A set of electrocardiographic criteria for the diagnosis of coronary artery disease was evaluated in two different groups of patients examined by computer aided 12 lead exercise electrocardiographic stress testing and coronary arteriography. One group consisted of patients with severe angina pectoris and the other of patients who had suffered a myocardial infarction three years before the study...

Fechtrup C, Ostermann H, van de Loo J. Prothrombin activation fragment 112 and thrombin-antithrombin III complexes in patients with angina pectoris: relation to the presence and severity of coronary atherosclerosis. Thromb Haemostasis 1993;70:550–3. 9. Merlini PA, Bauer KA, Oltrona L, Ardissino D, Cattaneo M, Belli C, et al. Persistent activation of coagulation mechanism in unstable angina and ...

Of 2744 patients seen in clinic practice, 37 were found to have a prolonged PR interval. The causes of prolongation of the PR interval were: congenital heart disease, 6; chronic rheumatic heart disease, 2; digitalis induced, 4; miscellaneous, 5; and coronary heart disease, 20. Of the 20 associated with coronary heart disease, 8 (2I.6% of all the patients with prolonged PR interval) had myocardi...

same test, after each individual rested 30 min and took 0.4 mg nitroglycerin sublingually, increased V02 max in patients with angina (by 14.5%, P <0.001) and in patients with prior infarction (by 6%, P < 0.005) but not in healthy persons. Angina at VO2 max was prevented in 12 patients. Maximal heart rate was increased by 11% in the angina group and by 4% in the myocardial infarction group; the ...

Platelets have been implicated in the formation of occlusive intracoronary thrombi leading to unstable angina pectoris and acute myocardial infarction. Evidence of platelet involvement in these syndromes includes increased thromboxane A2 synthesis during ischemic events and enhanced in vitro sensitivity to agonists. To determine the density and affinity of platelet thromboxane A2/prostaglandin ...

The appropriate management of the individual patient presenting with unstable angina remains challenging for physicians, despite improved knowledge of the pathophysiology of acute coronary syndromes and considerable increased availability of diagnostic techniques and treatment regimens. Unstable angina is most frequently the consequence of acute disruption of a vulnerable, usually lipid-rich, a...

We correlated clinical parameters with angiographic findings in 108 men with a previous isolated inferior myocardial infarction, to determine if these parameters could predict accurately which patients had multivessel disease. Of 71 men in angina class 2-3, 42 had three vessel disease versus only seven of the 37 who were either asymptomatic or angina class 1 (P less than 0.001). Multivessel dis...

OBJECTIVE To observe the long-term prognosis of patients with unstable angina and select simple criteria to identify high and low risk subgroups. DESIGN A six month prospective survey with three year follow up. SETTING One eleven bed coronary care unit. PATIENTS All patients admitted with chest pain in whom no infarct was confirmed by subsequent electrocardiographic or enzyme changes and ...

Background—Earlier reports have shown that the outcome of balloon angioplasty or bypass surgery in unstable angina is less favorable than in stable angina. Recent improvements in percutaneous treatment (stent implantation) and bypass surgery (arterial grafts) warrant reevaluation of the relative merits of either technique in treatment of unstable angina. Methods and Results—Seven hundred fifty-...

Over the past 35 years, the view has evolved that the acute coronary syndromes, ie, unstable angina pectoris, myocardial infarction, and sudden death, are caused by plaque rupture and formation of a platelet thrombus. There is at least a transient total or subtotal coronary occlusion in all cases of acute myocardial infarction. Q-wave infarcts are thought to differ from non–Q-wave infarcts by m...