Invasive reperfusion study. II. Multicentre European randomized trial of anistreplase vs streptokinase in acute myocardial infarction.

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.

Effect of cadralazine on brachial artery hemodynamics and forearm venous tone in essential hypertension.

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.

Myocardial map derived from two-dimensional echocardiography: reproducible and standardized description of infarction topographies.

The aim of this study was to improve the reproducibility and the standardization of the topographical assessment of myocardial infarctions in routine two-dimensional echocardiography. A myocardial map of the left ventricle was derived from a necropsy study of normal human hearts; interventricular grooves and papillary muscles were used as anatomical landmarks defining 16 segments with similar planimetered surfaces. A reporting sheet was prepared, with diagrams of standardized echo sections and with a map showing the position of the corresponding outlines. The echocardiographic method consisted in identifying on each section the regions without systolic thickening, and displaying the results on the map, until a coherent picture of the abnormal areas was obtained. Interobserver reproducibility was studied in 50 consecutive patients with prior myocardial infarction; segments were classified as fully abnormal, partly abnormal, non-visualized, and normal. Among the 800 segments there were 1% severe and 12% moderate discrepancies; discrepancies were significantly lower for segments with confrontation in two different sections intersecting on the map. A classification of infarction topographies was obtained in 100 consecutive patients; it was compared with the data of two reanalysable pathologic series from the literature; a similar presentation of the results showed similar typical patterns of myocardial involvement, for which a nomenclature was proposed. A myocardial map may be used to provide a simple and reproducible description of infarction topographies; the results obtained lead us to recommend an echocardiographic standardization of ventricular segmentation and of nomenclature of infarction topographies, similar to that of pathological studies.

[Changes in passive left ventricular pressure-volume relations in acute volume expansion]. / Modifications de la relation pression-volume passive ventriculaire gauche lors d'une expansion volumique aiguë.

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.

[Surgery of truncus arteriosus in the first 2 years of life. Analysis of a consecutive series of 22 patients]. / Trattamento chirurgico del truncus arteriosus nei primi due anni di vita. Analisi di una serie consecutiva di 22 pazienti.

At the Laennec Hospital in Paris, between 1976 and 1980 twenty-two children with Truncus Arteriosus Communis (TAC) underwent primary total repair during the first twenty-four months of life, according to the technique described by McGoon in 1968. All infants operated before the age of three months (group A: 7 patients) were in severe cardiac insufficiency with respiratory distress. Eleven patients (group B) were electively operated between four and nine months of age. Only four patients (group C) underwent surgical treatment after twelve months and before twenty-four months of age. The hospital mortality was very high in group A, because of the severity of the preoperative conditions. In three patients who underwent total repair at eight and eighteen months of age respectively, irreversible pulmonary hypertension (stage IV according to Edwards classification) was the cause of death. In our experience, severe postoperative myocardial ischemia was often associated with complete atrio-ventricular block (BAV): the possible causes are discussed. Furthermore, all patients, to a variable extent, had some manifestations of left ventricular (LV) insufficiency, which was always reversible after medical treatment. For several days, almost systematically, mechanical ventilation is necessary after a total repair of TAC. The result in the nine surviving patients is excellent: they had a strictly normal life, without any therapy. In conclusion, we believe that elective surgery for TAC can be performed more safely between six and nine months of age: if medical treatment cannot control heart failure, surgery must be performed urgently in order to avoid severe ventilatory disturbances. After twelve months of age, total repair is performed only if a pulmonary biopsy confirms the possibility of regression of the pulmonary vascular lesions.

Influence of positive end-expiratory pressure on left ventricular performance.

Although left ventricular dysfunction is common during ventilatory support with positive end-expiratory pressure (PEEP), the mechanism of this disorder remains unclear. In 10 patients with the adult respiratory-distress syndrome we studied the effects of a stepwise increase in PEEP from 0.to 30 cm H2O on left ventricular output, intracardiac transmural pressures, and two-dimensional echocardiographic measurements of left ventricular cross-sectional area at end-systole and at end-diastole. Increasing PEEP was associated with progressive declines in cardiac output, mean blood pressure, and left ventricular dimensions and with equalization of right and left ventricular filling pressures. The radius of septal curvature decreased at both end-diastole and end-systole, implying a leftward shift of the interventricular septum. At the highest PEEP, blood-volume expansion did not restore cardiac output, although left ventricular transmural filling pressures had returned to base-line values. We conclude that decreased cardiac output during PEEP is mediated by a leftward displacement of the interventricular septum, which restricts left ventricular filling.

[Indices of left venticular performance and evaluation myocardial quality in mitral valve insufficiency, chronic aortic valve insufficiency and stenosis]. / Indices de performance ventriculaire gauche et appréciation de la qualité du myocarde dans l'insuffisance mitrale, l'insuffisance et le rétrécissement aortiques chroniques.

132 patients with pure mono-valvular cardiopathies (mitral incompetence, aortic stenosis and aortic incompetence) were classified into two groups according to the values of the systolic work index/myocardial mass ratio (SWI/MLV). Normal values of the ejection function (EF) and mean velocity of circumferential fibre shortening (VCF) for each cardiopathy were so obtained. Only patients with aortic stenosis of group I (SWI/MLV greater than or equal to 0.75 gm . g-1) had normal EF. All the other patients had EF and VCF values below normal although this did not always imply impaired myocardial function. Therefore the myocardial mass should also be considered in the evaluation of myocardial function and it would seem desirable to take this parameter into account in the management of these patients.