What does this research mean for the field?

Concentric and eccentric left ventricular hypertrophy are distinct clinical phenotypes with differing risk profiles and racial predispositions, and both independently predict worse long-term all-cause mortality in individuals with subclinical cardiovascular disease. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

January 31, 2022Open Access

Left ventricular hypertrophy subtype and long-term mortality in those with subclinical cardiovascular disease: The Multi-Ethnic Study of Atherosclerosis (MESA)

Structured PICO

Do concentric and eccentric left ventricular hypertrophy phenotypes increase long-term all-cause mortality in individuals with subclinical cardiovascular disease?

Population

4,979 participants with subclinical cardiovascular disease and available cardiac MRI data for left ventricular mass and wall thickness, from the multicenter, prospective MESA study in the United States.

Intervention

Concentric hypertrophy (CH) and eccentric hypertrophy (EH) derived from cardiac MRI

Comparator

No left ventricular hypertrophy

Outcome

All-cause death over 15 years follow-uphard clinical

Both concentric and eccentric left ventricular hypertrophy are distinct clinical phenotypes associated with significantly worse long-term all-cause mortality in individuals with subclinical cardiovascular disease.

Abstract

Abstract The clinical and biochemical profile of differing LVH phenotypes and its effect on long term outcomes is ill-defined. The study investigated the differences in risk profiles and prognostic effect of concentric (CH) and eccentric hypertrophy (EH) on long-term adverse outcomes in a contemporary, ethnically diverse cohort. We analyzed follow-up data over 15 years from the Multi-Ethnic Study of Atherosclerosis study, an ongoing multicenter, prospective population-based study in the United States that enrolled 6,814 participants with subclinical cardiovascular disease between 2000 and 2002. 4,979 participants with left ventricular mass and wall thickness, derived from cardiac MRI at baseline enrollment were included. Descriptive statistics, Kaplan-Meier curves, and regression models were applied. Independent variables associated with CH were Black and Hispanic race/ethnicity, systolic blood pressure, and metabolic syndrome. Independent variables associated with EH were systolic blood pressure, urine creatinine, whereas serum creatinine had an inverse association. The primary endpoint of all-cause death (n=1,137, 22.8%) occurred in 21.7%, 47.4%, and 56.6% of participants with no, concentric, or eccentric hypertrophy, respectively (p<0.001). Age (HR per year = 1.10 1.09, 1.11, p<0.001), male gender (HR=1.48 1.29, 1.69, p<0.001), Black race (HR=1.17 1.005,1.36, p=0.04), fasting glucose (HR=1.005 1.003, 1.007, p<0.001), baseline creatinine (HR per mg/dL = 1.29 1.15-1.46, p<0.001), LVEF (HR per 1% = 0.98 0.98, 0.99, p=0.005), IL-6 (HR per pg/mL = 1.17 1.12, 1.22, p<0.001), concentric hypertrophy (HR=1.84 1.41-2.41, p<0.001), and eccentric hypertrophy (HR=2.58 1.77-3.76, p<0.001) were significant predictors of all-cause mortality. We conclude that CH and EH are two distinct clinical phenotypes of left ventricular hypertrophy with differing gender and racial predisposition, both associated with worse long-term adverse outcomes.

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