Blog Highlight: Effect of Biventricular Pacing on Ventricular Tachycardia and Ventricular Fibrillation

Blog by Timm Dickfeld, MD, PhD Chief of Electrophysiology at the VA Baltimore, Associate Professor of Medicine at the University of Maryland, and Founder of the Maryland Arrhythmia and Cardiology Imaging Group (MACIG) Baltimore, Maryland
Blog by Timm Dickfeld, MD, PhD Chief of Electrophysiology at the VA Baltimore, Associate Professor of Medicine at the University of Maryland, and Founder of the Maryland Arrhythmia and Cardiology Imaging Group (MACIG) Baltimore, Maryland

So finally, what is the effect of biventricular (BiV) pacing on VT and VF?

Most electrophysiologists can remember a case or two in which biventricular pacing significantly reduced the amount of ventricular tachycardia. However, while several studies suggested an antiarrhythmic effect, other reports questioned if the dispersion of repolarization and the prolongation of the QT interval associated with BiV pacing may actually have proarrhythmic effects. A recent analysis from the MADIT-CRT investigators1 shed new light on this clinical conundrum.

In the MADIT-CRT study, 1,820 patients with ischemic or non-ischemic cardiomyopathy (EF <30%), NYHA class I–II and a QRS duration of >130ms were randomized to either BiV-ICD or ICD implantation with a 3:2 randomization. Based on the reduction of the left ventricular end-systolic volume (LVESV) at 1 year, the patients were divided into high responders with >25% reduction (n=529), low responders with <25% reduction in LVESV, apart from the “regular” ICD patients (n=623).

During the two-year follow-up, 13% of patients experienced ventricular arrhythmia after a median time of 1.24 years. Using a categorical analysis, ventricular arrhythmias were most likely in low responders (28%), less frequent in ICD-only patients (21%), and least likely in high responders to BiV pacing (12%) with a p-value of <0.001. In a continuous analysis, each incremental 10% reduction of LVESV reduced the risk of subsequent ventricular arrhythmia by about 20%.

First, the good news: 71% were high responders with a significant reduction of the LVESV. It appears that there is a close correlation between the mechanical and the electrical improvement and that the reduction in HF seems to go hand-in-hand with a decrease in ventricular arrhythmia. However, these positive effects were only seen in patients with positive response to BiV pacing. Therefore, a good response to resynchronization therapy seems to be critical. No information was available in the study about lead placement, but it is reasonable to conclude that every effort should be made in achieving the best possible CS lead location.

The million dollar question is, of course, if those results also apply to patients with class III and IV heart failure symptoms. Unfortunately, this study cannot answer the question, but this question will have to be answered in upcoming trials. For now, one may have to assume that the same observations hold true for more advancing stages of HF.

Interestingly, there was a trend for more ventricular arrhythmias in the low responders versus the ICD patients, raising the question if resynchronization therapy might indeed be proarrhythmic in this subgroup. MADIT-CRT has identified several predictors of high clinical response such as female gender, left bundle branch block, a wider QRS and non-ischemic CMP. Clearly, we should use those clinical criteria — and others that will come forward — for careful patient selection to minimize the group of low responders. My personal feeling is that those will also be eventually reflected in the BiV guidelines to allow an even more tailored approach to BiV implantation.

Reference

  1. Barsheshet A, Wang PJ, Moss AJ, et al. Reverse remodeling and the risk of ventricular tachyarrhythmias in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy). J Am Coll Cardiol 2011;57:2416-2423.