Technical Briefs

In Vitro Investigation of the Impact of Aortic Valve Stenosis Severity on Left Coronary Artery Flow

[+] Author and Article Information
E. Gaillard

Laboratory of Biomedical Engineering, Clinical Research Institute of Montreal, University of Montreal, 110 Avenue des Pins Ouest, Montreal, QC, H2W 1R7, Canadaemmanuel.gaillard@ircm.qc.ca

D. Garcia

CRCHUM, Research Centre, University of Montreal Hospital, 2099 Alexandre de Seve, Montreal, QC, H2L 2W5, Canada

L. Kadem

Laboratory of Cardiovascular Fluid Dynamics, Concordia University, 1515 St. Catherine Street West, Montreal, QC, H3G 1M8, Canada

P. Pibarot

Quebec Heart Institute, Laval Hospital,  Laval University, 2725 Chemin Sainte-Foy, Sainte-Foy, QC, G1V 4G5, Canada

L.-G. Durand

Laboratory of Biomedical Engineering, Clinical Research Institute of Montreal, University of Montreal, 110 Avenue des Pins Quest, Montreal, QC, H2W 1R7, Canada

J Biomech Eng 132(4), 044502 (Mar 17, 2010) (4 pages) doi:10.1115/1.4000990 History: Received October 23, 2009; Revised January 11, 2010; Posted January 12, 2010; Published March 17, 2010; Online March 17, 2010

Patients with aortic valve stenosis (AS) may experience angina pectoris even if they have angiographically normal coronary arteries. Angina is associated with a marked increase in the risk of sudden death in AS patients. Only a few in vitro models describing the interaction between the left ventricular and aortic pressures, and the coronary circulation have been reported. These models were designed for specific research studies and they need to be improved or modified when other specific studies are required. Consequently, we have developed an in vitro model that is able to mimic the coronary circulation in presence of aortic stenosis. First, we have validated the model under physiological conditions. Then, we have examined and quantified the hemodynamic effects of different degrees of AS (from normal to severe AS) on the coronary flow using a model of the normal left coronary artery. In the coronary in vitro model without AS (normal valve), the amplitude and shape of coronary flow were similar to those observed in in vivo measurements obtained under physiological conditions, as described by Hozumi (1998, “Noninvasive Assessment of Significant Left Anterior Descending Coronary Artery Stenosis by Coronary Flow Velocity Reserve With Transthoracic Color Doppler Echocardiography,” Circulation, 97, pp. 1557–1562). The presence of an AS induced an increase in the maximum and mean coronary flow rates (97% and 73%, respectively, for a very severe AS). Furthermore, when AS was very severe, a retrograde flow occurred during systole. This study allowed us to validate our coronary in vitro model under physiological conditions, both in the absence and presence of AS. These changes could explain the fact that even if patients have angiographically normal epicardial coronary arteries, we can observe the occurrence of angina pectoris in these patients in the presence of an AS.

Copyright © 2010 by American Society of Mechanical Engineers
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Grahic Jump Location
Figure 2

Schema of the locking system of the aortic valve leaflets

Grahic Jump Location
Figure 3

On the left: aortic and coronary flow rates in normal conditions (without AS) obtained from the in vitro model (notice that scales are not the same for the aortic (L/min) and coronary (mL/min) flow rates); on the right: aortic and LV pressures in normal conditions obtained from the in vitro model

Grahic Jump Location
Figure 4

Coronary flow rate for the four different AS severities obtained from the in vitro model

Grahic Jump Location
Figure 1

Schema of the in vitro flow model



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