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Localized abnormalities of motion of the left ventricular wall commonly follow inadequate or absent coronary blood flow to a region of the heart, and may greatly impair the overall function of the heart as a pump.1 These localized areas of wall dysfunction may be transient, as in the setting of angina pectoris or an evolving myocardial infarction, or may be persistent as the presence of true aneurysm formation. When coronary-artery disease is present, various stresses that raise oxygen demands of the heart, such as increased heart rate or augmented contractility, may induce transient localized ischemia with abnormal wall motion, although . . .
Edmund H. Sonnenblick (Thu,) studied this question.
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