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The effect of preoperative left ventricular function on early and late prognosis was assessed in 103 patients with aortic stenosis who underwent left ventricular cineangiography before homograft replacement of the aortic valve. The patients were separated into two groups: Group A (58 patients) with an ejection fraction of 0.46 or more and Group B (45 patients) with an ejection fraction of 0.45 or less. The two groups were compared with respect to clinical and hemodynamic data as well as operative result. There was poor correlation between clinical data and left ventricular function. In Group A there were three early deaths (5.2 percent) and three late deaths (5.2 percent) compared with no early and six late deaths (13.3 percent) in Group B during the follow-up period of 12 to 102 months (mean 43 months). Most patients in Group B showed considerable symptomatic improvement but less than that observed in Group A. Forty-two patients (13 in Group A and 29 in Group B) underwent repeat cardiac catheterization and coronary angiography. Improvement in left ventricular function as assessed by radial analysis of segmental wall motion and ejection fraction was observed in 20 of the 29 patients in Group B. Failure of left ventricular function to improve was associated with additional coronary artery disease in the majority of patients. It is concluded that poor left ventricular function does not increase the risk of aortic valve replacement for aortic stenosis and that improvement in left ventricular function can be expected in the majority of patients.

Ten patients with symptoms of acute myocardial infarction of less than 6 hours duration were randomised to receive either anisoylated plasminogen streptokinase activator complex [APSAC] (30U) or streptokinase (1,500,000U) intravenously. The aims of the study were to compare the angiographic patency of the infarct-related coronary arteries and to monitor drug safety and tolerance for up to 24 hours. The left anterior descending artery was occluded in 3, the left circumflex in 3 and right coronary artery in 4 patients. Time between onset of pain and treatment ranged from 150 to 330 minutes. At 90 minutes, 8 patients, 3 of 5 (60%) of the APSAC group and all of the streptokinase group, had patent arteries. No significant differences were found in measurements of coagulation. There were no haemorrhagic complications. One patient of the APSAC group had reinfarction 6 hours after treatment and died in cardiogenic shock. APSAC seems safe and is easier to use than streptokinase, and both agents result in patency in the majority of patients, although too few patients were included to allow a valid comparison. However, thrombolysis should be considered only a temporary solution in acute myocardial infarction, associated mainly with 3-vessel disease.

The hemodynamic effects of verapamil and practolol were investigated in a group of 10 selected patients (7 with coronary artery disease) undergoing cardiac catherization. The drugs were given i.v. in a dose of 0.1 mg/kg, alone or in combination, before and after controling the heart rate by atrial pacing. Measured hemodynamic parameters included aortic and left ventricular pressure and its first derivative, cardiac output, and echocardiographically derived left ventricular dimensions. Each drug given individually caused minor hemodynamic changes, but the combination of practolol and verapamil when the heart rate was fixed by atrial pacing invaribly caused a reduction in LV dp/dt max which was independent of preload and afterload. It is concluded that both drugs have a mildly negative inotropic effect when administered at this dose intravenously to patients with normal or mildly impaired left ventricular function. The myocardial depression was more apparent when practolol preceded verpamil. Caution must be exercised when using these drugs in combination in patients with impaired myocardial function.