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232 consecutive patients with acute myocardial infarction were treated either with 2 x 10(6) IU urokinase as an intravenous bolus injection, or 250,000 IU streptokinase intracoronary, or 60 mg recombinant tissue-type plasminogen activator (rt-PA) over 90 min. All patients enrolled had chest pain for more than 30 min and less than 3 h before admission and a typical electrocardiogram. Contra-indications to thrombolytic treatment were absent. All bleeding complications occurring within 24 h after admission were assumed to be due to thrombolytic therapy. Bleeding complications occurred in 14 patients (6.5%). Only seven patients received a blood transfusion (3%). No correlation was evident between previous hypertension, diabetes mellitus, smoking, sex, age, fibrinogen level before and 24 h after thrombolytic therapy and bleeding complications. The risk of bleeding was not significantly different between the different thrombolytic regimens despite marked differences in the fall of the fibrinogen level. The decrease of fibrinogen following thrombolytic therapy did not influence the patency rate of the infarct vessel. Thrombolytic therapy in acute myocardial infarction is a safe treatment even among patients advanced in years and with medically controlled hypertension and diabetes mellitus, irrespective of the kind of thrombolytic treatment.

To study the haemodynamic and neurohumoral effects of nisoldipine (2 X 10 mg) vs captopril (3 X 25 mg), 24 patients with heart failure (New York Heart Association class II and III) due to coronary artery disease were treated in a randomized double-blind trial over 3 months. Both drugs were well tolerated. Clinical status was similarly improved in both groups, nisoldipine exerted an additional antiischaemic effect. Nisoldipine lowered the mean arterial pressure and capillary wedge pressure acutely and also after long-term treatment. The increase in cardiac index and stroke volume index, however, which was pronounced after acute administration, was no longer present after 3 months of therapy at rest and was abolished during exercise. Norepinephrine plasma concentration increased after the first dose, plasma renin activity did not change, and aldosterone plasma concentration showed a small insignificant decrease. Urine concentrations of norepinephrine and vasopressin were slightly elevated after the 3-month therapy. After captopril, mean arterial pressure and pulmonary capillary wedge pressure decreased acutely and at follow up. Cardiac index and stroke volume index increased significantly only during exercise at follow-up. Plasma renin activity was significantly elevated and aldosterone plasma concentration only slightly lowered. In contrast to what was seen with nisoldipine, plasma norepinephrine concentration and urine catecholamine and vasopressin concentrations remained unchanged. In conclusion, the pronounced haemodynamic effects seen after the first dose of nisoldipine are mostly abolished after long-term treatment, probably due to neurohumoral counterregulation. The haemodynamic response to captopril is complete only after long-term treatment, without evidence of activation of the neurohumoral systems.

As part of a prospective randomized double-blind trial (PRIMI) to study the early patency rate of the infarct-related artery after saruplase (INN for recombinant unglycosylated full-length human single-chain urokinase-type plasminogen activator) vs streptokinase in a subgroup of patients, left ventricular function was compared between both treatment groups at 90 min and 24 h after thrombolysis and at discharge, and ventricular function was related to the coronary perfusion grade. Despite a higher patency rate in the saruplase group 60 min after initiating thrombolysis, neither global ejection fraction nor hypokinesia at the infarct site were significantly different between the treatment groups at any of the three time points when function was measured. Hypokinesia at the infarct site remained almost equally severe throughout the study in patients with perfusion grade O, I, and II, and was consistently significantly milder in patients with perfusion grade III. In contrast, in patients with perfusion grade II there was a significant drop in hyperkinesia at the opposite wall at 24 h after thrombolysis and before discharge despite unchanged wall motion at the infarct site. Although patients treated with saruplase had a higher patency rate in the infarct related vessel shortly after the start of thrombolysis, no difference was found in left ventricular function compared to patients treated with streptokinase. Complete reperfusion (TIMI grade III) seems to be a prerequisite for left ventricular function recovery after thrombolysis, whereas only an occluded vessel (TIMI grade O and I) seems to be related to a longer lasting hyperkinesia at the opposite wall.

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