William Arguelles1, Maria M Llabre2, Frank J Penedo2, Martha L Daviglus3, Ralph L Sacco4, Kiang Liu5, Moyses Szklo6, Joseph F Polak7, John Eng8, Gregory L Burke9, Neil Schneiderman2. 1. Department of Psychology, University of Miami, United States. Electronic address: warguelles@psy.miami.edu. 2. Department of Psychology, University of Miami, United States. 3. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, United States; Department of Medicine, University of Illinois at Chicago, United States. 4. Department of Neurology, University of Miami Miller School of Medicine, United States. 5. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, United States. 6. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, United States. 7. Radiology, Tufts University School of Medicine, United States. 8. Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, United States. 9. Division of Public Health Sciences, Wake Forest School of Medicine, United States.
Abstract
BACKGROUND/ OBJECTIVES: Data describing relationships between change in risk factors and coronary artery calcification (CAC) are lacking and could inform optimal cardiovascular disease prevention and treatment strategies. This study aimed to examine how change in traditional cardiometabolic risk factors related to change in CAC among individuals with detectable subclinical atherosclerosis. METHODS: Latent growth modeling was used to examine change in cardiometabolic risk factors (waist circumference, body mass index, systolic and diastolic blood pressure, high- and low-density lipoprotein cholesterol, triglycerides, and glucose) related to change in CAC up to an average 4.9-year follow-up in a multi-ethnic cohort of 3398 asymptomatic individuals (57.8% men) who had detectable CAC (score>0) at baseline, adjusting for baseline risk factor levels and CAC values, age, gender, race/ethnicity, smoking, family history of CVD, income, and use of antihypertensive, lipid-lowering, and glucose-lowering medications. RESULTS: Greater declines in blood pressure (systolic and diastolic) and low-density lipoprotein cholesterol at follow-up were each associated with greater CAC progression. The observed inverse associations were attributable to greater CAC progression in participants taking antihypertensive and lipid-lowering drugs who, as expected, had declines in blood pressure and lipid levels, respectively. These inverse associations did not emerge in participants not taking these medications. CONCLUSIONS: Among individuals with subclinical atherosclerosis, the unexpected inverse associations observed between change in blood pressure and lipid levels with CAC progression emphasize the importance of considering medication use, and, when feasible, the severity and duration of disease, in exploring associations between risk factors and CAC change.
BACKGROUND/ OBJECTIVES: Data describing relationships between change in risk factors and coronary artery calcification (CAC) are lacking and could inform optimal cardiovascular disease prevention and treatment strategies. This study aimed to examine how change in traditional cardiometabolic risk factors related to change in CAC among individuals with detectable subclinical atherosclerosis. METHODS: Latent growth modeling was used to examine change in cardiometabolic risk factors (waist circumference, body mass index, systolic and diastolic blood pressure, high- and low-density lipoprotein cholesterol, triglycerides, and glucose) related to change in CAC up to an average 4.9-year follow-up in a multi-ethnic cohort of 3398 asymptomatic individuals (57.8% men) who had detectable CAC (score>0) at baseline, adjusting for baseline risk factor levels and CAC values, age, gender, race/ethnicity, smoking, family history of CVD, income, and use of antihypertensive, lipid-lowering, and glucose-lowering medications. RESULTS: Greater declines in blood pressure (systolic and diastolic) and low-density lipoprotein cholesterol at follow-up were each associated with greater CAC progression. The observed inverse associations were attributable to greater CAC progression in participants taking antihypertensive and lipid-lowering drugs who, as expected, had declines in blood pressure and lipid levels, respectively. These inverse associations did not emerge in participants not taking these medications. CONCLUSIONS: Among individuals with subclinical atherosclerosis, the unexpected inverse associations observed between change in blood pressure and lipid levels with CAC progression emphasize the importance of considering medication use, and, when feasible, the severity and duration of disease, in exploring associations between risk factors and CAC change.
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