Publication Date

2011-01-01

Availability

Open access

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Psychology (Arts and Sciences)

Date of Defense

May 2010

First Committee Member

Neil Schneiderman - Committee Chair

Second Committee Member

Maria M. Llabre - Committee Co-Chair

Third Committee Member

Frank J. Penedo - Committee Member

Fourth Committee Member

Ralph L. Sacco - Committee Member

Abstract

There are few published data describing the progression of cardiovascular disease (CVD) risk factors, the progression of coronary artery calcification (CAC; a measure of subclinical CVD), and how these processes relate to one another. Most previous studies have been limited by cross-sectional designs and small or restricted samples. The few prospective studies examining these relationships have used baseline CVD risk factor values to predict CAC change scores, and have yielded inconsistent findings. This study used latent growth modeling to examine how progression in specific cardiometabolic risk factors (CRFs; waist circumference, body mass index, systolic and diastolic blood pressure, high-density and low-density lipoprotein cholesterol, triglycerides, and glucose) relates to incidence and progression of CAC in a multi-ethnic cohort of 4,560 asymptomatic individuals, controlling for baseline risk factor and CAC values, age, race/ethnicity, smoking, family history of CVD, income, and time-varying use of antihypertensive, lipid-lowering, and glucose-lowering medications. All analyses were conducted separately on men (n = 2,132) and on women (n = 2,428). Consistent with an earlier study of this sample (Kronmal et al., 2007), several CRFs at baseline were associated with CAC incidence and progression. Some gender differences in these associations were further outlined. Among individuals that had undetectable CAC at baseline, change over time in CRFs was not related to incidence of CAC in either men or women. Among women who had detectable CAC at baseline, regression (or less progression) in systolic (B = -3.173, p < .05) and diastolic blood pressure (B = -8.558, p < .05), as well as low-density lipoprotein cholesterol (B = -2.485, p < .05), was each univariately associated with greater CAC progression. These associations appeared to be influenced by medication use, such that women taking antihypertensive and lipid-lowering medications exhibited greater CAC progression despite showing average decreases in respective CRF levels over time. Furthermore, when change in blood pressure and change in low-density lipoprotein cholesterol level were both included as predictors of CAC progression, only change in low-density lipoprotein cholesterol level remained inversely associated with CAC progression. No significant associations between change in CRFs and CAC progression were observed in men who had detectable CAC at baseline. To our knowledge, this is the first study systematically reporting on how change in various CVD risk factors relates to progression of CAC. A brief discussion regarding these findings, as well as suggestions for future research, are provided.

Keywords

Growth Modeling; Progression; Cardiovascular Disease; Risk Factors; Coronary Artery Calcification

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