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      Prevalence of Total Coronary Occlusion during the Early Hours of Transmural Myocardial Infarction

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          Abstract

          To define the prevalence of total coronary occlusion in the hours after transmural myocardial infarction, we used coronary arteriography to study the degree of coronary obstruction in 322 patients admitted within 24 hours of infarction. Total coronary occlusion was observed in 110 of 126 patients (87 per cent) who were evaluated within four hours of the onset of symptoms; this proportion decreased significantly, to 37 of 57 (65 per cent), when patients were studied 12 to 24 hours after the onset of symptoms. Among 59 patients with angiographic features of coronary thrombosis, the thrombus was retrieved by Fogarty catheter in 52 (88 per cent) but was absent in seven (12 per cent false positive). Among an additional 20 patients without angiographic features of thrombosis, a thrombus was discovered in five (25 per cent false negative). Thus, total coronary occlusion is frequent during the early hours of transmural infarction and decreases in frequency during the initial 24 hours, suggesting that coronary spasm or thrombus formation with subsequent recanalization or both may be important in the evolution of infarction.

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          Most cited references22

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          Treatment of myocardial infarction in a coronary care unit

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            Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of "preinfarction" angina.

            To investigate the pathogenesis of myocardial infarction we undertook a systematic study of patients with angina at rest, a syndrome known to evolve frequently into infarction. Among 187 consecutive patients, 37 had infarction, all in the area that showed electrocardiographic changes during angina. In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented. In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks. One patient in whom spasm was observed at the onset of infarction died six hours later; at post-mortem examination, a fresh laminar thrombus was found at the site of the spasm. After infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiography.
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              Acute myocardial infarction: intracoronary application of nitroglycerin and streptokinase.

              In five patients with acute myocardial infarction, the effects of both intracoronary nitroglycerin (NTG) and subsequent intracoronary streptokinase application were evaluated. In addition, transluminal recanalization was performed in one of these patients. Injection of NTG into the infarct-related coronary artery resulted in improved distal filling of the subtotally occluded left circumflex artery in one patient, and in transient patency of the completely occluded right coronary artery in a second patient. In a third patient patency of the totally occluded left anterior descending artery (LAD) was achieved by transluminal recanalization with a guide wire. In a forth patient with occulsion of the LAD, there was no response to intracoronary NTG and mechanical recanalization was not attempted. Subsequent intracoronary infusion of streptokinase (1,000--2,000 U/min for 15--60 min) resulted in a further and long-term reduction of narrowing at the site of acute occlusion in patients I-III and in opening of the completely occluded LAD in patient IV. Improvement of lumen was paralleled by alleviation of symptoms. In a fifth patient, in whom the LAD was subtotally occluded, the degree of coronary obstruction could not be changed by intracoronary application of NTG or by lysis. In this patient, symptoms and ECG changes improved with reduction of pathologically elevated blood pressure values. The findings suggest that myocardial infarction had been caused by thrombotic occulsion in four patients, and that spasm of the infarct vessel could have been an additional factor in two of these patients. In the fifth patient, an increase of afterload in the presence of a subtotal lesion might have caused the critical imbalance between oxgen supply and demand, resulting in cell death.
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                Author and article information

                Journal
                New England Journal of Medicine
                N Engl J Med
                Massachusetts Medical Society
                0028-4793
                1533-4406
                October 16 1980
                October 16 1980
                : 303
                : 16
                : 897-902
                Article
                10.1056/NEJM198010163031601
                7412821
                14c5a9ce-e4e4-4b96-a02e-264b1ea81984
                © 1980

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