Original Contribution |
From the National Institute of Health and Medical Research (INSERM), Unit 258 (M.Z., C.B.-K., D.C., P.D.); Centre de Diagnostic et de Prévention Neurovasculaire (P.-J.T.), Paris; and Centre d'examen EVA-INSERM (I.R.), Nantes, France.
Correspondence to Mahmoud Zureik, MD, PhD, INSERM U 258, Hôpital Broussais, 96 rue Didot, 75674 Paris Cedex 14, France. E-mail zureik{at}hbroussais.fr
AbstractFamilial aggregation of coronary heart disease (CHD) has been reported in several studies. The specific underlying mechanisms and the relative contribution of atherosclerosis to the subsequent CHD events in subjects with family history are not well established. This study examined the association of parental history of premature death from CHD with ultrasound carotid measurements of atherosclerosis in a population of 1040 subjects aged 59 to 71 years. Ultrasound examination included measurements of intima-media thickness at the common carotid arteries (at sites free of plaques) and assessment of atherosclerotic plaques in the extracranial carotid arteries. Subjects who reported that 1 or both parents had sudden death or died of myocardial infarction before the age of 65 years were considered positive for parental history of premature death from CHD (n=53, 5.1%). The prevalence of atheromatous plaques was higher in subjects with history of premature death from CHD compared with those without history (41.5% versus 20.5%, P<0.001). Age- and sex-adjusted odds ratio of atheromatous plaques associated with parental history of premature death from CHD was 2.85 (95% confidence interval, 1.60 to 5.08; P<0.001). Multivariate adjustment for major known cardiovascular risk factors did not markedly alter the results (odds ratio, 2.70; P<0.002). In contrast, common carotid intima-media thickness was not associated with parental history of premature death from CHD (0.66±0.11 versus 0.66±0.12 mm, P=0.76). These findings were observed in both men and women. In conclusion, parental history of premature death from CHD is strongly associated with carotid plaques. Familial transmission of CHD risk does not seem to be specifically mediated by arterial wall thickening measured at sites free of plaques.
Key Words: carotid arteries atherosclerosis coronary disease ultrasonics epidemiology
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