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.

Key Clinical Message

• Post‐infarction inflammatory remodeling is temporally associated with the onset of short‐coupled VF (SC‐VF).

• Recognizing ultra‐short coupling intervals (< 300 ms) on ECG is a critical diagnostic clue.

• Verapamil effectively suppresses this lidocaine‐refractory arrhythmic phenotype.

• Definitive long‐term management mandates ICD implantation.

1. Introduction

Ventricular arrhythmias remain a primary driver of mortality following acute myocardial infarction (AMI) [1]. Although ischemia‐induced reentrant tachycardia is the most recognized mechanism [2], distinct electrophysiological phenotypes often emerge during the subacute phase of infarction. One such phenotype, short‐coupled ventricular fibrillation (SC‐VF), is characterized by ultra‐short premature ventricular contraction (PVC) coupling intervals (< 300 ms). Notably, SC‐VF is traditionally regarded as an idiopathic condition occurring in structurally normal hearts [3, 4]; however, its manifestation in the context of structural damage is rare. Herein, we report a unique case of SC‐VF triggered not by acute primary ischemia, but by the inflammatory remodeling phase post‐infarction.

2. Case History/Examination

A 49‐year‐old male with a history of hypertension and type 2 diabetes presented with acute‐onset chest pain. The electrocardiogram (ECG) demonstrated an acute anterior STEMI (Figure 1A), with a peak troponin I of 7.731 μg/L. Emergency coronary angiography revealed a proximal occlusion of the left anterior descending (LAD) artery and a chronic total occlusion of the right coronary artery (RCA) (Figure 2A,B). Primary percutaneous coronary intervention (PCI) was performed, successfully restoring TIMI 3 flow in the LAD (Figure 2C). Post‐procedural echocardiography revealed a dilated left ventricle (66 mm) with an LVEF of 43%.

FIGURE 1.

Patient's Electrocardiogram (ECG) Recordings. (A) 12‐lead ECG on admission, showing acute anterior ST‐segment elevation. (B) Cardiac monitoring strip on post‐procedure Day 5, showing ventricular bigeminy. (C) Cardiac monitoring strip during cardiac arrest, showing a short‐coupled PVC triggering Torsades de Pointes, which degenerated into ventricular fibrillation, followed by conversion to sinus rhythm after defibrillation. (D) Magnified rhythm strip showcasing the critical “R‐on‐T” phenomenon. The red arrow indicates the triggering extrasystole, and the red calipers highlight the ultra‐short coupling interval of 240 ms. Note the normal QT interval preceding the extrasystole, distinguishing this from pause‐dependent Long QT syndromes. (E) 12‐lead ECG at discharge, showing the evolution of the anterior myocardial infarction.

FIGURE 2.

Patient's Coronary Angiography and Device Images. (A) Acute occlusion in the proximal‐mid Left Anterior Descending (LAD) artery. (B) Chronic total occlusion of the proximal Right Coronary Artery (RCA) with collateral circulation. (C) Restoration of TIMI grade 3 flow in the LAD after stent implantation. (D) Chest X‐ray confirming single‐chamber ICD lead placement in the right ventricular apex.

The patient was stabilized on a regimen of dual antiplatelet therapy, high‐intensity statins, and sacubitril/valsartan. However, on post‐procedural Day 5, telemetry captured the sudden onset of PMVT rapidly degenerating into VF, necessitating emergency defibrillation. The inciting event was an ultra‐short‐coupled PVC with a coupling interval of 240 ms, occurring near the peak of the preceding T‐wave (the “R‐on‐T” phenomenon) (Figure 1B–D). Morphologically, as recorded on the telemetry strip, the triggering PVC exhibited a wide, predominantly positive complex (tall R wave) in lead II. This morphology indicates a superior‐to‐inferior depolarization vector, strongly suggesting an origin from the anterior or anteroseptal region. Crucially, this anatomical origin aligns topographically with the ischemic border zone of the patient's anterior STEMI.

3. Differential Diagnosis, Investigations, and Treatment

Reversible and alternative causes of polymorphic ventricular tachycardia (PMVT) were systematically evaluated and excluded. Acute ischemia‐induced PMVT was deemed highly unlikely, as the patient reported no recurrent angina, the ST segments remained stable, and the LAD stent was confirmed to be patent. Furthermore, reperfusion‐related ventricular arrhythmia typically occurs within the first 48 h following revascularization; in contrast, our patient's electrical storm manifested abruptly on Day 5. Electrolytes, including serum potassium (4.9 mmol/L) and magnesium (1.07 mmol/L), were within physiological ranges. The QTc interval was normal (420 ms), effectively excluding Long QT Syndrome‐related arrhythmias. Consequently, the delayed presentation, combined with the distinctive ultra‐short coupling interval, pointed toward a Purkinje‐related trigger unmasked during the subacute post‐infarction period. Notably, CRP levels peaked at 72.63 mg/L on Day 6, closely aligning with the onset of the electrical storm (Table 1).

TABLE 1.

Dynamic changes of key laboratory parameters during hospitalization.

Parameter	Day 0 (Emergency/Pre‐PCI)	Day 1 (Post‐PCI/ICU admission)	Day 6 (Post‐cardiac arrest/Peak inflammation)	Day 16 (Pre‐discharge)
hs‐cTnI (μg/L)	5.912	7.731	2.555	0.222
BNP (pg/ml)	1030.50	1552.61	2217.0 (NT‐proBNP)	552.73
K+ (mmol/L)	4.1	4.5	3.7	4.9
Mg2+ (mmol/L)	—	0.77	1.04	1.07
CRP (mg/L)	—	19.28	72.63	22.17
Scr (μmol/L)	99	86	102	108

Note: Serum Mg²⁺ and CRP levels were not routinely assessed during the initial emergency admission (Day 0) for acute ST‐segment elevation myocardial infarction. The initial value for hs‐cTnI represents the peak level recorded on Day 1.

Abbreviations: BNP, Brain Natriuretic Peptide; CRP, C‐Reactive Protein; hs‐cTnI, High Sensitivity Cardiac Troponin I; Scr, Serum Creatinine.

Following initial defibrillation, lidocaine was administered (1.5 mg/kg bolus followed by 2 mg/min maintenance). However, the patient remained recalcitrant, experiencing three additional self‐terminating episodes of SC‐VF. Recognizing the short‐coupled phenotype and its association with calcium‐dependent triggered activity, the clinical team initiated oral verapamil (40 mg q8h) under close hemodynamic monitoring. Metoprolol was temporarily suspended to mitigate the risk of bradycardia. Within 12 h of verapamil initiation, the PVC burden decreased significantly, with no further episodes of SC‐VF. Given the malignant nature of the arrhythmia and adherence to guideline [5], a single‐chamber ICD was implanted (Figure 2D).

4. Conclusion and Results

At the 3‐month follow‐up, the patient remained stable on a combined regimen of verapamil, metoprolol, and guideline‐directed medical therapy (GDMT). The patient reports clear symptomatic improvement and is satisfied with the outcome.

5. Discussion

This case illustrates an atypical manifestation of SC‐VF during the subacute phase of AMI. While SC‐VF is traditionally defined as an idiopathic arrhythmia occurring in structurally normal hearts, our findings suggest that the pathophysiological milieu post‐MI can interact with a pre‐existing electrophysiological substrate to facilitate lethal arrhythmias.

5.1. The “Two‐Hit” Pathophysiological Model

To explain this phenomenon, we propose a “Two‐Hit” hypothesis. The “first hit” likely involves a latent, subclinical vulnerability within the Purkinje network, such as an undetected channelopathy or microstructural abnormality [6]. The “second hit” was the physiological stress of the transmural anterior wall MI, which served as the critical trigger.

Notably, the electrical storm did not manifest during the acute reperfusion phase; instead, it emerged on Day 5. This onset closely preceded the peak inflammatory response, as indicated by a C‐reactive protein (CRP) level of 72.63 mg/L on Day 6. While we propose this “Two‐Hit” pathophysiological model, we acknowledge that the causal relationship between inflammatory remodeling and the onset of SC‐VF remains inferential rather than definitively proven. However, this strong temporal correlation suggests that border‐zone remodeling and mechanical stretch—potentially mediated by pro‐inflammatory cytokines such as IL‐6 or TNF‐α may have significantly lowered the threshold for triggered activity, thereby unmasking the previously silent SC‐VF substrate [7].

5.2. Electrophysiological Mechanisms and Differential Diagnosis

From an electrophysiological perspective, the electrical storm was initiated by an ultra‐short‐coupled PVC (240 ms) and exhibited a morphology resembling Torsades de Pointes (TdP). Although a full 12‐lead ECG was not obtainable during the hemodynamic collapse, the telemetry recordings (Figure 1B–D) captured a wide, predominantly positive complex in lead II during the triggering PVC, indicating a superior‐to‐inferior depolarization vector. Crucially, when correlated with the standard 12‐lead ECGs (Figure 1A,E) which unequivocally localize the structural damage to the anterior wall, this specific vector strongly points toward an origin within the anterior or anteroseptal region. This topographical concordance provides robust clinical evidence for our hypothesis: the localized inflammatory remodeling at the infarct border zone acted as the precise pro‐arrhythmic substrate, unmasking the latent vulnerability of the local Purkinje network and triggering the electrical storm. However, because the patient's QTc interval was within normal limits, the arrhythmia is more accurately classified as PMVT triggered by SC‐PVCs.

Regarding cellular mechanisms, while calcium‐dependent early afterdepolarizations (EADs) are considered the primary drivers, delayed afterdepolarizations (DADs) or Phase 2 reentry cannot be definitively excluded without invasive mapping. Nevertheless, the clinical response serves as a diagnostic surrogate: the failure of lidocaine strongly suggests that the arrhythmia was not driven by conventional sodium‐channel‐dependent ischemic reentry [8], which typically characterizes the acute phase of MI.

5.3. Therapeutic Dilemma and the Rationale for Verapamil

The clinical management of this patient presented a significant therapeutic paradox. Given the patient's mildly reduced LVEF (43%) and ventricular dilation, non‐dihydropyridine calcium channel blockers are generally contraindicated due to their negative inotropic effects. However, the therapeutic decision to administer verapamil involved a critical risk–benefit assessment. The patient was experiencing a lethal, lidocaine‐refractory electrical storm. We reasoned that the immediate risk of sudden cardiac death from recurrent VF far outweighed the potential risk of transient hemodynamic compromise. Previous reports have demonstrated the unique efficacy of verapamil in suppressing Purkinje‐related PMVT and SC‐VF by blunting calcium‐dependent triggered activity [9, 10].

By inhibiting L‐type calcium channels, verapamil directly suppresses the triggers of SC‐VF. Under strict hemodynamic monitoring, the rapid and sustained suppression of the arrhythmia following verapamil administration corroborates the dominance of calcium‐mediated triggered activity in this specific phenotype [11]. This justifies its cautious emergency use as a salvage therapy even in the setting of moderate structural dysfunction, while it is traditionally avoided in HFrEF [12].

5.4. Limitations

Despite the clinical success, this report has inherent limitations. First, due to hemodynamic instability, high‐density electrophysiological mapping was not performed, which prevented the definitive localization of the trigger to the Purkinje system. Second, genetic screening for SC‐VF‐associated variants, such as DPP6 or RYR2 [13], was unavailable; consequently, a definitive genetic predisposition could not be confirmed.

5.5. Conclusion

SC‐VF may present as a rare but fatal complication during the remodeling phase of myocardial infarction. Clinical recognition of ultra‐short coupling intervals (< 300 ms) is life‐saving, as it necessitates a strategic shift from traditional sodium channel blockers (lidocaine) toward mechanism‐oriented calcium channel blockade (verapamil), followed by ICD implantation for definitive secondary prevention.

Author Contributions

ZiYu Zhao: conceptualization, investigation, visualization, writing – original draft, writing – review and editing. Ming Ni: investigation, writing – original draft, writing – review and editing. Bo Li: investigation, resources, writing – review and editing. Songhua Li: conceptualization, project administration, supervision, validation, writing – review and editing.

Funding

The authors have nothing to report.

Consent

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor‐in‐Chief of this journal.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.