Family history of coronary heart disease and the incidence and progression of coronary artery calcification: Multi-Ethnic Study of Atherosclerosis (MESA)

Abstract

Objective We evaluated family history as a predictor of incident and progressive coronary artery calcium (CAC) using data from the Multi-Ethnic Study of Atherosclerosis (MESA). Background MESA is a multi-center prospective study of 6,814 asymptomatic individuals. The relationship between family history of coronary heart disease (CHD) and CAC incidence or progression has not been described previously. Methods A total of 5,099 participants had detailed information about family history of CHD (late versus premature and parental versus sibling history). The mean time between CAC scans was 3.1 ± 1.3 years. The association of late versus premature family history was assessed against CAC change using multivariate regression model adjusted for demographics and cardiac risk factors. Results A family history of premature CHD was associated with an odds ratio (OR) of 1.55 (p < 0.01) for incident development of CAC after adjusting for risk factors and demographics. A premature family history was associated with 14.4 units (p < 0.01) greater volume scores compared to those with no family history in similarly adjusted models by median regression analysis. A combined parental and sibling family history was associated with the greatest incidence and progression in demographic-adjusted models. Caucasians demonstrated the most consistent predictive relationship between family history of premature CHD and incidence (p < 0.01) and progression (p < 0.05) of CAC, though no significant interaction with ethnicity was noted. Conclusions Family history of premature CHD is associated with enhanced development and progression of subclinical disease, independent of other risk factors, in a multiethnic, population-based study.

Protective Effect Of Aabresham (Bombyx Mori) Against Atherosclerosis

“…Both active smoking and exposure to smoke are associated with the progression of atherosclerosis. The outcome of our observation are quite similar to that of George Howard et al (1998) 16 where, although most of the participants were females yet developed atherosclerosis as they were passively exposed to smoking. 36%(18) of subjects virtually belonged to upper lower class (IV), 24% (12) to upper middle class(II), 20%(10) from lower middle class (III), 16% (8) upper class I and 4% (two) from lower class(V).…”

Association Between Family History, a Genetic Risk Score, and Severity of Coronary Artery Disease in Patients With Premature Acute Coronary Syndromes

“…Parikh et al 25 demonstrated that a FHx of CAD was associated with increased subclinical coronary disease as measured by coronary artery calcification in the Framingham Offspring Study, which has also been confirmed in the MultiEthnic Study of Atherosclerosis. 28 Otaki et al 29 prospectively evaluated a subset of young patients (n=6308, men aged <55 years and women aged <65 years) from the Coronary CT Angiography Evaluation For Clinical Outcomes: An International Multicenter Registry (CONFIRM) who underwent CCTA for suspected CAD. They found that compared with patients without a positive FHx, patients with a positive FHx had a higher prevalence of any CAD (40% versus 30%; .…”

Prevalence and risk of cardiovascular risk factors and events in offspring of patients at high vascular risk and effect of location of parental vascular disease

“…Offspring of parents with hypertension more often showed signs of hyperinsulinemia [23], high-normal blood pressure, increased serum CRP and leptin plasma levels compared with offspring without such parental history [8,[24][25][26][27]. In addition, it was recently demonstrated that family histories of premature and late coronary heart disease are associated with a progression of coronary artery calcium in offspring [28]. In offspring of patients who experienced a heart attack, increased levels of total cholesterol, VLDL cholesterol and LDL cholesterol from the age of 18 years were demonstrated previously [29].…”