Wave-intensity analysis: a new approach to coronary hemodynamics

Author:

Sun Yi-Hui1,Anderson Todd J.1,Parker Kim H.2,Tyberg John V.1

Affiliation:

1. Departments of Medicine and Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada T2N 4N1; and

2. Physiological Flow Studies Group, Department of Biological and Medical Systems, Imperial College of Science, Technology, and Medicine, London SW7 2BY, United Kingdom

Abstract

In 10 anesthetized dogs, we measured high-fidelity left circumflex coronary (PLCx), aortic (PAo), and left ventricular (PLV) pressures and left circumflex velocity ( U LCx; Doppler) and used wave-intensity analysis (WIA) to identify the determinants of PLCx and U LCx. Dogs were paced from the right atrium ( control 1) or right ventricle by use of single ( control 2) and then paired pacing to evaluate the effects of left ventricular contraction on PLCx and U LCx. During left ventricular isovolumic contraction, PLCx exceeded PAo, paired pacing increasing the difference. Paired pacing increased ΔPX(the PLCx-PAo difference at the PAo-PLV crossover) and average dPLCx/d t ( P < 0.0001 for both). During this time, WIA identified a backward-going compression wave (BCW) that increased PLCx and decreased U LCx; the BCW increased during paired pacing ( P < 0.0001). After the aortic valve opened, the increase in PAo caused a forward-going compression wave that, when it exceeded the BCW, caused U LCx to increase, despite PLV and (presumably) elastance continuing to increase. Thus WIA identifies the contributions of upstream (aortic) and downstream (microcirculatory) effects on PLCx and U LCx.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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