Left ventricular hypertrophy is an independent cardiovascular risk factor. In hypertensives, the pattern of hypertrophy is influenced by central haemodynamic characteristics. Central haemodynamics may also determine physiological differences in left ventricular structure and predispose to particular responses of the left ventricle to pathological increases in load. M-mode echocardiography was used to measure left ventricular diastolic dimension and to estimate left ventricular mass index, relative wall thickness and stroke volume in 159 healthy volunteers aged between 19 and 74 years. Tonometric sphygmography was used to estimate augmentation index, central end-systolic and mean arterial blood pressure. Effective arterial elastance was calculated as the ratio of end-systolic pressure to stroke volume. Left ventricular mass index and relative wall thickness were adjusted for variation in age, sex and blood pressure before analyses. Left ventricular diastolic dimension exhibited significant inverse correlations with both effective arterial elastance (r =-0.72, P < 0.0001) and augmentation index (r =-0.23, P = 0.004). Adjusted left ventricular mass index was inversely correlated with effective arterial elastance (r =-0.35, P < 0.0001), but no correlation was observed between left ventricular mass index and augmentation index (r = 0.04). Adjusted relative wall thickness correlated with increasing effective arterial elastance (r = 0.32, P < 0.0001) and augmentation index (r = 0.18, P = 0.02). Relative wall thickness (r = 0.34, P < 0.0001), but not left ventricular mass index, correlated with age. Higher elastance and augmentation correlates with relatively smaller left ventricular cavity size but larger relative wall thickness. Age-related changes in left ventricular afterload may affect relative wall thickness more significantly than left ventricular mass index and may contribute to a particular change in left ventricular geometry with age.
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July 2001
Research Article|
June 12 2001
Physiological relationships between central vascular haemodynamics and left ventricular structure
Jenny A. DEAGUE;
Jenny A. DEAGUE
*Department of Physiology, University of Melbourne, Parkville, Victoria 3010, Australia
†Department of Cardiology, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia
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Catherine M. WILSON;
Catherine M. WILSON
†Department of Cardiology, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia
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Leeanne E. GRIGG;
Leeanne E. GRIGG
†Department of Cardiology, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia
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Stephen B. HARRAP
Stephen B. HARRAP
*Department of Physiology, University of Melbourne, Parkville, Victoria 3010, Australia
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Clin Sci (Lond) (2001) 101 (1): 79–85.
Article history
Received:
November 06 2000
Revision Received:
February 07 2001
Accepted:
March 22 2001
Citation
Jenny A. DEAGUE, Catherine M. WILSON, Leeanne E. GRIGG, Stephen B. HARRAP; Physiological relationships between central vascular haemodynamics and left ventricular structure. Clin Sci (Lond) 1 July 2001; 101 (1): 79–85. doi: https://doi.org/10.1042/cs1010079
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