Abstract 13509: Association of Systemic Inflammation with Speckle Tracking Derived Left Ventricular Peak Systolic Strain In Young Adults Over a 10-Year Follow-Up Period: The CARDIA Study
Objective: We hypothesized that in young adults, increasing severity of a systemic inflammatory state, assessed by levels of C-reactive protein (CRP), would be associated with a greater reduction in left ventricular 4-chamber peak longitudinal systolic strain (PSS) 10 years later.
Methods: Baseline CRP values were obtained from Year-15 (2000-2001) data of the CARDIA study and were related to PSS measured from echocardiograms performed in Year-25 (Y25). Multivariable models were used to assess the linear association between CRP (normalized using a logarithmic scale) and PSS. Baseline CRP values were then further dichotomized to values ≥5mg/L vs. <5mg/L and multivariable models were used to evaluate if a more severe systemic inflammatory state was associated with a greater reduction in PSS. Multivariable models were initially adjusted for age, sex, systolic blood pressure (SBP), total cholesterol, HDL cholesterol, number of cigarettes currently smoked, diabetic status, and use of antihypertensive medications. BMI was added to the previous models to evaluate the influence of obesity on the association between systemic inflammation and PSS.
Results: We included 1742 patients with complete data at Y15. 5.3% were diabetics and 7.2% used anti-hypertensive medication; mean±SD values for age, SBP, BMI, CRP, HDL cholesterol, and total Cholesterol were 40±3.6 years, 112±14mm Hg, 28.3±6.4 Kg/m2, 2.0±2.9 mg/L, 50±14mg/dl, and 185±36 mg/dl, respectively. There were 368 smokers at baseline, smoking an average of 12.6 cigarettes per day. 245 patients had CRP ≥5mg/L. Mean PSS at Y25 was -14±2.6 %. Associations between CRP and PSS, in models with and without BMI are shown in Table1.
Conclusion: In models including traditional risk factors, CRP is associated with reduction in PSS over a 10-year follow-up period. However, part of this association is mediated by obesity.
- © 2012 by American Heart Association, Inc.