Left ventricular (LV) function is the major determinant of prognosis in patients with myocardial infarction. Despite recent advances in medical therapy of heart failure, mortality rates of patients with poor ejection fraction (EF) remains high. We hypothesised that systematic revascularisation of the stenosis of the infarct-related artery would result in improved LV contractility. From 1991 to 1997, 14 consecutive patients had severe Q wave anteroseptal myocardial infarction with EF⩽36%. The mean age of the 14 patients was 55±12 years (range 38–73 years). There were 12 men and 2 women. Forty-three percent had a previous coronary history. Ten (71%) underwent thrombolytic treatment 4.8±3.9 h after the onset of symptoms, 5 with streptokinase and 5 with rt-PA. Four (28%) had heart failure and 2 (14%) cardiogenic shock at the time of presentation. The patients with heart failure received diuretics and angiotensin converting enzyme inhibitors. They had no residual ischemia. Coronary arteriography revealed a significant stenosis (⩾70%) of the left anterior descending artery (LAD) in 11 patients (79%) and a complete occlusion in 3 (21%). Associated lesions were a stenosis of the second acute marginal artery in 1 patient, a stenosis of the first marginal artery in 1 and a complete occlusion of the right coronary artery in 4. Global LV EF was assessed 5.2±4.3 days after the onset of symptoms; it was measured by LV angiography in 12 patients and by gated blood single-photon emission computed tomography (G-SPECT) in 2. The EF was 31.4±5.8% (range 16–36%). Preoperative viability studies were not used for patient selection. Coronary angioplasty of LAD alone was performed 12.5±7.8 days after the onset of infarction. Patients with heart failure clinically improved at the time of intervention. Coronary angioplasty (PTCA) was successful in all patients. The diameter stenosis, assessed by quantitative angiography, decreased from 85.0±11.4 to 8.6±9.7% (P<0.0001). Follow-up averaged 7.2±5.1 months. Angina pectoris was absent and exercise stress testing was negative. Eight patients (58%) had no cardiac failure, 3 (21%) were in New York Heart Association (NYHA) class II, 2 (14%) class III and 1 (7%) class IV. EF was assessed by angiography in 5 patients and by G-SPECT in 7. It was significantly increased from 31.4±5.8 to 45.6±10.4% (P<0.001) (Fig. 1). Few studies have been designed to analyse the improvement of LV function after successful angioplasty of the residual stenosis after myocardial infarction (Table 1). In 1992, Montalescot 1 and Ellis 2 were not able to show that deferred angioplasty, following fibrinolysis, would improve the EF and obtain clinical benefits. However, three studies (Linderer 3, Miketic 4 and Meijer 5) have shown that deferred angioplasty following fibrinolysis produced an improvement in EF, but this benefit disappeared in the case of restenosis. It is worth noting that in Linderer's 3 and Miketic's 4 studies, the EF prior to angioplasty was only slightly altered. In Fath-Ordoubadi's 6 study, the viability was evaluated by positron emission tomography and the contractility evaluated by sonography. The EF increased from 41±10 to 45±10% (P=0.04) and the segment contractility index improved. Danchin 7 studied the effect of unblocking completely occluded arteries using angioplasty, on EFs. He noted an improved contractility in patients who retained an open artery upon control; however, this benefit disappeared in the case of reocclusion. Our study differs from the others in that we selected the most severe patients, whose EF was very low (<36%) and who were likely to develop severe cardiac insufficiency. The limitations of this study are the small number of patients and the lack of a control group. Moreover, two different techniques were used to assess left EF. However, the values obtained by the two methodologies are very well correlated in our departments. Despite its limitations, our study suggests that systematic coronary angioplasty of the stenosis of the infarct-related artery in patients with severely impaired LV function is able to produce a significant improvement in systolic function. It may avoid the development of severe cardiac failure in the majority of patients. Randomised controlled trials are now required to ensure that percutaneous revascularisation is of benefit in addition to medical therapy and that the risk is as low as observed in this patient series.

Persistence of a thrombus after coronary angioplasty can be treated by transcatheter aspiration. This technique has been used in the right coronary artery of three patients. Coronary arteriography showed the occlusion of the proximal segment in two patients and a stenosis in one. In the two patients with an occlusion, there was no residual stenosis after balloon angioplasty, but a long thrombus remained: in the third patient, the thrombosis of the mid‐segment of the right coronary artery was secondary to a spasm of the proximal and mid‐segments. In all patients, the guiding catheter was gently advanced up to the thrombus that was aspirated with a syringe. The immediate result was excellent, and the control angiogram performed after a delay of 1 to 15 months showed the patency of the artery and the absence of residual stenosis.

Myocardial infarction is being increasingly reported in younger women. Eleven women younger than 40 years who were admitted for recent myocardial infarction between 1989 and 1993 were studied, Results of this study and of a literature review demonstrated risk factors also found in men (primarily smoking, but also genetic predisposition, dyslipidemia, and arterial hypertension), as well as risk factors specific to women, including oral contraception (particularly in smokers) and peripartal events (toxemia of pregnancy, treatment with adrenoceptor agonists). Selective coronary arteriography usually showed lesions of a single vessel or intact coronary arteries. Although atherosclerosis may be a contributory factor, the frequently normal appearance of the coronary arteries suggests a predominant role of acute thrombosis and/or spasm. The treatment should be the same as in men, except during pregnancy, Female gender may be a factor of adverse prognostic significance.

Previous small clinical trials have suggested that treatment with nitric oxide donors in suspected myocardial infarction can reduce mortality by 30-35%. To confirm this finding in a large-scale trial, we compared molsidomine and its active metabolite linsidomine (a nitric oxide donor) with placebo in 4017 patients with acute myocardial infarction.In our trial, patients without signs of overt heart failure (Killip III/lV) were randomly assigned in a double-blind design within 24 h of symptom onset to receive linsidomine 1 mg/h intravenously for 48 h, followed by 16 mg molsidomine by mouth daily for 12 days (n = 2007), or an identical placebo (n = 2010). All other treatments could be used at the responsible physician's discretion with the exception of systematic vasodilator treatment. The molsidomine and placebo groups showed similar all-cause 35-day mortality (168 [8.4%] vs 176 [8.8%] deaths, p = 0.66), and adjustment for baseline variables in a Cox model had no effect. Similarly, we found no difference for long-term mortality(mean follow-up 13 months; 294 [14.7%] vs 285 [14.2%] deaths, p = 0.67). The two groups showed similar frequencies of major and minor adverse events; only headache was significantly more common in the molsidomine group.Changes in treatment practices and the lower risk profile of our study subjects than of participants in previous trials may explain the results. It is still not clear whether nitric oxide donors can improve survival in higher-risk myocardial infarction patients.

The association of tetralogy of Fallot and mitral stenosis is extremely rare. This is probably the first description of this association. The clinical and haemodynamic presentation is similar to that of cyanotic heart disease with pulmonary stenosis and post-capillary pulmonary hypertension. The mitral stenosis was probably congenital as it was diagnosed at 14 months of age.

L'association d'un retrecissement mitral a une tetralogie de Fallot est exceptionnelle. L'observation rapportee ici est vraisemblablement la premiere description de cette association. Le tableau clinique et hemodynamique est celui d'une cardiopathie cyanogene avec stenose pulmonaire et hypertension arterielle pulmonaire de type postcapillaire. Cette stenose mitrale est vraisemblablement congenitale, puisqu'elle a ete diagnostiquee a l'âge de 14 mois

The association of tetralogy of Fallot and mitral stenosis is extremely rare. This is probably the first description of this association. The clinical and haemodynamic presentation is similar to that of cyanotic heart disease with pulmonary stenosis and post-capillary pulmonary hypertension. The mitral stenosis was probably congenital as it was diagnosed at 14 months of age.