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Dynamic tomographic images of the heart may be obtained by computerised treatment of a number of projections and planes recorded by a gamma camera rotating around a patient whose blood is labelled with radioactive technetium. This new technique of assessing cardiac function was tested in a group of 40 coronary patients and the results compared with standard contrast angiography. The following parameters were compared : LV volume, global and regional ejection fractions. The zones of interest were easily defined on the tomographic images and correction for background noise was negligible. Two different methods have been developed to measure volume. The first consists in counting the matrix units in three dimensions on serial planes through a given cavity. The second is based on the reconstruction of thick slices integrating all the ventricular radioactivity, the counting of which is calibrated with reference to an orthogonal plane. The correlations with angiography were excellent with both methods (R = 0,85 and 0,87 respectively). An equally good correlation was observed for ejection fraction (r = 0,85). A segmental model acceptable for both gamma line angiography, gamma tomography and contrast angiography comprises 6 segments : septal, apical, antero-lateral, postero-lateral, posterior, and inferior. The sensitivity and specificity of both isotopic methods of detection of major wall abnormalities (akinesia and dyskinesia) were assessed.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibrinolysis is a physiological process which aims at dissolving intravascular thrombi and is mediated by activation of plasminogen to plasmin. Streptokinase (SK) and urokinase (UK) are non-specific plasminogen activators. They have proved effective as thrombolytic agents, but their use is limited by the risk of haemorrhages due to systemic fibrinogenolysis. More fibrin-specific drugs have recently been developed. One is a tissue plasminogen activator (t-PA), the other is a urokinase precursor (pro-UK), also called single chain urokinase plasminogen activator (scu-PA). Genetic engineering techniques have resulted in the large-scale production of a "recombinant t-PA" (rt-PA) and a "recombinant scu-PA" (r scu-PA) for therapeutic use, notably in acute myocardial infarction. In vitro, these two drugs exhibit a thrombolytic activity that is equal to, or greater than that of SK or UK. In vivo, their fibrinogenolytic effect is less pronounced, and their thrombolytic effect greater than those of SK or UK. "Acyl-enzymes" have more recently emerged. These are inactive acylated SK-plasminogen complexes which progressively become effective in plasma after deacylation. So far, the most extensively studied of these complexes is BRL 26921 (anisoylated plasminogen streptokinase activator complex, or APSAC) which is administered by bolus intravenous injection. It is more thrombolytic than SK but produces systemic fibrinogenolysis to an equivalent degree. Injected intravenously (by infusion or bolus) during the first hours of a coronary infarction these three new thrombolytic agents have proved effective in promoting coronary reperfusion, with an early coronary patency rate of 70-75%.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventriculo-atrial (VA) conduction was studied by ventricular stimulation at increasing rate and atrial mapping in 126 patients either without ventricular preexcitation (WPW) and supraventricular tachycardia (SVT) (Group I: 60 cases) or with the WPW syndrome with or without SVT (Group II: 30 cases) or with SVT without WPW (Group III: 53 cases) or with short PR intervals (Group IV: 3 cases). In Group I, 22 patients had VA block, 10 had concealed accessory pathways and 28 had nodal VA conduction. In Group II, 2 patients had VA block, 6 had nodal VA conduction and 22 had preferential retrograde conduction through the Kent bundle. In Group III, 9 patients had concealed Kent bundles and 24 had nodal retrograde conduction. In Group IV, the results were varied. The characteristics of retrograde VA conduction are therefore often different from those of anterograde conduction. 52 attacks of SVT were recorded; in the 18 cases of Group II, 5 septal, 3 right lateral, 8 left lateral Kent bundles and 2 intranodal reentries were demonstrated. In the 33 cases of SVT without overt WPW (Group III) a concealed accessory pathway was demonstrated in 9 cases. In all, approximately a half (25 out of 52) of all SVT were due to reentry involving an accessory pathway which was concealed in about one third of cases (9 out of 25) and more often situated on the left border than on the right or in the septum.

Four brothers with a maximum age difference of 20 years, the eldest of whom has been re-examined after a 10 year interval, have sinoatrial block, a supra-hisian atrioventricular block and paroxysmal atrial arrhythmias which have led to partial atrial standstill in the eldest: left anterior hemiblock is also present in the two youngest brothers. The condition is very well tolerated. This family is compared to the other 12 reported cases of familial idiopathic binodal block in the adult, an autosomal dominant condition with variable penetration. The diagnosis is reserved and justifies endocavitary investigation of the sinus node function and atrioventricular conduction in the four brothers and the most exposed members of their family. The mechanism of the condition is unknown. It seems to arise from variable degrees of nonspecific of the nodal and atrial tissues.

In a multicentre randomized open study conducted on two parallel groups the effectiveness of APSAC was compared with that of streptokinase (SK) in 116 cases of myocardial infarction treated during the first 2.75 hours. APSAC (30 IU) was administered by intravenous bolus injection over 2 to 5 minutes, and SK (1.5 million IU) by intravenous infusion over 60 minutes. The patency of the coronary artery responsible for myocardial infarction was evaluated by coronary arteriography performed 1.74 h on average after the beginning of treatment; it was 70 p. 100 in the APSAC group and 51 p. 100 in the SK group (p less than 0.05). The fall in plasma fibrinogen was similar in both groups (mean minimum level; 0.2 g/l). Haemorrhages occurred in 9/58 patients treated with APSAC (15.5 p. 100) and in 13/58 patients treated with SK (22.4 p. 100); these haemorrhages took place during the first 24 hours in 4 patients of the APSAC group and in 10 patients of the SK group. Five patients died: 2 in the APSAC group and 3 in the SK group. In a subgroup of 38 patients who underwent 3 control coronary arteriographies (at 90 min, 24 hours and 3 weeks), the patency rates were 63 p. 100, 82 p. 100 and 93 p. 100 respectively with APSAC and 44 p. 100, 86 p. 100 and 92 p. 100 respectively with SK (NS). No coronary reocclusion occurred in the APSAC group, as against 3 (1 early, 2 delayed) in the SK group. It is concluded that APSAC seems to be more effective than intravenous streptokinase; it is easier to administer (bolus injection) and does not carry a higher risk of haemorrhage.

The incidence of binodal, sinoatrial (SA) and atrioventricular (AV), block was determined in a series of 362 patients, 90 of whom had chronic sinoatrial block (group I), 162 suprahisian, infrahisian or diffuse AV block (group II), 38 with paroxysmal supraventricular tachycardia (group III), and 70 with slow atrial fibrillation, 54 of whom were studied in sinus rhythm (group IV). Electrophysiological investigation revealed: overt or latent AV block in 71% of group I, 48% of group III, and 100% of group IV; overt or latent SA block in 40 to 61% of group II, 87% of group III and 78% of group IV; paroxysmal atrial fibrillation in 61% of group I, 25% of group II and 50% of group IV; intra-atrial block in 26% of group I, 20% of group II, 16% of group III and 31% group IV. An ECG syndrome associating binodal block and disturbances or atrial conduction and excitability is suggested. The pathogenesis and anatomical basis are discussed, the prime lesion of which may be fibrosis of the atrial tissues which may ultimately result in partial or total atrial standstill.

The authors report a case of massive haemolytic anaemia with acute mitral valve regurgitation and left cardiac failure, which occurred one year after surgical reconstruction of the mitral valve for rupture of smaller leaflet chordae. Anaemia, mitral regurgitation and cardiac failure disappeared after mitral valve replacement, using a Carpentier Edwards No. 29 valve. Haemolytic anaemia following mitral valve reconstruction is exceptional. It seems to be due to the suture material lying in a turbulent regurgitation stream when mitral incompetence develops again.

18 of 39 cases of ischaemic papillary muscle dysfunction reported elsewhere underwent cardiac catheterisation and angiography. Fifteen patients had previous myocardial infarction. The average age of the patients was less than in the overall series (69 vs 73 years) but the incidence of infarction and the degree of cardiac disease were greater. The absence of catheter data in the other patients is explained by their older age (76.4 years) and the longer period of recruitment. Their results and outcome of medical or surgical treatment are reported. The pathogenesis of the syndrome is reconsidered in the perspective of paroxysmal forms. A protocol for investigation is suggested to guide the therapeutic options. Right heart catheterisation at rest (n = 16), on exercise (n = 12), under vasodilator therapy (n = 6) and during angiography (n = 2) does not show a specific profile. These investigations only provide haemodynamic data related to therapy but they are essential for the interpretation of ventriculography. Ventriculography (n = 8) demonstrated 4 cases of mitral regurgitation (2 major and 2 minor), a reduced EF (0.47 +/- 0.17), asynergy of 36.1 p. 100 of segments analysed, predominantly in the inferior and lateral zones. Coronary angiography showed triple vessel disease in 6 cases, double vessel disease in 1 case and 1 stenosis of the left main coronary artery. Stenosis was commonest on the left circumflex (87.5 p. 100) and right coronary arteries (87.5 p. 100) but also frequently involved the left anterior descending artery (75 p. 100). Of the 12 patients treated medically, 8 died (66.6 p. 100) and the survivors remain symptomatic (33.3 p. 100), half with and half without attacks. After surgery (n = 8) comprising coronary bypass surgery (n = 6) or mitral valve replacement (n = 2), patients were asymptomatic. 1 patient died of cancer. These paroxysmal forms of mitral regurgitation may be explained by the association of aggravating, reversible ischaemic or haemodynamic factors to organic mitral lesions. Mitral valve replacement is justified when dysfunction becomes permanent and coronary bypass surgery is advocated whenever possible. The indications for surgery can only be taken into account after complete haemodynamic and angiographic investigation. A protocol for the interpretation of these investigations is suggested.

Many investigators have reported about beneficial results with thrombolytic therapy in patients with acute pulmonary embolism. Streptokinase and urokinase have been used for more than 15 years, but the conditions of use of these agents still remain controversial. Optimal dosage and treatment schedule are still evolving. For streptokinase most investigators adopt a fixed dosage schedule: a loading dose of 250,000 units followed by a maintenance infusion of 100,000 units per hour for 24 to 72 hours. For urokinase numerous dosage regimens have been used such as: high dosage schedule 4,400 units per kilogram per hour for twelve to 24 hours with or without loading dose; moderate dosage 1,600 to 2,000 units per kilogram per hour for 24 hours and low dosage in bolus. With these treatments there is a trend to reduced in-hospital-mortality in massive pulmonary embolism; the early pulmonary revascularization and the hemodynamic improvement are higher than those noticed with heparin. These results are obtained with a minimum of complication essentially bleeding in 10 or 15%; most bleeding being located at puncture site. More recently, new thrombolytic agents have been used in acute pulmonary embolism. Only four studies have tested rt-PA which is effective and relatively safe, but the optimal dose regimens remain to be determined. Less information is available concerning Anisoylated Plasminogen Streptokinase Activator Complex (APSAC), the angiographic improvement seems to be rapid and important (50% on average) but the decrease of fibrinogen is important too and comparable with streptokinase. Considering the good results of thrombolytic treatment of acute submassive and massive pulmonary embolism, there is a doubt as to whether the pulmonary embolectomy has any place in the pulmonary embolism patients except in those with cardiac arrest. In the near future new thrombolytic drugs could be more efficient on pulmonary embolism and deep venous thrombosis, and thus the bleeding risk might be decreased.

The authors report a case of total anomalous pulmonary venous return (TAPVR) draining into the innominate (brachiocephalic) vein, discovered in a 40-year old male patient and successfully treated by surgery. This type of cardiopathy is usually suspected in the neonatal period, being badly tolerated, and such a prolonged survival is quite exceptional. Survival is conditioned by the site of the TAPVR, by the size of the atrial septal defect and also by the presence or absence of an obstacle to the pulmonary venous return and of pulmonary arterial hypertension. In the absence of pulmonary vascular disease, surgical correction is mandatory and results in regression of the symptoms and of the pulmonary arterial hypertension.

In a case of right ventricular infarction, a negative lung image was observed on the resting thallium-201 scan, with a pulmonary activity much lower than the surrounding background. The myocardial image showed only a moderate inferior hypoactivity and the left ventricular ejection fraction was normal. This seems to be related to right ventricular failure with normal left ventricular function. It represents the opposite mechanism to the increased pulmonary thallium uptake commonly seen in severe left ventricular impairment.

Sixty-seven patients with recent acute pulmonary embolism (within 5 days) and an angiographic deficit of over 30% were included in a randomised study designed to compare the efficacy of the associations of urokinase-heparin (Group I) and lysyl-plasminogen-urokinase-heparin (Group II). Plasminogen was administered as an intravenous bolus of 150 microkatal units at the beginning of the urokinase infusion, the dosage of which was set at 2 700 000 IU over 24 hours. Both groups received anticoagulant doses of heparin. The efficacy of treatment was judged by early revascularisation on pulmonary angiography performed during the 24 hours after the end of treatment and by changes in the parameters of fibrinolysis and its inhibitors. The clinical features of the two groups were comparable but the angiographic changes were more pronounced in Group I (deficit: 68.5 +/- 10.4% vs 62.3 +/- 10.9%, p less than 0.02). Treatment had to be stopped before the 24th hour in 4 cases (3 early deaths and 1 severe haemorrhage). The average revascularisation was 30.5 +/- 6.8% in Group I and 38.3 +/- 31.1% in Group II (NS). The alpha-2-antiplasmins were lower (NS) in Group II as were the fibrinogen levels (p less than 0.01 at the 12th and 24th hour) whilst the plasminogen levels and surface of fibrin plateaux were higher (p less than 0.01 at the 6th hour and p less than 0.05 at the 12th hour, respectively). These results show that moderate doses of urokinase associated with heparin are effective in the treatment of acute pulmonary embolism.(ABSTRACT TRUNCATED AT 250 WORDS)

From 1982 to 1984 included, 31 patients under 70 years of age were admitted during the first three hours of a primary myocardial infarction (MI) and are the subject of a randomized prospective study. 16 patients are treated with 5,000 U of heparin given in intravenous bolus, followed with 150,000 IU of urokinase (UK) in intravenous bolus, then 12,000 IU of UK/min for 90 min or a total dose of 1,230,000 IU. 15 patients are treated with heparin alone (intravenous bolus of 5,000 U). Repeated titrations of creatine phosphokinase (CPK) and the coagulation parameters are performed during the first 24 hours. A coronary angiography with ventriculography (RAO 30 degrees) is performed on the 1st day (D1) and the 3rd week (W3). Study of the left ventricular kinetics (LV) is carried out according to the Stanford method. At D1, the rate of coronary patency is 56 p cent (n = 9) in the UK (A) group and 53 p. cent (n = 8) in the control group B (heparin alone). The percentage of late re-thrombosis is 0 p. cent in group A and 12.5 p. cent in group B (heparin alone). 1 patient died in each group. The CPK peak is less high in case of coronary patency in group A than in case of thrombosis (1,444 +/- 413 vs 1,710 +/- 120 U -heparin alone) and occurs earlier (16 +/- 2 h vs 21 +/- 1 h). In group A a significant decrease of fibrinogen (p. 0.01) as well as plasminogen and alpha-2-antiplasmins (p less than 0.001), is noted. No severe haemorrhagic complications nor sustained rhythm disorders are noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimental studies on rabbits have shown that CY 222, a low molecular weight heparin (mean: 2.500 daltons), has the anti-thrombosis properties of heparin but reduces the risk of haemorrhage in optimal doses of 1.000 AXa IC (Institut Choay) units/kg/day. The safety and effectiveness of CY 222 were tested in 47 patients presenting with a less than 5 days' old pulmonary embolism. The patients were divided into three groups according to dosage: group I (n = 16) received 500 AXa ICu/kg/day; group II (n = 17), 750 AX ICu/kg/day, and group III (n = 14), 1.000 AXa ICu/kg/day. The drug was administered by continuous intravenous infusion during 10 days. Its effectiveness was assessed from the Miller index calculated on conventional pulmonary angiograms on days 0, 5 and 10. On the 10th day of treatment, the percentage of revascularization was similar in all three groups (group I 65.9 +/- 9.9 p. 100; group II 71 +/- 6.8 p. 100; group III 68 +/- 8.5 p. 100), but the improvement was significantly more rapid in group III patients. Embolism recurred in 5 cases (2 in group I, 1 in group II, 2 in group III) and was fatal in 1 case (group I). Haemorrhagic complications were noted in 3 cases (group III patients). Except for thromboelastography, all coagulation tests were unmodified by CY 222. The anti Xa and the (very low) anti IIa activities of the drug were directly related to the doses administered.(ABSTRACT TRUNCATED AT 250 WORDS)

In a 62 years old patient suffering from stenocardia and paroxysms of atrial fibrillation, coronary angiography disclosed two coronary-pulmonary fistulas associated with a tritruncal stenotic coronary atheroma. During the operation consisting of a double aortocoronary shunt and closing the anomalous pulmonary ostium, a control coronary angiography confirmed the shunt permeability and showed the absence of opacifications at the passage of the fistulas. In the immediate postoperative period the recurrence of paroxysmal atrial fibrillation was no longer accompanied by stenocardia which did not reappear one year after operation. This observation illustrates the fact that coronary-pulmonary fistulas may aggravate a fortuitously associated coronary insufficiency.

Two cases of arteriovenous fistula arising from the internal mammary artery are described. The detection of the continuous subclavian murmur was preceded by therapeutic procedures in both cases; difficult subclavian vein catheterisation in the first; reoperation of sternotomy for postoperative haemorrhage after open heart mitral commissurotomy in the second. Oxymetry after sampling at, above and below the subclavian vein confirmed the presence of a shunt and allowed estimation of shunt flow, which was minimal in both cases, 11 and 32% of cardiac output respectively. The origin of the fistula at the internal mammary artery and the communicating vein were identified by semi-selective angiography. The latter was superior vena cava in the first case and the internal mammary vein in the second. The low shunt flow probably explains the outcome: spontaneous closure in both cases. This is exceptional in any form of arteriovenous fistula.

The authors report the case of a 49 year old woman who presented with congestive cardiac failure and hypertension. Clinical examination revealed a high output state and an abdominal mass with a continuous murmur which angiography showed to be a very vascular right renal tumour with a large and early venous return. Catheter studies confirmed the increased cardiac output (cardiac index 5.37 l/mn/m2), an increase in right heart and mean pulmonary capillary pressures (28 mmHg), decreased peripheral arterial resistances and a left-to-right shunt effect at the level of the suprarenal inferior vena cava (+ 3.8 volumes of oxygen per 100 ml). After radical right nephrectomy, the cardiac failure and hypertension regressed and the haemodynamic parameters returned to normal.

Twenty six patients with acute (less than 5 days) pulmonary embolism (PE) confirmed by bilateral pulmonary angiography with a Miller index greater than 15 were given tissue plasminogen activator (Alteplase) (rt-PA) intravenously (n = 20) or directly into the pulmonary artery (n = 6). The dosage was 100 mg/7 hours (bolus 10 mg + 40 mg/2 hours + 50 mg/5 hours). Heparin (5000 IV as a bolus and 1000 IV/hour) was associated in all cases. The Miller index decreased from 24 +/- 1 (n = 26) before treatment to 12 +/- 1 (n = 25) (p less than 0.001) after 100 mg of Alteplase, and from 25 +/- 0.4 (n = 14) to 22 +/- 0.5 (n = 14) (p less than 0.001) after 50 mg. The mean pulmonary arterial pressures fell from 30 +/- 2 mmHg to 21 +/- 2 mmHg after 50 mg (n = 26) (p less than 0.001) and to 14 +/- 1 (n = 25) (p less than 0.001) after 100 mg of Alteplase. A decrease in mean pulmonary artery pressures (-22%, p less than 0.001) and total pulmonary resistances (-29%, p less than 0.001) was obtained after one hour of thrombolysis in 12 monitored patients. There were no fatalities. Severe haemorrhage occurred in 6 cases. Therefore, Alteplase induced a rapid dissolution of recent intrapulmonary thrombi without inacceptable haemorrhagic complications. Its action could be particularly beneficial in patients with right ventricular failure due to life threatening pulmonary embolism.

A case of leiomyosarcoma of the pulmonary artery in a 64-year old man without previous cardiovascular disease is reported. The clinical picture, which comprised episodes of paroxysmal dyspnoea associated with acute cor pulmonale, suggested pulmonary embolism. Radioisotope perfusion study and pulmonary angiography seemed to confirm this diagnosis, but no improvement was obtained with a prolonged thrombolytic treatment. The presence of a median mass at CT led to exploratory thoracotomy and to the finding of a tumour in the pulmonary artery, which turned out to be a leiomyosarcoma. The disease rapidly took an unfavourable course. Comparison of this case with data from the literature showed that primary tumours of the pulmonary artery are extremely rare, that they are diagnosed with difficulty and often at a late stage and that their prognosis is usually very sombre.

44 patients with refractory heart failure (RHF) were treated with a conversion enzyme inhibitor, captopril. Prior to treatment, 26 patients had stage IV RHF and 18 patients had stage III RHF (NYHA). The course of the trial was marked by early deaths (6 months) in 9 cases (20.4%), early treatment failure in 8 cases (18.2%), intolerance in 3 cases (6.8%) and 3 patients (6.8%) were lost to follow-up. 21 patients (48%) were improved by the treatment and were followed for a mean of 16 months +/- 8.6. The mean dosage of captopril was 157 mg per day in 3 oral doses (range: 75 to 300 mg per day). The pulmonary capillary pressure dropped, on average, from 30 +/- 10 mm Hg to 21 +/- 7 mm Hg (p less than 0.01) by the 8th day and remained stable thereafter. The cardiac index increased by 40%. The heart rate decreased by a mean of 10.4%, by the time of the first examination. The mean blood pressure was not significantly modified. Side effects which resolved after changing the dosage were seen in one third of cases: renal failure (4 cases), hypotension (2 cases), hyperkalaemia (1 case). In the long term, 6 patients (2.6%) died after a mean delay of 15.6 +/- 5.3 months.

The study of two cases of young patients with renal transplants who, successively and a few months after the procedure, presented a thrombophlebitis of the lower extremities (with or without pulmonary embolism), then an acute coronary insufficiency, without any encouraging or triggering factor, raises the hypothesis that this is not a mere coincidence. In fact, in the literature, numerous cardiovascular risk factors) inherent in complicated chronic renal failure, dialysis, steroid therapy and immuno-suppressive treatment (Azathioprime, under these circumstances) were demonstrated. In addition, abnormalities of the platelets aggregation, hemostasis and fibrinolysis, were at the origin of thrombo-embolic accidents. Besides any specific cardiovascular risk factor or any obvious biological anomaly, there is still a predisposition of patients with renal transplants, to arterial as well as venous thrombo-embolic accidents.

Two cases of anterior transmural myocardial infarction occurring after closed chest injuries in young adults (26 and 29 years) are reported. In one case, the infarct was detected after 42 days when the patient gradually developed left ventricular failure after thoracic injury (fracture of the left 9th rib). In the other case, the diagnosis was made during the initial evaluation of a patient with multiple injuries by routine electrocardiography. Radio-isotopic investigations showed an antero-septo-apical and lateral defect with akinetic wall motion in the first case, and apical hypofixation with limited akinesis in the second one. Coronary angiography with left ventriculography was performed after 2 and 3 months respectively, and showed a prolonged non-atheromatous stenosis of the proximal left anterior descending artery with anterior wall hypokinesia, apical akinesia and mitral incompetence (Case n 1) and slight changes of the distal part of the left anterior descending artery with apical hypokinesia (Case n 2). These two cases bring the number of documented reported cases to 37 and illustrate the two possible mechanisms of myocardial infarction after closed chest trauma: direct trauma to the coronary arteries with vascular lesions and secondary myocardial infarction associated with a poor prognosis, and myocardial contusion resulting in random myocardial lesions which usually carry a better prognosis.

44 cases of paroxysmal sinoatrial tachycardia (PAT) due to reentry within the sinus node or between the sinus node and the atrium are reported; these tachycardias are usually quite well tolerated clinically as the rhythm is rarely faster than 140/min and they are often degraded by functional AV block. They can be triggered and terminated by one (or two) atrial stimuli, and reduced by carotid sinus massage but relapse in the short term. They often alternate with a disturbance of atrial excitability in patients who also have binodal disease. Their diagnosis implies endocavitary investigation showing sinusal anterograde atrial activation and atrial and ventricular stimulation to differentiate them from other types of paroxysmal tachycardia, especially those due to reentry involving concealed right sided Kent bundles. Studies of sinus node function by atrial extrastimulus techniques in 38 patients usually showed an isolated and prolonged Zone I followed, without a transitional plateau, by a Zone IV of sinus echos during which the tachycardia could be triggered. This type of tachycardia, without doubt as common as junctional tachycardia, may respond to treatment with Quinidine, Amiodarone, Verapamil, or beta-blockers, associated with permanent pacing in cases of binodal block.

Episodic mitral regurgitation due to ischaemia of one or both papillary muscles was studied in a review of 39 cases with complementary investigations and compared with previously reported data. The condition occurred after myocardial infarction in 69 p. 100 of cases (usually after inferior infarction: 54 p. 100) associated with ischaemia of the controlateral territory; there was no history of myocardial infarction in 31 p. 100 of cases. The patients were usually elderly (73 years), often hypertensive (77 p. 100) and diabetic (62 p. 100). The clinical syndrome was that of severe anginal pain, mitral regurgitation and left ventricular failure which was critical in some cases. The ECG showed typical ST depression (4.1 +/- 1.6 mm) especially in the antero-lateral leads; left bundle branch block (28 p. 100) with left axis deviation (18 p. 100), sometimes associated with changes of chronic infarction (64 p. 100) was also recorded. Mitral regurgitation and left ventricular failure regressed almost completely in typical cases between attacks, whilst the ECG showed slight residual sub-endocardial ischaemia (ST depression of 1.5 +/- 0.4 mm) in 30 cases and/or subepicardial ischaemia observed in the anterolateral leads in 13 cases. Phonomechanographic recordings (n = 32) showed moderate mitral regurgitation (1-2/6), usually parasystolic (47 p. 100) or early and mid systolic (36 p. 100) in 87.5 p. 100 of cases between attacks, aggravated by handgrip exercise and improved by trinitrin administration. Echocardiography (n = 27) only showed mitral valve changes in 2 patients (increased density of the papillary muscle in 1 case and prolapse of the anterior leaflet in 1 case); however, segmental wall hypokinetic (51 p. 100) or dyskinetic (15 p. 100) motion, was common with increased left ventricular end diastolic dimensions (mean 56.3 +/- 8.0 mm) and decreased fractional shortening (mean 0.30 +/- 0.07) (67 p. 100). Left atrial dimensions were increased (mean 39.7 +/- 6.4 mm) in 52 p. 100 of patients. Thallium 201 myocardial scintigraphy (n = 32) showed hypofixation in 57 (36 p. 100) and a lacuna in 23 (14 p. 100) of the 160 segments analysed. Left ventricular angioscintigraphy (n = 27; 135 segments) showed hypokinesia in 72 segments (53 p. 100); 2.7 segments per patient), akinesia in 19 segments (15 p. 100; 0.7 segment per patient) and dyskinesia in 2 segments (1.5 p. 100); 0.1 segment per patient). The global ejection fraction was 46 +/- 13 p. 100. Coronary angiography (n = 8) showed significant diffuse atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)

The prourokinase-urokinase system physiologically contributes to fibrinolysis activation. It is therefore rational to envisage the use of urokinase in thrombotic diseases, and notably in the acute phase of myocardial infarction (MI) where coronary thrombosis is virtually constant. The main studies on this subject were published in 1975 and in 1985, thus reflecting the changes in therapeutic concepts that have occurred during these 10 years. The older studies concerned patients who were admitted within the first 12 hours of MI and had no early angiographic examination; the results were evaluated indirectly on clinical and enzymatic criteria and on the regression of electrical signs of myocardial suffering. The more recent studies concern patients who are treated at an early stage, often within the first 3 hours of the accident, on the basis of experimental data which favoured early coronary reperfusion as a means of protecting the myocardium; in these studies coronary arteriography is performed immediately after the thrombolytic treatment; computer-assisted studies of the left ventricular function are also carried out, so that the results of thrombolysis are expressed in terms of coronary patency and improvement in segmental kinetics. The results of these different sets of studies have proved to be similar with time. Urokinase, notably when injected intravenously, has a beneficial effect in the acute phase of MI when compared to the conventional treatment. The coronary reperfusion obtained with urokinase is favourable to the myocardium, and the sooner it occurs the better. This benefit is demonstrated by clinical, electrical, enzymatic and angiographic data. Thus, despite its cost, urokinase remains useful in the treatment of MI, notably because it is well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)