Chronically decreased aortic distensibility causes deterioration of coronary perfusion during increased left ventricular contraction
S Ohtsuka,
M Kakihana,
H Watanabe,
and
Y Sugishita
Department of Internal Medicine, University of Tsukuba, Japan.
OBJECTIVES. This study investigated the long-term effects of decreased aortic distensibility on the heart in relation to coronary perfusion. BACKGROUND. Aortic distensibility is decreased in patients with atherosclerosis and hypertension and in the elderly. However, the effect of a long-term decrease in aortic distensibility on coronary perfusion has not been fully investigated. METHODS. Twelve anesthetized dogs underwent thoracotomy and were allocated to two groups: Group I included six control dogs with a normal aorta; Group II included six dogs with decreased aortic distensibility produced by banding the descending aorta. After 4 to 6 weeks, the dogs had a second operation to measure coronary artery flow and transmural flow distribution. Because the effect of decreased aortic distensibility on coronary perfusion may be affected by ventricular contractility, measurements were performed at baseline and during increased ventricular contraction induced by isoproterenol infusion. RESULTS. At baseline, arterial compliance was reduced by 35% in Group II, but there was no change in total mean arterial resistance. Hemodynamic variables, regional wall motion and coronary flow were also similar in both groups. However, during isoproterenol infusion, coronary flow increased more in Group II than in Group I (p < 0.01), and the coronary flow reserve ratio (maximal peak hyperemic flow divided by rest flow) decreased more in Group II than in Group I (mean [+/- SD] 1.9 +/- 0.4 vs. 2.4 +/- 0.3, p < 0.05). Moreover, although the transmural flow distribution was similar in the two groups at baseline, during isoproterenol infusion the endocardial flow increased less in Group II than in Group I (p < 0.05), and the endocardial/epicardial flow ratio was significantly decreased in Group II compared with Group I (mean [+/- SD] 0.70 +/- 0.18 vs. 0.99 +/- 0.22, p < 0.05). The subendocardial electrocardiogram showed ST segment elevation during isoproterenol infusion in Group II (p < 0.05) but not in Group I. CONCLUSIONS. These results demonstrate that during increased ventricular contraction, chronically decreased aortic distensibility contributes to a further decrease in the coronary flow reserve ratio, impairs endocardial blood flow and may induce subendocardial ischemia even in the absence of coronary artery stenosis.
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