Natural History of Myocardial Function in an Adult Human Population: Serial Longitudinal Observations From MESA

Abstract

ObjectivesThe aim of this longitudinal study was to define the determinants of aging-related left ventricular (LV) remodeling and function in a large multiethnic population. BackgroundThe influence of risk factor exposure on myocardial remodeling and function in humans across adult life remains incompletely understood. MESA (Multi-Ethnic Study of Atherosclerosis) is a longitudinal population-based cohort of asymptomatic adults at baseline. MethodsWe examined 757 participants who were free of clinical cardiovascular disease and underwent tagged cardiac magnetic resonance both at baseline and at the 10-year follow-up as part of the MESA study. LV remodeling, circumferential shortening (CS), and torsion were assessed by tagged cardiac magnetic resonance. Multivariable linear regression was used to determine the association of changes in risk factors with changes in cardiac geometry and function. ResultsThe mean age of participants was 63 ± 9 years at baseline; 50% were women. Overall, the LV mass-to-volume ratio increased by 10% over 10 years (p < 0.01). CS was unchanged (17.8% to 17.9%, p = 0.246), whereas torsion increased by 13% (3.8°/cm to 4.3°/cm, p < 0.001). Increased systolic blood pressure was associated with reduced CS (−0.02%/mm Hg, p < 0.01). Participants who remained on antihypertensive therapy during the whole study had a greater decrease in LV mass-to-volume ratio (−0.045 vs. no medication, p < 0.05) with a greater increase in CS (0.78% vs. no medication, p < 0.01). Moreover, greater LV mass at baseline was significantly associated with reduced CS (−0.02%/g, p < 0.01) and torsion (−0.02°/cm/g, p < 0.01) independently of risk factors. ConclusionsLongitudinal observation demonstrates that LV mass and worsening risk factors are fundamental determinants of reduced regional myocardial shortening over 10 years. Increased torsion of the myocardial wall is seen with progressive concentric remodeling and may explain why systolic function is maintained with aging.