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

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.