P-3 MP-38: Beat to beat viscous damping is modulated by ace inhibitors in human hypertension

Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. Arterial wall viscosity is a source of energy dissipation associated with vascular smooth muscle (VSM). Our aim was to evaluate the role of VSM viscous damping and its energy dissipation in the human common carotid artery (CCA) during control and ACEI treatment conditions. Noninvasive CCA pressure (tonometry) and diameter (B mode echography) waveforms were obtained in normotensive subjects (NT group) and in hypertensive patients (HT group) single-blind randomized into HT-placebo or HT-treated (ramipril, 5–10 mg/day during 3 months). Assessment of arterial wall dynamics was made by measuring its viscous (η), inertial (M) and elastic (E) properties. Viscous energy dissipation during the heart beat (W) was computed as 4ωηA, where ω is [2η(heart rate)], and A is the arterial cross sectional area. The effects of viscous damping on the overall arterial wall were evaluated by a normalized damping calculated as η/[2(EM)0.5]. (See Table 1) Viscous damping parameters NT group HT group HT-treated (n = 12) (n = 22) (n = 12) Arterial wall viscosity (mmHg s/mm) 7.2±3.2 13.1±2.8b 9.6±3.4ac Energy dissipation (105 erg/cm2) 10.9±5.8 31.9±11.61b 16.4±6.4ac Normalized damping 0.72±0.19 0.73±0.23 0.77±0.25 Values are expressed as mean ± standard deviation. a P < 0.05 b P < 0.01 respect to NT group c P < 0.01 respect to HT group Arterial wall viscosity and energy dissipation were greater in HT than in NT, and remained near normal in HT-treated, whereas no changes were observed in the HT-placebo group. The constancy of the normalized damping independently from pressure levels is thought to prevent damages of the arterial wall caused by the deleterious high frequency components present in the pulse waveform. In conclusion, our results suggest that smooth muscle modulates energy dissipation. This apparent disadvantage could positively contribute to maintain the cushioning exerted by the arterial wall. The energy dissipation improvement by ramipril in HT could be partially related to smooth muscle relaxation induced by angiotensin converting enzyme inhibition.