[Show abstract][Hide abstract] ABSTRACT: Paroxysmal episodes of atrial frequently cause severe functional disturbance because of their recurrent nature. Propafenone (Rythmol) is a very active anti-arrhythmic at the ventricular level which acts by decreasing the rate of atrio-ventricular and intra-ventricular conduction and by prolonging the refractory period of the right atrium and the accessory pathways. The authors conducted an open study of this drug in 20 cases with resistant, recurrent atrial fibrillation. All of the patients were known to have recurrent episodes of atrial fibrillation which could not be prevented by a variety of antiarrhythmic agents. They performed a clinical, electrocardiological and laboratory evaluation of these patients. Holter monitor recordings were performed prior to entry into the study, during the first week of treatment, between the 4th day and the 8th day, on the 20th day, at the 2nd month and between the 3rd and 6th months. Propafenone was prescribed at a dose of 900 mg per day and the initial dose was reduced to 600 mg after the 3rd month of treatment. Five patients can be classified as therapeutic failures, as the arrhythmia recurred. These patients presented a "vagal" atrial fibrillation preceded by an episode of bradycardia. 15 patients can be considered to have obtained a successful result, as no recurrences were detected during the 6 month observation period. The electrical and laboratory tolerance was satisfactory. The most frequent side effects were minor transient gastrointestinal disturbances.
No preview · Article · Jan 1985 · Annales de Cardiologie et d Angéiologie
[Show abstract][Hide abstract] ABSTRACT: The reestablishment of anterograde arterial flow by intraluminal coronary repermeabilitation during the constitution of an infarct represents a direct method of myocardial revascularisation aiming to reduce the mass of infarcted tissue. Twenty patients underwent coronary angiography during the initial phase of myocardial infarction (on average 4.6 hours after the onset of symptoms). There was total occlusion of the artery responsible for the infarct in 17 cases, and subtotal stenosis in 3 cases. The protocol included an initial intracoronary injection of 0.5 mg of trinitin, an attempt to pass a flexible guide wire past the obstruction, and then local administration of streptokinase (a bolus injection of 25,000 units followed by an infusion of 2,000 units per minute, for 1 to 2 hours). Coronary repermeabilisation was obtained in 11 cases after partial relief of the obstruction by trinitrin (2 cases) or passage of the guide wire (4 cases). The immediate effects of revascularisation were: 1) the relief of pain in all cases; 2) normalisation of the ST changes in 10 out of 11 cases; no QRS changes were observed in only 3 cases; 3) an early rise in serum creatinine phosphokinase in all cases; 4) slight or no significant residual stenosis was observed in 6 out of 11 cases. One patient had recurrent infarction 10 hours after intracoronary thrombolysis but the other 10 patients have remained asymptomatic over a follow-up period of 6 to 18 months. Control coronary angiography on the 10th day showed that the affected artery remained patent in all cases, that the degree of residual stenosis decreased in 2 cases and that the ejection fraction remained unchanged: 55 ± 9% before, compared to 59 ± 8% at control. The reported incidence of coronary revascularization by intracoronary thrombolysis varies from 53 to 95% of cases with no associated prohibitive risk to patients. The long term effects of this procedure of revascularisation during the acute phase of myocardial infarction on the myocardium and mortality rate need evaluation by detailed multicentre trials. Intravenous thrombolytic therapy, allowing a more widespread application of the method, deserves fresh assessment. Finally, the multifactorial mechanism of coronary occlusion responsible for infarction is demonstrated with the participation of spasm, almost constant intraarterial thrombosis and the atheromatous plaque, which, from the angiographic point of view, was only slightly or non-occlusive in half the cases in this series.
No preview · Article · Jul 1983 · Archives des maladies du coeur et des vaisseaux
[Show abstract][Hide abstract] ABSTRACT: 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 (> 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.
No preview · Article · Mar 1983 · Archives des maladies du coeur et des vaisseaux
[Show abstract][Hide abstract] ABSTRACT: Thirty patients with threatening myocardial infarction were treated with intravenous isosorbide trinitrate. Eight patients had increasingly severe angina, 6 had de novo crescendo angina, 3 had Prinzmetal angina and 13 had signs of impending extension of a previous infarct. In all cases the anginal attacks occurred spontaneously. The drug was administered in association with a beta-blocker or a calcium antagonist. The initial dosage was 33 mcg/min and dosage adjustments ranged from 16 to 130 mcg/min. the main duration of treatment was 3.6 days. Pain was controlled in all patients. Anginal attacks ceased completely and permanently in 24, but the remaining 6 became isosorbide dinitrate-dependent and could only be weaned by aortocoronary bypass. The effects on the drug on heart rate and blood pressure remained moderate and never interfered with dosage adjustments. Coronary artery angiography was performed without any trouble in 25 patients, 21 of whom underwent myocardial revascularization by venous grafts.
No preview · Article · Jul 1982 · La Nouvelle presse médicale
[Show abstract][Hide abstract] ABSTRACT: Twenty patients with chronic congestive heart failure resistant to conventional treatment with digitalis, diuretics and vasodilators received captopril, an oral inhibitor of the angiotensin-converting enzyme, in daily doses of 200 mg and were followed up for 2 months or more. At 2 months, there was a significant reduction in functional symptoms (NYHA classification), bodyweight and left ventricular filling pressure, with an equally significant rise in cardiac output and sodium urinary excretion. There was no fall in systemic blood pressure, nor tachycardia. These effects were sustained in 8 patients followed up for 6 months. They seem to indicate that captopril is both effective and well tolerated in chronic congestive heart failure.
No preview · Article · May 1981 · La Nouvelle presse médicale
[Show abstract][Hide abstract] ABSTRACT: Although rupture of a mitral papillary muscle during myocardial infarction is well known, and post-infarction transmural ruptures causing false aneurysms occasionally reported, the association of rupture of the anterior papillary muscle and a underlying transmural parietal rupture giving rise to a false aneurysm is quite exceptional, and, to the best of our knowledge, has not previously been reported. Despite the serious nature of the disease, surgical cure of the aneurysm with mitral valve replacement was successful, due to the limitation of the anatomical disruption by early pericardial symphysis.
No preview · Article · Nov 1979 · Archives des maladies du coeur et des vaisseaux
[Show abstract][Hide abstract] ABSTRACT: Echocardiography detected a mobile left ventricular tumour. The tracing showed a cluster of echoes in the left ventricular outflow tract corresponding to the location of the tumour as confirmed by cineangiograms. At operation, a thrombus was discovered, attached to a chorda tendineae.
[Show abstract][Hide abstract] ABSTRACT: Bacterial endocarditis due to Staphylococcus epermidis is rare and severe. In a first patient, a 58-year-old-man, it developed 40 days after the insertion of a double prosthesis (mitral and aortic). Cure was obtained by medical treatment using a combination of vancomycin and gentamicin, followed by pristinamycin and tobramycin. The second patient, a 50-year-old-woman, suffering from cirrhogenic hepatitis and treated with corticosteroids. Staphylococcus epidermidis endocarditis developed without any portal of entry being discovered. After the failure of various antibiotic combinations (even though bactericidal in vitro), a mitral Starr valve was inserted which resulted in cure. None of the patients showed any sign of valvular mutilations or disinsertion of prosthesis.
No preview · Article · Jun 1979 · La Nouvelle presse médicale