We evaluated the functional capacity of the intercoronary collateral vasculature in response to graded exercise 2 weeks after acute circumflex coronary artery occlusion. Acute myocardial infarction was produced in 11 chronically instrumental awake dogs by abrupt occlusion of the left circumflex coronary artery. Two weeks later regional myocardial blood flow was measured at rest and during three levels of graded treadmill exercise by injection of radionuclide-labeled microspheres, 7-10 μm in diameter, into the left atrium. The region of collateral-dependent myocardium was determined by injection of Evans blue dye into the coronary artery distal to the occluder, and the extent of infarction by histological examination. At rest, blood flow to collateral-dependent regions was directly proportional to the amount of viable myocardium present. In regions containing <25% infarcted myocardium, blood flow increased progressively with exercise as in normally perfused control areas from the anterior left ventricular wall. In regions containing >75% infarcted myocardium, blood flow did not increase significantly during exercise, and in over one-half flow, during exercise, actually fell below the resting level. In areas containing 26-75% infarcted myocardium, blood flow demonstrated an intermediate ability to increase in response to exercise. Thus, the capacity of the coronary collateral circulation to deliver blood to its dependent myocardium was compromised progressively in proportion to the degree of infarcted myocardium. Collateral-dependent areas containing relatively small proportions of infarcted myocardium had normal blood flow response to exercise, whereas regions containing extensive infarction had little or no functional reserve so that increasing hypoperfusion commonly occurred during exercise.
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Acknowledgements. This work was supported by the Swedish Childhood Cancer Foundation (Barncancerfonden), the Swedish Research Council (Vetens-kapsrådet), governmental grants from Agreement concerning research and education of doctors (ALF), the Sahlgrenska Academy at the University of Gothenburg, the Sten A Olsson’s Foundation, the King Gustav V Jubilee Clinic Research Foundation (JK-fonden), the Frimurare Barnhus Foundation, the Wilhelm and Martina Lundgren Foundation, the Gothenburg Medical Society, Sahlgrenska Foundations (SU-fonden), the Aina Wallström’s and Mary-Ann Sjöblom’s Foundation, the Ulla and Rune Amlöv Foundations, AFA Insurance and the Swedish Society of Medicine. We are grateful for the skillful technical assistance of Rita Grandér.