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Traumatic aortic valve regurgitation is a rare complication of non-penetrating thoracic trauma. The most frequent lesion is the isolated injury of the non-coronary cusp. Actually, the transoesophageal echocardiography is the procedure of choice to confirm the diagnosis and to reveal the associated cardiovascular lesions. Surgical management with early operation is the best policy, however this surgery can be delayed for treatment of other life-threatening injuries. Up today, aortic valve replacement (AVR) was recommended to repair traumatic aortic valve regurgitation; nevertheless, in the recent international literature, the number of cases reports with conservative surgery (CS) is increasing: 10 AVR (group I) and 10 CS (group II). Analysis of the post-operative and long term periods shows good results: it confirms the excellent clinical evolution in the group I (mean time of follow-up: 18.2 +/- 16.3 months), and reveals satisfactory results in the group II for patients with isolated lesion (mean time of follow-up: 29.1 +/- 30.7 months). In conclusion, each time the traumatic aortic regurgitation is due to an isolated lesion, the conservative surgery should be performed in order to avoid aortic valve replacement and its potential complications especially in young patients with healthy valves. However, the aortic valve replacement is the safest technique for complex or multiple injuries of the aortic valve.

Anticancer chemotherapy continues to advance. One of the new therapeutic orientations is the targeting of receptors which regulate the tumoral activity of the malignant cells. Trastuzumab is the prototype of these new chemotherapeutic agents. It is a monoclonal antibody directed against a tyrosine kinase receptor related to the EGF (Epidermal Growth Factor): the HER receptor. This receptor is also present in myocardial cells. Blockade of this myocardial receptor could cause severe cardiotoxicity about which some information is available but which continues to pose many problems. This data should be known as cardiologists will be consulted before the prescription of Trastuzumab and could also be confronted by these cardiotoxic effects. Precise physiopathological explanations have already been published from experimental studies which show the deleterious effects of the suppression of certain HER receptors on the heart. These studies not only explain all the clinical signs of Trastuzumab's cardiotoxicity but also suggest ways of preventing and treating some of these cases of cardiac failure.

Can the biochemical evidence for "new thrombophilic factors" influence the duration of AVK treatment following the occurrence of a first pulmonary embolus? Certainly for the classic but very rare antithrombin defects as well as for the existence of circulating anticoagulant. Possibly for protein C and S defects. On the other hand, the existence of a heterozygotic "Leiden" mutation of factor V, or factor II, and an increase of factors VIII, IX, or XI, do not at present warrant a change in AVK prescription. In effect, in the case where the existence of a thrombogenic state implies a prolongation of AVK treatment with its significant potential complications, it is indispensable that the risk/benefit ratio is well founded, which is not the case for these "new" thrombophilic states. The coexistence of several of these new biochemical anomalies (for example the association of a factor V and factor II mutation) probably represents an excess risk of thrombosis, but in this situation the reasoning remains the same. On the other hand, faced with a confirmed recurrence, the studies in the literature tell us that very long term treatment should be debated independently from the biochemical results. It is conceivable that there are biochemical anomalies (sometimes quite frequent which should be viewed as "normal variants") which, although they have great significance for improving the understanding of venous thrombo-embolic disease, do not at present warrant a change in our therapeutic protocols. Another facet of the problem concerns the use of D-dimers following the first months of AVK treatment in order to possibly distinguish patients at low risk of recurrence. The first results of this approach are interesting, but require confirmation before they can be used in practice.

An atrial arrhythmia could be encountered during the atrial lead implantation. The lead placement must subsequently be delayed after restitution of the sinus rhythm or completely abandoned. The authors investigate the atrial lead placement during atrial arrhythmia and the lead performance at 6-month follow-up. The study population was 65 patients aged 78.5 years, 42 males and 28 structural heart diseases. They were implanted for sick sinus syndrome (n=14), atrioventricular block (n=44), infra-hisian conduction abnormality (n=7) in association with an atrial fibrillation (63.1%), an atrial flutter (24.6%) or an atrial tachycardia (12.3%). The onset of the arrhythmia was < or = 7 days (47.7%) or > 7 days (52.3%). An atrial lead was placed in the right atrial appendage under fluoroscopic control. If the sinus rhythm was not restored at 1 month, an electrical cardioversion was performed. The per-implantation atrial signal amplitude was 2.2+/-1.5 mV (range 0.5 mV to 7 mV). Sinus rhythm was restored in 54 patients. At 1 month, one patient was in an incessant atrial fibrillation. The 53 patients in sinus rhythm had a good atrial lead performance. Out of 46 patients who completed the 6-month follow-up, 4 had an arrhythmia recurrence. The 42 patients in sinus rhythm had a good atrial lead performance. At 1 and 6-month follow-up, the atrial pacing threshold (1.1+/-0.7 V vs 1.2+/-1.0 V, ns) and the atrial signal amplitude (2.1+/-1.0 mV and 2.1+/-0.9 mV, ns) were stable. Comparing the patients with a recent or a chronic arrhythmia, the pacing thresholds (1.2+/-1.1 V vs 1.14+/-0.8 V, ns), the atrial signal amplitudes (2.17+/-0.9 mV vs 2.05+/-0.9 mV, ns) and the proportion of satisfactory pacemaker performance in DDD(R) mode for the patients in sinus rhythm (100% vs 100%, ns) did not statistically differ between the two groups at 6 months. In conclusion, the placement of an atrial lead in the right atrial appendage during an atrial arrhythmia is feasible with a good lead performance at 6 months in sinus rhythm regardless the onset time of the arrhythmia and provides a satisfactory atrial-based pacing with the preservation of the atrioventricular synchrony.

Malignant disease predisposes to deep venous thrombosis (DVT) or pulmonary embolism (PE) in several ways. One classical situation is that of DVT or PE with no apparent cause which may be the first sign of an occult cancer. In this domain, although the epidemiological data is well known, it is important to recognise the limitations of "blind" investigations. Another situation is more common. The patients have a diagnosed malignancy and thromboembolic disease is the main extra-cancer complication. The approach to this problem is changing, both in primary prevention where many trials have already reported encouraging results, and in the treatment after the event where classical therapeutic protocols are not always well adapted. Ancestral fears of the prescription of anticoagulants in cancer patients must cede to a more objective benefit/risk analysis which seems to be very favourable in some situations. Moreover, some publications have demonstrated a chance finding of a possible anticancer effect of antithrombotic agents.

The necessity of anticoagulant treatment after a pulmonary embolus or a deep venous thrombosis has been demonstrated. The modalities of this treatment have been well established, especially the usefulness of initial heparin therapy followed by a period of antivitamin K treatment with an "ideal target INR" between 2 and 3. One of the last questions in this therapeutic protocol is the duration of antivitamin K treatment. The choice of duration of treatment must be made on numerous criteria. It is necessary to distinguish the circumstances of the occurrence of the DVT or the PE and the context. It is thus possible for less than 3 months treatment in secondary venous thrombo-embolic disease, which occurs in precise, recognised circumstances for which the cause will have been controlled. Otherwise, in so-called idiopathic venous thrombo-embolic disease, which is distinguished by a higher prevalence of recurrences, it is known that long-term antivitamin K treatment is effective for the thrombo-embolic recurrences but at the price of a risk of haemorrhage. Finally thrombo-embolic recurrences also benefit from a long treatment. These circumstances of occurrence are thus important in order to decide the choice of treatment duration. But, in our opinion, the compliance to antivitamin K treatment remains the primary criterion to consider. The dilemma facing the prescriber is to evaluate the risk-benefit ratio of each patient, asking especially if the antivitamin K treatment surveillance of a particular patient will be done as well as in the randomised studies. For the future, long-term antivitamin K does not perhaps represent the only therapeutic option. The results of studies evaluating the durations of long-term treatment with less intense levels of anticoagulation (INR < 2) as well as therapeutic alternatives to antivitamin K (antiaggregants or other antithrombins) are awaited.

In the cardiac patient, there are clinical situations where antivitamin K is indicated more by the co-existing pathological associations or by a particular thrombogenic situation than by the cardiac disease itself. The presence of an embologenic abnormal rhythm, an apical thrombus or a large anterior akinesis are recognised as situations where antivitamin K must be discussed and, except for absolute contraindication, initiated. The studies undertaken for several decades are highly instructive and their contributions are considerable in the different questions which could be asked regarding the efficacy of antivitamin K. In particular they have the merit of signalling the correct directions to take and the errors to avoid. Concerning the evolution of cardiac disease, it must be admitted that the very good results of antivitamin K treatment alone at high dose are to be balanced against their haemorrhagic risk. The studies testing the association of low-dose aspirin with moderate-dose antivitamin K (INR 2 to 2.5) are to date very promising. The evaluation of the understanding of the treatment by patient education remains a major stage when initiating antivitamin K treatment in the cardiac patient.

Masquerading bundle branch block associates left bundle branch block in the standard lead and right bundle branch block in the precordial leads. Mr R., 67 year old, was referred for investigation of syncope. He had a history of idiopathic dilated cardiomyopathy (normal coronary arteries; EF: 14%, CI: 2.2 l/min/m2 at later investigations). The ECG showed LBBB with left axis deviation, a PR interval at the upper limits of normal and ventricular premature beats. During observation, he had another syncopal episode and the ECG showed wide complex tachycardia (160 bpm) reduced by external cardioversion. Electrophysiological investigations showed inducible VT due to bundle branch reentry. The HV interval in sinus rhythm was 80 ms. Radiofrequency ablation of the right bundle led to first degree AVB with masquerading bundle branch block with an increased HV interval of 120 ms. The usual facility of ablation of the right bundle branch block is an argument in favour of the hypothesis whereby masquerading bundle branch block is a variety of RBBB with severe conduction defects of the two branches.

Circulating endothelin-1, a very strong peptide vasoconstrictor first discovered in 1988, is raised in cardiac failure. This increase contributes to the deleterious effects of cardiac failure. Although specific anti-endothelin drugs are under development in this condition, the effects of more commonly used drugs on circulating endothelin-1 levels are not well known. The aim of this study was to evaluate the effects of ACE inhibitor therapy on plasma endothelin-1 levels in cardiac failure. The plasma endothelin-1 levels were measured in 24 patients (stages III and IV of the NYHA classification), before and after treatment with angiotensin converting enzyme inhibitor (Captopril: test doses, then 75 mg/day). A control group of 10 paired patients was used to shake off the effects of bed rest and hospital salt-free diet. The initial endothelin-1 levels were high but equivalent in the control and study groups: 9.13 +/- 1.87 fmol/mL vs 8.98 +/- 1.92 fmol/mL. Plasma endothelin-1 decreased significantly in the study group 72 hours after beginning ACE inhibitor therapy (7.44 +/- 1.95, p < 0.02) but remained higher than normal (p < 0.01), whereas the values in the control group remained the same. This study demonstrates a decreases in plasma endothelin-1 levels 72 hours after onset of ACE inhibitor therapy in patients with stable severe cardiac failure. This results, already suggested by many experimental studies and certain ancillary clinical trials, could explain some of the beneficial effects of ACE inhibitors in this condition.

Objectives: High blood levels of homocysteine have been recently described as a risk factor for thromboembolic events and early development of atherosclerosis. The aim of this work was to study homocysteine blood levels in patients under 55 years of age with acute coronary artery disease., Patients and Methods: The study included 110 patients (98 men, 12 women) with poorly controlled angina pectoris (n = 35) or in the acute phase of myocardial infarction (n = 65). Homocysteine was assayed by liquid chromatography in all patients on the day of the acute episode and 24 hours later. Homocysteine levels were also determined in 40 controls under 55 years of age with no history of coronary artery disease., Results: Blood level of homocysteine was 10.6 +/- 6.2 mumol/l in the patients and 7.7 +/- 2.5 mumol/l in the controls (p < 0.01). The difference was greater in the 30-40 year age rang with 14.4 +/- 2 mumol/l in patients versus 6.4 +/- 1.5 mumol/l in controls (p < 0.001). The assays were reproducible at 24 hours (difference less than 10%). The levels were significantly higher in patients with several diseased arteries than those with single-artery disease. The difference between patients and controls was especially remarkable for non-smokers and those with high cholesterol levels., Conclusion: Hyperhomocysteinemia would be a factor favoring early development of coronary atherosclerosis.

The tilt test is a widely used diagnostic tool for the investigation of syncope of suspected vasovagal origin. Some workers suggest that the sensitivity should be increased at the price of the loss of some specificity. Passive (non-sensitised) or isoproterenol (sensitised) protocols have not been widely studied on a large scale. The authors report the respective results of two protocols (passive and sensitised with isoproterenol proposed by Benditt et al.) applied to the same subject at 24 hours' interval in a random order in a series of 108 patients (age 56 +/- 19.3 years, 72 men) with unexplained syncope or malaise. After 30 minutes in decubitus, an 80 degrees tilt was maintained for 45 minutes for the passive test and for 25 minutes for the sensitised test, followed by a continuous infusion of isoproterenol in 10 minutes intervals of decubitus and inclination at successive doses of 1.3 and 5 micrograms/min. One or both tests were positive in 62 patients (57.4%). The overall concordance of the two tests (both positive or both negative) was 53.7%. In a subgroup of 60 subjects with clinically suggestive vasovagal attacks, the sensitivity of the passive test was 25% compared with 73.3% with the isoproterenol test (p < 0.001). Based on this difference of sensitivity between the two protocols, and knowing the good specificity of the isoproterenol test, the authors recommended the isoproterenol test as being of great practical value.

The authors report the case of a non-Hodgkin malignant lymphoma (NHL) of the heart presenting with syncope. The diagnosis of a cardiac tumours was made by echocardiography. Myocardial biopsy enabled diagnosis of a highly malignant NHL in a patient with a history of low grade NHL. Chemotherapy with CNOP (Cyclophosphamide, Novantrone, Oncovin, Prednisone) induced total regression of the tumour. The patient is in total remission 23 months later. The authors emphasise the value of echocardiography in the diagnosis and follow-up of this pathology. The case is also noteworthy because of the unusual transformation of a low grade to a high grade cardiac NHL.

Cerebral emboli, regardless of their nature, can be detected by transcranial Doppler by performing long-term recordings of the middle cerebral artery. The signals detected, called HITS (high intensity transient signals) described in vitro and in vivo have particular physical characteristics. These embolic signals have been identified in patients with prosthetic heart valves, in patients with atrial fibrillation, following myocardial infarction, following cerebrovascular accident, in patients with carotid stenosis or aortic plaques, during cardiac and carotid surgery and during carotid angiography. During assessment of a cerebrovascular accident, the discovery of HITS could be an argument in favour of an embolic origin. This new technique raises great hopes for establishing the relationship between the discovery of emboligenic heart disease and their neurological clinical manifestations. This new technique has many fields of application: investigation of asymptomatic emboli in patients with emboligenic heart disease, efficacy of antiaggregant, anticoagulant or surgical treatments.

The necessity for anticoagulant treatment after pulmonary embolism or deep vein thrombosis has been demonstrated. The modalities of this treatment have been established, especially the value of initial heparin relayed by oral antivitamin K therapy with a target INR value between 2 and 3. The last question remaining in this protocol is that of the duration of anticoagulant treatment. The choice of duration of anticoagulation should take into consideration two potential complications: haemorrhage due to over-anticoagulation and excessive duration of therapy, and recurrent thromboembolism which could result from an inadequate duration of therapy. Several trials have addressed this question and have led to a consensus of opinion: therefore, secondary venous thrombo-embolic disease, occurring under known, special circumstances, the cause of which has been treated, should be given 4 to 6 weeks anticoagulant therapy. In the other cases, so-called idiopathic venous thromboembolism (the proportion of which is on the increase), recent studies are inadequate to reach a consensus. These "idiopathic" forms are characterised by a higher incidence of recurrent thromboembolism of "secondary" cancer and coagulation abnormalities. The search for the optimal duration of anticoagulant therapy in these forms requires prospective trials taking their features into account and should lead to further therapeutic options. The evaluation of longer treatment protocols with less intensive degrees of anticoagulation and of alternatives to oral vitamin K antagonists is justified.

There are few conditions in medicine as difficult to diagnose as pulmonary embolism. This is certainly not due to the rarity of the disease which is probably as common as myocardial infarction in France. The circumstances surrounding pulmonary embolism and the risk factors of deep venous thrombosis have been well identified. The risk of thromboembolic venous disease has been assessed for each type of surgery. The methods of treatment and prevention have progressed over a number of years. However, in practice, these advances have not "transformed" the frequency of the disease or reduced its mortality. Further progress could come from improved identification of patients at risk, especially by biological tests and new abnormalities of blood coagulation.

The authors describe a case of sinus tachycardia, an unusual cardiac complication of mediastinal radiotherapy; occurring in two patients by the first days of treatment and persisting for several years. No other cause for this tachycardia could be detected in either case. Electrophysiological investigation of one of the two patients was normal. Despite the risk of a high-degree conduction disorder, "symptomatic" beta-blocker treatment was prescribed, but only induced a limited effect.

The lack of knowledge of the origin of venous thrombosis (VT) causes frustration and distress to the clinician. Some results published in the literature suggest a lot of potential aetiologies. Anyhow, we are far from getting a proof that a systematic and exhaustive search for a potential cause, for instance impairment of blood coagulation or infraclinical cancer, could be of benefit for the patient and could present a good cost/efficacy ratio. Consensus recommendations limit the extent of blood coagulation studies only to some precise clinical situations. New biological data evidencing a resistance to activated C protein in 20 to 50 per cent of VT cases, will likely bring new rules. As far as infraclinical cancers are concerned and whether their relationship to idiopathic VT is well-established, it is still doubtful that such systematic heavy and expensive checking up could be of any benefit.

The prevalence of arrhythmia increases with age. Considered as an "ordinary" event in elderly patients, these arrhythmias may nevertheless have serious consequences. This study was undertaken to determine the clinical, aetiological and prognostic features of serious arrhythmias in a population of elderly subjects (> or = 70 years) hospitalised over a 20 months period and comprising 202 patients (103 women, 99 men, mean age 79.6 +/- 5.9 years). Supraventricular arrhythmias are the most common by far (84.2%): 51.4% of patients had atrial fibrillation, 15.3% had atrial flutter; 12.9% had focal atrial tachycardia, 4.5% had junctional tachycardia. Of the ventricular arrhythmias (15.8%), there were 12 sustained ventricular tachycardias, 4 torsades de pointes and 1 ventricular fibrillation. The increased duration of hospital stay (10 +/- 6 days on average) is related not to age but to the type of arrhythmia (longer for ventricular arrhythmias) and to left ventricular dysfunction. The main complications of arrhythmias were cardiac failure (52.4%), neurological deficits (37.4%) and angina (18.6%). Electrocardiographic signs of atrioventricular block were present in 62% of cases and QRS changes in 47.3% of cases. Ventricular arrhythmias were more commonly associated with intraventricular conduction defects, signs of myocardial necrosis and prolongation of the QT interval; they were also common in patients with left ventricular dysfunction and when the left ventricle was dilated. The aetiology of ventricular arrhythmias was mainly iatrogenic (50%) and ischaemic (21.8%), whereas the aetiologies of the supraventricular arrhythmias were varied, 14.7% of cases being idiopathic. Conversion to stable sinus rhythm was obtained in half the patients. A pacemaker was implanted in 10.8% of cases. The hospital mortality was 4.9%.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors report a case of severe pulmonary hypertension (PHT) in a couple of HIV seropositive heroin addicts. The parallel clinical course in these two patients with only mild immunodeficiency and the fact that they both had the same supplier were in favour of PHT secondary to talcoma. In the light of these cases, one wonders whether, as suggested by certain epidemiological studies currently underway, drug addiction should be considered to be a cause of PHT in its own right. According to the authors, this approach would underestimate the incidence of this disease in this particular population and would therefore bias the epidemiological data.

Myocardial infarction is a common and serious condition in patients over 70 years of age. The aim of this study was to assess the feasibility and efficacy of angioplasty without thrombolysis for revascularising an occluded artery in this age group. Between March 1986 and December 1989, 32 patients over 70 years of age (average 76 +/- 3 years) underwent angioplasty without thrombolysis in the acute phase of myocardial infarction. During the same period, 83 patients under 70 years of age were treated in the same manner. In the elderly subjects, the initial lesion was a total occlusion in 26 out of 32 cases (81%) and 99% stenosis in the other 6 cases (19%), and was successfully revascularised in 28 of the 32 patients (87.5%). Three episodes of ventricular fibrillation occurred during the procedure, one of which was lethal. A recurrence of pain during the hospital period was observed in 3 patients, 1 of whom died and the other 2 underwent repeat angioplasty. The hospital mortality was 5 patients (16%), all of whom were over 75 years of age. The comparison with patients under 70 years of age showed a comparable primary success rate, 87.5% (28/32) versus 92% (76/83) (p = 0.5), but a higher mortality, 16% (5/32) versus 4% (4/83) (p < 0.05) and a tendency to worse left ventricular function (ejection fraction 51% versus 62%) and to more extensive coronary artery disease; on the other hand, the post-hospital outcome was the same in both groups; Globally, emergency coronary angioplasty is a valuable alternative to thrombolysis for the treatment of myocardial infarction in patients over 70 years of age.

Objectives: We conducted this study to evaluate the role of transoesophageal echocardiography in the aetiologic diagnosis of ischaemic cerebral vascular events in young subjects., Methods: Over a 16-month period, 70 consecutive patients under 55 (mean age 49 years; range 32-55; 34 females, 36 males) underwent transoesophageal echocardiography as part of a complete work-up after a recent (< 1 month) cerebral event considered to be ischaemic in nature. Exclusion criteria were age over 55, vascular stenosis or ulcerated plaque, embologenic heart disease and valve prosthesis. 24-h Holter recordings were also obtained in all patients., Results: The cerebral event was temporary in 11 subjects and permanent in the other 59. The ischaemic nature of the event was confirmed in all patients with computed tomography or magnetic resonance imagery. All patients were in sinus rhythm at examination and supraventricular paroxysmal arrhythmia was observed in 7 during the Holter recordings. The transoesophageal echocardiography was normal in 37 patients (52%) and pathologic in 33 (48%). The source of the embolus was identified in 4 cases (6%) and the probable cause of the cerebral event was found in 29 (42%). Among the abnormal structures observed were permeable oval foramens, inter-atrial septum aneurysms and plaques on the ascending aorta., Conclusions: In our selected population of patients under 55 years of age, transoesophageal echocardiography detected the certain or probable source of the ischaemic cerebral event in 48% of the cases, a diagnostic yield better than most other methods. Nevertheless, there is no known therapeutic response to several of the potential sources of embolus observed.

The authors report a case of severe pulmonary hypertension after long-term dexfenfluramine treatment in a 48 year old man with no previous medical history. Dexfenfluramine, which has previously been reported to cause pulmonary hypertension, is an amphetamine-like anorexic agent, a pharmacological group known to predispose to this type of side effect. The possibility of this complication should be born in mind before prescribing the drug. In particular, it would seem to be particularly important not to exceed the recommended length of treatment especially as potential reversibility of pulmonary hypertension on withdrawal of the drug has been reported in one case.

Myocardial ischaemia may occur during spasm or thrombosis of the coronary arteries. The vascular endothelium plays an essential role in the lesions observed during ischaemia and myocardial reperfusion by the intermediary of the numerous endothelium-derived vasoactive factors. These include the "endothelium-derived relaxing factors" (EDRFs) nitrous oxide, prostacyclin, which are vasodilators and platelet antiaggregants ant the "endothelium-derived contracting factors" (EDCFs), endothelin, PGH2, oxygen-free radicals which are vasoconstrictive. The endothelial cells also produce the platelet activating factor and factors essential for coagulation. The metabolism and biological properties of these different mediators are reviewed. During the phenomena of myocardial ischemia-reperfusion, endothelial regulation is activated by tissue hypoxia and reduction of coronary flow and perfusion pressure. This regulation also depends on the functional state of the arteries (macroscopically normal or pathological). These vasomotor phenomena are associated with the effects of platelet aggregation and myocardial accumulation of neutrophil polynuclear blood cells. During the second phase of reperfusion cellular lesions are produced by the generation of cytotoxic oxygen-free radicals. Assays of mediators present a clinical interest when the modalities of sampling have been fixed (systemic blood samples or during cardiac catheterisation, sites of sampling, choice of timing of sampling with respect to the biological half lives of the mediators). Determining a correlation between the in vitro biological effects on those in isolated organs and clinical data has become possible with the improvement in techniques of sampling and the increasing collaboration between biologists and clinicians.

Interferon, a fairly recent drug, is used in some cancers and other diseases. The adverse effects include cardiotoxicity which was recognized from phase-I trials. Some of these complications are very common and not serious at the dose levels administered: transient hypotension at the beginning of the treatment, atrial extrasystole. Other effects are less common and not dangerous: low-level conduction impairment or reversible hypertension as the authors recalled. There are also a much more serious forms of toxicity which may be life-threatening, one of which seems to be dose-dependent and consists of the onset of cardiomyopathy, which is usually reversible when treatment is stopped, the other is uncontrollable and usually occurs in high-risk cardiac patients from the first few injections and results in sudden death induced by acute coronary artery failure and/or serious ventricular arrhythmia. The physiopathology of this cardiotoxicity remains unknown, but as it is known to exist, rigorous cardiological monitoring of all patients receiving this treatment is necessary.

The results of epidemiologic studies on the efficacy of different strategies of prevention or improvement of the prognosis of coronary artery disease are generally expressed in terms of percentage reduction of risk; for example, the treatment of hypercholesterolaemia reduces the risk of coronary death by 21%. In order to improve the assessment of the efficacy of these approaches the authors propose to take into account the number of subjects which needs to be treated each year to prevent one cardiovascular event more than the control group (for example, in hypercholesterolaemia, 1,736 patients). This number depends on the reduction of risk and also on the incidence of complications in the control group. Using this method, the authors classified different therapeutic strategies in order of their efficacy: thrombolytic therapy in the acute phase of myocardial infarction, then aortocoronary bypass grafting of left main coronary or triple vessel disease, secondary prevention with stopping smoking, and betablocker therapy. Finally, primary prevention with anti-smoking campaigns, treatment of hypertension and hypercholesterolemia. Based on this figure and knowing the annual cost of patient treatment, it is possible to calculate a cost-effectiveness ratio for each of these therapeutic interventions.

The case of a young woman with clinical and biological manifestations suggestive of a pheochromocytoma primarily producing dopamine is reported. Whether endogenous production of dopamine was due to a tumor or to a metabolic abnormality remained unclear.

This study reports 15 cases of ischaemic clinical forms of hypertrophic cardiomyopathy (HCM). In this retrospective study over a 3 year period, 15 patients with HCM presented with clinical and electrocardiographic signs simulating unstable angina (N = 5) or myocardial infarction (N = 10). All patients had chest pain lasting at least 20 minutes with pseudo-ischaemic ECG changes. Two patients were given thrombolytic therapy. The clinical and enzymatic outcome and results of complementary investigations (including coronary angiography) confirmed the absence of coronary artery disease. The diagnostic of HCM was made by echocardiography. These cases were all apparently primary forms of HCM without intraventricular pressure gradient under basal conditions. Three of the patients were known cases of HCM but the condition was diagnosed after the ischaemic presentation in the other cases. Eight of them had however been considered to have had coronary insufficiency for an average of 5 years. The clinical presentation of HCM represents a difficult differential diagnostic problem with myocardial infarction. Echocardiography is of little help in distinguishing the 2 diseases as septal hypokinesis is often observed in HCM. The clinical course usually reestablishes the diagnosis within a few hours but the delay is often too long in this situation of therapeutic emergency and the indications of thrombolysis may be wrongly posed. Although there is no available formal means of distinguishing the two conditions, this study underlines that this clinical form of HCM is not rare and that the diagnosis should be keep in mind with the other differential diagnoses of myocardial infarction.

The classification of hypertrophic cardiomyopathies remains a thorny nosological problem. Within this extensive diagnostic group, it is felt that the very special sub-group of "Japanese" apical hypertrophic forms must be subject to the strictest possible criteria in order to avoid improper use. The case reported here of biventricular apical hypertrophic cardiomyopathy in a 60-year-old woman with a family history of HCM, in whom the clinical, ECG and above all angiographic features were typically those of AHCM but where the existence of an intraventricular gradient was found during challenge manoeuvres emphasises this classification problem. Pseudo-AHCM in a context of OCM or pseudo-OCM in a context of AHCM? The discussion is not merely of nosological interest in view of the recently documented clear prognostic differences between these two conditions. Main series from the literature are reviewed.

The authors report the case of a myocardial abscess in an infectious endocarditis with a double localization, mitral and aortic. The way it is revealed, by severe and recurring ventricular arrhythmias, differs from the conduction disorders usually described. The diagnosis is suspected by non-invasive examinations, echocardiography and nuclear magnetic resonance. It is backed up by angiographic exploration. The intervention confirms the data obtained by cardiac imaging, and enables the ablation of the abscess which is cleaned out, and the cure of the valvular lesions. Taking into account the gravity of this complication, a close clinical, electrocardiographic and echocardiographic surveillance of all infectious endocarditis is necessary.

Arteriovenous fistula is one of the main causes of high output cardiac failure. The authors report a case following lumbar disc surgery. There are a number of features which may suggest this complication both during surgery and in the immediate postoperative period which are important because the patient may only become symptomatic a long time after operation with a clinical presentation which leads to a cardiological rather than to a surgical referral.

Cardiogenic shock is a very serious complication of acute myocardial infarction because of its prevalence (10-15% of cases) and the associated mortality of 80 to 90 per cent despite the availability of new inotropic drugs and intra-aortic balloon counterpulsation. The aim of this study was to show that revascularisation by percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction complicated by cardiogenic shock completely changes the prognosis. Between April 1985 and February 1988 emergency PTCA was carried out in 25 patients in cardiogenic shock defined as systolic hypotension (less than 80 mmHg) and clinical signs of peripheral or cerebral hypoperfusion. The patients were 21 men and 4 women with an average age of 62.7 +/- 6.7 years. The average delay before hospital admission was 122 mn (range 30 to 240 mn--40%--). External cardiac massage for ventricular arrhythmias or circulatory arrest was required in 56 per cent of cases and 20 per cent underwent balloon angioplasty during resuscitation. Five patients died in the catheter laboratory and 7 others during the hospital period. Thirteen patients (53%) survived and were discharged home. There have been no late deaths during the 24 month follow-up period; 46 per cent asymptomatic, 38 per cent in Class II and 16 per cent in Class III. Survival was better in the last 15 patients undergoing emergency angioplasty: 66 per cent compared with only 30 per cent in the first 10 patients in whom the decision to perform PTCA was then late, after failure of thrombolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

The beta-adrenoceptors are now well individualized. They are divided into three distinct units: the receptor site, a regulating protein and a catalytic unit. The receptor density of the cell membrane varies according to the degree of stimulation of the receptor by agonists or the degree of blockade by antagonists. The myocardial or lymphocytic beta-adrenoceptor density is measured by "radioreceptor" assay using a radioactive beta-blocker. The myocardial beta-receptor density falls during heart failure, mainly to the detriment of beta 1 receptors. The density of beta 2 receptors remains unchanged. This fall in beta 1 receptors is related to the increase in the circulating catecholamines (down regulation) and is proportional to the severity of the disease. These physiological and physiopathological consequences can be directly applied to the treatment of heart failure by positive inotopic drugs or by beta-blockers.

Following insertion of a Leveen's valve after surgical portocaval anastomosis, a male patient with alcoholic cirrhosis developed dyspnoea with hypoxaemia. An interstitial syndrome was present in the lower lobes. Other findings were: polycythaemia (Hb 20 g/100 ml), subnormal spirometric values, decrease in CO transfer capacity, normal pulmonary compliance, absence of intracardiac shunt and pulmonary arterial hypertension and absence of bronchial or alveolar lesions on a surgical lung biopsy. Blood gas measurements and radioisotope explorations led to the conclusion that the patient had an anatomical shunt predominant in the lower parts of the lungs, associated with a shunt effect and a transfer disorder. The anatomical shunt was due to pulmonary arteriovenous microfistulae, some of which were visualized by superselective angiography. Catheterization of the portocaval anastomosis eliminated any shunt between the portal system and the pulmonary veins.

A new case of bi-directional tachycardia is reported. Intracavitary recordings show that the site of the disorder lies below the main trunk of the bundle if His. Analysis of the surface electrocardiogram and of electrical stimulation has led to a number of arguments for the hypothesis of a reentry circuit which uses the right branch in the reverse direction, and then the anterior and posterior sub-branches alternately in the normal direction. The recurrent attacks of tachycardia can be prevented by permanent ventricular stimulation at a rate above that which occurs between the attacks. However, the relief which this affords has not altered the prognosis of this arrhythmia, which remains very poor.

The tolerance and efficacy of propafenone were studied in cases of chronic ventricular extrasystoles of the elderly (age greater than 70 years). Only patients presenting more than 1,000 extrasystoles per day and requiring a treatment, were included in this study. Patients presenting non-compensated cardiac insufficiency, hypotensive patients, patients with conduction disorders without pacemakers as well as patients presenting a severe renal or hepatic insufficiency, were excluded. After making sure that the rhythm disorder was chronic, a control Holter was performed, then, 600 mg of propafenone per day, in 3 doses were prescribed for 5 days. On the 5th day, a Holter was performed as well as a blood propafenone level. Some patients received then 900 mg per day with a new Holter and plasma propafenone titration on the 10th day. 11 patients were studied in this fashion. The tolerance to 600 mg was good in 10 out of 11 cases. The efficacy, appreciated by the decrease of the number of isolated ventricular extrasystoles (-69%), doublets (-95%), triplets (-98%) and salvos of ventricular tachycardias (-100%), was excellent in 6 cases, average in 2 cases and mediocre in 3 cases. Increase of the dosage to 900 mg does not improve significantly the anti-arrhythmic efficacy while the side effects seem more frequent. It is not possible to establish a relationship between plasma concentrations and efficacy. At a dosage of 600 mg per day, propafenone is therefore effective in the treatment of ventricular extrasystoles in elderly patients and its tolerance is good. Higher doses are not advisable as they seem much less well tolerated without any additional advantage.

The rate association of a "type A" W.P.W. syndrome with a left bundle branch block gives a characteristic electrocardiographic picture:--the left bundle branch block is partially masked, the delay in the basial region of the left ventricle being in part cancelled by pre-excitation--the features of the W.P.W. syndrome are also modified, since the ventricular axis is corrected by the left bundle branch block. The electrocardiographic tracings taken during the various tachycardias and during treatment for arrhythmia, together with the intra-cavitary recordings allow a precise diagnosis to be made. In this case, vectocardiography was particularly useful as it gave a clear demonstration of the median delay of the ventricular loop, the only pathognomic feature of left bundle branch block, during a period when the left bundle of Kent was functioning.

The aim of this study was to compare the efficacy and safety of enalapril and a combination of a thiazide diuretic (altizide) and a diuretic that reduce potassium excretion (spironolactone), in patients presenting moderate essential hypertension. The four-month, double-blind study of two parallel groups involved 20 patients (12 males, 8 females) of mean age 54 years. All patients first received placebo for 15 days. Subsequently, 10 patients received 20 mg enalapril per day and 10 patients 15 mg altizide combined with 25 mg spironolactone in the same tablet. Blood pressure was measured every five minutes for 30 minutes with an automatic apparatus (Dynamap 845), before administration of placebo, before treatment and one, two and three months after treatment. There was no significant change of pulse rate with enalapril or with the diuretic combination. Both treatments produced an identical significant drop in systolic pressure. On the other hand enalapril seemed more efficacious in reducing diastolic pressure at the fourth month: respective pressures 98.2 +/- 13.3 mmHg and 81.0 +/- 8.5 mmHg (p less than 0.005) with enalapril, 98.6 +/- 7.4 mmHg and 86.0 +/- 6.1 mmHg (p less than 0.001) with the diuretic association (17% versus 12%, p less than 0.05). Safety was good with both medicinal preparations and the few side-effects noted did not necessitate withdrawal of treatment.