Left ventricular hypertrophy and sudden cardiac death

Abstract

Sudden cardiac death (SCD) is among the leading causes of death worldwide, and it remains a public health problem, as it involves young subjects. Current guideline-directed risk stratification for primary prevention is largely based on left ventricular (LV) ejection fraction (LVEF), and preventive strategies such as implantation of a cardiac defibrillator (ICD) are justified only for documented low LVEF (i.e., ≤ 35%). Unfortunately, only a small percentage of primary prevention ICDs, implanted on the basis of a low LVEF, will deliver life-saving therapies on an annual basis. On the other hand, the vast majority of patients that experience SCD have LVEF > 35%, which is clamoring for better understanding of the underlying mechanisms. It is mandatory that additional variables be considered, both independently and in combination with the EF, to improve SCD risk prediction. LV hypertrophy (LVH) is a strong independent risk factor for SCD regardless of the etiology and the severity of symptoms. Concentric and eccentric LV hypertrophy, and even earlier concentric remodeling without hypertrophy, are all associated with increased risk of SCD. In this paper, we summarize the physiology and physiopathology of LVH, review the epidemiological evidence supporting the association between LVH and SCD, briefly discuss the mechanisms linking LVH with SCD, and emphasize the need to evaluate LV geometry as a potential risk stratification tool regardless of the LVEF.

Keywords: Arrest; Arrhythmias; Concentric; Eccentric; Echocardiography; Geometry; Left ventricular hypertrophy; Prediction; Remodeling; Risk stratification; Sudden cardiac death; Tachycardia; Ventricular fibrillation.