[Topographic aspects of threatened extension of transmural myocardial infarction. Electrocardiographic and coronarographic data]. / Aspects topographiques de la menace d'extension d'infarctus du myocarde transmural. Données électrocardiographiques et coronarographiques.

The topographical and physiopathological aspects of the danger of extension of infarction of the myocardium are defined with the aid of data collected by electrocardiogram and coronarography in 50 patients. The danger of extension in situ, observed in 64% of the cases, is the most frequent and complicates particularly the progression of anterior infarcts. In fact, it is located in the same area as the initial infarct in 91% of the cases for anterior infarcts and in 40% of the cases for inferior infarcts. It is expressed by an elevation of the ST segment in 84% of the cases and corresponds to a monotruncular attack in 63% of the cases. The downstream bed of the vessel destined for the infarcted area and threatened secondarily remains permeable in the anterograde sense. Apart from infarcts, the danger of extension is less frequent, found in 36% of the cases, and complicates preferentially the progression of inferior infarcts. It finds expression in a depression of the ST segment in 77% of the cases and the coronary attack is always pluritruncular. The mortality in one month is 35% of 17 patients treated medically and 3% of 33 patients who have been equipped with a shunt or angioplasty. In situ the danger of extension denotes the presence of cellular islets, which are still healthy, in the region of an infarcted myocardial zone, the viability of which may be threatened secondarily by a phenomenon of coronary occlusion, which is intermittent and repeated. Except for an infarct, the danger of extension implies the diffusion of an atheromatous effect. The good results of surgical treatment or dilatation argues in favour of an early coronarographic exploration.

[Anti-arrhythmia and electrophysiological effects of encainide in supraventricular tachycardias]. / Effets électrophysiologiques et anti-arythmiques de l'encaïnide dans les tachycardies supraventriculaires.

In order to assess the electrophysiologic effects and anti-arrhythmia effects of encainide after acute IV injection and chronic oral therapy, a group of 10 patients (mean age 54) with recurrent supraventricular tachycardia was studied. Seven patients had more than 2 attacks per month, and supraventricular tachycardia (SVT) resulted in severe symptoms in the three remaining SVT was due to AV nodal re-entry in 6 patients and to concealed accessory pathway in 4. After a control study, SVT was initiated, and encainide (0.75 mg/kg) was infused intravenously in attempt to stop the tachycardia. A second study was achieved. After 4 days of oral therapy (25 or 50 mg T.I.D.) a third study was performed, including SVT initiation attempts. Encainide depressed conduction in all cardiac tissues, and this effect was more evident after oral administration. Antegrade I:I conduction cycle length increased of 13.9% (p less than 0.05), and the same parameter in retrograde conduction increased of 30.03% (p less than 0.05). IV injection interrupted 2 of 10 SVT only. However, after 30 minutes, 5 re-initiated SVT were nonsustained, and mean cycle length increased from 326 +/- 21 to 397 +/- 51 (p less than 0.01). After oral therapy, SVT was initiated in 4 of 10 patients, nonsustained in 3. During long term follow-up (one year or more), no severe adverse effect has been reported. Three patients are still experiencing short events of well-tolerated SVT. Hence, moderate or low doses or oral encainide may safely control recurrent supraventricular tachycardia.

[Effects of amrinone administered orally and by injection in heart failure]. / Effets de l'amrinone utilisée par voie orale et injectable dans l'insuffisance cardiaque.

Amrinone is a new positive inotropic agent available in oral and intravenous preparations. Twelve patients with Stage III cardiac failure of ischaemic (6 cases), myocardial (5 cases) or valvular (1 case) origin, were treated with oral amrinone. The protocol included a complete clinical, radiological and biochemical work-up, an exercise stress test, cardiac catheterisation and echocardiography before entering the trial. The patients underwent clinical examination, stress testing and echocardiography at the 4th, 8th and 12th week of treatment with 300 mg daily of amrinone. Two patients had to be withdrawn from the trial because of thrombocytopaenia; one patient deteriorated and eventually died of pulmonary embolism. There was a marked improvement in the 8 patients who achieved the trial, with an average gain of 40 watts on exercise testing, a mean reduction of 16 mm Hg in diastolic pulmonary pressures, and an increase of 11 p. 100 in EF and velocity of circumferential fibre shortening. Four additional patients were given intravenous amrinone (1 cc/kg relayed with an infusion of 1 ng/kg/min). Ventricular end-diastolic pressures fell by 9 mm Hg and cardiac index rose by 1.02 1/min/m2. Tolerance was good with no arrhythmic complications or significant variations in mean arterial pressure or heart rate. Although certain reserves have to be made with regards of tolerance of oral amrinone, the drug would seem to be useful and effective in the intravenous form. Further studies are under way.

[Myocardial revascularization in the developing phase of myocardial infarction using intracoronary thrombolytic therapy]. / Revascularización miocárdica en fase de constitución del infarto de miocardio por tratamiento trombolítico intracoronario.

The author's experience on intracoronary thrombolysis on 71 patients that underwent coronary angiography in the first six hours of myocardial infarction is presented. The coronary artery responsible for the infarction was totally occluded in 66 cases and presented a subtotal occlusion in the remaining 5 cases. The protocol included the intracoronary injection of 2 mg isosorbide dinitrate and 78.000-385.000 U of streptokinase. An early reperfusion occurred in 66% of the patients, without mortality in the acute phase. ST-segment returned to normal in 41 of the 47 reperfused cases, but a Q wave developed in 42 cases. Hospital mortality was 6,4%, and the reocclusion rate was 17%.

[So-called rudimentary or nontransmural myocardial infarction. Coronary lesions, course and prognosis]. / L'infarctus du myocarde "rudimentaire" ou non transmural. Lésions coronariennes, évolution et pronostic.

Eighty patients admitted to hospital between 1975 and 1980 for "non-transmural" myocardial infarction (72 men, 8 women, mean age 56 +/- 9 years) were studied. The diagnosis was based on a severe attack of pain of over 30 minutes duration, increased serum cardiac enzyme levels (CKMB greater than 24 U; SGOT greater than 60 U), pyrexia and signs of inflammation. The patients were divided into two groups according to their ECG changes: Group A: "rudimentary" infarction with prolonged T wave inversion from V1 to V5, narrow transient Q waves and reduction of R wave amplitude in the corresponding leads; Group B: persistant prolonged, intercritical ST depression greater than 2.5 mm (subendocardial infarct). All patients underwent selective coronary angiography and left ventriculography in the RAO projection within 15 days of admission. The angiographic data (coronary score, ejection fraction, alinetic perimeter) were compared to those of 2 randomly chosen control groups: Group C: 30 inferior wall infarcts with coronary angiography and regularly followed-up; Group D: 30 transmural anterior infarcts with coronary angiography, regularly followed-up. Four factors were analysed during follow-up: the incidence of death after discharge from hospital, transmural infarction, unstable angina and cardiac failure. All patients were treated medically (nitrate derivatives, betablockers, calcium antagonists). Sixteen patients in Group A (p less than 0,025) were operated and excluded from the prognostic study. The angiographic data showed a high incidence of isolated, severe LAD disease in Group A (59.2% of cases) and that multivessel disease was commoner in Group B (78.4%). A collateral circulation revascularising the LAD was observed in 42% of patients in Group A. (ABSTRACT TRUNCATED AT 250 WORDS)

[Electrophysiological effects of encainide in man]. / Effets électrophysiologiques de l'encaïnide chez l'homme.

Encainide is an antiarrhythmic agent under evaluation; it is effective in ventricular and supraventricular arrhythmias. Its electrophysiological effects seem to differ according to the route of administration, oral or intravenous, probably because of the effects of active metabolites. Two electrophysiological studies were carried out in 20 patients, under basal conditions, and after 4 to 10 days oral administration at doses ranging from 75 to 300 mg/day. Encainide depressed intra-atrial conduction (prolongation of the P-A interval from 29,7 +/- 2,2 to 36 +/- 4,5 ms, p less than 0,01), slowed conduction in the atrioventricular mode (prolongation of the A-H interval from 74 +/- 14 to 98 +/- 15 ms, p less than 0,01) and the His-Purkinje system (lengthening of H-V from 50 +/- 3 to 70 +/- 6,2 ms, p less than 0,001). The sinus node function was depressed with lengthening of the corrected sinus node recovery time (297 +/- 64 to 387 +/- 71 ms, p less than 0,01) and of the sinoatrial conduction time (173 +/- 25 to 219 +/- 43, p less than 0,01). The atrial and ventricular refractory periods were significantly longer (245 +/- 16 ms to 273 +/- 10 ms, p less than 0,001, and 237 +/- 12 to 266 +/- 19 ms, p less than 0,01, respectively). This new antiarrhythmic agent therefore seems to act at all levels which suggests that it may have wide ranging antiarrhythmic effects.

[Oral and injectable amrinone in cardiac insufficiency]. / Etude de l'amrinone orale et injectable dans l'insuffisance cardiaque.

The authors report the results of a study of amrinone which was prescribed orally and by injection. 12 patients with stage III congestive heart failure were treated with oral amrinone. Prior to inclusion in the trial, all of the patients underwent a complete clinical, radiological and laboratory examination. They were examined by ergometric haemodynamic tests with measurement of the cardiac output and by echocardiography. After discharge from hospital, the patients were reviewed clinically every week and cyclo-ergometric and echocardiographic examinations were performed at 4, 8 and 12 weeks. At the end of the study, a further haemodynamic survey was performed in 8 patients. Two patients left the trial because of thrombocytopenia which appeared between the 10th and 25th day of treatment and 2 others left the trial (1 death, 1 treatment failure). In the 8 patients who completed the trial, the authors found: a functional improvement (improvement by one NYHA class within 3 months), a mean gain of 40 Watts at the last stress test, an 11% improvement in the ejection fraction and in the rate of circumferential shortening, a decrease in the filling pressure (16 mm Hg) and an improvement in the cardiac index (mean of 700 ml). A haemodynamic study was conducted in 4 patients who received amrinone by injection (1 mg/kg by slow intravenous injection, followed by an infusion of 10 ng/kg/min). The authors observed a mean drop in left ventricular end-diastolic pressure of 9 mm Hg an increase in the cardiac index of 1.02 l/min/m2, without any significant variation in the mean blood pressure or the heart rate.

[Myocardial infarction before the age of 35. Clinical and coronarographic aspects]. / Infarctus du myocarde avant l'âge de 35 ans. Aspects cliniques et coronarographiques.

Myocardial infarction under the age of 35 is no longer a rarity. A series of 22 patients exhibited all the usual epidemiological, clinical and angiographic features of the disease: risk factors, predominantly excessive smoking associated with dyslipoproteinaemia in 50% of the cases; onset during exercise in one quarter of the cases, more frequently than in elderly people; and absence of significant lesions at angiography in one third of the cases. Angiography of the coronary arteries, performed in the early stages of infarction in 5 patients, demonstrated the presence of several factors in the pathogenesis of arterial occlusion in young people, i.e. thrombosis in almost every case, arterial spasm in 10% of the patients and atheromatous plaques with little or no stenosis in one half.

[Are calcium inhibitors useful in the treatment of effort angina pectoris]. / Les inhibiteurs calciques sont-ils utiles dans le traitement de l'angine de poitrine d'effort?

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.