ABSTRACT
IRS II (Invasive reperfusion study II) was a multicentre randomized trial comparing the efficacy of a 2-5-min 30 U anistreplase intravenous injection with a 1,500,000 U 60-min streptokinase (SK) intravenous infusion in acute myocardial infarction. 116 patients were randomized within 6 h of onset of symptoms. Early coronary patency was assessable in 107 patients by coronary angiogram performed 102 min after thrombolytic treatment (range: 30-297 min) in the anistreplase group and 93 min (range: 22-330 min) in the SK group. The early coronary patency rate was significantly higher in the anistreplase group than in the SK group: respectively, 70% (38/54) and 51% (27/53), P less than 0.05). Fifty patients had assessable coronary angiograms at 90 min and 24 h. The 24-h patency rate was 92.3% (24/26) in the anistreplase group vs 87.5% (21/24) in the SK group. No early reocclusion occurred in the anistreplase group vs 15.4% (2/13) in the SK group (NS). Fibrinogen fell to 13.2 +/- 19.8% on anistreplase vs 9.4 +/- 10.3% on SK (NS). Bleeding complications occurred in 12% (7/58) of treated patients in the anistreplase group vs 20.7% (13/58) in the SK group (NS). Two cerebrovascular accidents occurred after thrombolytic treatment with anistreplase (3.4%) vs one after SK (1.7%) (NS). Thus, anistreplase is more effective than intravenous SK and easier to administer.
Subject(s)
Anistreplase/administration & dosage , Coronary Circulation/drug effects , Myocardial Infarction/therapy , Streptokinase/administration & dosage , Adult , Aged , Coronary Angiography , Female , Follow-Up Studies , Hemodynamics/drug effects , Humans , Infusion Pumps , Injections, Intravenous , Male , Middle Aged , Myocardial Infarction/mortality , Recurrence , Survival RateABSTRACT
Forearm venous tone and brachial artery hemodynamics, including determinations of the arterial diameter and compliance by the use of pulsed Doppler systems, were measured in 16 patients with sustained essential hypertension before and after acute oral cadralazine dosing. Systolic and diastolic blood pressures significantly decreased, whereas heart rate increased. Brachial artery diameter and vascular resistance decreased, respectively, from 0.501 +/- 0.015 to 0.485 +/- 0.015 cm (P less than 0.001) and from 124.8 +/- 13.8 to 99.3 +/- 11.9 mm Hg/ml . sec (P less than 0.01). Blood flow velocity increased (P less than 0.05) but volumic flow, pulse wave velocity, and brachial artery compliance did not change. Forearm venous tone increased but the increase was inversely related to the degree of arteriolar vasodilatation. Our results indicate that, with cadralazine, forearm vascular resistance decreased while forearm blood flow was unchanged, the dilatation of small arteries contrasted with a significant reduction in the diameter of the large brachial artery, and the decrease in blood pressure was associated with a lack of increase in arterial compliance and changes in venous tone. This suggests an overriding influence of the activation of the autonomic nervous system on the action of cadralazine on large arteries and veins.
Subject(s)
Brachial Artery/drug effects , Hemodynamics/drug effects , Hypertension/drug therapy , Pyridazines/therapeutic use , Administration, Oral , Adult , Blood Flow Velocity , Blood Pressure/drug effects , Drug Evaluation , Female , Heart Rate/drug effects , Humans , Hypertension/physiopathology , Male , Middle Aged , Pyridazines/pharmacology , RheologyABSTRACT
The passive left ventricular pressure-volume relationship characterises left ventricular distensibility. However, it has recently been shown that acute pharmacological intervention can significantly change the position of the diastolic pressure-volume curve. We studied the effects of acute volumic expansion on the passive left ventricular pressure-volume relationship. In fact, the interpretation of left ventricular function curves during acute volumic expansion assumes that the left ventricular pressure-volume relationship remains unchanged. We measured the heart rate, cardiac output, left and right ventricular pressures with micromanometers, ventricular volumes by cineangiography 50 frames/sec (n = 6) or ventricular diameters by M mode echocardiography (n = 6) in 12 patients without valvular or coronary heart disease during rapid volumic expansion, and calculated stroke volumes and indices of left ventricular performance; the passive left ventricular pressure-volume or pressure-diameter relationship was adjusted to an exponential function P = a.ekp.V or P = a'.ek'p.De. After volumic expansion the cardiac output rose due to an increase in heart rate and stroke volume. The increase in stroke volume was related to that of end diastolic volume, the end systolic volume remaining unchanged: there was little difference in the indices of left ventricular performance. The pressure-volume and pressure-diameter curves were considerably shifted upwards and to the left during acute volumic expansion: this seemed to be due mainly to an increased intrapericardial pressure secondary to the increase in intrapericardial content. The relationship obtained by subtracting the simultaneous right ventricular from the instantaneous left ventricular pressure after volumic expansion was identical to the basal left ventricular pressure-volume curve. These observations demonstrate the importance of external factors of left ventricular compression in the changes in the passive left ventricular diastolic relationship during acute volumic expansion and invalidate the use of function curves obtained under these conditions for the assessment of left ventricular systolic function. The end diastolic pressure cannot be considered to reflect end diastolic volume and the function curves, in fact, illustrate changes in diastolic distensibility.
