Family History of Premature Coronary Heart Disease and Coronary Artery Calcification

Multi-Ethnic Study of Atherosclerosis (MESA)

Published in: Circulation, v. 116, no. 6, Aug. 7, 2007, p. 619-626

Posted on on January 01, 2007

by Khurram Nasir, Matthew J. Budoff, Nathan D. Wong, Maren T. Scheuner, David Herrington, Donna K. Arnett, Moyses Szklo, Philip Greenland, Roger S. Blumenthal

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BACKGROUND: A family history of premature coronary heart disease (CHD) is a known risk factor for CHD events. The purpose of this study was to assess the strength of the association between a family history of premature CHD and coronary artery calcification (CAC) in a multiethnic cohort of asymptomatic individuals. We also sought to determine whether individuals with a reported family history of premature CHD have an increased atherosclerotic burden among those classified as being at low to intermediate risk on the basis of the conventional Framingham risk score. METHODS AND RESULTS: The association of family history of premature CHD with CAC was assessed in 5347 asymptomatic individuals (47% men; mean age 62+/-10 years) in the Multi-Ethnic Study of Atherosclerosis (MESA). The demographics (age, gender, and race)-adjusted OR for CAC >0 with versus without a family history of premature CHD was 1.94 (95% CI, 1.64 to 2.29). On adjustment for CHD risk factors, the association was slightly attenuated to an OR of 1.84 (95% CI, 1.55 to 2.19). Family history of premature CHD was significantly associated with CAC in all ethnic groups. The age-, gender-, and race-adjusted prevalence of CAC >0 was significantly higher with presence of any family history of premature CHD than for those with no family history of premature CHD among individuals classified as low risk (35% versus 23%, P<0.0001) and among those at intermediate risk (70% versus 60%, P=0.01). Similarly, the prevalence of age-gender-race-based CAC >/=75th percentile in low-risk (24% versus 14%, P=0.0003) and intermediate-risk (34% versus 20%, P<0.001) individuals was also higher among those with a family history of premature CHD. Compared with those without a family history of premature CHD, the association with the presence of CAC was strongest in participants reporting such history in both a parent and a sibling (odds ratio, 2.74; 95% CI, 1.64 to 4.59), followed by those reporting a family history in a sibling only (odds ratio, 2.06; 95% CI, 1.64 to 2.58) and those reporting a family history of premature CHD only in a parent (odds ratio, 1.52; 95% CI, 1.19 to 1.93). CONCLUSIONS: An association between family history of premature CHD and the presence of any CAC, as well as advanced CAC, was observed in the present population-based multiethnic study. The relationship was independent of other risk factors and Framingham risk score, which supports the utility of including information on family history of premature CHD in current methods of global risk assessment and practice guidelines.

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