1)
Ultra-short-coupled premature ventricular contractions (<300 ms) can trigger lethal ventricular fibrillation during post-infarction inflammatory remodeling, which may be successfully suppressed by verapamil despite mildly reduced LVEF.
May warrant verapamil consideration in refractory post-MI short-coupled VF; extends phenotype beyond idiopathic cases but leaves open need for prospective trials.
This case illustrates the rare clinical emergence of the short-coupled ventricular fibrillation (SC-VF) phenotype during the subacute remodeling phase following acute myocardial infarction (AMI). Although SC-VF is traditionally characterized as an idiopathic syndrome occurring in structurally normal hearts, we report the case of a 49-year-old male who experienced sudden cardiac arrest 5 days after successful revascularization for an anterior ST-segment elevation myocardial infarction (STEMI). Despite documented coronary patency, the patient manifested an electrical storm of polymorphic ventricular tachycardia (PMVT) and VF, triggered by ultra-short-coupled premature ventricular contractions (PVCs) (coupling interval = 240 ms). The arrhythmia proved refractory to conventional lidocaine therapy. However, prompt recognition of the SC-VF phenotype facilitated the cautious administration of verapamil-notwithstanding a mildly reduced left ventricular ejection fraction (LVEF 43%)-which successfully suppressed the rhythmic instability. Following the implantation of an implantable cardioverter-defibrillator (ICD) for secondary prevention, this case suggests that post-AMI inflammatory remodeling is temporally associated with the unmasking of latent electrophysiological vulnerabilities. Ultimately, the detection of an ultra-short coupling interval (< 300 ms) serves as a pivotal clinical marker for transitioning from standard sodium channel blockade to mechanism-driven calcium channel antagonism.
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Zhao et al. (2026) conducted a case report in Short-coupled ventricular fibrillation post-AMI (n=1). Verapamil was evaluated on Suppression of ventricular fibrillation. Verapamil successfully suppressed refractory short-coupled ventricular fibrillation triggered by ultra-short-coupled premature ventricular contractions following an acute myocardial infarction.
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