OBJECTIVE: Arterial stiffness is an emerging major risk factor for cardiovascular morbidity and mortality. The aim of the present study was to assess if coronary artery plaque load correlates with non-invasive measures of arterial stiffness. DESIGN: Prospective investigational study. SETTING: Tertiary university hospital centre. PATIENTS: Patients undergoing elective diagnostic coronary angiography. INTERVENTIONS AND MAIN OUTCOME MEASURES: Coronary artery plaque burden was assessed using a 30 MHz intravascular ultrasound catheter during an automated pullback. Proximal coronary artery plaque volume was determined using a validated edge-detection algorithm following three-dimensional computerized reconstruction. Central arterial stiffness was assessed in each patient using applanation tonometry to radial, carotid and femoral pulses, with derivation of aortic pressure augmentation and pulse wave velocity using pulse wave analysis. RESULTS: In 35 patients (61 +/- 2 years), proximal coronary arterial plaque volume was 5.9 +/- 0.6 mm3/mm of vessel. Plaque volume correlated positively with carotid-radial pulse wave velocity (r = 0.47, P = 0.008) and appeared to correlate with carotid-femoral pulse wave velocity (r = 0.34, P = 0.07). Aortic augmentation (r = 0.24, P = 0.16), augmentation index (r = 0.3, P = 0.08), and pulse pressure (r = 0.22, P = 0.2) did not correlate significantly with proximal coronary artery plaque volume. CONCLUSIONS: Non-invasive measures of carotid-radial pulse wave velocity correlate with the extent of coronary artery plaque volume and may be a useful non-invasive surrogate marker for the extent of coronary atherosclerosis. Our findings are consistent with the suggestion that central aortic stiffness may promote the development of coronary atherosclerosis and ischaemic heart disease.
OBJECTIVE: Arterial stiffness is an emerging major risk factor for cardiovascular morbidity and mortality. The aim of the present study was to assess if coronary artery plaque load correlates with non-invasive measures of arterial stiffness. DESIGN: Prospective investigational study. SETTING: Tertiary university hospital centre. PATIENTS: Patients undergoing elective diagnostic coronary angiography. INTERVENTIONS AND MAIN OUTCOME MEASURES: Coronary artery plaque burden was assessed using a 30 MHz intravascular ultrasound catheter during an automated pullback. Proximal coronary artery plaque volume was determined using a validated edge-detection algorithm following three-dimensional computerized reconstruction. Central arterial stiffness was assessed in each patient using applanation tonometry to radial, carotid and femoral pulses, with derivation of aortic pressure augmentation and pulse wave velocity using pulse wave analysis. RESULTS: In 35 patients (61 +/- 2 years), proximal coronary arterial plaque volume was 5.9 +/- 0.6 mm3/mm of vessel. Plaque volume correlated positively with carotid-radial pulse wave velocity (r = 0.47, P = 0.008) and appeared to correlate with carotid-femoral pulse wave velocity (r = 0.34, P = 0.07). Aortic augmentation (r = 0.24, P = 0.16), augmentation index (r = 0.3, P = 0.08), and pulse pressure (r = 0.22, P = 0.2) did not correlate significantly with proximal coronary artery plaque volume. CONCLUSIONS: Non-invasive measures of carotid-radial pulse wave velocity correlate with the extent of coronary artery plaque volume and may be a useful non-invasive surrogate marker for the extent of coronary atherosclerosis. Our findings are consistent with the suggestion that central aortic stiffness may promote the development of coronary atherosclerosis and ischaemic heart disease.
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