TY - JOUR
T1 - Increased Wave Reflection Rather Than Central Arterial Stiffness Is the Main Determinant of Raised Pulse Pressure in Women and Relates to Mismatch in Arterial Dimensions A Twin Study
AU - Cecelja, Marina
AU - Jiang, Benyu
AU - McNeill, Karen
AU - Kato, Bernet
AU - Ritter, James
AU - Spector, Tim
AU - Chowienczyk, Phil
PY - 2009/8/18
Y1 - 2009/8/18
N2 - Objectives Our aim was to examine the relative contributions of the first systolic shoulder (P1) and augmentation pressure (Delta P-aug) to central pulse pressure (cPP), their relation to central arterial stiffness (pulse wave velocity [PWV]) and arterial diameters, and their respective heritability estimates.
Background cPP is augmented above P1 by Delta P-aug due to pressure waves reflected from the periphery of the circulation.
Methods Women (n = 496) from the Twins UK adult twin registry (112 monozygotic, 135 dizygotic pairs) age 21 to 81 years were studied. cPP, P1, and Delta P-aug were estimated using the SphygmoCor system (Atcor, West Ryde, Australia) from transformed radial waveforms. Carotid-femoral PWV was measured using the same system. Aortic and femoral artery diameters were measured by ultrasonography. Heritability was estimated using structural equation modeling.
Results P1 and Delta P-aug accounted for 22% and 76%, respectively, of the variance in cPP. After adjustment for mean arterial pressure and heart rate, P1 strongly independently positively correlated with PWV (standardized regression coefficient, beta = 0.4, p <0.0001), whereas Delta P-aug did not independently correlate with PWV but independently negatively correlated with the ratio of the diameter of the femoral to that of the abdominal aorta (beta = -0.12, p <0.001). Estimates of heritability (h(2)) of cPP, PWV, P1, and Delta P-aug were 0.43, 0.34, 0.31, and 0.62, respectively, after adjustment for mean arterial pressure and heart rate.
Conclusions These results suggest that, in women, Delta P-aug is highly heritable, is associated with the ratio of distal to proximal arterial diameters, and, independent of PWV, is a major determinant of cPP. (J Am Coll Cardiol 2009; 54: 695-703) (C) 2009 by the American College of Cardiology Foundation
AB - Objectives Our aim was to examine the relative contributions of the first systolic shoulder (P1) and augmentation pressure (Delta P-aug) to central pulse pressure (cPP), their relation to central arterial stiffness (pulse wave velocity [PWV]) and arterial diameters, and their respective heritability estimates.
Background cPP is augmented above P1 by Delta P-aug due to pressure waves reflected from the periphery of the circulation.
Methods Women (n = 496) from the Twins UK adult twin registry (112 monozygotic, 135 dizygotic pairs) age 21 to 81 years were studied. cPP, P1, and Delta P-aug were estimated using the SphygmoCor system (Atcor, West Ryde, Australia) from transformed radial waveforms. Carotid-femoral PWV was measured using the same system. Aortic and femoral artery diameters were measured by ultrasonography. Heritability was estimated using structural equation modeling.
Results P1 and Delta P-aug accounted for 22% and 76%, respectively, of the variance in cPP. After adjustment for mean arterial pressure and heart rate, P1 strongly independently positively correlated with PWV (standardized regression coefficient, beta = 0.4, p <0.0001), whereas Delta P-aug did not independently correlate with PWV but independently negatively correlated with the ratio of the diameter of the femoral to that of the abdominal aorta (beta = -0.12, p <0.001). Estimates of heritability (h(2)) of cPP, PWV, P1, and Delta P-aug were 0.43, 0.34, 0.31, and 0.62, respectively, after adjustment for mean arterial pressure and heart rate.
Conclusions These results suggest that, in women, Delta P-aug is highly heritable, is associated with the ratio of distal to proximal arterial diameters, and, independent of PWV, is a major determinant of cPP. (J Am Coll Cardiol 2009; 54: 695-703) (C) 2009 by the American College of Cardiology Foundation
U2 - 10.1016/j.jacc.2009.04.068
DO - 10.1016/j.jacc.2009.04.068
M3 - Article
VL - 54
SP - 695
EP - 703
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 8
ER -