|| Checking for direct PDF access through Ovid
The increased risk of cardiovascular disease (CVD) among individuals with a family history of CVD is well known. Whether parental premature CVD is associated with vascular calcification in offspring has not, however, been established.To investigate the relationship between parental premature CVD and coronary heart disease (CHD) and the presence of coronary artery calcification (CAC) and abdominal aortic calcification (AAC) in offspring.This was a retrospective analysis of data from the multidetector CT (MDCT) substudy of the Framingham Heart Study. Participants were enrolled in either the Framingham Offspring or the Framingham Third Generation (Gen3) cohort. Between June 2002 and April 2005, measurements of CAC and AAC were performed using 8-slice MDCT. Inclusion criteria were age older than 35 years for females and 40 years for males, and weight less than 320 lbs (145.2 kg). Participants were excluded if their mother was younger than 65 years of age or if their father was younger than 55 years of age at the time of MDCT, or if only one of their parents was enrolled in the Framingham Heart Study. Pregnancy was an additional exclusion criterion for female participants.The primary end points were the presence of CAC and AAC.Among the 3,483 participants who underwent MDCT, 797 Framingham Offspring and 1,238 Gen3 individuals were eligible for inclusion in the analysis. The mean age in the Offspring and Gen3 cohorts was 62.5 years and 46 years, respectively. The incidence of diabetes was higher in the Offspring cohort than in the Gen3 cohort (8.2% vs 2.7%), as was the incidence of hypertension (35.5% vs 17.8%). Mean total cholesterol was also higher among individuals in the Offspring cohort than among Gen3 individuals (202.5 mg/dl vs 193.8 mg/dl). Current cigarette smoking was, however, more common in the younger cohort (11% vs 13%). The occurrence of parental premature CVD was associated with a more than twofold increase in the risk of CAC in Gen3 participants, independent of other CVD risk factors (odds ratio [OR] 2.17, 95% CI 1.41-3.33; P = 0.0004). Parental premature CHD also independently increased the risk of CAC in Gen3 individuals (OR 2.22, 95% CI 1.22-4.01; P = 0.009). In an analysis adjusted for age and sex, parental premature CVD was an independent predictor of AAC among Gen3 individuals (OR 1.80, 95% CI 1.25-2.60; P = 0.002) as was parental premature CHD (OR 1.81, 95% CI 1.11-2.93; P = 0.02); however, the significance of these associations diminished when the model was adjusted for other CVD risk factors. There were no significant associations between parental premature CVD or CHD and occurrence of CAC or AAC in the Offspring cohort. Notably, paternal CVD and CHD were found to have a more pronounced effect on the risk of CAC and AAC in Gen3 participants than were maternal CVD and CHD, but this effect was not evident in the Framingham Offspring.Parental premature CVD and CHD are significant independent predictors of arterial calcification, particularly in younger adults.