Overdrive pacing for ventricular fibrillation storm after myocardial infarction

Polymorphic ventricular arrhythmias (ventricular fibrillation and polymorphic ventricular tachycardia) are serious complications following myocardial infarction (MI). These arrhythmias should be recognized as a distinct arrhythmic entity with a specific pathophysiology, time course, and evolution, different from organized scar-related ventricular tachycardias.1–4 They represent a challenging situation due to the frequent progression to an arrhythmic storm, characterized by recurrent sustained ventricular arrhythmias (VAs) (>3 episodes/24 h).5 These storms are often refractory to conventional antiarrhythmic drugs,2–5 and therapeutic options are still limited. Quinidine has recently been reported as efficient,4 and catheter ablation is now increasingly proposed but remains complex and challenging.2,6 Overdrive pacing has been proposed to control arrhythmias in these cases, but clinical evidence for this therapeutic strategy remains limited to case reports.3–6 This multicentre retrospective study aimed at determining the effectiveness of overdrive pacing in post-MI polymorphic ventricular tachycardia and fibrillation storms. We retrospectively included patients from 5 French medical centres who presented post-MI arrhythmic storms between 2012 and 2023. Inclusion required an arrhythmic storm post-MI (<30 days) with attempted overdrive pacing. All patients experienced ventricular fibrillation or polymorphic ventricular tachycardia storms, triggered by short-coupled premature ventricular contractions (PVC). No additional ECG parameters were required. Overdrive pacing was performed using a temporary transvenous pacing lead, a temporary external pacemaker with an active lead, or by reprogramming a previously implanted device. Overdrive pacing attempts were initiated at the physicians’ discretion, following institutional protocols. Pacing frequency was set ∼40% above baseline rate, and gradually increased until PVC/VA disappearance. Positive response was defined as no arrhythmia recurrence during continuous pacing, excluding events triggered by pacing interruptions. Pacing-induced haemodynamic degradation was defined as a ≥10 mmHg drop in systolic blood pressure or a ≥10% reduction in left ventricular ejection fraction. The study was approved by the Institutional Review Board. Quantitative variables are presented as median [first–third quartile] or mean ± standard deviation. The impacts of prior treatment regimen (number of failed drugs/interventions before pacing), heart rate, and QTc on therapeutic success were assessed using logistic regression. Odds ratios (OR) are presented with 95% confidence intervals. A Wilcoxon signed rank test was used to compare number of shocks before and after overdrive. Significance level was set at 5%. Fifty-one patients met inclusion criteria. Baseline characteristics are presented in Figure 1. Arrhythmic storms began 8 [5; 11] days after MI diagnosis. Median revascularization time was 48.0 [8.5; 60.0] h. Patients’ characteristics and treatment prior to overdrive onset are detailed in Figure 1. Pacing was initiated after the failure of 2.8 ± 1.5 treatment regimens. Median electrical storm duration was 2.0 [1.0; 4.7] days. Mean overdrive pacing rate was 94.5 ± 9.3 b.p.m. and was maintained for 5.0 [3.0; 8.7] days, i.e. 3.7 days after arrhythmia control. Eighteen patients were stimulated in AAI mode, 23 in VVI, and 10 in DDD. Left: patient characteristics. OP, overdrive pacing; LCSD, left cardiac sympathetic denervation; SD, standard deviation; IQR, interquartile range; temp., temporary. Right: ECG tracings of arrhythmia onset and overdrive pacing ‘ON–OFF’ effect on VA recurrences. (A) Sinus rhythm, heart rate 55 b.p.m., QTc 426 ms, PVC coupling 320 ms, onset of ventricular fibrillation requiring immediate defibrillation. (B) Short-coupled PVC initiating non-sustained polymorphic ventricular tachycardia, ventricular pacing is immediately switched ‘on’ and suppressed PVC/VA recurrence. (C) Ventricular pacing is stopped, and immediate monomorphic short-coupled PVC recurrence is observed. A few seconds later, we observed ventricular fibrillation onset requiring immediate defibrillation Nine patients died from cardiovascular causes; 42 patients (82%) survived to discharge. Number of shocks after overdrive pacing onset was significantly reduced, (7 [4; 15] vs. 0 [0; 1]; P < .0001). Overdrive pacing effectively suppressed recurrent arrhythmias, with no on-treatment recurrence in 47 patients (92%). This response was not significantly modulated by the number of therapies prior to pacing initiation (OR: 0.93 [0.49–1.78]; P = .83). Neither heart rate (OR: 1.03 [0.96–1.12]; P = .37) nor QTc intervals (OR: 0.98; [0.95–1.02]; P = .33) were related to pacing response. Two patients died of refractory storm despite overdrive pacing, amiodarone, lidocaine, and deep sedation (prior to overdrive) and undergoing catheter ablation (after overdrive). Twenty-one patients (41%) had VA recurrence during pacing weaning attempts, which corresponded to transient pacing cessation or rate decrease. Seventeen patients received additional therapy after overdrive pacing initiation due to VA recurrence upon transient interruption: two patients received extracorporeal life support, one patient was sedated, and 14 patients underwent catheter ablation. Four patients presented pacing related haemodynamic degradation. We observed 10 lead-related complications, Figure 1. No iatrogenic pericardial effusion, vascular, or infectious complications were observed. After the storm, 28 patients (55%) received an implantable cardioverter-defibrillator. Two patients had been implanted prior to the event. Nine patients died before implantation; one underwent emergency heart transplantation. Eight were not implanted because VA started within 48 h after MI. Three either declined or were ethically ineligible for implantation. After a median follow-up of 393 [117; 645] days, which included remote monitoring of 30 patients (59%), only one patient had ventricular arrhythmia recurrence, more than a year after the initial event. This multicentre observational study is the first to review a population of post-MI ventricular fibrillation storms treated with overdrive pacing. Mortality appears lower than expected given the notorious severity of this clinical scenario,2,4 with overdrive pacing providing immediate arrhythmia control in the vast majority of patients. The arrhythmia phenotype in this cohort shares similarities with that already documented in quinidine responsive pseudo-torsade de pointes (TdP).4,7 ECG data resembled those associated with pseudo-TdP, featuring a slightly prolonged QT interval and short-coupled PVC (Figure 1). Despite the observed VA rate-dependence with frequent recurrences upon pacing rate reduction or interruption, the majority of patients exhibited normal baseline heart rates before VA appearance (Figure 1). This may suggest a broader therapeutic scope for overdrive pacing, beyond solely bradycardia/pause dependent arrhythmias. Notably, only a single patient failed quinidine treatment, and only two patients had failed stellate ganglion blockade prior to pacing initiation. Furthermore, the number of patients benefiting from deep sedation may seem relatively low given the severity of these storms. Our study underscores the efficiency of overdrive pacing for arrhythmia management in this context, and additional work must endeavour to identify the optimal treatment sequence from the available therapeutic arsenal. We noted that VA recurrences were very rare after discharge, even though a minority of patients underwent ablation. This suggests that arrhythmogenicity gradually disappears with myocardial healing and scar stabilization. Overdrive pacing therefore enables physicians to achieve acute control over arrhythmia recurrence and effectively ‘wait out the storm’ until recovery. This strategy limits the need for other invasive therapies, such as circulatory assistance or challenging emergency catheter ablation procedures. All authors declare no disclosure of interest for this contribution. The data that support the findings of this study are available from the corresponding author, upon reasonable request. All authors declare no funding for this contribution. The study was approved by our Institutional Review Board. None supplied.