OBJECTIVE: Increased pulse pressure has been associated with increased cardiovascular risk in individuals with diabetes. Changes in central aortic properties can increase central pulse pressure and may adversely affect microvascular perfusion and cardiac performance. This study was performed to define early changes in central arterial properties in a group of young individuals with type 1 diabetes. RESEARCH AND DESIGN METHODS: Seventeen individuals with type 1 diabetes and their nondiabetic control subjects who were participating in the Cardio-Diab Study had arterial stiffness and pulsatile hemodynamics measured with calibrated tonometry and pulsed Doppler. Aortic characteristic impedance (Z(c)) was calculated from the ratio of change in carotid pressure and aortic flow in early systole. Pulse wave velocity (PWV) was assessed from tonometry and body surface measurements. RESULTS: Duration of type 1 diabetes was 15.3 +/- 0.7 (mean +/- SD) years. In type 1 diabetic subjects, central pulse pressure was elevated (45 +/- 11 vs. 36 +/- 10 mmHg in control subjects, P = 0.02), as was peripheral pulse pressure (54 +/- 13 vs. 43 +/- 10 mmHg, P = 0.002). Z(c) was elevated in type 1 diabetes (179 +/- 57 vs. 136 +/- 42 dynes x s/cm5 in control subjects, P = 0.004), whereas PWV was not different (5.9 +/- 0.9 vs. 5.9 +/- 0.7 m/s in type 1 diabetic vs. control subjects, respectively; NS). There was a moderate correlation between Z(c) and urinary albumin excretion (coefficient 0.39, P = 0.02). CONCLUSIONS: Z(c) appears to be increased early in type 1 diabetes, before elevation of PWV and is associated with higher pulse pressure, which may contribute to renal microvascular damage in diabetes.
OBJECTIVE: Increased pulse pressure has been associated with increased cardiovascular risk in individuals with diabetes. Changes in central aortic properties can increase central pulse pressure and may adversely affect microvascular perfusion and cardiac performance. This study was performed to define early changes in central arterial properties in a group of young individuals with type 1 diabetes. RESEARCH AND DESIGN METHODS: Seventeen individuals with type 1 diabetes and their nondiabetic control subjects who were participating in the Cardio-Diab Study had arterial stiffness and pulsatile hemodynamics measured with calibrated tonometry and pulsed Doppler. Aortic characteristic impedance (Z(c)) was calculated from the ratio of change in carotid pressure and aortic flow in early systole. Pulse wave velocity (PWV) was assessed from tonometry and body surface measurements. RESULTS: Duration of type 1 diabetes was 15.3 +/- 0.7 (mean +/- SD) years. In type 1 diabetic subjects, central pulse pressure was elevated (45 +/- 11 vs. 36 +/- 10 mmHg in control subjects, P = 0.02), as was peripheral pulse pressure (54 +/- 13 vs. 43 +/- 10 mmHg, P = 0.002). Z(c) was elevated in type 1 diabetes (179 +/- 57 vs. 136 +/- 42 dynes x s/cm5 in control subjects, P = 0.004), whereas PWV was not different (5.9 +/- 0.9 vs. 5.9 +/- 0.7 m/s in type 1 diabetic vs. control subjects, respectively; NS). There was a moderate correlation between Z(c) and urinary albumin excretion (coefficient 0.39, P = 0.02). CONCLUSIONS: Z(c) appears to be increased early in type 1 diabetes, before elevation of PWV and is associated with higher pulse pressure, which may contribute to renal microvascular damage in diabetes.
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