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Experimental study demonstrates coronary artery stasis driven by microvascular vasospasm in canine infarct models, suggesting a mechanism for secondary coronary thrombosis.
After induced myocardial infarction in the dog, there was marked reduction of flow in the anatomically patent coronary artery supplying the area of infarct. This coronary artery stasis offers a possible mechanism for the secondary development of coronary artery thrombosis after myocardial infarction. Evidence that this flow abnormality was due to vasospasm involving small intramyocardial arteries is presented.
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H. Richard Hellstrom (1971) studied this question.
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