Abstract 2373: Cardiac Structural and Functional Correlates of C-reactive Protein in a Population with High Prevalence of Diabetes and Hypertension: The Strong Heart Study
Background Inflammatory mediators are involved in the pathogenesis of congestive heart failure. There are, however, conflicting findings about the relationship between left ventricular structure and function and C-reactive protein (CRP) levels.
Methods We investigated the relationship of CRP with echocardiographic measures of cardiac structure and function in 3,104 American Indian participants in the Strong Heart Study.
Results Participant characteristics were: age 60±8 years, 62% female, diabetes in 49%, hypertension in 48%, coronary heart disease in 7%, congestive heart failure in 4%. In univariate analysis, CRP (median 3.9 mg/L; interquartile range 2.1 – 7.3 mg/L) had significant inverse associations with left ventricular ejection fraction (EF) and stress-correct mid-wall shortening (scMWS) and significant positive associations with left ventricular end-diastolic and end-systolic dimensions (LVIDd and LVIDs), left atrial dimension (LA) and left ventricular mass/height2.7 (LVM/ht2.7; all p<0.05). In addition, participants with EF<35% had higher CRP than those with EF≤55% (9.5±11.1 mg/L vs. 6.6±9.3 mg/L; p<0.05). CRP had no significant relationship with mitral E-wave deceleration time and CRP levels were not significantly different in the three mitral E/A categories (normal, abnormal relaxation and restrictive filling). In multivariate linear regression analysis, adjusted for age, sex, renal function, body mass index, diabetes and hypertension status, there were persistent significant relations between CRP and EF, scMWS, LVIDd, LVIDs, LA and LVM/ht2.7 (Table⇓).
Conclusions This is the largest study to date to demonstrate significant independent relations between CRP and larger cardiac size and worse left ventricular systolic function in a population-based sample of adults with high prevalence of diabetes and hypertension. These findings suggest a possible mediating role of inflammation in both LV remodeling and systolic dysfunction.