[Isolated right heart failure in acute lymphocytic myocarditis]. / Décompensation cardiaque droite isolée lors d'une myocardite aiguë lymphocytaire.

The authors report a case of acute myocarditis, presenting with signs of isolated right heart failure which was progressive and fatal. This is a very rare observation which poses diagnostic problems. A review of the literature showed only 4 previous reports, all diagnosed at autopsy, in which the diagnosis was not suspected in vivo. In our case, echocardiography raised the possibility of myocarditis at an early stage, although the initial clinical signs were atypical and did not indicate right ventricular disease. It is particularly important to detect right ventricular involvement, especially when associated with left ventricular disease, as the prognosis is very poor. This case report illustrates the difficulty of the differential diagnosis and shows the diagnostic and prognostic value of echocardiography when interpreted in the clinical and electrocardiographic context.

[Value of the analysis of pulmonary venous flow in the evaluation of hemodynamics in dialysed patients]. / De l'intérêt de l'analyse du flux veineux pulmonaire dans l'estimation d'un état hémodynamique. Exemple de la dialyse.

The aim of this study was to assess the value of analysis of pulmonary venous flow in the evaluation of the haemodynamic status of patients with chronic renal failure with normal left ventricular function, treated by haemodialysis. Pulmonary venous flow was recorded immediately before and after haemodialysis in 27 patients with chronic renal failure and a mean age of 44 years. Three groups of patients were defined according to the change in mitral E/A ratio: Group I (E/A < 1 before and after dialysis), Group II (E/A > 1 before and < 1 after dialysis) and Group III (E/A > 1 before and after dialysis). There was a significant difference between these subgroups before dialysis with respect to age, S, D, VTI S, Total VTI, VTI S/Total (p < 0.05). However, because the values overlapped, only a VTI S/Total ratio greater than 59% differentiated patients in Group II from those in group III (p < 0.05). After dialysis, the change in S/D and VTI S/Total ratios increased in Groups I and II and decreased in Group III. The authors concluded that 63% of patients without LV dysfunction on haemodialysis have abnormalities of relaxation which are latent in 47% of cases due to increased filling pressures diagnosed by a VTI S/Total ratio > 59% or simply because the patients are over 50 year old.

Von Willebrand factor in diabetic angiopathy.

Diabetes mellitus is a complex disease characterised by chronic hyperglycaemia responsible for complications affecting the kidneys, eyes, peripheral nerves and micro- and macrovascular systems. Von Willebrand factor (vWf), a multimeric glycoprotein mainly synthesised by endothelial cells, is involved in platelet adhesion and aggregation and acts as the carrier of coagulation factor VIII in plasma. Increased levels of vWf, reflecting activation of or damage to endothelial cells, have been described in association with atherosclerosis and diabetes. vWf appears to be a predictive marker of diabetic nephropathy and neuropathy, although not of retinopathy, which suggests that endothelial dysfunction precedes the onset of diabetic microangiopathy. This dysfunction could be especially involved in the pathogenesis of renal abnormalities of diabetes. vWf is not a predictive marker of macroangiopathy when diabetes is associated with atherosclerotic risk factors. In the presence of chronic diabetic complications, vWf levels are not associated with any grade of retinopathy but increase with the severity of nephropathy and would appear to be a risk factor for macrovascular mortality in these patients. The endothelial dysfunction of diabetes can generate atherosclerotic lesions responsible for damage to the arterial wall, atheroma and formation of platelet microaggregates. Concomitant with high vWf levels, other possible mechanisms of endothelial damage include reduced synthesis or release of nitric oxide, hyperglycaemic pseudohypoxia and protein kinase-C activation, increased synthesis of proteins bearing advanced glycosylation end-products or transforming growth factor-beta (TGF-beta) activation of coagulation and inhibition of fibrinolysis. At present, it is not known whether high vWf levels are inherent to the physiopathology of diabetes, nor whether diabetes induces endothelial dysfunction through other pathways. However, since angiopathy resulting from endothelial dysfunction is the main cause of morbidity and mortality in diabetic patients, appropriate therapy is necessary to reduce these complications. Glycaemic control seems to be insufficient to normalise plasma vWf, whereas a decrease can be obtained by ingestion of diets rich in oleic acid or by treatment with statins. Inhibition of the binding of vWf to the GPlba receptor by synthetic peptides, aurin tricarboxylic acid or monoclonal antibodies has been proposed to prevent the thrombosis induced by high levels of plasma vWf. Thus, vWf probably represents an interesting target for the inhibition of thrombosis in diabetes.

Sensitivity and long-term prognostic value of cardiac troponin-I increase shortly after percutaneous transluminal coronary angioplasty.

BACKGROUND: After successful coronary interventions, minor elevations of creatine kinase MB (CK-MB) identified a population with a worse long-term prognosis than that in patients without enzyme elevations. In that setting, cardiac troponin-I (cTn-I), a highly specific marker for myocardial injury, was considered for a small study; the results did not support the view that significant myocardial damage occurred during successful percutaneous transluminal coronary angioplasty (PTCA). HYPOTHESIS: The present study was designed to assess the rate of elevated values of cTn-I after successful PTCA and to determine its prognostic value. METHODS: CTn-I and CK-MB were measured in 44 patients before and daily for 3 days after PTCA. Two groups of patients were considered according to the presence or absence of elevated levels of cTn-I. The rate of free-event survival was estimated for the two groups using the Kaplan-Meier method and was compared with the log rank test. RESULTS: Globally, 36% of patients had an increase in cTn-I (normal values 0.35 ng/ml) and 9% had an increase in CK-MB, p = 0.002. The mean time to maximal enzyme level was 1.8 days for cTn-I and 2.2 days for CK-MB. Over a follow-up of 1375 +/- 416 days, 18% of patients experienced adverse events, and cTn-I did not identify a population of worse long-term prognosis. CONCLUSION: These results suggest that cTn-I is more sensitive than CK-MB in identifying minor myocardial damage after PTCA, but these elevated concentrations of cTn-I in the short-term aftermath of angioplasty do not seem to be a marker of worse long-term prognosis.

Comparative efficacy of a two-hour regimen of streptokinase versus alteplase in acute massive pulmonary embolism: immediate clinical and hemodynamic outcome and one-year follow-up.

OBJECTIVES: This study sought to compare the efficacy of 2-h regimens of alteplase and streptokinase in acute massive pulmonary embolism. The primary end point was immediate hemodynamic improvement, and secondary end points included early clinical efficacy and safety, as well as 1-year clinical outcome. BACKGROUND: Several thrombolytic regimens have been compared for the past 10 years in randomized studies, showing that 2-h infusion regimens of alteplase or urokinase lead to faster hemodynamic improvement than former 12- to 24-h administration protocols in acute massive pulmonary embolism. Many trials have focused on immediate hemodynamic and angiographic outcomes, but none has addressed long-term follow-up after thrombolysis. METHODS: Sixty-six patients with acute massive pulmonary embolism (Miller score > 17 and mean pulmonary artery pressure >20 mm Hg) were randomly assigned to receive either a 100-mg 2-h infusion of alteplase (n = 23) or 1.5 million IU of streptokinase over 2 h (n = 43). In both groups, heparin infusion was started at the end of thrombolytic infusion and adapted thereafter. Total pulmonary resistance was monitored over a 12-h period. Pulmonary vascular obstruction was assessed 36 to 48 h after thrombolytic therapy. One-year follow-up information included death, cause of death, recurrent pulmonary embolism, chronic thromboembolic pulmonary hypertension, stroke and bleeding. RESULTS: Both groups had similar baseline angiographic and hemodynamic characteristics of severity, with maintained cardiac output in 64 (97%) of 66 patients. The results (mean +/- SD) demonstrated that despite a faster total pulmonary resistance improvement observed at 1 h in the alteplase group compared with the streptokinase group (33+/-16% vs. 19 16%, p = 0.006), a similar hemodynamic efficacy was obtained at 2 h when both thrombolytic regimens were completed (38+/-18% vs. 31+/-19%). There was no significant difference in either pulmonary vascular obstruction at 36 to 48 h or bleeding complication rates. One-year event-free survival was similar in both groups, as most events were related to concomitant diseases. CONCLUSIONS: These results suggest that a 2-h regimen of streptokinase can be routinely used in patients with massive pulmonary embolism and maintained cardiac output without obviously compromising efficacy or safety.

Effect of pravastatin on angiographic restenosis after coronary balloon angioplasty. The PREDICT Trial Investigators. Prevention of Restenosis by Elisor after Transluminal Coronary Angioplasty.

OBJECTIVES: This study sought to determine whether pravastatin affects clinical or angiographic restenosis after coronary balloon angioplasty. BACKGROUND: Experimental data and preliminary clinical studies suggest that lipid-lowering drugs might have a beneficial effect on restenosis after coronary angioplasty. METHODS: In a multicenter, randomized, double-blind trial, 695 patients were randomized to receive pravastatin (40 mg/day) or placebo for 6 months after successful balloon angioplasty. All patients received aspirin (100 mg/day). The primary angiographic end point was minimal lumen diameter (MLD) at follow-up, assessed by quantitative coronary angiography. A sample size of 313 patients per group was required to demonstrate a difference of 0.13 mm in MLD between groups (allowing for a two-tailed alpha error of 0.05 and a beta error of 0.20). To allow for incomplete angiographic follow-up (estimated lost to follow-up rate of 10%), 690 randomized patients were required. Secondary end points were angiographic restenosis rate (restenosis assessed as a categoric variable, > 50% stenosis) and clinical events (death, myocardial infarction, target vessel revascularization). RESULTS: At baseline, clinical, demographic, angiographic and lipid variables did not differ significantly between groups. In patients treated with pravastatin, there was a significant reduction in total and low density lipoprotein cholesterol and triglyceride levels and a significant increase in high density lipoprotein cholesterol levels. At follow-up the MLD (mean +/- SD) was 1.47 +/- 0.62 mm in the placebo group and 1.54 +/- 0.66 mm in the pravastatin group (p = 0.21). Similarly, late loss and net gain did not differ significantly between groups. The restenosis rate (recurrence > 50% stenosis) was 43.8% in the placebo group and 39.2% in the pravastatin group (p = 0.26). Clinical restenosis did not differ significantly between groups. CONCLUSIONS: Although pravastatin has documented efficacy in reducing clinical events and angiographic disease progression in patients with coronary atherosclerosis, this study shows that it has no effect on angiographic outcome at the target site 6 months after coronary angioplasty.

Comparison between abnormalities in segmental endocardial motion and abnormalities in segmental wall thickening after anterior myocardial infarction. A cine-magnetic resonance study.

In this study, two patterns of regional contract on of the left ventricle have been studied: endocardial motion and wall thickening, in order to check which of these was the most affected after myocardial infarction. The clinical relevance of this comparison was to assess which parameter of the regional contraction abnormality would best depict the severity of the infarction. Long axis cine-magnetic resonance slices were used to assess segmental systolic left ventricular endocardial motion and segmental systolic wall thickening in 39 normal subjects and in 30 patients at the chronic stage of an anterior myocardial infarction. In the group of normal subjects, endocardial motion and wall thickening showed significant regional heterogeneity. Overall endocardial motion was greater than overall wall thickening: 9.5 +/- 2.0 mm vs 7.1 +/- 1.8 mm. P = 4 x 10(-12) (3.1 +/- 1.2 mm vs 2.0 +/- 0.7 mm, P = 9 x 10(-5) after infarction). A significant linear correlation was found between these two parameters. In the infarction group, abnormality scores for endocardial motion and for wall thickening were calculated. These scores were defined as the average values exceeding the mean minus two standard deviations of the normal range for segments corresponding to the antero-septal-apical walls. The abnormality score for endocardial motion greater than the abnormality score for wall thickening: 0.31 +/- 0.12 vs 0.20 +/- 0.07, P = 9 x 10(-4). We conclude that, in clinical practice, endocardial motion is affected to a greater degree by myocardial infarction than is wall thickening and therefore constitutes a more discriminant index in the assessment of post-infarction patients.

A study of biochemical markers of reperfusion early after thrombolysis for acute myocardial infarction. The PERM Study Group. Prospective Evaluation of Reperfusion Markers.

BACKGROUND: In acute myocardial infarction (AMI), early noninvasive identification of patients with occluded infarct-related arteries (IRAs) after thrombolysis has important prognostic and therapeutic implications. The aims of this study were to evaluate biochemical methods for the early diagnosis of patency after thrombolysis prospectively and to establish the optimal diagnostic criteria retrospectively. METHODS AND RESULTS: In 97 patients with AMI treated with thrombolytic agents < or = 6 hours after the onset of symptoms, myoglobin, troponin T, creatine kinase, the MB isoenzyme and MM isoforms of creatine kinase were measured just before thrombolysis began and 90 minutes later. IRA patency was assessed by means of 90-minute coronary angiography. For each marker, compared with the expected sensitivity and specificity based on published thresholds for the diagnosis of patency, the observed values were consistently lower but were markedly improved in a subset of patients treated > 3 hours after the onset of symptoms. With receiver-operator characteristic curve analysis of the slopes of increase and relative increases in each marker over 90 minutes, the best diagnostic performance was achieved by use of the relative increase in myoglobin, troponin T, and MM3/MM1 creatine kinase isoforms in patients treated > 3 hours after onset (areas under the curve of 0.84, 0.83, and 0.85, respectively). CONCLUSIONS: Effective early noninvasive diagnosis of patency after thrombolysis is possible in patients treated > 3 hours after symptom onset by use of criteria derived from the relative increase over 90 minutes in plasma markers, particularly myoglobin, troponin T, and MM3/MM1 creatine kinase isoforms. The diagnostic performance of the relative increase in myoglobin appears to be less susceptible to small changes in the diagnostic threshold value.

Prognostic factors of chronic heart failure in NYHA class II or III: value of invasive exercise haemodynamic data.

UNLABELLED: Various parameters have been found useful for establishing the prognosis of patients with chronic heart failure, in particular haemodynamic parameters measured at rest. However, few studies deal with the prognostic value of invasive exercise haemodynamic parameters in such patients. Our aim was to test the value of such parameters to assess the prognosis of patients with chronic heart failure in functional class II or III of the New York Heart Association. METHODS: Between December 1990 and June 1993, 50 patients fulfilled the criteria for inclusion in the study. The average age and ejection fraction of the population were 54 +/- 2 years and 20 +/- 0.5% respectively. All patients were examined clinically; their invasive haemodynamic parameters were measured at rest and during exercise, and their exercise peak VO2, validated by reaching the anaerobic threshold, was determined. They were followed up for 21.2 +/- 1.17 months (ranges 3-26 months). The assessment criteria employed were mortality and the occurrence of major events (heart failure, pulmonary oedema or severe ventricular arrhythmia). RESULTS: The population consisted of 32 men and 18 women. No gender-related differences were found. Two groups could be distinguished in terms of prognosis: G1: n = 31 living patients with no events, and G2: n = 19 deceased or with major events. G1 and G2 were comparable with regard to age, sex ratio and ejection fraction. Several of the 52 parameters tested were different in the two groups, in particular peak VO2, exercise duration, the workload developed during the cardiopulmonary test and all the invasive exercise haemodynamic parameters except heart rate (P < 0.0001). Haemodynamic parameters at rest had no prognostic value in this series. The ROC curves, the survival curves and the Cox analysis showed that exercise cardiac power output, exercise left ventricular work indices and exercise peak VO2 were the most useful factors for assessing the prognosis of patients with NYHA II or III chronic heart failure. An exercise cardiac power output < 2 watts accurately identified those patients with a short-term poor prognosis, and exercise peak VO2 was almost as accurate. To a lesser extent, the NYHA functional class was also an independent prognostic parameter during multivariate analysis. In conclusion, it appears that invasive haemodynamic parameters are best for determining the prognosis of patients with chronic heart failure. Peak VO2 can, however, be as useful. Moreover this is an easily obtainable non-invasive parameter, which makes it more useful in the evaluation and the follow up of such patients.

[4-year mortality of heart failure with intact systolic function: a retrospective studies]. / Mortalité à 4 ans de l'insuffisance cardiaque à fonction systolique conservée. Etude rétrospective.

Heart failure with normal systolic function has been recognised in 30-40% of patients investigated for congestive heart failure. The authors undertook a retrospective study of global and cardiovascular mortality at 4 years in two groups of patients with a history of congestive heart failure documented by equilibrium angioscintigraphy: group I (n = 109) with poor left ventricular systolic function (EF = 26 +/- 9%) and group II (n = 40) with normal systolic function (EF = 58 +/- 8%). The 4 year cardiovascular mortality was less in group II (21.6% vs 49%; p < 0.004) whereas the global mortality was comparable in the two groups. The only discriminating parameters for cardiovascular mortality between the two groups were age of more than 60 years and values of diastolic blood pressure exceeding 90 mmHg which were associated with a higher mortality in the group with normal systolic function. These results indicate a better prognosis in terms of cardiovascular mortality from congestive heart failure in patients with normal systolic function compared with those with poor systolic function.

Variation in von Willebrand's Factor according to the treatment of acute myocardial infarction: physiopathological and clinical implications.

To investigate whether von Willebrand's Factor (vWF) changes as a result of the reperfusion strategy during acute myocardial infarction (AMI), vWF was measured on days 0, 1, 2, 3, 4, 5 and 15 in 34 patients with AMI. Thrombolysis was initiated in 22 patients and followed by a coronary angiogram 90 min later. In 13 patients the infarct-related artery was then patent (THR group). In nine patients the infarct-related artery was occluded and rescue percutaneous transluminal coronary angioplasty was performed (group THR+rPTCA). In 12 patients, primary PTCA was carried out (pPTCA group). Admission values of vWF were similarly high in the three groups, while changes in vWF over the following days were statistically different among the groups. No significant change was observed in THR, whereas a significant and prolonged increase was found after failed thrombolysis with PTCA (peak increase at day 5:1.54 +/- 0.04 U.ml-1). In the pPTCA group, a significant increase could only be found on day 3 (0.96 +/- 0.04 U.ml-1). Absence of a statistical rise in vWF might be a late indicator of successful thrombolysis. The prolonged increase in vWF after failed thrombolysis needing rescue PTCA probably reflects a higher resistance to thrombolysis, while the slight but significant increase in vWF following primary PTCA could be due to vascular injury.

Exercise peak VO2 determination in chronic heart failure: is it still of value?

The prognostic value of exercise peak VO2 is still controversial. We therefore prospectively studied 75 patients in New York Heart Association functional class II or III with chronic heart failure stabilized by drug treatment. The patients (mean age of 58 +/- 10 years) were submitted to a clinical examination, a radionuclide determination of left ventricular ejection fraction, and a haemodynamic study at rest (right side catheterization); their plasma sodium, plasma creatinine and blood urea nitrogen levels were measured in addition to exercise peak VO2. An exercise peak VO2 threshold value of 14 ml.kg-1.min-1 was used to define two groups: GI (23 patients), with an exercise peak VO2 < or = 14 ml.kg-1.min-1 and G2 (52 patients) with an exercise peak VO2 > 14 m.kg-1.min-1. G1 and G2 were comparable in terms of age, heart rate, left ventricular ejection fraction, cardiac index and mean arterial pressure. Apart from exercise peak VO2, G1 and G2 also showed differences in right and left ventricular filling pressures, plasma sodium, plasma creatinine, blood urea nitrogen levels and exercise duration (all P < 0.01). Moreover the prognosis was worse in G1 than in G2: nine deaths vs 0, and seven major events--major events being defined as pulmonary oedema, hospitalization for heart failure, or severe ventricular arrhythmias--vs three (P < 0.001). A sub-group analysis (deceased patients, living patients with and without major events) was performed. Out of 20 clinical and paraclinical parameters, exercise peak VO2 proved to have the greatest prognostic value.(ABSTRACT TRUNCATED AT 250 WORDS)

[Von Willebrand factor in coronary disease]. / Le facteur de Willebrand en pathologie coronaire.

The value of studying factors of haemostasis and thrombosis in patients with coronary artery disease is established. The endothelial lesion and evolution of the thrombus play key roles in acute coronary syndromes and coronary angioplasty. The von Willebrand factor (VWF) is known for its participation in primary haemostasis. Deficits of this factor lead to a haemorrhagic syndrome, von Willebrand's disease. This glycoprotein is mainly synthesised by the endothelial cells. Its polymeric composition allows identification of two types of multimeres. The high molecular weight, active multimeres are liberated from the endothelium after stimulation by thrombin. Low molecular weight multimeres are less active and are secreted continuously. The VWF promotes platelet adhesion and facilitates platelet aggregation. Experimental pig models with VWF deficiency show that this factor is essential for the constitution of an occlusive thrombus. Several physiopathological mechanisms interact to increase VWF concentrations during thrombosis: the endothelial lesion, adrenergic stimulation, acute phase reaction. Increased VWF concentrations have been reported in many clinical situations. The results are most demonstrative in coronary artery disease. The VWF is abnormally high from the time of hospital admission in patients with acute myocardial infarction and continues to increase up to the 5th day before falling, without returning to normal values, at the 15th day. It is a sensitive though not specific late diagnostic marker of myocardial infarction. Increased VWF concentrations are not proportional to the severity of coronary atherosclerosis. They are, however, related to the infarct size, to the inflammatory reaction and to the prothrombotic phase.(ABSTRACT TRUNCATED AT 250 WORDS)

[Left ventricular filling in young insulin-dependent diabetics]. / Le remplissage ventriculaire gauche chez le diabétique insulino-dépendant jeune.

Left ventricular function indices were measured by pulsed Doppler-echocardiography in 17 young patients (mean age: 25 +/- 5) with insulin-dependent diabetes and 17 controls (identical mean age: 25 +/- 5) free of heart disease. All subjects had normal left ventricular systolic function. Twenty three per cent of diabetics showed a left ventricular filling anomaly on the basis of at least two abnormal indices. Isovolumic relaxation time was significantly prolonged in diabetics as compared with normal individuals (83 +/- 7 v. 68 +/- 9 ms, p < 0.00015). Half-pressure time was also prolonged in the patients (46 +/- 9 v. 38 +/- 6 ms, p < 0.01), the same applying to rapid filling deceleration time (158 +/- 32 v. 136 +/- 29 ms, p < 0.05). Peak rapid filling rate, the proportion of total filling accounted for by rapid filling, peak atrial systole velocity and the atrial contribution to total filling did not differ between the diabetics and controls. Systolic blood pressure was significantly higher in diabetics as compared with controls (124 +/- 8 v. 114 +/- 10 mmHg, p = 0.007), although remaining within normal limits. This would not, however, explain the differences seen between the 2 groups regarding left ventricular profile. The filling anomalies reported here were not correlated with the duration of diabetes nor with other parameters such as glycosylated hemoglobin or 24-hour microalbuminuria. Our results suggest that approximately 20 p. cent of young diabetics have sub-clinical left ventricular anomalies.(ABSTRACT TRUNCATED AT 250 WORDS)

[Dynamic cartography of flow patterns by cine-MRI. Presentation of the technique and preliminary results for major vessels]. / Cartographie dynamique des flux par ciné-IRM. Présentation de la technique et résultats préliminaires sur les gros vaisseaux.

The authors report the principles, experimental evaluation and clinical approach of a method for dynamic imaging of flow patterns by NMRI, based upon the phase modulation technique. The imaging method is based upon gradient echo, functioning in "cine" and "flow compensated" mode. Modifications in this sequence enable attribution to the moving spins phase of a value which is considered to be proportional to the flow rate. A map of rates is then obtained from the phase image. Calibration of this sequence in vitro has shown excellent correlations between flow rate and the phase information thus obtained: r always > 0.98 for rates up to m/s. The first results obtained in vivo for the thoracic and abdominal aorta, in 11 control subjects, show that the technique is suitable for the study of pulsatile blood flow, providing very detailed information concerning the spatial distribution of flow rates. Mean flow in the suprarenal abdominal aorta (4.6 +/- 1.6 l/min) is 32% greater than that in the inferior vena cava (3.1 +/- 1 l/min), corresponding to an estimation of portal vein flow of 1.5 l/min. Practical limitations related to the use of a resistive magnet are nevertheless stressed and the authors list the technical aspects necessary for the better clinical utilisation of this non-invasive flowmetric technique. A review of the current literature forms the basis for an assessment of the potential importance of dynamic and quantitative NMRI of flow patterns in the cardiovascular area.

[Acute myocardial infarction in patients over 70 years of age treated by immediate primary angioplasty]. / Infarctus du myocarde aigu chez les patients de plus de 70 ans traités par angioplastie primaire immédiate.

Twenty consecutive patients aged over 70, admitted for acute myocardial infarction, underwent coronary arteriography within less than 6 hours after the onset of pain to confirm the diagnosis and determine the indications for other than thrombolytic reperfusion treatment, the risk of thrombolysis seeming theoretically prohibitive. In all cases, the artery responsible was found to be obstructed and, based upon this criterion, primary reperfusion angioplasty was performed. The criterion for success of angioplasty was the reappearance of distal flow (grade > 1 of the TIMI classification--Thrombolysis in Myocardial Infarction). The reperfusion rate obtained by angioplasty was 85%. Follow-up coronary arteriography during hospitalisation (between D10 and D15) in 17 patients revealed neither restenosis nor re-occlusion. In case of successful reperfusion, left ventricular ejection fraction improved by 16% (in absolute values). Hospital mortality was 15% (6 patients were in cardiogenic shock from the time of admission). Mortality (after a follow-up of 27.3 +/- 17.5 months) was 20%. Complications of the procedure during the acute phase included one femoral hematoma and one moderate coronary dissection, with an uncomplicated outcome. Angioplasty is an effective reperfusion method in patients aged over 70, and is an alternative to thrombolysis which, in this age group, is accompanied by a risk of hemorrhagic complications, cerebral in particular. Thus angioplasty can be suggested as first line treatment in elderly patients provided they have been admitted to a unit where operational cardiology is available on a continuous basis.