[Influence of sex on the prognosis of high risk acute coronary syndromes treated by early angioplasty]. / Influence du sexe sur le pronostic des syndromes coronaires aigus à haut risque traités par angioplastie précoce.

The aim of this study was to evaluate the influence of sex on the prognosis of high risk acute coronary syndromes treated early with angioplasty. Over a period of two years, 694 consecutive patients (151 female, 543 male) underwent revascularisation within the first 24 hours of an acute coronary syndrome without permanent ST elevation (ST depression (52.5%) or relapse of angina despite medical treatment (47.5%). The females were older than the males (67.9 vs 62.3 years; p < 0.0001), smoked less (7.3 vs. 32.8%; p < 0.001) and had a higher prevalence of hypertension (53 vs. 42.1%; p = 0.017). The angiographic characteristics were equivalent in both sexes, except for a lower frequency of thrombus in the females (6.9 vs. 15.2%; p < 0.0001). All lesions were treated with endoprosthesis implantation. The angiographic success rate was comparable (94 vs. 93.7%) as was the rate of major cardiac events while in hospital (3.8 versus 4%). With an average survival of 2 years, the incidence of major cardiac events remained identical in both sexes (15.4 vs 15.7%: p = 0.43): cardiac mortality (3.2 vs 2%; p = 0.18), myocardial infarction (7.3 vs 6.7%; p = 0.37), further revascularisation (8.3 vs 7.2%; p = 0.47). The survival without major cardiac event was comparable at 1 year (87 +/- 0.1 vs 88 +/- 0.3%) and at 2 years (78 +/- 0.2 vs 83 +/- 0.3%; p = 0.58). In conclusion, the progression both in hospital and at two years with a strategy of early revascularisation for high risk acute coronary syndromes was comparable in males and females.

Prognostic value of ventricular arrhythmias in systemic hypertension.

OBJECTIVE: Hypertensive left ventricular hypertrophy is associated with an increased risk of arrhythmias and mortality. However, no clinical study has demonstrated a significant relationship between ventricular arrhythmias and mortality in systemic hypertension. DESIGN AND METHODS: To evaluate the prognostic value of arrhythmogenic markers, we included, prospectively, 214 hypertensive patients aged (mean+/-SD) 59.1+/-12.8 years, without symptomatic coronary disease, myocardial infarction, systolic dysfunction or electrolyte disturbances. At inclusion, a 12-lead electrocardiogram (ECG) with QT dispersion calculation, a 24 h Holter ECG (204 patients) with Lown classification of ventricular arrhythmias, echocardiography (reliable in 187 patients) and a signal-averaged ECG (125 patients) with ventricular late potentials were recorded. RESULTS: At baseline, echocardiographic left ventricular hypertrophy was found in 63 patients (33.7%). Non-sustained ventricular tachycardia (Lown class IVb) was recorded in 33 patients (16.2%) and late potentials in 27 patients (21.6%). After a mean follow-up of 42.4+/-26.8 months, all-cause mortality was 11.2% (24 patients); 17 patients died of cardiac causes (7.9%); of these, nine (4.2%) died suddenly. In univariate analysis, age, Lown class IVb and a QT dispersion > 80 ms were significantly related to global, cardiac and sudden death (P < 0.01). The left ventricular mass index was related to cardiac mortality (P= 0.002). In multivariate analysis, only Lown class IVb was an independent predictor of global and cardiac mortality, increasing the risk of global death 2.6-fold (95% confidence interval 1.2-6.0) and cardiac death 3.5-fold (95% confidence interval 1.2-9.7). CONCLUSION: In hypertensive patients the presence of non-sustained ventricular tachycardia has prognostic value.

Lack of haemodynamic effects of nitric oxide on post-capillary pulmonary hypertension induced by acute sino-aortic denervation.

1. The aims of the present experiments were to define a new experimental model of pulmonary hypertension induced by a post-capillary mechanism and to assess the haemodynamic effects of nitric oxide on post-capillary pulmonary hypertension. 2. Cardiopulmonary variables of 28 male beagle dogs, anaesthetized with chloralose, 16 spontaneous breathing and 12 with assisted ventilation, were studied before and after sino-aortic denervation (SAD). The haemodynamic effects of inhaled nitric oxide (25 p.p.m., 10 min). N(omega)-nitro-L-arginine methyl ester (20 mg kg-1, i.v.), urapidil (0.5 mg kg-1-, i.v.) and propranolol (300 micrograms kg-1, i.v.) were studied after SAD. 3. SAD induced an acute and transient pulmonary hypertension, more marked in spontaneous breathing dogs. This pulmonary hypertension involved a post-capillary mechanism, secondary to the left ventricular haemodynamic effects of the acute increase of left ventricular after-load induced by systemic hypertension. In fact, the increase of mean pulmonary arterial pressure after SAD and the decrease of this parameter after urapidil or propranolol were strongly correlated with the variations of pulmonary capillary wedge pressure. Furthermore, no significant change in pulmonary vascular resistance was found after SAD or administration of alpha or beta-adrenoceptor antagonists. 4. Inhaled nitric oxide did not reverse pulmonary hypertension induced by SAD. N(omega)-nitro-L-arginine methyl ester had no significant haemodynamic effect of pulmonary circulation. 5. In conclusion, the lack of effect of inhaled nitric oxide and nitric synthase inhibitor on pulmonary circulation parameters SAD suggest that endothelium-derived oxide is not involved in the mechanisms leading to post-capillary pulmonary hypertension.

Cardiac beta-adrenoceptors and adenylyl cyclase activity in human left ventricular hypertrophy due to pressure overload.

The effect of left ventricular hypertrophy (LVH) due to chronic pressure overload on right atrial (RA) and left ventricular (LV) myocardial beta-adrenergic receptor (beta-AR) density and subtypes, adenylyl cyclase (AC) activity and ADP-pertussis toxin ribosylated proteins was investigated in humans with LVH due to aortic stenosis and in patients without LVH undergoing heart surgery for mitral stenosis or coronary artery disease taken as controls. Both groups presented normal systolic function or plasma catecholamine levels. In LVH and controls, beta-AR density was similar in RA (62 +/- 6 vs 77 +/- 12 fmol.mg-1 protein) and LV (39 +/- 7 vs 32 +/- 2 fmol.mg-1 protein). In LVH, beta 1-AR percentage was < than in controls in LV (35 +/- 11 vs 73 +/- 5%, P < 0.05) but not in RA (79 +/- 5 vs 73 +/- 8%). Basal AC activity in RA (19 +/- 4 vs 21 +/- 6 pmol.mg-1 protein) and LV (22 +/- 5 vs 27 +/- 3 pmol.mg-1 protein) was similar in LVH and in controls. Isoprenaline-induced stimulation of AC in RA was similar in LVH and in controls (51 +/- 18 vs 36 +/- 18%) but < in LV of LVH (7 +/- 6 vs 45 +/- 6%, P < 0.05). In the presence of ICI-118,551 (a beta 2-adrenoceptor antagonist), isoprenaline failed to induce any increase in cAMP in LVH. The quantification of ADP-pertussis toxin ribosylated proteins indicated a lower concentration of substrates in LV myocardial membranes from LVH. These data indicate that in LVH due to pressure overload, there is a down-regulation of beta 1-AR and an increase in beta 2-AR density. This is associated with alterations of the transmembrane signalling marked by a decreased capacity of isoprenaline to stimulate AC and an impaired expression of Gi proteins.

Nasal nitric oxide concentration is decreased in heart failure patients receiving nitrates.

Nitric oxide (NO) is a free radical gas and a short-lived messenger which has many paracrine functions. Direct assessment of NO production is very difficult in vivo. However, the paranasal cavities generate a high amount of NO which diffuses in the nasal cavity where it can be easily measured. Several studies have suggested alterations of the NO production in heart failure. Thus, we assessed nasal NO concentration in normal subjects and in heart failure patients. The nasal NO concentration averaged 227 +/- 10 ppb in the control group (n = 20), and 210 +/- 10, 198 +/- 20 and 159 +/- 54 ppb in New York Heart Association (NYHA) class II (n = 30), III (n = 28) and IV (n = 7) patients, respectively (mean +/- standard error [SE], not significant using analysis of variance [ANOVA]). Nasal NO level was not influenced by age, sex or etiology of the heart failure or by treatment with frusemide, angiotensin-converting enzyme inhibitor or digoxin. However, treatment with NO-releasing drugs (nitrates or molsidomine) significantly decreased the nasal NO level in heart failure patients. A two-way ANOVA revealed that treatment with a NO-releasing drug influenced nasal NO concentration (P = 0.0005), whereas NYHA class did not (P = 0.23), with a trend towards an interaction between the two parameters (P = 0.09): the inhibitory effect of NO-releasing drug on nasal NO concentration was more pronounced in severe heart failure. In an additional group of 12 patients (NYHA class II or III), the nasal NO concentration was 174 +/- 19 ppb during NO-releasing drug treatment and increased to 231 +/- 27 ppb 3 days after withdrawal of the nitrates (P = 0.0007 using paired t-test). Conversely, the nasal NO concentration in another group of seven patients (NYHA class II or III) was 219 +/- 32 ppb without nitrate treatment and decreased to 188 +/- 28 ppb 7 days after nitrate addition (P = 0.02 using paired t-test). In contrast, the nasal NO concentration in another group of ten ischemic patients without heart failure was 203 +/- 25 ppb without nitrate treatment and was similar (207 +/- 28 ppb) 7 days after nitrate addition (not significant using paired t-test). In conclusion, nasal NO production is normal in heart failure, except in patients receiving NO-releasing drugs. Nasal NO concentration could be useful for investigating the mechanism(s) by which exogenous NO donors decrease endogenous NO production.

Prognostic value of heart rate variability in time domain analysis in congestive heart failure.

AIMS: Analysis of heart rate variability is a noninvasive tool that allows to study autonomic control of the heart. Several studies have shown disturbed heart rate variability in patients with chronic heart failure (CHF). We sought to assess the prognostic value of time domain measures of heart rate variability in CHF. METHODS AND RESULTS: We prospectively enrolled 190 patients with CHF in sinus rhythm, mean age 61+/-12 years, 109 (57.4 %) in NYHA class II and 81 (42.6 %) in class III or IV, mean cardiothoracic ratio 57.6+/-6.4 % and mean left ventricular ejection fraction 28.2+/-8.8 %, 85 (45 %) with ischemic and 105 (55 %) with idiopathic dilated cardiomyopathy. Time domain measures of heart rate variability were obtained from 24 h Holter ECG recordings. During follow-up (22+/-18 months), 55 patients died. In multivariate analysis, independent predictors for all-cause mortality were: ischemic heart disease, cardiothoracic ratio > or =60 % and standard deviation of all normal RR intervals <67 ms (RR=2.5, 95 % CI 1.5--4.2). CONCLUSIONS: Depressed heart rate variability has independent prognostic value in patients with CHF.

[Perindopril and chronic heart failure]. / Périndopril et insuffisance cardiaque chronique.

Haemodynamic studies performed in patients with cardiac failure have shown that perindopril decreases right and left ventricular filling pressures, systemic blood pressure and peripheral resistances, slightly reduces the heart rate and increases cardiac output. Flammang showed that these haemodynamic changes are sustained after 12 months' treatment. A randomised double blind multicenter trial versus placebo was carried out over 3 months following a 15 days pre-inclusion period in 125 patients with NYHA Stage II and III cardiac failure stabilised by digitalis and diuretic therapy. Perindopril was administered at a dosage of 2 or 4 mg according to initial systolic blood pressure and efficacy was evaluated at 1 and 3 months according to the NYHA classification, a score of clinical severity, the duration of two exercise stress tests on a bicycle ergometer or treadmill and the cardiothoracic ratio. There were no cases of cardiac decompensation (NYHA Stage IV) in the group of perindopril whilst 3 cases were observed in the placebo group. Significant improvements in the clinical scores and effort capacity were observed in the perindopril group. The duration of exercise on the treadmill was 778 seconds with perindopril compared to 544 seconds in the placebo group. Systolic blood pressure did not change and there was a slight decrease in standing diastolic pressures. No significant increases in blood urea or creatinine levels were observed. To study the effects on blood pressure, a major factor in the management of a patient with cardiac failure, McFadyen compared the changes in blood pressure after a single dose of perindopril, enalapril, captopril and placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

[Is the treatment of left ventricular systolic dysfunction different according to the etiology?]. / Le traitement de l'insuffisance cardiaque avec altération de la fonction systolique est-il différent selon l'étiologie?

Cardiac failure is the terminal stage of evolution, the finality of many valvular, vascular, myocardial, general, congenital or acquired conditions. The therapeutic decisions should be based on the search for a curable cause of a predisposing factor and the evaluation of the severity of the cardiac failure. At advanced stages of ventricular dysfunction when the myocardial lesions are constituted, when cardiac and vascular remodelling has occurred, the aetiological treatment, which is the constant objective, is unfortunately too late. The treatment is the same, whatever the aetiology, in order to improve functional problems. At early stages, and, if possible, preventively, surgery, revascularisation techniques, the correction of an arrhythmia, the suppression of a cardiotoxic factor, are essential. The different therapeutic classes used could have different efficacies depending on the aetiology, but, finally, this point is negligible: the medications are based on the results of large scale, controlled, therapeutic trials.

[Angiotensin converting enzyme inhibitors and ischemic heart diseases]. / Inhibiteurs de l'enzyme de coversion et cardiopathies ischémiques.

Experimental studies and molecular biological techniques have demonstrated the importance of angiotensin II in ventricular and vascular remodelling and in atherogenesis. Large scale clinical trials analysing the effects of converting enzyme inhibitors on the mortality and morbidity in post-infarction left ventricular dysfunction, have shown beneficial effects of these agents on major events of coronary artery disease. Experimental studies have shown reduction of intimal thickening and of the multiplication and migration of smooth muscle cells and of vascular fibrosis. Converting enzyme inhibitors seem to restore endothelial function by acting as donors of NO and could play a role in the stabilisation of atheromatous plaque, the prevention of platelet aggregation and on the activation of intravascular fibrinolytic systems. Large scale clinical trials (SOLVD and the prevention and treatment arms of SAVE) have also shown a 23% reduction in the risk of reinfarction and a 15% reduction in the risk of unstable angina. The results of ongoing trials in patients with coronary artery disease without cardiac failure are awaited with great impatience.

[Action of converting enzyme inhibitors on myocardial ischemia and reperfusion injuries]. / Actions des inhibiteurs de l'enzyme de conversion sur l'ischémie myocardique et les lésions de reperfusion.

During myocardial ischaemia, either in chronic coronary insufficiency or the acute phase of myocardial infarction, the renin-angiotensin system is activated which, by its deleterious cardiac effects, aggravates the ischaemia. Angiotensin Converting Enzyme (ACE) inhibitors, by their indirect effects (improved conditions of left ventricular load, negative inotropism, attenuation of catecholaminergic stimulation), reduce myocardial oxygen consumption, and by their direct coronary vasodilator effect reduce myocardial ischaemia. In addition, by attenuating the formation of oxygen-free radicals, by participating in the inactivation of some of them and protecting the lysosomal membranes, they combat reperfusion injury. In the animal model of acute myocardial infarction, they reduce myocardial infarct size and the prevalence of reperfusion arrhythmias. In the clinical situation, their effects on the ischemic response to effort in anginal patients remain controversial, appear to be more marked in abnormalities of the coronary micro-circulation especially in syndrome X and in hypertensive heart disease. In ischemic heart disease, long-term treatment may be beneficial by their trophic coronary and myocardial effects and two large scale trials report a decrease in the recurrence of myocardial infarction with ACE inhibitors. In the acute phase of myocardial infarction if their possible actions on reducing the infarct size and reperfusion arrhythmias require further confirmation, they do limit expansion of the infarct and decrease early left ventricular dilatation. However, the appreciation of tolerance is variable and the timing of their introduction remains controversial.

[Left ventricular hypertrophy and myocardial ischemia (coronary atherosclerosis excluded)]. / Hypertrophie ventriculaire gauche et ischémie myocardique (en dehors de l'athérosclérosecoronaire).

The diagnosis of myocardial ischemia due to coronary artery disease in the presence of left ventricular hypertrophy associated with chest pain and ST-T wave changes is difficult. Resting and exercise ST changes are not specific and even stress or dipyridamole Thallium scintigraphy may give erroneous results. In fact, the changes of myocardial perfusion induced by left ventricular hypertrophy reflect a reduction of coronary vasodilator reserve and the increased coronary vascular resistance explains the angina with normal coronary arteries observed in these patients. The reduction of coronary reserve is the result of complex and controversial processes: increased vascular compression, reduction of capillary density: hypertrophy of the arteriolar media or simply changes in coronary vasomotricity. Understanding these abnormalities implies appropriate antihypertensive treatment: lowering the blood pressure, reducing the myocardial hypertrophy and improving subendocardial perfusion.

[Calcium channel inhibitors and ventricular filling]. / Inhibiteurs calciques et remplissage ventriculaire.

Abnormalities of ventricular relaxation and compliance often precede changes in systolic function in ischemic and hypertrophic or hypertensive heart disease. Several studies using non-invasive methods have confirmed the beneficial effects of calcium channel blockers on left ventricular diastolic function in ischemic and primary hypertrophic cardiomyopathies. Their usefulness remains controversial in secondary cardiac hypertrophy such as in hypertensive heart disease. Improved left ventricular isovolumic relaxation and filling results more from the coronary and peripheral vasodilatory effects of calcium channel blockers than from a direct action on the cardiac muscle.

[Treatment of cardiac insufficiency: does treatment depend on whether its cause is ischemic or idiopathic?]. / Le traitement de l'insuffisance cardiaque est-il différent selon sa cause, ischémique ou idiopathique?

Angiotensin converting enzyme (ACE) inhibitors are associated with a greater reduction in mortality in non-ischaemic cardiomyopathy than in ischaemic cardiomyopathy after the results of the V-HeFT-II and SOLVD trials in symptomatic patients. However, a recent analysis of the global, symptomatic and therapeutic, results of the SOLVD trials, demonstrated a similar reduction in mortality with ACE inhibitors in ischaemic and non-ischaemic cardiomyopathies. Moreover, after myocardial infarction, the beneficial effects of ACE inhibitors have been well established in patients with left ventricular dysfunction. Betablockers, especially bisoprolol in the CIBIS-I trial, also seem to be more effective in non-ischaemic cardiomyopathy. However, CIBIS-II and the US Carvedilol Heart Failure Trial Program clearly showed that the benefits of betablockade were identical whether ischaemic or not. The beneficial effects of betablockers in the post-infarction period are more marked when left ventricular dysfunction is severe. The PROVED and RADIANCE trials suggest that digitalis is more effective in non-ischaemic cardiomyopathy. These results were not confirmed by the DIG trial which showed a significant reduction in the combined criterion, mortality and hospital admission for aggravation of cardiac failure, both in ischaemic and in non-ischaemic cardiomyopathy. However, the use of digitalis should be prudent during ischaemic cardiomyopathy, the neutral effect on global mortality in the DIG trial masking divergent results with a tendency to reducing mortality due to aggravation of cardiac failure and a significant increase of other causes of cardiac death, especially from myocardial infarction and arrhythmias. Amiodarone could also be useful in non-ischaemic cardiomyopathy. The reduction in risk of death in the GESICA study, which comprised 60% of patients with non-ischaemic cardiomyopathy, contrasting with the absence of an effect with this molecule in the STAT-CHF trial which only comprised 29% of patients with non-ischaemic cardiomyopathy. The new generation of calcium antagonists could also be more effective in non-ischaemic cardiomyopathy. Although amlodipine significantly reduced mortality in the PRAISE trial in non-ischaemic cardiomyopathy, there was no favourable effect with felodipine in the V-HeFT-III tria. Finally, if in the earlier studies oral anticoagulants were more effective in non-ischaemic cardiomyopathy, the recent results of the SOLVD trial showed that warfarin decreased the mortality in both ischaemic and non-ischaemic cardiomyopathy. The value of anti-aggregant therapy is not questioned in coronary artery disease, but its role in dilated cardiomyopathy has not yet been established. In conclusion, apart from the use of digitalis which must be prudent in post-infarction cardiomyopathy or in patients with ventricular arrhythmias, the treatment of cardiac failure differs little with respect to its ischaemic or non-ischaemic aetiology, and should be based on the NYHA (New York Heart Association) classification.

[Can ventricular dysfunction be prevented or delayed in course?]. / Peut-on prévenir ou ralentir l'évolution de la dysfonction ventriculaire?

Left ventricular dysfunction is asymptomatic or paucisymptomatic for a long time. It would be beneficial if progression to the symptomatic stages could be prevented. This is only possible when the abnormal conditions of cardiac load or perfusion which cause the myocardial disease, can be corrected. The treatment of hypertension or valvular disease is an example of this approach. Another approach is to reduce the perverse effects of the neurohormonal adaptations to cardiac failure. The treatment of chronic myocardial infarction by angiotensin converting enzyme inhibitors is an example of this approach.

[Therapeutic choices in silent ischemia]. / Choix thérapeutiques dans l'ischémie silencieuse.

Silent or painless myocardial ischaemia is a common presentation of coronary insufficiency. Repeated episodes lead to anatomical and functional myocardial changes and are associated with the risk of ischemic cardiomyopathy, infarction, arrhythmias and sudden death. The physiopathology is complex and involves transient changes in coronary flow secondary to abnormalities of coronary vasomotricity. It is commonly observed in association with symptomatic angina, in unstable angina and after acute myocardial infarction. In all cases, appropriate treatment is required, the aim being to decrease and suppress not only pain but also ischaemia. Treatment is guided by the ischemic episodes. "Isolated" silent myocardial ischaemia as the only sign of coronary insufficiency justifies accurate evaluation of the coronary status, risk factors and a therapeutic trial, followed by systematic coronary angiography if the ischaemia persists. Silent myocardial ischaemia has modified classical therapeutic attitudes in which the choice of treatment is based on the severity of functional impairment. Priority should now be given to treating the severity of the ischaemia and of the anatomical lesions.

[Anticoagulant treatment and cardiac insufficiency]. / Traitements anticoagulants et insuffisance cardiaque.

In cardiac failure, should conventional therapy be associated systematically with anticoagulant or antiplatelet therapy? Embolic complications are uncommon (1 to 2.5% per year) and the benefit/risk ratio seems to be marginal. The absence of prospective randomised controlled trials makes it impossible to give a definitive reply to this question. The indications of oral anticoagulants are based on experience, good sense, the recognition of known embolic risk factors: severe cardiac failure, atrial fibrillation, EF < 0.30 and low VO2 max, mitral valve disease or prosthetic valve, detection of intracavitary thrombus or spontaneous contrast on transoesophageal echocardiography. Aspirin does not seem to be mandatory even if it reduces the thromboembolic risk non-significantly. In this elderly population with a high co-morbidity, the risks of haemorrhage cannot be ignored, and, if oral anticoagulants are prescribed, biological surveillance must be intensive.

[Congestive cardiomyopathies originating from arrhythmia]. / Cardiomyopathies congestives d'origine arythmique.

Arrhythmia-induced cardiomyopathy is partially or totally reversible left ventricular dysfunction after normalisation of the tachycardia or arrhythmia. On the one hand, there are pure forms in which the arrhythmia occurs in apparently normal hearts and, on the other hand, the more common form in which there is minimal underlying cardiac disease associated with the arrhythmia. Total or partial recovery after reduction of the arrhythmia or "ablation" of its substrate remains a key feature of the diagnosis. Many experimental studies of the functional and structural myocardial and neurohormonal effects of prolonged tachycardias or tachyarrhythmias have provided insight into the modes of occurrence and the characteristics of this type of "reversible" left ventricular dysfunction. But, in fact, there is a lack of anatomical, clinical and follow-up data of this syndrome, the diagnosis of which is always difficult and essentially retrospective after recovery of left ventricular function.

[The CAPITOL study (Captopril Post Infarction Tolerance). A trial of progressive titration of captopril after myocardial infarct with left ventricular dysfunction]. / L'étude CAPITOL. Essai de titration progressive du captopril après infarctus du myocarde avec altération de la fonction ventriculaire gauche.

The objective of CAPITOL (Captopril Post Infarction Tolerance) multicentre open trial was to study the tolerance of a protocol of titration of Captopril in patients with recent myocardial infarction complicated by left ventricular dysfunction. Five hundred and four patients, with a mean age of 62 +/- 12 years, were included during the hospital period in the 74 participating intensive care units, 9 +/- 6 days after myocardial infarction (ejection fraction 34 +/- 6%). After a 6.25 mg test dose of Captopril, the dosage was progressively increased to the target dose of 150 mg at the end of the first month. Of the 504 patients included, 343 finished the trial and 161 stopped the trial prematurely. At the end of the hospital period, 73% received 75 mg/day: at the first follow-up visit (27 +/- 16 days after inclusion), 59% had attained 150 mg/day, this proportion increasing to 71% at the end of the trial (79 +/- 33 days after inclusion). There was no significant change in blood pressure for the whole study population. However, the systolic blood pressure of the patients receiving 150 mg/day of Captopril at the end of the trial was slightly higher than that observed at the end of the hospital period (126 +/- 17 mmHg and 116 +/- 17 mmHg respectively, p = 0.006). Severe Intercurrent events were observed in 89 patients: 24 deaths, 7 recurrent infarctions, 58 hospital admissions (21 for cardiac failure, 15 for recurrence of angina, 11 aorto-coronary bypass operations, 7 coronary angioplasties, 2 cerebro-vascular accidents, 2 systemic emboli). Of the benign complications, hypotension was observed in 25% of patients, nearly half of which occurred during the hospital admission. The drugs prescribed in association with Captopril were Aspirin (78%), betablockers (57%), nitrate derivatives (42%) and diuretics (27%). Multivariate analysis showed 3 factors associated with good tolerance of the 150 mg dosage of Captopril: Killip Class I or II on admission, an ejection fraction > 30% and an initial systolic blood pressure > 100 mmHg. In conclusion, in this trial of dose titration, 3 out of 4 patients with myocardial infarction and left ventricular dysfunction, tolerated the 150 mg/day dosage of Captopril. Patients in the trial could also be treated with drugs recommended after myocardial infarction, in particular the betablockers. Arch Mal Coeur 1999: 92: 395-403.

[Contribution of perindopril to the treatment of chronic congestive cardiac insufficiency. Multicenter pilot double blind study versus placebo]. / Apport du perindopril au traitement de l'insuffisance cardiaque chronique congestive. Etude pilote multicentrique en double aveugle contre placebo.

Cardiac decompensation occurred in three patients of the placebo group, but not in the perindopril group. The effectiveness of perindopril in heart failure was demonstrated by the improvement observed in exercise test and severity score and by the decrease of cardiothoracic ratio. Changes in SAP, and serum creatinine levels, in particular, showed that the drug was well tolerated.

[Inferior wall myocardial infarction and atrioventricular block; angiography and prognosis]. / Infarctus inférieurs et blocs auriculo-ventriculaires; données angiographiques et pronostic.

This study was based on 42 cases of 2nd or 3rd degree atrioventricular block out of 292 cases of inferior wall myocardial infarction. The criteria of selection were monitoring in the intensive care unit during the acute phase, selective coronary angiography in the first 48 hours to 5 days, and regular clinical follow-up during the first year after infarction. The conduction defect was either immediately recorded on the first ECG, delayed (between the 12th and 24th hour) or late (after the 3rd day). These 42 inferior wall infarcts with atrioventricular block (incomplete in 14 and complete in 28 cases) differed from inferior infarction without block by: - the severity of the clinical signs during the acute phase (35% with cardiac failure, 19% with cardiogenic shock); - the severity of the coronary lesions (71.4% with triple vessel disease in infarction with atrioventricular block compared with 32% in those without block, p < 0.02); - the prevalence of the association of > 70% stenosis of the right coronary and left anterior descending arteries; - the alteration of left ventricular function (53% patients with atrioventricular block had ejection fraction of under 30%); - the severity of these infarcts was not related to the atrioventricular block which regressed in 95% of cases but to the severity of the coronary disease, the left ventricular dysfunction and the advanced age of the patients (72.3 +/- 8 years).