Key result
Adding arterial calcium to Framingham models improves CHD risk prediction ~15% but not cerebrovascular risk.
Why the study?
Risk prediction for cardiovascular disease may improve by targeting multiple atherosclerosis components across vascular beds for both coronary heart disease and cerebrovascular disease.
Does the addition of coronary, aortic arch, or carotid artery calcification improve the prediction of coronary heart disease and cerebrovascular events in asymptomatic adults?
Cohort (n=2,153)
Does the addition of coronary, aortic arch, or carotid artery calcification improve the prediction of coronary heart disease and cerebrovascular events in asymptomatic adults?
Effect estimate: NRI 15%
p-value: p=<0.01
Calcification in the coronary arteries, aortic arch, and carotid arteries significantly improves risk prediction for coronary heart disease but not for cerebrovascular events in asymptomatic older adults.
May enhance CHD risk stratification; extends Framingham models but requires prospective validation before practice change.
AIMS: Since atherosclerosis is a systemic process, risk prediction would benefit from targeting multiple components of cardiovascular disease simultaneously. To this end, it is useful to examine the predictive value of non-invasive measures of atherosclerosis in various vascular beds for both coronary heart disease (CHD) and cerebrovascular disease. METHODS AND RESULTS: Between September 2003 and February 2006, 2153 asymptomatic participants (69.6±6.6 years) from the Rotterdam Study underwent a multi-detector computed tomography scan. During a median follow-up of 3.5 years, 58 CHD events (myocardial infarction and CHD death) and 52 cerebrovascular events (TIA and stroke) occurred. Participants were classified into low (<5%), intermediate (5-10%), and high (>10%) 5-year risk categories based on a refitted Framingham risk model. The model was extended by coronary, aortic arch, or carotid calcium and reclassification percentages were calculated. For the outcome CHD, the C-statistic improved from 0.693 for the Framingham refitted model to 0.743, 0.740, and 0.749 by addition of coronary, aortic arch, and carotid calcium, respectively. Reclassification was most substantial in the intermediate risk group where addition of coronary calcium reclassified 56% of persons [net reclassification improvement (NRI): 15%; P<0.01)]. Adding aortic arch calcium led to a reclassification of 32% of persons (NRI: 8%; P=0.01) and adding carotid calcium reclassified 51% (NRI: 9%; P=0.02). In contrast, calcification in any of the three vascular beds did not improve cerebrovascular risk prediction. CONCLUSION: Coronary, aortic arch, and carotid artery calcification significantly improved risk prediction of CHD but not of cerebrovascular events.
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Elias‐Smale et al. (2011) conducted a cohort in Asymptomatic cardiovascular risk (n=2,153). Coronary, aortic arch, or carotid calcium vs. Framingham risk model alone was evaluated on Coronary heart disease (CHD) events (myocardial infarction and CHD death) (NRI 15%, p=<0.01). Adding coronary, aortic arch, or carotid artery calcification to a Framingham risk model significantly improved risk prediction for CHD (e.g., coronary calcium NRI 15%, P<0.01) but not cerebrovascular events.
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