[Occlusive spasm of a coronary artery not treated during angioplasty. Apropos of a case]. / Spasme occlusif d'une artère coronaire non abordée au cours d'une angioplastie. A propos d'une observation.

The authors report the case of a patient who, during percutaneous transluminal angioplasty of the circumflex artery, developed sudden occlusion of the anterior interventricular artery without stenosis and not touched by the operator. The fact that this occlusion was completely reversible after an intra-coronary injection of nitroglycerin suggests that this was due to spasm. This case suggests the possibility of consequences of angioplasty at a point distant from the dilated site. The authors use this case and a review of the literature to discuss the pathophysiological mechanisms which could be responsible for such consequences.

Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty.

In an attempt to discern biological (such as thrombotic or fibrinolytic) risk factors in patients developing restenosis after percutaneous transluminal coronary angioplasty, the following factors were measured prior to angiography in a population of 23 patients (20 men, 3 women, mean age 57 +/- 5 yr) treated by a successful angioplasty (gain > 20% and residual stenosis < 50%) for stable angina pectoris and who had a routine angiographic restudy. The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. Also studied were clinical characteristics: age, gender, diabetes, hypertension, smoking habits, previous myocardial infarction; angiographic data: global extent of coronary artery disease, location of the stenosis in a bend or branch point, complexity of the lesion, initial and residual stenosis and treatment during follow-up. The coronary angiograms were analyzed by a computer-assisted method with automatic edge detection. On angiographic criteria, 6 patients (restenosis group) were judged to have developed a restenosis (30% decrease in diameter and/or return to a 50% stenosis). The other 17 patients (those without restenosis) were considered to have a persistent success. Apart from age (group without restenosis: 55 +/- 6; restenosis group 61 +/- 5, p < 0.04), there were no differences in clinical, angiographic or treatment variables. There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). These findings indicate that patients developing restenosis after coronary angioplasty tend to have an imbalance in the prothrombotic-antithrombotic equilibrium prior to the procedure.

Evaluation of plasmatic leucocyte elastase levels in coronary artery disease.

Leucocyte elastase may be involved in the structural modification observed in the atherosclerotic process. Therefore, we tested the usefulness of leucocyte elastase plasma level determination as a marker for atherosclerosis. Plasma levels of elastase were determined by ELISA in 100 consecutive patients (mean age 56 +/- 9.8 years) admitted to hospital for coronary angiographic investigation of chest pain. Eighty-seven patients had evidence of atherosclerosis, and 13 patients had normal coronary vessels. No significant difference in leucocyte elastase was found between the 2 groups, nor was there any relationship between elastase levels and the severity of atherosclerosis. However, relationships between plasma leucocyte elastase levels and various lipid fractions (Apo AI, LDL) and daily tobacco consumption were found. Leucocyte elastase may thus play a role not only by direct modification of the vessel wall, but also indirectly via risk factors such as dyslipoproteinemia and leucocyte toxicity.

Biological risk factors for sudden death in patients with coronary artery disease and without heart failure.

In a study of biological risk factors for sudden death in patients with coronary artery disease, 320 patients were, prospectively, recruited and followed-up over two years. None of the patients had heart failure or recent myocardial infarction. The following variables were recorded: previous acute myocardial infarction, hypertension, smoking habits, ventricular arrhythmia; the angiographic variables included: left ventricular ejection fraction, Jenkins' and mean atherosclerotic scores; lipid profile: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoproteins Al and B; hemostatic profile: fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2-antiplasmin, euglobulin clot lysis time and tissue plasminogen activator before and after venous occlusion, tissue plasminogen activator inhibitor, platelet factor 4, beta-thromboglobulin. During the follow-up period, 12 of the patients died suddenly. In these patients, ejection fraction was lower: 49 +/- 16% versus 61 +/- 14% for the other patients (P less than 0.02), fibrinogen higher: 3.9 +/- 0.8 g/l versus 3.5 +/- 0.8 for the living patients (P less than 0.05) and protein C lower: 89 +/- 39% versus 111 +/- 39% (P = 0.06) for the other patients. In multivariate analysis: lower ejection fraction (P less than 0.008), older age (P less than 0.03) and lower protein C (P less than 0.01) were correlated with sudden death. Among the patients with coronary artery disease, the raised fibrinogen and the decreased protein C appeared to be risk factors for sudden cardiac death. These alterations reflected a prothrombotic state which might increase the ischemic risk, due to an acute thrombosis, leading to the fatal ventricular arrhythmia. Determination of these hemostatic variables might be a useful adjunct for assessment of the vital prognosis of patients with coronary artery disease, especially the risk of sudden death in addition to other known clinical, electrocardiographic, hemodynamic risk factors. This would also guide both the instigation of complementary investigations and appropriate therapy in such high risk group of patients.

[Mitral valve prolapse and angina with normal coronary arteries: research of a thrombogenic factor]. / Prolapsus valvulaire mitral et angor à coronaires saines: recherche d'un facteur thrombogène.

The potential thrombotic risk of mitral valve prolapse may, in certain circumstances, require preventive treatment. This study was aimed at determining whether the presence of angina in patients with mitral valve prolapse and healthy coronary vessels was accompanied by a high-risk thrombogenic profile. Forty two patients (19 women and 23 men) with anginal chest pain and angiographically normal coronary vessels were divided into two populations according to the presence (18 patients) or absence (24 patients) of mitral valve prolapse (MVP) shown by angiography. Before angiography, all patients underwent laboratory studies to detect any possible abnormality of plasma coagulation and of prothrombotic physiological fibrinolysis. Study of subgroups, according to sex and/or the presence of MVP, revealed no significant difference in the profile of laboratory parameters. Thus the presence of angiographic MVP in symptomatic patients free of atherosclerosis is not associated with the existence of any particular thrombotic profile and, theoretically, does not require preventive anti-thrombotic treatment.

[Cardiac lesions in Takayasu's disease. A case with initial pericarditis and tamponade]. / Atteintes cardiaques de la maladie de Takayasu. Un cas de pancardite inaugurale avec tamponnade.

The authors report the case of 21-year old female patient with a particular form of Takayasu's disease remarkable for its initial presentation and its cardiac and coronary lesions. The disease began with miscarriage at the 5th months of pregnancy, followed by acute pericarditis with tamponade. Subsequently, lesions of the aortic and mitral valves developed, while the myocardium became involved with left ventricular dilatation and hypokinesia confirmed by echocardiography and cineangiography. Coronary arteriography revealed large coronary aneurysms which are exceptional in this disease. This case prompted the authors to discuss the various cardiac lesions and the relationship of Takayasu's disease with pregnancy.

Echocardiographic study of left ventricular function in type 1 diabetes mellitus: hypersensitivity of beta-adrenergic stimulation.

Systolic left ventricular function was investigated by echocardiography in 23 young, type 1 diabetics and 11 control subjects. A stimulation by isoproterenol was performed in order to study beta-adrenergic cardiac responsiveness. M-mode recordings were digitized and analyzed by computer. Systolic parameters such as left ventricular fractional shortening and mean velocity of circumferential shortening were not different, but maximal velocity of shortening was increased both at rest (P less than 0.01) and with isoproterenol (P less than 0.05) in the diabetics. An abnormal systolic anterior motion of the mitral valve was found during administration of isoproterenol in 65% of the diabetics and in only one control. These findings are suggestive of a hyperkinetic state, associated with a poor metabolic control (high value of HbA1), together with adrenergic hypersensitivity in type 1 diabetes mellitus.

A case of the Budd Chiari syndrome attributed to a deficit in protein C.

We report a case of Budd Chiari syndrome associated with a deficit in protein C, in a young women admitted to hospital for investigation of thromboembolic disease and ascites. This coagulation defect was thought to be an aetiological factor in the suprahepatic vein thrombosis. The diagnosis and treatment of this rare form of the syndrome are discussed.

[Fibrinolytic treatment with urokinase and streptokinase for recurrent thrombosis in two valve prostheses for the aortic and mitral valves during pregnancy]. / Traitement fibrinolytique par urokinase et streptokinase d'une thrombose récidivante sur double prothèse valvulaire aortique mitrale au cours de la grossesse.

The authors report a case of a patient who had two episodes of valvular thrombosis successfully treated with fibrinolysis using urokinase and streptokinase. They emphasise how efficient these treatments are in spite of the gravity of the initial picture and also point out the dangers and difficulties that can occur because of the risk of haemorrhage in pregnancy, and particularly during delivery and post-partum. They show once more that the treatment is harmless for the fetus. They conclude that using fibrinolytic treatment should be considered first when there is great danger to the patient, and the advantages and disadvantages of thrombolysis should be weighed up.

Cardioprotective effect of trimetazidine in severe ischemic cardiomyopathy.

The aim of this study was to assess the value of long-term treatment with 60 mg per day of trimetazidine, a cellular antiischemic agent, in comparison with placebo, in patients with ischemic cardiomyopathy controlled by conventional treatments. Twenty patients, with a mean age of 59.5 +/- 1.6 years, suffering from severe ischemic cardiomyopathy (NYHA IV, 6 patients; NYHA III, 14 patients) confirmed by coronary angiography, were included in the study; four of them suffered from residual angina. All of these patients were receiving long-term treatment with long-acting nitrates associated with digitalis (9 patients), diuretics (15 patients), anticoagulants (13 patients), and antiarrhythmics (11 patients), and were considered to be stabilized at the time of inclusion in the study. The examinations consisted of clinical and laboratory assessment, resting ECG, 24-hour ECG monitoring, X-ray evaluation of cardiac volume (CV), and evaluation of echocardiographic left ventricular shortening (ELVS) and of isotopic ejection fraction (EF). These three parameters were expressed as a percentage variation with respect to the initial value, and their variation between the two groups was compared by means of two-way analysis of variance. Clinically, the therapeutic benefit provided by trimetazidine resulted in: a) an improvement of dyspnea in all patients treated with trimetazicine compared with only one patient with placebo (p less than 0.001), b) resolution of residual angina, which was unchanged with placebo, c) reduced requirements for complementary treatments (a single case versus eight cases in the placebo group; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Risk factors for progression of atherosclerosis six months after balloon angioplasty of coronary stenosis.

To assess the possible progression of coronary artery disease after percutaneous transluminal coronary angioplasty (PTCA) and its relation to risk factors and restenosis, 124 patients who underwent a first successful PTCA were studied. All had routine follow-up angiography 5 to 8 months after PTCA. Restenosis was defined as a 30% decrease in diameter stenosis or a return to greater than 50% stenosis, and progression (in any nondilated site) as a 20% decrease in diameter stenosis, assessed by a video-densitometric computer-assisted technique. Univariate and multivariate analysis with respect to progression was carried out for age, sex, initial unstable angina, previous myocardial infarction, diabetes mellitus, hypertension, hypercholesterolemia (greater than or equal to 6.2 mmol), smoking habits, Jenkins' score, dilated artery and restenosis. Forty-one patients (33%) had restenosis, and 23 (19%) had evidence of progression; 20 (87%) of these latter patients had restenosis and 3 (13%) did not. Univariate correlates of progression were: previous myocardial infarction (p less than 0.05), higher Jenkins' score (p less than 0.0003) and restenosis (p less than 0.0001). Restenosis was the only multivariate correlate (p less than 0.00003). Progression at routine angiography after PTCA is not rare, and appears to be related to both the initial extent of coronary artery disease and restenosis.

Therapeutic value of a cardioprotective agent in patients with severe ischaemic cardiomyopathy.

Trimetazidine (TMZ) has been shown to have anti-ischaemic properties improving exercise tolerance without haemodynamic effects. A 6-month double-blind placebo-controlled study was carried out in 20 patients, mean age 59 +/- 6 years, to examine the benefit of adding 60 mg of TMZ vs placebo to the classical therapy, excluding those previously treated with calcium-antagonists, conversion enzyme inhibitors, vasodilators and antiplatelet agents. All patients had severe ischaemic cardiomyopathy, confirmed by coronary angiography; six were in NYHA class IV; 14 in NYHA class III; four had mild recurrent angina pectoris. assessment included clinical and biological evaluation, electrocardiography (ECG), 24-h ECG monitoring, cardiac volume evaluation with chest X-ray, left ventricular fractional shortening by echocardiography, left ventricular ejection fraction by radionuclide angiography. Baseline characteristics were similar in placebo (11 patients) and TMZ (nine patients) groups. Eighteen patients (nine in each group) were followed up for 6 months. In eight patients of the placebo group, treatment had to be modified (addition of calcium antagonists: four patients, conversion enzyme inhibitors: two patients; digitalics: one patient; diuretics: one patient). In the TMZ group, digitalic therapy was withdrawn in one patient and added in one patient (P less than 0.01). At 6 months, all TMZ group patients were free from angina; dyspnoea was improved in all TMZ patients and in only one placebo patient (P less than 0.001). Ejection fraction, increased by 9.3% in the TMZ group and decreased by 15.6% in the placebo group (P less than 0.018), CV decreased by 7% with TMZ, increased by 4% with placebo. (P = 0.034).(ABSTRACT TRUNCATED AT 250 WORDS)

Study of the electrophysiological properties of intravenous bisoprolol in patients with and without coronary artery disease by programmed stimulation.

The objective of this study was to assess the electrophysiological properties of intravenous bisoprolol in patients with and without coronary artery disease (CAD) by programmed stimulation. Sixteen inpatients subjected to an electrophysiological investigation because of dizziness or palpitations were given 10 mg of intravenous bisoprolol after basal measurement and were checked again 15 and 45 min after infusion. Eight patients with CAD (seven males and one female; mean age of 60+/-4 years) and eight patients without CAD (five males and three females; mean age of 59+/-4 years) were investigated after washout of prior antiarrhythmic drugs. For coronary patients, the CAD was documented by a history of myocardial infarction or by a confirmatory coronary arteriography. Main outcome measures were parameters of invasive electrophysiological exploration, with measurement of conduction intervals at rest and during pacing and of refractory periods by means of extrastimulus technique. No significant difference was noted at baseline between the two groups except for CSNRT. After infusion of 10 mg of bisoprolol, with the exception of CSNRT (increased in the group without CAD), no significant differences were noted on comparison between coronary and noncoronary patients. Bisoprolol significantly increased the sinus cycle length, SACT, and FRP of the atria. Regarding atrioventricular nodal conduction, bisoprolol significantly increased the AH 100, ERP, and FRP and significantly decreased the Wenckebach point. In the right ventricle, bisoprolol moderately, but significantly, decreased the corrected QT and induced a small, temporary, significant increase in ERP. Bisoprolol appears to be a very potent beta-blocker that is well tolerated at an intravenous dose of 10 mg. Its depressant effects concern mainly the atrial function and the nodal conduction, without significant differences between the two groups of patients. The decrease in QTc may be a favorable aspect regarding its electrophysiologic tolerance especially in the acute phase of myocardial infarction.

[Low molecular weight heparin: an real alternative in thrombolysis in hemodialyzed patients. A trial of coronary thrombolysis]. / L'héparine de bas poids moléculaire: alternative réelle dans la thrombolyse chez le dialysé? Essai de thrombolyse coronaire.

Fibrinolytic treatments pose serious problems in subjects at high risk for hemorrhage, such as those requiring chronic dialysis. A 36-year-old patient requiring dialysis for the last 14 years due to chronic kidney failure was hospitalized for unstable angina combined with calcified mitral stricture. Prompt coronary arteriography revealed recent intracoronary thrombi. The failure of drug treatment and the surgical indication in light of unstable angina led the authors to use low-molecular-weight heparin b.i.d. for 12 days with monitoring of laboratory parameters (anti-Xa activity, APTT). No thrombotic or hemorrhagic episode was recorded. Control angiography indicating partial lysis of the left and right intracoronary thrombi led to exact evaluation of the residual underlying stenoses. A double aortocoronary bypass was subsequently performed combined with replacement of the mitral valve. This case gives a glimpse of the potential value of low-molecular-weight heparin as a valid alternative to conventional fibrinolysis in subjects requiring dialysis.

[von Willebrand's disease and coronary atherosclerosis. Apropos of 3 cases]. / Maladie de Willebrand et athérosclérose coronarienne. A propos de trois cas.

The von Willebrand factor (VWF) is a link in the platelet-vessel wall interaction which plays an essential role in the response of the vessel wall to an atherosclerosis-including aggression. However, can von Willebrand's disease really prevent the development of atherosclerosis? The authors report 3 cases of young men aged 36, 40 and 51 years with atherogenic risk factors and von Willebrand's disease (two mild and one severe form). The three patients developed both atherosclerotic lesions and thrombosis. This would suggest that VWF deficiency does not protect humans from atherosclerosis.

Risk factors for myocardial infarction during coronary artery bypass graft surgery.

Patients with a particular thrombotic profile may be at greater risk of myocardial infarction during coronary artery bypass graft surgery. The thrombotic profile of 50 patients admitted to hospital with stable angina pectoris was determined prior to haemodynamic investigation. ECG results and determination of cardiac enzymes showed that 12 patients had suffered a perioperative myocardial infarction. These patients had a higher mean atherosclerotic score (42.1 +/- 10.5 vs 32.9 +/- 13, P less than 0.02), a longer aortic cross clamp time (59 +/- 15.2 vs 45.7 +/- 16.3 min, P less than 0.05), lower serum levels of protein C (101.2 +/- 26 vs 124.7 +/- 31.4%, P less than 0.05) and tissue plasminogen activator (322 +/- 580 vs 2307 +/- 2830 IU ml-1, P less than 0.01). There were no differences between the two groups in Jenkin's coronary score, the number and type of grafts, ejection fraction, left ventricular end-diastolic pressure, lipid profile or levels of markers of platelet release. In addition to a more severe distal coronary atheroma and a longer aortic cross-clamp time, patients with impaired endothelial fibrinolytic activity appeared to be at greater risk of myocardial infarction during coronary artery bypass graft surgery.

[Data of programmed ventricular stimulation in left ventricular hypertrophy of hypertensive origin]. / Les données de la stimulation ventriculaire programmée dans l'hypertrophie ventriculaire gauche d'origine hypertensive.

Various studies have established the increase of sudden death in hypertensive patients with left ventricular hypertrophy (LVH). In order to specify its most important factors, an electrophysiological study consisting of Holter recording (HR) and programmed ventricular stimulation (PVS), was performed in 24 patients with hypertension: 12 with LVH and 12 without LVH, on ultrasonography. In all patients, coronary angiography was normal. The results are the following: 1) LVH increases the ventricular vulnerability, this arrhythmogenic substrate and its stability are explored by PVS; 2) HR and PVS are not correlated, therefore HR does not explore the arrhythmogenic substrate of LVH, but rather the potential triggering factors of severe rhythm disorders; 3) it has not been possible to evaluate the role of the autonomous nervous system in this study; 4) finally, a significant correlation was found between the degree of anatomical hypertrophy of the LV and the duration of the interval AH.

Prostacyclin-mediated effect of high density lipoproteins as cellular cholesterol acceptors on aortic smooth muscle cells.

Low (LDL) and high (HDL) density lipoproteins stimulate prostacyclin (PGI2) synthesis in cultured rabbit and human aortic smooth muscle cells. In this respect, the efficacy of HDL exceeded that of LDL, HDL3 being the most effective. HDL3 obtained from hypoalphacholesterolemic patients' serum had a lesser stimulative effect on PGI2 synthesis as compared with HDL3 of normolipidemic subjects. Partially purified apoprotein A-1 stimulates the metabolism of 14C-arachidonic acid accompanied with enhanced formation of prostaglandins, especially 6-keto-PGII alpha. Within a 24 h incubation in the fetal calf serum-free medium, prostaglandins I2 and E1 (1 x 10(-7) M) reduce the intracellular cholesterol level in human aortic smooth muscle cells by 30%. Total HDL fraction as well as HDL3 and HDL2b applied in combination with prostaglandins have a synergistic effect resulting in a 50% fall in intracellular cholesterol. Hypothetically, the uptake of cholesterol by HDL may include the following stages: (1) HDL interacts with the cell and activates the intracellular PGI2 synthesis probably via apo A-1 modulatory action on arachidonic acid metabolism; (2) newly synthesized PGI2 activates cholesteryl ester hydrolase leading to the formation of free cholesterol; (3) HDL takes up free cholesterol.

[Value of trimetazidine in the long-term treatment of cardiomyopathies of ischemic origin]. / Intérêt de la trimétazidine dans le traitement au long cours des myocardiopathies d'origine ischémique.

The effect of a cellular anti-ischemic, trimetazidine (TMZ) in ischemic cardiomyopathies, was evaluated in a double-blind versus-placebo (P) trial, over a period of six months. 20 patients, mean age: 59.5 years, with advanced ischemic cardiomyopathy, demonstrated by left catheterization and coronary angiography, with a past history of myocardial infarction, received either 60 mg per day of TMZ (nine patients) or the placebo (eleven patients) in addition to a basic treatment of digitalis, diuretics and nitrated medications. A complete, clinical, biological and paraclinical evaluation, including chest X-ray, ultrasonography, isotopic ventriculography and 24 h-ECG, was performed upon inclusion in the study; and after three and six months of treatment. Two patients from the placebo group were not reevaluated at six months. The clinical condition, according to the NYHA classification, improved in all patients from the TMZ group, deteriorated in eight on nine patients from the placebo group (p less than 0.001). The isotopic stroke volume is preserved with TMZ, deteriorated with P. The cardiac volume decreases with TMZ, increasing with P. TMZ is beneficial clinically and functionally in advanced ischemic cardiomyopathies.