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Provides a pathophysiological perspective on the cessation or persistence of angina following coronary thrombosis.
That attacks of angina pectoris may cease after the occurrence of coronary thrombosis has been pointed out by McKeen 1 and by Wolff and White. 2 This is probably explained by the fact that the branch of the coronary which, by its narrowed condition, was responsible for pain on an increased demand for function of the heart, is obliterated by the thrombosis. After obliteration of the vessel by a thrombosis there is an infarct of that part of the heart muscle which it supplies and, if the patient survives, this is followed by scar tissue replacement. The infarct or the scar is physiologically inactive and increased physiologic demand on the heart does not result in the attacks of angina pectoris to which the patient was previously subject, unless other coronary branches are involved. On the other hand, we believe that it is not uncommon for patients who have suffered coronary
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LOWELL B. ECKERSON (1928) studied this question.
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