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Data on regional variations in the characteristics, management and early outcome of patients admitted with ST-elevation myocardial infarction (STEMI) in France are limited. We used data from the FAST-MI 2010 registry to determine whether regional specificities existed, dividing the French territory into 6 larger geographical regions. Variations in the patients' characteristics were found, partly related to regional variations in demography. Acute reperfusion strategy showed more use of primary percutaneous coronary intervention in the greater Paris area, compared to other regions, which would be expected owing to geography and local availability of catheterization laboratories. Overall, however, in-hospital management showed more similarities than differences across regions. Complications, and in particular in-hospital mortality, did not differ significantly among regions., (Copyright © 2015. Published by Elsevier SAS.)

Although surgical aortic valve replacement has been the standard of care for patient with severe aortic stenosis, transcatheter aortic valve implantation (TAVI) is now a fair standard of care for patients not eligible or high risk for surgical treatment. The decision of therapeutic choice between TAVI and surgery considers surgical risk (estimated by the Euro-SCORE and STS-PROM) as well as many parameters that go beyond the assessment of the valvular disease's severity by echocardiography: a multidisciplinary assessment in "Heart Team" is needed to assess each case in all its complexity.

Coronary syndromes without ST elevation, previously known as unstable angina, are now more frequent than ST elevation myocardial infarction. Evidence-based studies should guide their management after hospital discharge. This management seeks to fulfill precise objectives and has been demonstrated to be effective in terms of survival., (Copyright (c) 2009 Elsevier Masson SAS. All rights reserved.)

The electrical stimulation of the dorsal columns of the spinal cord exerts a dual analgesic and vasodilatory effect on ischemic tissues. It is increasingly considered a valuable method to treat severe and otherwise intractable coronary and peripheral artery disease. The quality of the results depends from both a strict selection of the patients by vascular specialists and the frequency and quality of the follow-up controls. However the indications, limits, mode of action and results of spinal cord stimulation are still poorly understood. This article, based on a personal experience of 164 implantations for peripheral and coronary artery disease, aims to draw attention to this technique and to provide information on recent and future developments.

The hybrid treatment of aortic aneurysms is indicated in patients having the ostia of supra aortic or visceral branches taken in to the aneurysm. Indeed, these lesions are not eligible for classic endovascular treatment because the existing endoprostheses cannot provide perfusion of the side branches without inducing major endoleaks. The surgical technique consists of 2 steps: firstly, a by-pass between normal aorta and the major aortic branches involved in the aneurysm is performed to guarantee the perfusion of the organs such as brain, bowel, and after endoprosthesis deployment. Secondly, the endoprosthesis is deployed using the classical technique to isolate the aneurysm. The hybrid approach provides safe and reliable treatment of complex aortic aneurysms with mortality and morbidity rate far below the classical open surgery.

Following acute myocardial infarction, necrotic cardiac tissue is replaced by scar leading to ventricular remodeling and pump failure. Transplantation of autologous bone marrow-derived cells into the heart, early post-infarct, aims to prevent ventricular remodeling. This strategy has been evaluated in four controlled, randomized clinical trials, which provided mixed results. A transient improvement in ventricular function was observed in one trial, and a modest improvement (the duration of which remains to be determined) in an additional trial, whereas two trials showed negative results. A modest benefit of bone marrow cell transplantation was also observed in patients with chronic ischemic heart disease. Despite mixed results reported so far, cell therapy of heart disease still is in its infancy and has considerable room for improvement.

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.

Although it is impossible to recall all the new developments of the year 2001 regarding thrombosis, we have selected certain results: several, with although "negative" results, are highly interesting because they contradict preliminary studies which could have predicted therapeutic perspectives that would considerably alter the management of a common and serious illness. In this sense, they remind us that the large randomised studies (RCT) remain the necessary and indispensable tool for validating a large scale therapy: others, because they come within the logic of certain earlier results, and in this sense it is good for a clinician to see that a certain logic still exists in cardiology; others again, because they define a certainly real benefit, but whose limits of applicability could sometimes escape clinicians.

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.

It is nearly impossible to follow and integrate all the new information in each subspeciality of cardiology. In the last months, important data has been published which may change clinical practice. In this domain, over half the cases of suspected coronary chest pain would only require a very short stay in a chest pain unit. The history, an accurate evaluation of symptoms, the application of Bayesian analysis, ECG interpretation and serum troponine measurement, associated with a degree of clinical experience, will allow orientation of the patient to a coronary care unit or hospital discharge (with possible out-patient referral). Patients with true unstable angina will no longer be treated by continuous intravenous injection of non-fractionated heparin because, in theory and in practice, this has been replaced with subcutaneous LMW heparin.... On the other hand, the electric syringe will continue to be required for the integration of the anti-GPIIB-IIIA for the treatment of unstable angina after the recommendations published concomitantly in the United States and Europe. This type of patient, especially with a "positive" troponine, will probably not be kept waiting long before referral to the catheter laboratory for coronary angiography and revascularisation. The long-term results of the FRISC II trial are confirmed by an even earlier invasive approach (Tactics-Timi 18) using anti-GPIIb-IIIa. In the first hours, and independently of other older prognostic factors, it will be possible to "predict or compare" the risk of coronary recurrence based on the results of certain biological "markers". In many centres, cases with ST elevation on the ECG could well be included in a phase III "medical protocol", associating a half-dose thrombolytic and an anti-GPIIb-IIIa. Finally, patients who will have been admitted to the chest pain unit with a suspected pulmonary embolism, for example because they had not been treated prophylactically with aspirin before hip surgery, will probably have the choice, after d-dimer measurement, between pulmonary scintigraphy and helicoidal CT scan. If the diagnosis of pulmonary embolism is confirmed, a single subcutaneous injection of LMW heparin could replace the conventional continuous intravenous injection of heparin. The earliest possible oral anticancer ... pardon me I anticoagulant treatment should be prescribed and explained.

1999 has been a good year in the field of innovation in thrombosis. In coronary syndrome without ST elevation: low molecular weight heparin has been confirmed to be more effective than non-fractionated heparin (enoxaparin) and to improve the prognosis of non-revascularised patients (dalteparin) after the hospital phase; hirudin has been shown to be more effective in terms of incidence of myocardial infarction and recurrence of angina than non-fractionated heparin without a higher incidence of bleeding complications; the anti-GP IIb-IIIa (abciximab) has confirmed all its advantages at 6 months and 1 year after a coronary event. The association of heparin and aspirin, which has been the mainstay of antithrombotic treatment of acute coronary syndromes without ST elevation, will soon be improved upon at the beginning of the third millennium. In myocardial infarction, medical thrombolysis has probably reached a turning point in its history. The association of half doses of rt-Pa and anti-GP IIb-IIIa has been shown to be more effective in obtaining good reflow than the thrombolytic agent alone at conventional doses. These results were obtained without any increase in bleeding complication. The same anti-GP IIb-IIIa also improve mechanical revascularisation by optimising reperfusion after the 24th hour. This benefit is rapidly transformed into reduced left ventricular dysfunction. Pulmonary embolism remains a critical illness as the ICOPER registry reports a 3 year mortality of nearly 16%. This emphasises the importance of early diagnosis which is usually possible without resorting to invasive procedures and by modulating all the results of paraclinical investigations with respect to the pretest clinical probability.

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.

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.

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.