OBJECTIVE: We previously demonstrated stronger relations of central vs. brachial blood pressure, particularly pulse pressure, to carotid artery hypertrophy and extent of atherosclerosis. Data regarding the relative impacts of central and brachial pressures on left ventricular hypertrophy and geometry are limited. METHODS: Echocardiography and radial applanation tonometry were performed in American Indian participants in the 4th Strong Heart Study examination. Left ventricular mass was calculated using an anatomically validated formula and adjusted for height. Brachial blood pressure was measured according to a standardized protocol. Central pressures were derived using a generalized transfer function. RESULTS: Of 2585 participants in the analysis, 60% were women, 21% had diabetes and 33% were hypertensive; the mean age was 40 +/- 17 years. All blood pressure variables were significantly related to left ventricular absolute and relative wall thicknesses and left ventricular mass index (all P < 0.001), with considerable variation in correlation coefficients (r = 0.135-0.432). Central and brachial systolic pressures were uniformly more strongly related to left ventricular wall thicknesses, diastolic diameter and mass index than their respective pulse pressures (all P < 0.005 by z statistics). Left ventricular relative wall thickness and mass index were more strongly related to central than brachial pressures. CONCLUSION: Left ventricular hypertrophy is more strongly related to systolic pressure than to pulse pressure. Furthermore central pressures are more strongly related than brachial pressures to concentric left ventricular geometry. These data suggest that absolute (systolic) pressure is more important in stimulating left ventricular hypertrophy and remodeling, whereas pulsatile stress (pulse pressure) is more important in causing vascular hypertrophy and atherosclerosis.
OBJECTIVE: We previously demonstrated stronger relations of central vs. brachial blood pressure, particularly pulse pressure, to carotid artery hypertrophy and extent of atherosclerosis. Data regarding the relative impacts of central and brachial pressures on left ventricular hypertrophy and geometry are limited. METHODS: Echocardiography and radial applanation tonometry were performed in American Indian participants in the 4th Strong Heart Study examination. Left ventricular mass was calculated using an anatomically validated formula and adjusted for height. Brachial blood pressure was measured according to a standardized protocol. Central pressures were derived using a generalized transfer function. RESULTS: Of 2585 participants in the analysis, 60% were women, 21% had diabetes and 33% were hypertensive; the mean age was 40 +/- 17 years. All blood pressure variables were significantly related to left ventricular absolute and relative wall thicknesses and left ventricular mass index (all P < 0.001), with considerable variation in correlation coefficients (r = 0.135-0.432). Central and brachial systolic pressures were uniformly more strongly related to left ventricular wall thicknesses, diastolic diameter and mass index than their respective pulse pressures (all P < 0.005 by z statistics). Left ventricular relative wall thickness and mass index were more strongly related to central than brachial pressures. CONCLUSION: Left ventricular hypertrophy is more strongly related to systolic pressure than to pulse pressure. Furthermore central pressures are more strongly related than brachial pressures to concentric left ventricular geometry. These data suggest that absolute (systolic) pressure is more important in stimulating left ventricular hypertrophy and remodeling, whereas pulsatile stress (pulse pressure) is more important in causing vascular hypertrophy and atherosclerosis.
Authors: Y Zhang; G Kollias; A A Argyris; T G Papaioannou; C Tountas; G D Konstantonis; A Achimastos; J Blacher; M E Safar; P P Sfikakis; A D Protogerou Journal: J Hum Hypertens Date: 2014-11-13 Impact factor: 3.012
Authors: Vernice R Peterson; Gavin R Norton; Michelle Redelinghuys; Carlos D Libhaber; Muzi J Maseko; Olebogeng H I Majane; Richard Brooksbank; Angela J Woodiwiss Journal: Am J Hypertens Date: 2014-11-05 Impact factor: 2.689