Mechanical Dispersion and Global Longitudinal Strain Improve Risk Stratification of Malignant Ventricular Arrhythmias and Sudden Cardiac Death Over Ejection Fraction Alone

2018 ◽  
Vol 27 ◽  
pp. S56
Author(s):  
R. Perry ◽  
S. Patil ◽  
M. Horsfall ◽  
C. Marx ◽  
D. Chew ◽  
...  
2021 ◽  
Vol 17 ◽  
Author(s):  
Issa Pour-Ghaz ◽  
Mark Heckle ◽  
Ikechukwu Ifedili ◽  
Sharif Kayali ◽  
Christopher Nance ◽  
...  

: Implantable cardioverter-defibrillator (ICD) therapy is indicated for patients at risk for sudden cardiac death due to ventricular tachyarrhythmia. The most commonly used risk stratification algorithms use left ventricular ejection fraction (LVEF) to determine which patients qualify for ICD therapy, even though LVEF is a better marker of total mortality than ventricular tachyarrhythmias mortality. This review evaluates imaging tools and novel biomarkers proposed for better risk stratifying arrhythmic substrate, thereby identifying optimal ICD therapy candidates.


Author(s):  
Hyun-Jung Lee ◽  
Hyung-Kwan Kim ◽  
Sang Chol Lee ◽  
Jihoon Kim ◽  
Jun-Bean Park ◽  
...  

Abstract Aims We investigated the prognostic role of left ventricular global longitudinal strain (LV-GLS) and its incremental value to established risk models for predicting sudden cardiac death (SCD) in patients with hypertrophic cardiomyopathy (HCM). Methods and results LV-GLS was measured with vendor-independent software at a core laboratory in a cohort of 835 patients with HCM (aged 56.3 ± 12.2 years) followed-up for a median of 6.4 years. The primary endpoint was SCD events, including appropriate defibrillator therapy, within 5 years after the initial evaluation. The secondary endpoint was a composite of SCD events, heart failure admission, heart transplantation, and all-cause mortality. Twenty (2.4%) and 85 (10.2%) patients experienced the primary and secondary endpoints, respectively. Lower absolute LV-GLS quartiles, especially those worse than the median (−15.0%), were associated with progressively higher SCD event rates (P = 0.004). LV-GLS was associated with an increased risk for the primary endpoint, independent of the LV ejection fraction, apical aneurysm, and 2014 European Society of Cardiology (ESC) risk score [adjusted hazard ratio (aHR) 1.14, 95% confidence interval (CI) 1.02–1.28] or 2011 American College of Cardiology/American Heart Association (ACC/AHA) risk factors (aHR 1.18, 95% CI 1.05–1.32). LV-GLS was also associated with a higher risk for the composite secondary endpoint (aHR 1.06, 95% CI 1.01–1.12). The addition of LV-GLS enhanced the performance of the ESC risk score (C-statistic 0.756 vs. 0.842, P = 0.007) and the 2011 ACC/AHA risk factor strategy (C-statistic 0.743 vs. 0.814, P = 0.007) for predicting SCD. Conclusion LV-GLS is an important prognosticator in patients with HCM and provides additional information to established risk stratification strategies for predicting SCD.


Heart ◽  
2019 ◽  
Vol 105 (14) ◽  
pp. 1063-1069 ◽  
Author(s):  
Simon Ermakov ◽  
Radhika Gulhar ◽  
Lisa Lim ◽  
Dwight Bibby ◽  
Qizhi Fang ◽  
...  

ObjectiveBileaflet mitral valve prolapse (MVP) with either focal or diffuse myocardial fibrosis has been linked to ventricular arrhythmia and/or sudden cardiac arrest. Left ventricular (LV) mechanical dispersion by speckle-tracking echocardiography (STE) is a measure of heterogeneity of ventricular contraction previously associated with myocardial fibrosis. The aim of this study is to determine whether mechanical dispersion can identify MVP at higher arrhythmic risk.MethodsWe identified 32 consecutive arrhythmic MVPs (A-MVP) with a history of complex ventricular ectopy on Holter/event monitor (n=23) or defibrillator placement (n=9) along with 27 MVPs without arrhythmic complications (NA-MVP) and 39 controls. STE was performed to calculate global longitudinal strain (GLS) as the average peak longitudinal strain from an 18-segment LV model and mechanical dispersion as the SD of the time to peak strain of each segment.ResultsMVPs had significantly higher mechanical dispersion compared with controls (52 vs 42 ms, p=0.005) despite similar LV ejection fraction (62% vs 63%, p=0.42) and GLS (−19.7 vs −21, p=0.045). A-MVP and NA-MVP had similar demographics, LV ejection fraction and GLS (all p>0.05). A-MVP had more bileaflet prolapse (69% vs 44%, p=0.031) with a similar degree of mitral regurgitation (mostly trace or mild in both groups) (p>0.05). A-MVP exhibited greater mechanical dispersion when compared with NA-MVP (59 vs 43 ms, p=0.0002). Mechanical dispersion was the only significant predictor of arrhythmic risk on multivariate analysis (OR 1.1, 95% CI 1.02 to 1.11, p=0.006).ConclusionsSTE-derived mechanical dispersion may help identify MVP patients at higher arrhythmic risk.


Author(s):  
Gustav Mattsson ◽  
Peter Magnusson

Heart failure implies a considerable burden for patients and resources for the health care system. Dilated cardiomyopathy is defined as left ventricular dilation and reduced systolic function, not solely explained by ischemic heart disease or abnormal loading conditions. Numerous genes have been identified in familial cases of dilated cardiomyopathy. Heart failure with reduced ejection fraction increases the risk for sudden cardiac death. Implantable cardioverter defibrillator therapy can provide a means of preventing sudden cardiac death in those deemed to be at high risk. Health care providers are in need of better tools in order to improve risk stratification. This chapter aims to provide an overview of the current knowledge about risk of arrhythmia and sudden death in patients with familial dilated cardiomyopathy, in particular for those patients with a specific mutation.


2020 ◽  
Vol 6 (5) ◽  
Author(s):  
Nabil El-Sherif ◽  
Mohamed Boutjdir ◽  
Gioia Turitto

Sudden cardiac death accounts for approximately 360,000 annually in the United States and is the cause of half of all cardiovascular deaths. Ischemic heart disease is the major cause of death in the general adult population. Sudden cardiac death can be due to arrhythmic or non-arrhythmic cardiac causes, for example, myocardial rupture. Arrhythmic sudden cardiac death may be caused by ventricular tachyarrhythmia (ventricular tachycardia/ventricular fibrillation) or pulseless electrical activity/asystole. The majority of research in risk stratification centers on ventricular tachyarrhythmias simply because of the availability of a successful management strategy, the implantable cardioverter/ defibrillator. Currently the main criterion of primary defibrillator prophylaxis is the presence of organic heart disease and depressed left ventricular systolic function assessed as left ventricular ejection fraction. However, only one third of eligible patients benefit from the implantable defibrillator, resulting in significant redundancy in the use of the device. The cost to the health care system of sustaining this approach is substantial. Further, the current low implantation rate among eligible population probably reflects a perceived low benefit-to-cost ratio of the device. Therefore, attempts to optimize the selection process for primary implantable defibrillator prophylaxis are paramount. The present report will review the most recent pathophysiology and risk stratification strategies for sudden cardiac death beyond the single criterion of depressed ejection fraction. Emphasis will be placed on electrophysiological surrogates of conduction disorder, dispersion of repolarization, and autonomic imbalance, which represent our current understanding of the electrophysiological mechanisms that underlie the initiation of ventricular tachyarrhythmias. Further, factors that modify arrhythmic death, including noninvasive risk variables, biomarkers, and genomics will be addressed. These factors may have great utility in predicting sudden cardiac arrhythmic death in the general public.


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