Dataset Information

Cardiovascular Event Prediction and Risk Reclassification by Coronary, Aortic, and Valvular Calcification in the Framingham Heart Study.

ABSTRACT:

Background

We determined whether vascular and valvular calcification predicted incident major coronary heart disease, cardiovascular disease (CVD), and all-cause mortality independent of Framingham risk factors in the community-based Framingham Heart Study.

Methods and results

Coronary artery calcium (CAC), thoracic and abdominal aortic calcium, and mitral or aortic valve calcium were measured by cardiac computed tomography in participants free of CVD. Participants were followed for a median of 8 years. Multivariate Cox proportional hazards models were used to determine association of CAC, thoracic and abdominal aortic calcium, and mitral and aortic valve calcium with end points. Improvement in discrimination beyond risk factors was tested via the C-statistic and net reclassification index. In this cohort of 3486 participants (mean age 50±10 years; 51% female), CAC was most strongly associated with major coronary heart disease, followed by major CVD, and all-cause mortality independent of Framingham risk factors. Among noncoronary calcifications, mitral valve calcium was associated with major CVD and all-cause mortality independent of Framingham risk factors and CAC. CAC significantly improved discriminatory value beyond risk factors for coronary heart disease (area under the curve 0.78-0.82; net reclassification index 32%, 95% CI 11-53) but not for CVD. CAC accurately reclassified 85% of the 261 patients who were at intermediate (5-10%) 10-year risk for coronary heart disease based on Framingham risk factors to either low risk (n=172; no events observed) or high risk (n=53; observed event rate 8%).

Conclusions

CAC improves discrimination and risk reclassification for major coronary heart disease and CVD beyond risk factors in asymptomatic community-dwelling persons and accurately reclassifies two-thirds of the intermediate-risk population.

SUBMITTER: Hoffmann U

PROVIDER: S-EPMC4802453 | biostudies-literature | 2016 Feb

REPOSITORIES: biostudies-literature

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Publications

Cardiovascular Event Prediction and Risk Reclassification by Coronary, Aortic, and Valvular Calcification in the Framingham Heart Study.

Hoffmann Udo U Massaro Joseph M JM D'Agostino Ralph B RB Kathiresan Sekar S Fox Caroline S CS O'Donnell Christopher J CJ

Journal of the American Heart Association 20160222 2

<h4>Background</h4>We determined whether vascular and valvular calcification predicted incident major coronary heart disease, cardiovascular disease (CVD), and all-cause mortality independent of Framingham risk factors in the community-based Framingham Heart Study.<h4>Methods and results</h4>Coronary artery calcium (CAC), thoracic and abdominal aortic calcium, and mitral or aortic valve calcium were measured by cardiac computed tomography in participants free of CVD. Participants were followed f ...[more]

PMID: 26903006

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Project description:ObjectivesThe aim of this study was to examine whether magnesium intake is associated with coronary artery calcification (CAC) and abdominal aortic calcification (AAC).BackgroundAnimal and cell studies suggest that magnesium may prevent calcification within atherosclerotic plaques underlying cardiovascular disease. Little is known about the association of magnesium intake and atherosclerotic calcification in humans.MethodsWe examined cross-sectional associations of self-reported total (dietary and supplemental) magnesium intake estimated by food frequency questionnaire with CAC and AAC in participants of the Framingham Heart Study who were free of cardiovascular disease and underwent Multi-Detector Computed Tomography (MDCT) of the heart and abdomen (n = 2,695; age: 53 ± 11 years), using multivariate-adjusted Tobit regression. CAC and AAC were quantified using modified Agatston scores (AS). Models were adjusted for age, sex, body mass index, smoking status, systolic blood pressure, fasting insulin, total-to-high-density lipoprotein cholesterol ratio, use of hormone replacement therapy (women only), menopausal status (women only), treatment for hyperlipidemia, hypertension, cardiovascular disease prevention, or diabetes, as well as self-reported intake of calcium, vitamins D and K, saturated fat, fiber, alcohol, and energy. Secondary analyses included logistic regressions of CAC and AAC outcomes as cut-points (AS >0 and AS ≥90th percentile for age and sex), as well as sex-stratified analyses.ResultsIn fully adjusted models, a 50-mg/day increment in self-reported total magnesium intake was associated with 22% lower CAC (p < 0.001) and 12% lower AAC (p = 0.07). Consistent with these observations, the odds of having any CAC were 58% lower (p trend: <0.001) and any AAC were 34% lower (p trend: 0.01), in those with the highest compared to those with the lowest magnesium intake. Stronger inverse associations were observed in women than in men.ConclusionsIn community-dwelling participants free of cardiovascular disease, self-reported magnesium intake was inversely associated with arterial calcification, which may play a contributing role in magnesium's protective associations in stroke and fatal coronary heart disease.

Project description:BackgroundLimited information is available regarding genetic contributions to valvular calcification, which is an important precursor of clinical valve disease.MethodsWe determined genomewide associations with the presence of aortic-valve calcification (among 6942 participants) and mitral annular calcification (among 3795 participants), as detected by computed tomographic (CT) scanning; the study population for this analysis included persons of white European ancestry from three cohorts participating in the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium (discovery population). Findings were replicated in independent cohorts of persons with either CT-detected valvular calcification or clinical aortic stenosis.ResultsOne SNP in the lipoprotein(a) (LPA) locus (rs10455872) reached genomewide significance for the presence of aortic-valve calcification (odds ratio per allele, 2.05; P=9.0×10(-10)), a finding that was replicated in additional white European, African-American, and Hispanic-American cohorts (P<0.05 for all comparisons). Genetically determined Lp(a) levels, as predicted by LPA genotype, were also associated with aortic-valve calcification, supporting a causal role for Lp(a). In prospective analyses, LPA genotype was associated with incident aortic stenosis (hazard ratio per allele, 1.68; 95% confidence interval [CI], 1.32 to 2.15) and aortic-valve replacement (hazard ratio, 1.54; 95% CI, 1.05 to 2.27) in a large Swedish cohort; the association with incident aortic stenosis was also replicated in an independent Danish cohort. Two SNPs (rs17659543 and rs13415097) near the proinflammatory gene IL1F9 achieved genomewide significance for mitral annular calcification (P=1.5×10(-8) and P=1.8×10(-8), respectively), but the findings were not replicated consistently.ConclusionsGenetic variation in the LPA locus, mediated by Lp(a) levels, is associated with aortic-valve calcification across multiple ethnic groups and with incident clinical aortic stenosis. (Funded by the National Heart, Lung, and Blood Institute and others.).

Project description:OBJECTIVES:To investigate the association between directly measured density and morphology of coronary artery calcium (CAC) with cardiovascular disease (CVD) events, using computed tomography (CT). METHODS:Framingham Heart Study (FHS) participants with CAC in noncontrast cardiac CT (2002-2005) were included and followed until 2016. Participants with known CVD or uninterpretable CT scans were excluded. We assessed and correlated (Spearman) CAC density, CAC volume, and the number of calcified segments. Moreover, we counted morphology features including shape (cylindrical, spherical, semi-tubular, and spotty), location (bifurcation, facing pericardium, or facing myocardium), and boundary regularity. In multivariate Cox regression analyses, we associated all CAC characteristics with CVD events (CVD-death, myocardial infarction, stroke). RESULTS:Among 1330 included participants (57.8?±?11.7 years; 63% male), 73 (5.5%) experienced CVD events in a median follow-up of 9.1 (7.8-10.1) years. CAC density correlated strongly with CAC volume (Spearman's ??=?0.75; p?<?0.001) and lower number of calcified segments (??=?-?0.86; p?<?0.001; controlled for CAC volume). In the survival analysis, CAC density was associated with CVD events independent of Framingham risk score (HR (per SD)?=?2.09; 95%CI, 1.30-3.34; p?=?0.002) but not after adjustment for CAC volume (p?=?0.648). The extent of spherically shaped and pericardially sided calcifications was associated with fewer CVD events accounting for the number of calcified segments (HR (per count)?=?0.55; 95%CI, 0.31-0.98; p?=?0.042 and HR?=?0.66; 95%CI, 0.45-0.98; p?=?0.039, respectively). CONCLUSIONS:Directly measured CAC density does not predict CVD events due to the strong correlation with CAC volume. The spherical shape and pericardial-sided location of CAC are associated with fewer CVD events and may represent morphological features related to stable coronary plaques. KEY POINTS:• Coronary calcium density may not be independently associated with cardiovascular events. • Coronary calcium density correlates strongly with calcium volume. • Spherical shape and pericardial-sided location of CAC are associated with fewer CVD events.

Project description:Background Arterial arteriosclerosis and atherosclerosis reflect vascular disease, the subclinical detection of which allows opportunity for cardiovascular disease (CVD) prevention. Larger cohort studies simultaneously quantifying anatomic thoracic and abdominal aortic pathologic abnormalities are lacking in the literature. Purpose To investigate the association of aortic wall area (AWA) and atherosclerotic plaque presence and burden as measured on MRI scans with incident CVD in a community sample. Materials and Methods In this prospective cohort study, participants in the Framingham Heart Study Offspring Cohort without prevalent CVD underwent 1.5-T MRI (between 2002-2005) of the descending thoracic and abdominal aorta with electrocardiogram-gated axial T2-weighted black-blood acquisitions. The wall thickness of the thoracic aorta was measured at the pulmonary bifurcation level and used to calculate the AWA as the difference between cross-sectional vessel area and lumen area. For primary or secondary analyses, multivariable Cox proportional hazards regression models were used to examine the association of aortic MRI measures with risk of first-incident CVD events or stroke and coronary heart disease, respectively. Results In 1513 study participants (mean age, 64 years ± 9 [SD]; 842 women [56%]), 223 CVD events occurred during follow-up (median, 13.1 years), of which 97 were major events (myocardial infarction, ischemic stroke, or CVD death). In multivariable analysis, thoracic AWA and prevalent thoracic plaque were associated with incident CVD (hazard ratio [HR], 1.20 per SD unit [95% CI: 1.05, 1.37] [P = .006] and HR, 1.63 [95% CI: 1.12, 2.35] [P = .01], respectively). AWA and prevalent thoracic plaque were associated with increased hazards: 1.32 (95% CI: 1.07, 1.62; P = .01) and 2.20 (95% CI: 1.28, 3.79; P = .005), for stroke and coronary heart disease, respectively. Conclusion In middle-aged community-dwelling adults, thoracic aortic wall area (AWA), plaque prevalence, and plaque volumes measured with MRI were independently associated with incident cardiovascular disease, with AWA associated in particular with stroke, and plaque associated with coronary heart disease. Clinical trial registration no. NCT00041418 © RSNA, 2022 Online supplemental material is available for this article. See also the editorial by Peshock in this issue.

Dataset Information

Cardiovascular Event Prediction and Risk Reclassification by Coronary, Aortic, and Valvular Calcification in the Framingham Heart Study.

Background

Methods and results

Conclusions

Publications

Cardiovascular Event Prediction and Risk Reclassification by Coronary, Aortic, and Valvular Calcification in the Framingham Heart Study.

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