Increased mechanical dispersion, with risk thresholds of 50 to 90 ms, consistently identifies higher arrhythmic risk in dilated and non-dilated left ventricular cardiomyopathy independent of LVEF.
Does mechanical dispersion predict ventricular arrhythmias and sudden cardiac death in patients with dilated and non-dilated left ventricular cardiomyopathy?
Mechanical dispersion derived from speckle-tracking echocardiography may enhance sudden cardiac death risk stratification in dilated and non-dilated left ventricular cardiomyopathy beyond conventional markers.
Background: Sudden cardiac death (SCD) is a major challenge in dilated (DCM) and non-dilated left ventricular cardiomyopathy (NDLVC). Current management strategies, based on left ventricular ejection fraction (LVEF), the presence or extent of myocardial scar, and selected high-risk genetic variants, are insufficient to accurately identify patients at risk. Mechanical dispersion (MD), derived from speckle-tracking echocardiography, is a potential marker of arrhythmic risk that reflects variability in regional myocardial contraction timing. Aim: The purpose of this narrative review is to synthesize current evidence on the predictive role of MD for ventricular arrhythmias (VA) and SCD in DCM and NDLVC, with particular emphasis on its relationship to myocardial fibrosis (MF) and established echocardiographic markers. Results: Across prospective and retrospective cohorts of DCM patients, increased MD has consistently identified individuals at higher arrhythmic risk, often independently of LVEF and global longitudinal strain (GLS). Reported threshold values for risk prediction range from 50 ms to 90 ms, with hazard ratios confirming incremental prognostic accuracy. The relationship between MD and MF assessed by late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) remains uncertain: some patients experience VA in the absence of LGE, while others display elevated MD despite no detectable focal MF, suggesting that additional mechanisms contribute to the arrhythmogenic substrate in DCM and NDLVC. Conclusions: MD may enhance SCD risk stratification in DCM and NDLVC by reflecting components of the arrhythmic substrate that are not detected by conventional markers.
Hart-Foia et al. (2026) studied this question. Increased mechanical dispersion, with risk thresholds of 50 to 90 ms, consistently identifies higher arrhythmic risk in dilated and non-dilated left ventricular cardiomyopathy independent of LVEF.