Higher carotid-femoral pulse wave velocity was strongly associated with thoracic aortic (OR 2.69), abdominal aortic (OR 1.47), and coronary artery calcification (OR 1.48) (all P<0.001).
Cross-Sectional (n=2,920)
Are arterial stiffness, pressure pulsatility, and wave reflection associated with arterial calcification in individuals free of cardiovascular disease?
Abnormal central arterial hemodynamics, particularly carotid-femoral pulse wave velocity, are strongly associated with vascular calcification even in younger individuals without prevalent cardiovascular disease.
Effect estimate: OR 2.69 per SD (for thoracic aortic calcification) (95% CI 2.17-3.35)
p-value: p=<0.001
OBJECTIVE: Arterial hemodynamics and vascular calcification are associated with increased risk for cardiovascular disease, but their inter-relations remain unclear. We sought to examine the associations of arterial stiffness, pressure pulsatility, and wave reflection with arterial calcification in individuals free of prevalent cardiovascular disease. APPROACH AND RESULTS: Framingham Heart Study Third Generation and Offspring Cohort participants free of cardiovascular disease underwent applanation tonometry to measure arterial stiffness, pressure pulsatility, and wave reflection, including carotid-femoral pulse wave velocity, central pulse pressure, forward wave amplitude, and augmentation index. Participants in each cohort (n=1905, 45±6 years and n=1015, 65±9 years, respectively) underwent multidetector computed tomography to assess the presence and quantity of thoracic aortic calcification, abdominal aortic calcification, and coronary artery calcification. In multivariable-adjusted models, both higher carotid-femoral pulse wave velocity and central pulse pressure were associated with greater thoracic aortic calcification and abdominal aortic calcification, whereas higher augmentation index was associated with abdominal aortic calcification. Among the tonometry measures, carotid-femoral pulse wave velocity was the strongest correlate of all calcification measures in multivariable-adjusted models (odds ratio per SD for thoracic aortic calcification, 2.69 95% confidence interval, 2.17-3.35; abdominal aortic calcification, 1.47 95% confidence interval, 1.26-1.73; and coronary artery calcification, 1.48 95% confidence interval, 1.28-1.72; all P<0.001, respectively). We observed stronger relations of carotid-femoral pulse wave velocity, central pulse pressure, and forward wave amplitude with nearly all continuous calcification measures in the younger Third Generation Cohort as compared with the Offspring Cohort. CONCLUSIONS: In community-dwelling individuals without prevalent cardiovascular disease, abnormal central arterial hemodynamics were positively associated with vascular calcification and were observed at younger ages than previously recognized. The mechanisms of these associations may be bidirectional and deserve further study.
Tsao et al. (Fri,) conducted a cross-sectional in Free of prevalent cardiovascular disease (n=2,920). Arterial hemodynamics (carotid-femoral pulse wave velocity, central pulse pressure, forward wave amplitude, augmentation index) was evaluated on Presence and quantity of thoracic aortic, abdominal aortic, and coronary artery calcification (OR 2.69 per SD (for thoracic aortic calcification), 95% CI 2.17-3.35, p=<0.001). Higher carotid-femoral pulse wave velocity was strongly associated with thoracic aortic (OR 2.69), abdominal aortic (OR 1.47), and coronary artery calcification (OR 1.48) (all P<0.001).