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Normokinesia adjacent to left ventricular aneurysm: a differential risk for sudden cardiac death
Constantine A Hassapoyannes1, Brent T McLaurin, Carlton A Hornung
1Division of Cardiology (111C), Department of Medicine, William Jennings Bryan Dorn Veterans Affairs Medical Center, WJB Dorn VAMC, 6439 Garners Ferry Road, Columbia, SC 29209-1639, USA. cahass@aol.com
Insights
In patients with left ventricular aneurysm (LVA), non-aneurysmal myocardial contractility predicts pump failure deaths. A normal segment adjacent to LVA independently predicts sudden cardiac death (SCD), possibly due to arrhythmogenic motion discordance.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
- Cardiovascular Imaging
Background:
- Ejection fraction (EF) predicts both sudden cardiac death (SCD) and non-sudden cardiac death (NSCD) post-myocardial infarction.
- Left ventricular aneurysm (LVA) independently predicts SCD, suggesting mechanical factors beyond global EF are involved.
Purpose of the Study:
- To test the hypothesis that mechanical factors, distinct from global left ventricular performance, predict SCD in patients with LVA.
- To investigate predictors of SCD and NSCD in LVA patients.
Main Methods:
- Secondary analysis of a prospective cohort study (66 patients with LVA).
- Ventriculography assessed LVA (diastolic eccentricity, systolic dyskinesia).
- Left ventricular segments evaluated for contractility; normal adjacent segments and EF assessed. Ventricular tachycardia documented via Holter.
Main Results:
- Median follow-up of 5.2 years yielded 12 NSCD and 8 SCD.
- Lower EF in deceased vs. survivors (31.5% vs. 39.7%).
- Similar EF but disparate residual contractility scores for NSCD and SCD groups (3.0 vs. 4.1). Decreasing contractility predicted NSCD (OR=17.06); normokinetic adjacent segment predicted SCD (OR=21).
Conclusions:
- Non-aneurysmal myocardial contractility differentiates pump failure deaths in LVA patients.
- A normal segment adjacent to LVA independently predicts SCD, likely via an arrhythmogenic substrate from motion discordance.
- Ventricular tachycardia significantly increased SCD prediction when combined with a normokinetic adjacent segment.
Background:
Following myocardial infarction, the ejection fraction (EF) is an indiscriminate predictor of both non-sudden cardiac death (NSCD) and sudden cardiac death (SCD). However, development of a left ventricular aneurysm (LVA) confers independent risk only for SCD. Thus, we tested the hypothesis that mechanical factors, other than the global left ventricular performance, are causally related to SCD in the presence of LVA.
Methods:
A secondary analysis was conducted from a longitudinal, prospective, long-term follow-up cohort study of 66 patients with LVA (diastolic eccentricity and systolic dyskinesia) diagnosed by ventriculography. The left ventricular contour was divided into five segments and contractility scores for the residual myocardium and the segments adjacent to the aneurysm were allocated along with assessment of the EF. A normal adjacent segment was considered present when at least one segment adjacent to the aneurysm exhibited normokinesia. Presence of ventricular tachycardia was documented by Holter recording.
Results:
At a 5.2-year median follow-up, there were 12 NSCD and 8 SCD. The EF was lower among patients who died vs. survivors (31.5% vs. 39.7%, P=0.01). Patients with NSCD and SCD, exhibited similar EF but disparate residual contractility scores (3.0 vs. 4.1, P<0.004). Among cardiac deaths, a decreasing residual contractility score differentially predicted NSCD (odds ratio=17.06, P<0.03), while a normokinetic adjacent segment differentially predicted SCD (odds ratio=21, P<0.02). Albeit a predictor of both NSCD and SCD, ventricular tachycardia increased markedly the model significance (P<0.004) only when tested with a normokinetic adjacent segment vis-a'-vis SCD.
Conclusions:
In the presence of LVA, the contractility of the non-aneurysmal myocardium is a differential predictor of death from pump failure. In contrast, a normal segment adjacent to LVA constitutes an independent and discriminate predictor of SCD, possibly through an arrhythmic substrate linked to the motion discordance between the expanding aneurysm and a normokinetic adjacent myocardium.