Abstract
To examine the effects of volume-overload hypertrophy on regional myocardial perfusion, we determined myocardial blood flows with microspheres at rest, during exercise, and during exercise with adenosine infusion in dogs with aortocaval fistulas for 12 wk (group 2) and sham-operated controls (group 1). A subgroup of six animals (group 3) was studied both before and after shunt closure in order to separate the influences of hypertrophy from the hemodynamic effects of the fistula. Epicardial blood flows in animals with patent fistulas were significantly greater than in controls under all conditions (P less than 0.05). However, endocardial blood flows were lower at maximal exercise and with adenosine, so that the endocardial-to-epicardial blood flow ratios were reduced 36 and 28%, respectively(P less than 0.05). These flow abnormalities were reversed by closing the fistula prior to regression of hypertrophy. Moreover, coronary resistance per unit of myocardium was not different for the three groups. These results suggest that the blood-flow abnormalities seen in the exercising dog with an aortocaval fistula are secondary to hemodynamic considerations and not to hypertrophy itself. Low aortic diastolic pressures and high myocardial oxygen demands during exercise may combine to produce subendocardial hypoperfusion in this model.
Published Version
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