Abstract 11058: Backward Propagation of Waves is Limited in the Human Arterial Tree
Modulation of the reflection of pressure waves back to the heart in the human arterial tree is thought to modify the arterial pressure waveform and contribute to cardiovascular morbidity. This assumes that waves propagate well in the backward direction. We directly measured the degree to which the reflected wave weakens with distance from a fixed site of reflection created by occlusion of a femoral artery by inflation of an external cuff. Pressure & Doppler velocity were measured with sensor-tipped intra-arterial wires from the femoral artery to the proximal aorta of 20 subjects (age 31-83 years) before and during femoral artery occlusion. Incident and reflected waves were identified and quantified using separated wave intensity analysis. Wave reflection index (WRI) expresses the backward compression wave as a percentage of the incident forward compression wave. Pd/Pp expresses pressure originating distal to the sensor relative to pressure originating proximally. Cuff inflation created a significant reflection evident in WRI (mean difference logWRI -5.59, 95% C.I. -8.1 to -3.1), Pd/Pp (0.23, 0.18 - 0.29) and earlier arrival of the reflected wave (46ms, 26 - 65) (p=0.0001 for all parameters) within 10cm of the occlusion site, when compared to the un-inflated cuff. This effect of femoral occlusion on WRI became statistically insignificant beyond 40cm from the reflection site (mean difference logWRI -1.14, 95% C.I. -3.8 - 1.5, p=0.39) (Figure). This was even less (20cm) for Pd/Pp (0.02, -0.01 - 0.58, p=0.19) & reflection time (3ms, -1 to 9, p=0.24). In conclusion, these data suggest that waves propagate poorly in a backward direction in the human arterial tree. This can be explained by the numerous bifurcations, designed for efficient forward wave propagation and consequently poor at wave propagation in the opposite (backward) direction. These findings challenge the prevalent view of distal arterial wave reflection adversely interacting directly with cardiac function.
- © 2011 by American Heart Association, Inc.