[Traumatic aortic regurgitation: diagnostic, management and treatment]. / Rupture traumatique de la valve aortique. Diagnostic, prise en charge et traitement.

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.

[Cardiotoxicity associated with trastuzumab (herceptin). An undesired effect leads towards a model of cardiac insufficiency]. / Toxicité cardiaque d'une nouvelle chimiothérapie anticancéreuse: le trastuzumab (Herceptin).

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.

[Atrial lead placement in the right atrial appendage during recent or chronic arrhythmia]. / Implantation de la sonde atriale dans l'auricule droit chez des patients en arythmie atriale récente ou chronique en vue d'une régularisation différée du rythme. Performance de la sonde à 6 mois.

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.

[Impact of biochemisty on the duration of treatment for pulmonary embolus]. / Impact de la biologie sur la durée du traitement d'une embolie pulmonaire. Le point de vue du clinicien.

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.

[When is antivitamin K therapy indicated in the stable coronary patient?]. / Quand faut-il utiliser les AVK chez le coronarien stable?

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.

[Duration of antivitamin K therapy in venous thromboembolic disease. Certainties and uncertainties]. / Durée du traitement AVK dans la maladie thromboembolique veineuse. Certitudes et incertitudes.

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.

[Venous thromboembolism and cancer]. / Maladie thromboembolique veineuse et cancer.

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.

Impact of attenuation correction by simultaneous emission/transmission tomography on visual assessment of 201Tl myocardial perfusion images.

UNLABELLED: It has been shown in clinical studies that for subjects with a low likelihood of coronary artery disease (CAD), attenuation correction (AC) improves the specificity of defect detection in the inferior wall (right coronary artery [RCA] region). The aim of this study was to investigate the effect of AC on the visual interpretation of the RCA and anteroseptal (corresponding to the left anterior descending artery [LAD]) regions in CAD patients. METHODS: Fifty-six patients with suspected CAD underwent 20Tl stress/4 h-delayed imaging SPECT using a simultaneous 201Tl emission/99mTc transmission imaging protocol. Images were reconstructed using the maximum likelihood-expectation maximum algorithm without and with AC. The stress/4 h-delayed images were interpreted blindly for reversible or fixed defects in the RCA and LAD regions by three experienced physicians. Coronary angiography, electrocardiography and enzyme findings were used to establish diagnoses of ischemia or infarction, and receiver operating characteristic (ROC) analyses were performed. RESULTS: Statistical testing of ROC curve areas showed that defect detection performance improved with AC when compared with performance without AC in the RCA region. This was mainly the result of a systematic increase in specificity of 12% or more (for any observer and any type of defect) for a similar sensitivity (no definite change in sensitivity values). However, defect detection performance significantly decreased in the LAD territory with AC images (P < 0.05) because of a systematic decrease in sensitivity of 20% or more, with no consistent change in specificity. Similar trends were observed when reversible and fixed defects were considered separately. CONCLUSION: AC significantly affects the visual interpretation of 201Tl stress/4 h-delayed SPECT images. This study confirmed the increase in specificity obtained with AC in the RCA territory. However, in the population considered, the studied AC was deleterious for the LAD territory assessment.

Atherosclerosis of the thoracic aorta and aortic debris as a marker of poor prognosis: benefit of oral anticoagulants.

OBJECTIVES: Our aim was to confirm the poor prognosis related to thoracic aortic plaques, in particular aortic debris, diagnosed by transesophageal echocardiography (TEE) and to evaluate patients' prognosis as a function of the antithrombotic treatment. BACKGROUND: Aortic atheroma (AA) has been widely studied. However, it is still not known which antithrombotic treatment should be adopted in this disease. METHODS: Patients referred for TEE and diagnosed with AA were followed. All thromboembolic events and deaths were recorded during a follow-up of 22+/-10 months. The antithrombotic treatment to be adopted was left to the discretion of the practitioner in charge of the patient. RESULTS: Aortic atheroma was found in 12% of all TEE performed and in 27.5% of TEE performed for stroke. This prevalence was higher when no other etiology existed to explain the stroke (p < 0.001). During follow-up, an end point occurred in 22.5% of patients. The more severe the AA the greater the incidence of events (p = 0.007). A higher mortality rate is shown in patients with aortic debris (p = 0.049). Compared with those treated with oral anticoagulants, patients with aortic plaques >4 mm thick treated with antiplatelets had more embolic events and combined events (p = 0.01 and p = 0.007, relative risk [RR] = 5.9, 95% confidence interval [CI] = 1.4 to 15, respectively); patients with aortic debris had more combined events and a higher mortality rate (p = 0.001, RR = 7.1, 95% CI = 1.2 to 19 and p = 0.019, RR = 9.1, 95% CI = 1.2 to 25, respectively). CONCLUSIONS: We confirm the high incidence of vascular events and deaths in patients with AA. We have demonstrated, for the first time in this condition, a better outcome among patients treated with oral anticoagulants versus antiplatelets.

Travel as a risk factor for venous thromboembolic disease: a case-control study.

BACKGROUND: The link between travel and the risk of venous thromboembolic disease (VTED) has been widely suspected. However, only cases or series of cases have been reported in the literature. STUDY OBJECTIVES: By means of a case-control study, we sought to confirm this relationship and to determine the main features, if any, of these posttravel VTEDs. DESIGN: The history, in particular the history of recent travel, of 160 patients presenting in our department with VTED was scrupulously investigated. All journeys undertaken during the preceding 4 weeks and lasting > 4 h by whatever means of transport were considered. The same questionnaire was submitted to a control group. RESULTS: When the two groups of patients are compared, a history of recent travel is found almost four times more frequently in the VTED group (p < 0.0001). The odds ratio for having a VTED in patients who traveled was 3.98 (95% confidence interval, 1.9 to 8.4). Means of travel used included the train in 2 cases, airplane in 9, and car in 28. Mean duration of travel was 5.4+/-2.1 h. These posttravel VTEDs are not confined to a specific location, seem to involve no particular predisposition, and are more often "idiopathic." This fact supports the hypothesis that travel alone can produce vein clot formation. CONCLUSIONS: A history of recent travel is a risk factor for VTED. Posttravel venous thrombotic events can occur after short journeys in patients with no other risk factors or concomitant disease

Usefulness of endocoronary electrocardiogram in the detection of myocardial viability and comparison with single-photon emission computed tomography Tl-201.

In 20 patients who had recently had an acute myocardial infarction, we compared endocoronary electrocardiographic modifications recorded during angioplasty with thallium-201 for the detection of myocardial viability. Our data demonstrate that endocoronary electrocardiography can be an easy and reliable tool to assess viability, with sensitivity, specificity, and positive and negative predictive values of 100%, 80%, 94%, 100%, respectively.

[Rapid decrease of serum endothelin-1 levels after treatment with ACE inhibitors in chronic cardiac failure]. / Diminution rapide des taux sériques d'endothéline-1 après traitement par inhibiteur de l'enzyme de conversion dans l'insuffisance cardiaque chronique.

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.

[Transformation of left bundle branch block into simulated bundle branch block after ablation of the right bundle in a patient with branch-to-branch reentry ventricular tachycardia]. / Transformation d'un bloc de branche gauche en bloc de branche déguisé après ablation de la branche droite chez un patient présentant des tachycardies ventriculaires par réentrée de branche à branche.

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.

Investigation of the thoracic aorta in cholesterol embolism by transoesophageal echocardiography.

OBJECTIVES: To examine the thoracic aorta of patients with severe cholesterol embolism (CE) by transoesophageal echocardiography (TOE). METHODS: The thoracic aorta of 20 consecutive patients with CE was compared with that in a control population matched for age and risk factors by TOE. Patients were prescribed steroids after CE was diagnosed. Follow up is reported and compared with results in the literature. RESULTS: Aortic plaques and debris were more common in patients with CE than in the control population (p < 0.001 and p < 0.0001, respectively). The mean (SD) number of aortic plaques in the CE patients was 2.6 (0.7). This aortic atheroma was found predominantly in the descending aorta. One patient died during a mean (SD) follow up of 24 (10) months. CONCLUSIONS: Aortic atheroma, as detected by TOE, should be considered as the main source of CE. In addition, the prognosis in our series, in which steroids were systemically prescribed, is much better than in others reported in the literature.

[Blood levels of homocysteine in patients under 55 years of age with acute coronary insufficiency]. / Taux d'homocystéine sanguine chez les patients de moins de 55 ans, atteints d'insuffisance coronarienne aiguë.

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.