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Journal ArticleDOI

Intracoronary thrombus in nontransmural myocardial infarction and in unstable angina pectoris

TLDR
The finding of thrombolysis in several patients with nontransmural MI and UA suggests that intracoronary thrombus formation plays a pathogenetic role in some patients with these ischemic syndromes.
Abstract
Although intracoronary thrombus formation plays a major role in acute transmural myocardial infarction (MI), its occurrence in unstable angina (UA) and nontransmural MI has not clearly been established. To determine whether intracoronary thrombus does occur in these syndromes, coronary arteriography was performed before, during, and after intracoronary nitroglycerin and streptokinase infusion in 17 patients. None of the 8 patients with nontransmural MI and 1 of the 9 patients with UA responded to intracoronary nitroglycerin. Seven of 8 patients with nontransmural MI and 4 of 9 patients with UA responded to streptokinase infusion with opening of an occluded vessel, an increase in stenotic diameter, dissolution of an intracoronary filling defect, or a combination of these. Serial opening and closing of ischemia-related vessels occurred spontaneously and in response to streptokinase in some patients in whom thrombolysis was demonstrated. Evidence of thrombolysis was not seen in any patient studied longer than 1 week from the onset of the rest pain syndrome. The finding of thrombolysis in several patients with nontransmural MI and UA suggests that intracoronary thrombus formation plays a pathogenetic role in some patients with these ischemic syndromes.

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Citations
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Journal ArticleDOI

Thrombosis and Acute Coronary-Artery Lesions in Sudden Cardiac Ischemic Death

TL;DR: The pathologic process in sudden ischemic death involves a rapidly evolving coronary-artery lesion in which plaque fissuring and resultant thrombus formation are present, and these findings have implications for the prevention of sudden cardiac death by antithrombotic therapy.
Journal ArticleDOI

Platelet activation in unstable coronary disease.

TL;DR: Data indicate that platelet activation occurs during spontaneous ischemia in patients with unstable angina, and the increment in prostacyclin biosynthesis during such episodes may be a compensatory response of vascular endothelium that limits the degree or effects of plateletactivation.
Journal ArticleDOI

Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion.

E Falk
- 01 Apr 1985 - 
TL;DR: The period of unstable angina before the final heart attack was, in all but one of 15 patients, characterized by such an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation seemed to have alternated with intermittentThrombus fragmentation.
Journal ArticleDOI

Coronary Angioscopy in Patients with Unstable Angina Pectoris

TL;DR: It is concluded that angioscopy frequently reveals complex plaques or thrombi not detected by coronary angiography, which suggests that anginal syndromes that are refractory to medical treatment can be caused by unstable pathologic processes in the intima.
Journal ArticleDOI

Angiographie morphology and the pathogenesis of unstable angina pectoris

TL;DR: In 110 patients with either stable or stable angina, the morphology of coronary artery lesions was qualitatively assessed at angiography and type II eccentric lesions were significantly more frequent in the 63 patients with unstable angina.
References
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Journal ArticleDOI

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

TL;DR: 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 ofinfarction.
Journal ArticleDOI

Nonoperative dilatation of coronary-artery stenosis: percutaneous transluminal coronary angioplasty.

TL;DR: It is estimated that only about 10 to 15 per cent of candidates for bypass surgery have lesions suitable for this procedure, and patients with single-vessel disease appear to be most suitable for the procedure.
Journal ArticleDOI

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

TL;DR: In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented, and after infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiographic.
Journal ArticleDOI

Selective intracoronary thrombolysis in acute myocardial infarction and unstable angina pectoris.

TL;DR: Intracoronary streptokinase application appears to be a safe and efficient method of achieving reperfusion and alleviating ischemia in the majority of patients with acute myocardial infarction and in five patients with unstable angina pectoris.
Journal ArticleDOI

Platelet aggregation in partially obstructed vessels and its elimination with aspirin.

J D Folts, +2 more
- 01 Sep 1976 - 
TL;DR: Histologic sections of the narrowed coronary artery obtained when coronary flow was reduced show an amorphous mass in the lumen which was thought to be a platelet aggregate, perhaps a similar process of platelet aggregation occurs in the stenosed coronary arteries in man, producing acute coronary obstruction, ischemia, and sudden death.
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