Evaluation of clinical factors involved in onset of myocardial infarction.
In order to discuss the mechanism of onset in myocardial infarction (MI), clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger. The majority of subjects did present conditions that constituted predispositions for MI, including a history of angina pectoris (especially unstable angina), poor therapeutic results for angina pectoris, organic stenosis of the coronary artery, life changes, and overwork. Patients with multiple factors tended to develop MI without a definite trigger, i.e., onset during sleep or rest whereas, in patients with fewer predisposing factors, it was obvious effort, excitation or stress that triggered MI. However, not a few of the patients presented with no organic stenosis of the coronary artery or no history of angina pectoris. There were patients without ST segment elevation at onset of MI, and patients in whom ST elevation was recorded after onset. These findings suggest the existence of mechanisms other than coronary occlusion in onset of MI. Occlusion of the coronary artery distributed to the infarct region occurred frequently among patients with delayed CPK efflux as well as prolonged chest pain and ST segment elevation. These lines of evidence suggest extension of infarction due to secondary coronary occlusion.
D000787:Angina Pectoris / Q000150:complications; D000789:Angina, Unstable / Q000150:complications; D003327:Coronary Disease / Q000150:complications; D003331:Coronary Vessels / Q000473:pathology; D003402:Creatine Kinase / Q000378:metabolism; D006801:Humans; D009203:Myocardial Infarction / Q000209:etiology* / Q000473:pathology; D009206:Myocardium / Q000201:enzymology; D011379:Prognosis; D013315:Stress, Psychological / Q000150:complications
D003402:Creatine Kinase