A Case Report of Short‐Coupled Ventricular Fibrillation Unmasked During Post‐Infarction Inflammatory Remodeling

ABSTRACT

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.