OBJECTIVE: Despite adequate glycemic and blood pressure control, diabetic hypertensives remain at increased cardiovascular risk. Aortic stiffness and pulse pressure (PP) amplification may provide complementary information to correct cardiovascular risk. We aim to determine whether these hemodynamic parameters are interrelated or not and to explore the factors related to pressure pulsatility. METHODS: A cross-sectional study was conducted in 351 patients, involving controls, hypertensives without diabetes and diabetic patients with or without hypertension. Hemodynamic parameters were determined by applanation tonometry. Multivariate regression analyses evaluated the interest of therapeutic strategies. RESULTS: Aortic stiffness and PP amplification were not interrelated (P = 0.32) in multivariate-adjusted analysis and were both independently associated with previous cardiovascular events. Although disproportionately increased aortic stiffness in diabetic hypertensives (P < 0.001), no difference was found for PP amplification. The present dissociation between these two hemodynamic parameters may be related to the effect of increased heart rate (P < 0.001) in the presence of diabetes, in men and women. In diabetic hypertensives, aortic stiffness was correlated with glycated hemoglobin level (P = 0.04), but not with blood pressure or heart rate. Antihypertensive and statin treatments were correlated with PP amplification but not with aortic stiffness. CONCLUSION: Aortic stiffness and PP amplification were not interrelated, suggesting that these markers may provide complementary information for cardiovascular risk. New therapeutic strategies targeting pressure pulsatility should take into account the impact of hyperglycemia and increased heart rate in diabetic hypertensives. Gender influence on the role of autonomic nervous system in attenuating pressure wave reflections remains to be further established.
OBJECTIVE: Despite adequate glycemic and blood pressure control, diabetic hypertensives remain at increased cardiovascular risk. Aortic stiffness and pulse pressure (PP) amplification may provide complementary information to correct cardiovascular risk. We aim to determine whether these hemodynamic parameters are interrelated or not and to explore the factors related to pressure pulsatility. METHODS: A cross-sectional study was conducted in 351 patients, involving controls, hypertensives without diabetes and diabeticpatients with or without hypertension. Hemodynamic parameters were determined by applanation tonometry. Multivariate regression analyses evaluated the interest of therapeutic strategies. RESULTS: Aortic stiffness and PP amplification were not interrelated (P = 0.32) in multivariate-adjusted analysis and were both independently associated with previous cardiovascular events. Although disproportionately increased aortic stiffness in diabetic hypertensives (P < 0.001), no difference was found for PP amplification. The present dissociation between these two hemodynamic parameters may be related to the effect of increased heart rate (P < 0.001) in the presence of diabetes, in men and women. In diabetic hypertensives, aortic stiffness was correlated with glycated hemoglobin level (P = 0.04), but not with blood pressure or heart rate. Antihypertensive and statin treatments were correlated with PP amplification but not with aortic stiffness. CONCLUSION: Aortic stiffness and PP amplification were not interrelated, suggesting that these markers may provide complementary information for cardiovascular risk. New therapeutic strategies targeting pressure pulsatility should take into account the impact of hyperglycemia and increased heart rate in diabetic hypertensives. Gender influence on the role of autonomic nervous system in attenuating pressure wave reflections remains to be further established.