[Thrombolysis in the acute phase of myocardial infarction].
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Biomedical subjects
Publications and source records attributed to B Letac.
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Seventy-six patients with anginalike chest pain (ALCP) and angiographically normal coronary arteries (NCA) had a study of the myocardial metabolism at rest and during maximal atrial pacing. The results were compared with pain characteristics, electrocardiogram, left ventricular, and coronary hemodynamic data. Coronary blood flow (CBF) was measured by continuous thermodilution. At maximal paced heart rate, the study of the myocardial metabolism distinguished two groups: (1) a first group of 50 patients whose lactate extraction coefficient was equal to or exceeded 9% and was considered as normal (Gr. I, K greater than or equal to 9%); (2) a second group of 26 patients whose lactate extraction coefficient was below 9% (Gr. II, K less than 9%), significant of myocardial ischemia. In group I (K greater than or equal to 9%), chest pain was usually atypical (typical in only 25% of cases) and rapid atrial pacing most often caused neither pain nor ECG changes. The hemodynamic and angiographic study showed minor alterations of the left ventricular cavity in 50% of cases. In group II (K less than 9%), chest pain was typical in 50% of the patients and maximal atrial pacing most often caused chest pain (85%) and ST-segment depression (80%). In almost every case, the left ventricular and the coronary angiograms were normal. Only in this group, which had clinical, electrical, and metabolic signs of myocardial ischemia, could the diagnosis of angina pectoris with angiographically normal coronary arteries be upheld.(ABSTRACT TRUNCATED AT 250 WORDS)
Twenty-three patients (ages 44-82) with angina-like chest pain with a negative stress test and a normal coronary angiogram were studied for myocardial lactate metabolism during atrial pacing and for esophageal motor function with manometric measurements and acid infusion test. Eight patients had an abnormal myocardial lactate metabolism during maximal atrial pacing. Esophageal motor anomalies were observed in six of these eight patients and nine of the 15 subjects with normal myocardial lactate metabolism. The frequency and type of these anomalies were not different between the two groups of patients. Perfusion of acid into the esophagus reproduced the spontaneous pain syndrome in three patients, independent of any simultaneous motor dysfunction. These results suggest that esophageal motor anomalies must be interpreted with caution in patients with angina-like chest pain before affirming the exclusively esophageal origin of the pain.
Captopril was administered to 23 patients in cardiac failure refractory to digitalo-diuretic therapy. Four patients had a large fall in systolic blood pressure (less than 70 mmHg) with a single dose of 25 mg of captopril. In the other 19 patients a significant fall in mean pulmonary capillary pressure (16,8 +/- 6,1 mmHg vs 27,2 +/- 8,5 mmHg, p less than 0,001), mean pulmonary artery pressure (26,3 +/- 11,3 mmHg vs 38,3 +/- 12,4 mmHg, p less than 0,001), mean right atrial pressure (5 +/- 5 mmHg vs 8 +/- 6 mmHg, p less than 0,01) was observed: there was a moderate fall in mean systemic arterial pressure (13%, p less than 0,001). There was a significant fall in pulmonary resistance (27%, p less than 0,001). The cardiac index increased (2,8 +/- 0,5 l/min/m2, p less than 0,001) and systemic resistance fell by 25% (p less than 0,001). The heart rate decreased by an average of 7 beats/min (p less than 0,02). The treatment was stopped in one patient because of the inefficacy of captopril at 100 mg per dose. The average daily dose in the 18 patients on long-term treatment was 212,5 +/- 106,8 mg. At the second month, the haemodynamic parameters were remeasured before the morning dose of captopril. The effects observed after the single dose were maintained apart from the systemic blood pressure, heart rate and systemic resistances which had returned to the value observed before administration of captopril. The mean pulmonary capillary pressure was significantly lower than before treatment but was higher than after the single dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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In order to study the circulatory changes induced by maximal atrial pacing in coronary patients, coronary sinus blood flow (CBF) measured by continuous thermodilution, lactate extraction coefficient (K), arteriovenous difference in oxygen (AVO2 diff), and aortic blood pressure (BP) were measured at basal state and at maximal heart rate (HRmax) in 11 patients without coronary disease (group I) and in 28 patients with severe coronary lesions, divided into two groups according to the absence (group IIa) or the presence (group IIb) of chest pain and ST-segment depression at HRmax X K was inverted in group IIb (24 +/- 17% vs -23 +/- 39%, p less than 0.001), but remained unchanged in group I and group IIa. Despite similar HRmax, percent increase in CBF was significantly lower in group IIb (54 +/- 34%), than in group I (113 +/- 54%, p less than 0.01). This contrasts with the higher values of the product of heart rate times systolic blood pressure (HR X SBP) as well as of diastolic blood pressure (DBP) in group IIb. The decrease in coronary resistances was lower in group IIb than in group I (p less than 0.001), and also lower than in group IIa (p less than 0.05). The ratio MVO2 X CBF/systolic BP X HRmax was significantly lowered only in group IIb (p less than 0.001) confirming the imbalance between myocardial oxygen supply and oxygen demand. In coronary patients, myocardial ischemia induced by atrial pacing is related to an insufficient increase in CBF, well evidenced by continuous thermodilution.
Since November 1979 left ventricular angiography and coronary arteriography have been performed in 80 patients with evolving acute myocardial infarction in order to attempt coronary recanalisation by local streptokinase infusion. The average delay between the onset of symptoms and streptokinase infusion was 3.6 hours. Thrombolysis was successful in 64% of cases. No serious complications related to the procedure were noted. Of the 12 patients in cardiogenic shock, recanalisation was achieved in only four, of whom two survived. To evaluate the left ventricular salvage resulting from early recanalisation the last 58 patients had a second left ventricular angiogram and further coronary arteriograms 21 +/- 10 days later and 16 patients had a third study three months later. From the left ventricular angiogram in the right anterior oblique projection the ejection fraction and two graphic variables of regional wall motion were computed quantifying the hypokinetic zone. Patients were divided into two groups, according to the patency of the infarct related artery at the second control: group 1 consisted of 28 patients with successful recanalisation confirmed, and group 2 of 30 patients in whom no recanalisation was achieved or secondary reocclusion had occurred. At the second study the ejection fraction was unchanged in group 1 but had significantly decreased in group 2. Regional wall motion improved in group 1 and worsened in group 2, more so in patients without recanalisation than in those in whom secondary reocclusion had occurred. The third study showed a further decrease in ejection fraction in group 2. A progressive decrease in percentage residual stenosis was observed in group 1. This sequential angiographic study confirms the partial myocardial salvage resulting from early coronary recanalisation during acute myocardial infarction.
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Sixty patients without organic heart disease presenting with chest pain suggestive of angina pectoris and angiographically normal coronary arteries underwent clinical, hemodynamic and metabolic investigation. The study of myocardial lactate metabolism during atrial pacing (168 +/- 14 bpm) allowed identification of two groups: --40 patients with a normal coefficient of lactate extraction (K greater than or equal to 9 per cent); --20 patients with a pathologically low coefficient of lactate extraction (K less than 9 per cent) reflecting myocardial ischemia. In the first group, chest pain was often atypical (75 per cent of cases). Hemodynamic investigation showed minor abnormalities of the left ventricle in 48 per cent of cases. The diagnosis of angina was rejected in these patients. In the second group, the majority of patients developed chest pain (85 per cent of cases) at the maximal heart rate with significant ST depression (80 per cent of cases). The chest pain was typical of angina pectoris in 50 per cent of cases. Hemodynamic and angiographic investigation of the left ventricle was completely normal in nearly all cases. Only these patients with clinical, electrocardiographic and metabolic signs of myocardial ischemia can be considered as having angina with normal coronary arteries. Although studies of myocardial lactate metabolism and other signs of myocardial ischemia distinguish clearly between these two groups of patients, the coronary hemodynamics were similar. Resting coronary flow, its increase for the same myocardial oxygen demands and coronary resistances were comparable in both groups, and not significantly different from the values obtained in a control group of patients without coronary artery disease or chest pain. These results confirm that about 30 per cent of patients investigated for chest pain suggestive of angina pectoris who have angiographically normal coronary arteries, develop signs of myocardial ischemia during atrial pacing. The physiopathological explanation remains unclear as coronary hemodynamics have been found to be normal.
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An angiographic study was carried out to evaluate myocardial recovery in 50 patients who had undergone coronary angiography in the first six hours of myocardial infarction with the object of attempting emergency revascularisation by a selective intracoronary infusion of streptokinase. Left ventriculography performed before initial coronary arteriography and 2 to 10 weeks later was compared. The ejection fractions and two indices obtained by quantitative analysis of regional contractility, the surface (SHK) and extent (EHK) of the ischemic zones were calculated. The patients were divided into two groups according to results: Group I, 25 patients with patent arteries at the second control, and Group II, 25 patients not revascularised or with a reobstructed artery at the second angiographic control. In Group I, the ejection fraction remained stable (47 +/- 11 p. 100 to 48 = 10 p. 100 N.S.) but SHK (13 +/- 6 cm2 to 10 +/- 5 cm2, p less than 0,01) and EHK in percentage of ventricular circumference (48 +/- 12 p. 100 to 42 +/- 11 p. 100, p less than 0,05) fell significantly. In Group II, the ejection fraction fell (55 +/- 9 p. 100 to 44 +/- 11 p. 100, p less than 0,001) whilst SHK (7 +/- 4 cm2 to 11 +/- 5 cm2, p less than 0,001) and EHK (34 +/- 11 p. 100 to 43 +/- 14 p. 100, p less than 0,001) increased significantly. These results show that revascularisation may result in significant functional myocardial recovery and, consequently, that some ischemic myocardium can be salvaged in these patients.
Since 1978, 17 patients have undergone surgery for massive pulmonary embolism in our department. Twelve patients survived and have been followed up for between 2 and 31 months postoperatively (mean 16 months). Reassessment of these patients included exercise tolerance test, pulmonary function test, perfusion scan, right heart catheterization and coagulation screening. Two survivors present major sequelae, namely vascular pruning and definite signs of pulmonary hypertension. The other 10 patients have minimal or no residual vascular occlusion, but show a high incidence of minor abnormalities: slight rise in pulmonary arterial pressure during exercise (3 cases), small angiographic and scintigraphic defects (5 cases), arterial hypoxemia (5 cases) and disturbances of pulmonary function (10 cases). Systemic venous problems were found to be frequent and to be a handicap in 5 cases, and an abnormal pattern of response to exercise was observed in 4 patients. These disturbances may be related to ligation of the vena cava. Various derangements of coagulation were found in all but one of the patients.
Acute coronary obstruction occurred in two patients during coronary angiography. In one case the obstruction was in the left main coronary artery; in the other it was close to the origin of the left anterior descending artery. In both cases acute cardiac ischaemia ensued, with electromechanical dissociation and collapse, which was not reversible by resuscitation. Rapid disobliteration of the occluded coronary artery was done with a guide-wire pushed through the obstruction via the coronary catheter. The recanalisation was completed by an intracoronary perfusion of streptokinase in one case. In both cases recovery was rapid and spectacular. The occurrence of acute ischaemia during coronary angiography should suggest accidental coronary occlusion. If a thromboembolic origin is suspected, transluminal disobliteration should be attempted. It is simple and can reverse a dangerous condition.
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The parameters of myocardial function in the initial phase of ventricular ejection are theoretically more sensitive than the indices calculated over the total systolic ejection period. The object of this study was to evaluate whether the calculation of the ejection fraction by thirds of systole, giving a separate assessment of left ventricular performance at the beginning, the middle and end of ejection, could reliably detect minor changes in ventricular function unrecognised by the usual holosystolic indices. Seventy left ventricular angiograms were analysed in 20 normal subjects (Group I) and 50 patients with coronary artery disease whose ventricular function estimated by the usual parameters was either decreased (Group II, 20 patients) or normal (Group III, 30 patients). In Group I, the ejection fraction in the first third of systole (FE1/3) was much higher than the ejection fraction in the second third (FE2/3). On the other hand, in Groups II and III, all patients had a FE1/3 lower than the FE2/3 (specificity: 100 p. 100). In these two groups, the reduction of FE1/3 and the increase of FE2/3 were very significant compared to Groupe I (p less than 0,001). The ejection fraction of the lest third was identical in the 3 groups. This abnormal distribution of ejection was detected in all coronary patients and was the only alteration of ventricular performance in each of the 30 patients in Group III. In this group, this abnormality was detected equally in patients with triple vessel disease (Subgroup III a, 20 patients) and in patients with isolated left anterior descending disease (Subgroup III b, 10 patients) illustrating the high sensitivity of this index for the detection of a minor abnormality of myocardial function.
Prazosine was studied in the treatment of chronic heart failure in 17 patients. The immediate effects were a reduction in pulmonary capillary pressure (22,9+/-8,8 mmHg to 15,5+/-7,4 mmHg, p less than 0,001), mean pulmonary artery pressure (34,2+/-10,6 mmHg to 23,8+/-9,2 mmHg, p less than 0,001), an increase in cardiac index (2,13+/-0,5 to 2,70+/-0,68 l/mn/m2 p less than 0,01), a reduction in mean systolic blood pressure (95,6+/-12,9 to 80,8+/-10,6 mmHg, p less than 0,001) and systemic resistance (1983+/-464 to 1 370+/-406 dynes.sec.cm-5). Heart rate did not change significantly. The long-term effects were assessed after 2 months continuous treatment in 14 patients. There was a clear-cut symptomatic improvement in the patients. This was without doubt related to the increase in cardiac output (+24 p. 100) which persisted at long term. On the other hand, the preload rose to its pre-treatment levels as did the blood pressure. This study confirms the value of Prazosine in the long-term treatment of chronic cardiac failure.
The authors report on a case of thrombosis of vena cava and renal vein associated with a nephrotic syndrome and complicated by a massive pulmonary embolism. Under emergency conditions, it was impossible to diagnose preoperatively a renal tumor, which is the most common cause of renal and vena caval obstruction or a thrombosis of the vena cava. Surgical treatment was carried out only because there were no arteriographic signs of renal neoplasm, and because thrombolytic treatment was contra indicated in a patient with greatly reduced vital capacity. Embolectomy was performed under cardiopulmonary by pass. The patient made a good recovery. Results of routine cardiac and pulmonary tests were normal after two months. Embolectomy must always be associated with as interruption of the vena cava, whose different forms are discussed. Partial interruptions using a De Weese clamp seems to be better tolerated than ligation.
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