Dyssynchrony: a risk marker for ventricular arrhythmias?

Editorial

Mechanical left ventricular dyssynchrony can result from conduction system abnormalities like left bundle branch block (LBBB), scarring in the left ventricle from ischemic or non-ischemic cardiomyopathy, and significant left ventricular dilatation resulting in changes in gap junctions and ion channels thereby affecting conduction velocity. The end result of these processes is dyssynchronous contraction of the left ventricle, causing inefficient pump function. Resynchronization either by treatment of underlying pathology or cardiac resynchronization therapy (CRT) has been shown to improve mortality and morbidity in this patient population.1 4 In MADIT-CRT study, patients with LBBB who had improvement in their dyssynchrony with CRT were also less likely to experience ventricular arrhythmias compared to those who did not have an improvement.5 This raises the question if dyssynchronous contraction of the left ventricle is arrhythmogenic?

Dyssynchrony in patients with purely conduction system abnormality and no myopathy as seen in right ventricular pacing or LBBB with normal left ventricular structure and function does not seem to be associated with increased risk of arrhythmias.6,7 In the presence of abnormal substrate, several studies have showed increased risk of adverse cardiovascular outcomes in patients with dyssynchrony but data on arrhythmic events are less convincing.8 11 A sub-study of MADIT-CRT showed no difference in the occurrence of ventricular arrhythmias in patients undergoing CRT implantation with or without baseline dyssynchrony.10 In REVERSE trial there was no difference in occurrence of ventricular arrhythmias in patients with CRT ON vs CRT OFF implying resynchronization had little impact on occurrence of ventricular arrhythmias. The study population in this trial included patients with mild heart failure (NYHA classes I and II) with QRS greater than 120 ms and since there was no baseline assessment of dyssynchrony it is plausible that most of these patients did not have significant dyssynchrony to begin with.12 In the InSync ICD trial, there was reduction in ventricular arrhythmias, which was related to the degree of the remodeling after CRT implantation.13 Most of these studies used strain imaging to assess and quantify dyssynchrony, which, in itself is limited by temporal resolution of echocardiography.

In the current study, Saurabh et al studied the impact of dyssynchrony as assessed by phase analysis of gated SPECT on ventricular arrhythmias in patients undergoing CRT. There results showed that most ventricular arrhythmias occurred in patients with dyssynchrony and at least some degree of myocardial scarring. Reversal of dyssynchrony was seen in only few patients post CRT-implant and these patients had decreased risk of ventricular arrhythmias. There are several limitations of the study including small sample size, retrospective design, significantly poor response to CRT, and lack of effect on mortality despite higher incidence of ventricular arrhythmias. But in spite of these limitations, this study reaffirms the complex interaction between dyssynchrony and substrate. Myocardial fibrosis, change in myocardial fiber orientation and conduction properties as seen in significant LV dilation, may result in heterogeneous propagation of depolarization and thus induce or enhance mechanical dyssynchrony. Same heterogeneity also promotes reentry and thus increases the propensity to ventricular arrhythmias.

Assessment of mechanical dyssynchrony can thus help us in risk stratification of patients with abnormal substrate. Absence of mechanical dyssynchrony may identify patients with less severe structural changes and subsequently lower risk of cardiovascular events and ventricular arrhythmias. Improvement in dyssynchrony may indicate improving substrate and serve as a marker for reverse remodeling. Further studies are needed to assess the contribution of myocardial substrate to dyssynchrony. Dyssynchrony assessment in patients with right ventricular pacing or LBBB pre- and post-acute myocardial infarction may serve to better understand this complex interaction.

Notes

Declaration

I declare no conflict of interest.

References

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Copyright information

© American Society of Nuclear Cardiology 2017

Authors and Affiliations

  1. 1.Division of Cardiovascular DiseasesUniversity of Alabama at BirminghamBirminghamUSA

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