Is left ventricular hypertrophy a modifiable risk factor in end-stage renal disease

Abstract

Purpose of review: Left ventricular hypertrophy (LVH) is common in end-stage renal disease (ESRD) and has been advocated as a therapeutic target. We review the considerations for targeting LVH as a modifiable risk factor in ESRD.

Recent findings: Pathologic myocardial changes underlying LVH provide an ideal substrate for the spread of arrhythmia and may be key contributors to the occurrence of sudden death in ESRD. LVH is present in 68-89% of incident hemodialysis patients and is frequently progressive, although regression is observed in a minority of patients. Higher degrees of baseline LVH, as well as greater increases in left ventricular mass index over time, are associated with decreased survival, but whether these associations are causal remains uncertain. Several interventions, including angiotensin blockade and frequent dialysis, can reduce the left ventricular mass index, but whether this is associated with improved survival has not been definitively demonstrated.

Summary: LVH is a highly prevalent and reversible risk factor, which holds promise as a novel therapeutic target in ESRD. Interventional trials are needed to provide additional evidence that LVH regression improves survival before prevention and reversal of LVH can be definitively adopted as a therapeutic paradigm in ESRD.

Figure 1. Contributors to Adverse Remodeling of the Left Ventricle in ESRD

Factors contributing to capillary dropout and left ventricular hypertrophy in ESRD. HTN-hypertension. LVH-left ventricular hypertrophy. ADMA-asymmetric dimethyl arginine. FGF-23-fibroblast growth factor 23. mTOR-mammalian target of rapamycin.