12.5 IMPAIRED REGULATION OF ARTERIAL WALL VISCOSITY DURING CHANGES IN BLOOD FLOW IN ESSENTIAL HYPERTENSIVE PATIENTS

Abstract

Background: Arterial wall viscosity (AWV) is a major source of cardiac energy dissipation along the arterial tree. Evolution of AWV during increase in blood flow and the impact of essential hypertension on this evolution have never been studied. Methods: Radial artery diameter, wall thickness and arterial pressure were simultaneous measured in 18 untreated essential hypertensive (HT) subjects and 14 frequency matched normotensive (NT) controls at baseline and during a sustained blood flow increase induced by hand skin heating. AWV was estimated by the ratio of the area of the hysteresis loop of the pressure-diameter relationship (viscous energy dissipated, WV) to the area under the loading phase of this relationship (elastic energy stored during the cardiac cycle, WE). Results: At baseline, WV and WE were higher in HT than in NT subjects (WV: 1.06±0.78 versus 0.66±0.49mmHg.mm2, p<0.01 WE: 2.33±1.47 versus 1.69±1.15mmHg.mm2, p<0.05) but WV/WE was similar (43.0%±10. 1% versus 39.4%±11.8%). Heating did not modify significantly WE in both groups but induced an increase in WV only in HT patients (HT: +0.39±0.67mmHg.mm2, p<0.05 NT: +0.24±0.43mmHg.mm2, p=0.14 HT versus NT: p=0.09). Subsequently, WV/WE increased in HT but not in NT subjects (HT: +9.2%±9.1%, p<0.01 NT: +3.9%±9.9%, p=0.22 HT versus NT: p<0.01). Midwall stress, used as index of wall loading conditions, similarly increased in both groups (HT: +19.0±7.8 kPa, p<0.001 NT: +28.1±7.7 kPa, p<0.01 HT versus NT: p=0.13). Conclusions: AWV is maintained during flow increase in NT subjects but increases in HT subjects. Excessive loss of energy may contribute to impair cardiovascular coupling during hypertension.