title: Left ventricular hypertrophy, subclinical atherosclerosis, and inflammation.
abstract: To elucidate mechanisms by which left ventricular (LV) hypertrophy (LVH) increases the risk of atherosclerotic heart disease, we sought to determine whether LVH is independently associated with coronary artery calcium (CAC) and serum C-reactive protein (CRP) levels in the general population. The Dallas Heart Study is a population-based sample in which 2633 individuals underwent cardiac MRI to measure LV structure, electron beam CT to measure CAC, and measurement of plasma CRP. We used univariate and multivariable analyses to determine whether LV mass and markers of concentric LV hypertrophy or dilation were associated with CAC and CRP. Increasing quartiles of LV mass indexed to fat-free mass, LV wall thickness, and concentricity, but not LV volume, were associated with CAC in both men and women (P<0.001). After adjustment for traditional cardiovascular risk factors and statin use, LV wall thickness and concentricity remained associated with CAC in linear regression (P<0.001 for each). These associations were particularly robust in blacks. LV wall thickness and concentricity were also associated with elevated CRP levels (P=0.001 for both) in gender-stratified univariate analyses, although these associations did not persist in multivariable analysis. In conclusion, concentric LVH is an independent risk factor for subclinical atherosclerosis. LVH is also associated with an inflammatory state as reflected in elevated CRP levels, although this relationship appears to be mediated by comorbid conditions. These data likely explain in part why individuals with LVH are at increased risk for myocardial infarction.
authors.affiliation: Donald W. Reynolds Cardiovascular Clinical Research Center and Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9047, USA.
authors.forename: Sameer K
authors.initials: SK
authors.lastname: Mehta
authors.forename: J Eduardo
authors.initials: JE
authors.lastname: Rame
authors.forename: Amit
authors.initials: A
authors.lastname: Khera
authors.forename: Sabina A
authors.initials: SA
authors.lastname: Murphy
authors.forename: Russell M
authors.initials: RM
authors.lastname: Canham
authors.forename: Ronald M
authors.initials: RM
authors.lastname: Peshock
authors.forename: James A
authors.initials: JA
authors.lastname: de Lemos
authors.forename: Mark H
authors.initials: MH
authors.lastname: Drazner
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D003331:Coronary Vessels / Q000378:metabolism; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000150:complications* / Q000473:pathology; D007249:Inflammation / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012307:Risk Factors; D013781:Texas; D014057:Tomography, X-Ray Computed
chemical_list: D002097:C-Reactive Protein; D002118:Calcium