Current status and needs for changes in critical care training: the voice of the young cardiologists.

AIMS: The implementation of the 2013 European Society of Cardiology (ESC) Core Curriculum guidelines for acute cardiovascular care (acc) training among European countries is unknown. We aimed to evaluate the current status of acc training among cardiology trainees and young cardiologists (<40 years) from ESC countries. METHODS AND RESULTS: The survey (March-July 2019) asked about details of cardiology training, self-confidence in acc technical and non-technical skills, access to training opportunities, and needs for further training in the field. Overall 614 young doctors, 31 (26-43) years old, 55% males were surveyed. Place and duration of acc training differed between countries and between centres in the same country. Although the majority of the respondents (91%) had completed their acc training, the average self-confidence to perform invasive procedures and to manage acc clinical scenarios was low-44% (27.3-70.4). The opportunities for simulation-based learning were scarce-18% (5.8-51.3), as it was previous leadership training (32%) and knowledge about key teamwork principles was poor (48%). The need for further acc training was high-81% (61.9-94.3). Male gender, higher level of training centres, professional qualifications of respondents, longer duration of acc/intensive care training, debriefings, and previous leadership training as well as knowledge about teamwork were related to higher self-confidence in all investigated aspects. CONCLUSIONS: The current cardiology training program is burdened by deficits in acc technical/non-technical skills, substantial variability in programs across ESC countries, and a clear gender-related disparity in outcomes. The forthcoming ESC Core Curriculum for General Cardiology is expected to address these deficiencies.

Organization of intensive cardiac care units in Europe: Results of a multinational survey.

BACKGROUND: The present survey aims to describe the intensive cardiac care unit organization and admission policies in Europe. METHODS: A total of 228 hospitals (61% academic) from 27 countries participated in this survey. In addition to the organizational aspects of the intensive cardiac care units, including classification of the intensive cardiac care unit levels, data on the admission diagnoses were gathered from consecutive patients who were admitted during a two-day period. Admission policies were evaluated by comparing illness severity with the intensive cardiac care unit level. Gross national income was used to differentiate high-income countries (n=13) from middle-income countries (n=14). RESULTS: A total of 98% of the hospitals had an intensive cardiac care unit: 70% had a level 1 intensive cardiac care unit, 76% had a level 2 intensive cardiac care unit, 51% had a level 3 intensive cardiac care unit, and 60% of the hospitals had more than one intensive cardiac care unit level. High-income countries tended to have more level 3 intensive cardiac care units than middle-income countries (55% versus 41%, p=0.07). A total of 5159 admissions were scored on illness severity: 63% were low severity, 24% were intermediate severity, and 12% were high severity. Patients with low illness severity were predominantly admitted to level 1 intensive cardiac care units, whereas patients with high illness severity were predominantly admitted to level 2 and 3 intensive cardiac care units. A policy mismatch was observed in 12% of the patients; some patients with high illness severity were admitted to level 1 intensive cardiac care units, which occurred more often in middle-income countries, whereas some patients with low illness severity were admitted to level 3 intensive cardiac care units, which occurred more frequently in high-income countries. CONCLUSION: More than one-third of the admitted patients were considered intermediate or high risk. Although patients with higher illness severity were mostly admitted to high-level intensive cardiac care units, an admission policy mismatch was observed in 12% of the patients; this mismatch was partly related to insufficient logistic intensive cardiac care unit capacity.

[Fatal surgical extraction of cardiac resynchronisation therapy defibrillator leads in a context of endocarditis due to methicillin-resistant Staphylococcus epidermidis. A case report and review of literature]. / Extraction chirurgicale fatale de sondes de défibrillateur cardiaque triple chambre dans un contexte d'endocardite à Staphylococcus epidermidis méthicilline-résistant. À propos d'un cas et revue de la littérature.

A 82-year-old man equipped with a cardiac resynchronisation therapy defibrillator for dilated cardiomyopathy with normal coronary arteries, in complete atrioventricular block, develops six months after a change of the generator-pocket a severe endocarditis due to a methicillin-resistant Staphylococcus epidermidis with a large lead vegetation. After 4 days of adapted antimicrobial therapy, a surgical device removal is realised with unfortunately a fatal end during extraction. This observation points out the severity of cardiovascular device infections in old and weak population, as well as the difficulty of treatment choices because of both infectious and rhythmic constraints. The lead extraction is a strong recommendation but the modality and timing of extraction are not consensual, especially in cardioverter defibrillator-dependent patients. Surgical removal remains an alternative to percutaneous lead extraction but with a higher operative risk.

Is There Still a Role for Fibrinolysis in ST-Elevation Myocardial Infarction?

OPINION STATEMENT: Fibrinolysis had long been the reference treatment in patients with ST-Elevation Myocardial Infarction (STEMI). It was associated with a large reduction in mortality as compared with delayed or no reperfusion in patients managed early, within the first 2 hours from the onset of symptoms. Fibrinolysis also had well-known potential complications: cerebral haemorrhage, especially in patients beyond 75 years, and reinfarction. Primary percutaneous intervention (PCI) has overcome most of these limitations, but at a price: PCI-related delays that can reduce the expected benefit of primary PCI compared with fibrinolysis. That primary PCI is today the treatment of choice in patients with STEMI is no longer discussed. However, fibrinolysis should still maintain a role in the management of acute myocardial infarction (AMI) for three reasons. First, fibrinolysis is no longer a stand-alone treatment. Modern fibrinolytic strategies combine immediate fibrinolysis, loading dose of thienopyridines, and transfer to a PCI hospital for rescue or early PCI within 24 hours. These strategies capitalize on the hub-and-spoke networks that have, or should have, been built everywhere to implement primary PCI. The overall clinical results of these modern fibrinolytic strategies are now similar to those of primary PCI. Second, a substantial number of patients cannot be managed with primary PCI within the reasonable time thresholds set by the guidelines. In the case of long PCI-related delays, patients will benefit from fibrinolysis before or during transfer to a PCI hospital. Third, modern fibrinolytic strategies-immediate fibrinolysis followed by rescue or early PCI-may even offer the best results of all in a subset of patients. Patients of less than 75 years, managed within the first 2 hours and who cannot have immediate PCI, will fare better with a modern fibrinolytic strategy than with primary PCI. Guidelines advocate regional networks between hospitals with and without PCI capabilities, an efficient ambulance service and standardization of AMI management through shared protocols. These regional logistics of care are essential to take full advantage of fibrinolysis strategies. In order to check that these strategies are correctly applied, networks need ongoing registries, as well as benchmarking and quality improvement initiatives.

Dicer-2- and Piwi-mediated RNA interference in Rift Valley fever virus-infected mosquito cells.

Rift Valley fever virus (RVFV) is a Phlebovirus (Bunyaviridae family) transmitted by mosquitoes. It infects humans and ruminants, causing dramatic epidemics and epizootics in Africa, Yemen, and Saudi Arabia. While recent studies demonstrated the importance of the nonstructural protein NSs as a major component of virulence in vertebrates, little is known about infection of mosquito vectors. Here we studied RVFV infection in three different mosquito cell lines, Aag2 cells from Aedes aegypti and U4.4 and C6/36 cells from Aedes albopictus. In contrast with mammalian cells, where NSs forms nuclear filaments, U4.4 and Aag2 cells downregulated NSs expression such that NSs filaments were never formed in nuclei of U4.4 cells and disappeared at an early time postinfection in the case of Aag2 cells. On the contrary, in C6/36 cells, NSs nuclear filaments were visible during the entire time course of infection. Analysis of virus-derived small interfering RNAs (viRNAs) by deep sequencing indicated that production of viRNAs was very low in C6/36 cells, which are known to be Dicer-2 deficient but expressed some viRNAs presenting a Piwi signature. In contrast, Aag2 and U4.4 cells produced large amounts of viRNAs predominantly matching the S segment and displaying Dicer-2 and Piwi signatures. Whereas 21-nucleotide (nt) Dicer-2 viRNAs were prominent during early infection, the population of 24- to 27-nt Piwi RNAs (piRNAs) increased progressively and became predominant later during the acute infection and during persistence. In Aag2 and U4.4 cells, the combined actions of the Dicer-2 and Piwi pathways triggered an efficient antiviral response permitting, among other actions, suppression of NSs filament formation and allowing establishment of persistence. In C6/36 cells, Piwi-mediated RNA interference (RNAi) appeared to be sufficient to mount an antiviral response against a secondary infection with a superinfecting virus. This study provides new insights into the role of Dicer and Piwi in mosquito antiviral defense and the development of the antiviral response in mosquitoes.

[Mortality of myocardial infarction]. / La mortalité des syndromes coronariens aigus.

Coronary disease is a major cause of death and disability. From 1975 to 2000, coronary mortality was reduced by half. Better treatments and reduction of risk factors are the main causes. This phenomenon is observed in most developed countries, but mortality from coronary heart disease continues to increase in developing countries. In-hospital mortality of ST elevation myocardial infarction (STEMI) is in the range of 7 to 10% in registries. In infarction without ST segment elevation (NSTEMI), in-hospital mortality is around 5%. More recent studies found a similar in-hospital mortality for STEMI and NSTEMI. Because of patient selection and monitoring, mortality in clinical trials is much lower. After adjustment for the extent of coronary disease, age, risk factors, history of myocardial infarction, the excess mortality observed in women is fading. Many clinical, biological and laboratory parameters are associated with mortality in myocardial infarction. They refer to the immediate risk of death (ventricular rhythm disturbances, shock…), the extent of infarction (number of leads with ST elevation on the ECG, release of biomarkers, ejection fraction…), the presence of heart failure, the failure of reperfusion and the patient's baseline risk (age, renal function…). Risk scores, and more specifically the GRACE risk score, synthesize these different markers to predict the risk of death in a given patient. However, their use for the treatment of myocardial only concerns NSTEMI. Only a limited number of mechanical or pharmacological interventions reduces mortality of heart attack. The main benefits are observed with reperfusion by thrombolysis or primary angioplasty in STEMI, aspirin, heparin, beta-blockers, angiotensin converting enzyme inhibitors. Some medications such as bivalirudin and fondaparinux reduce mortality by decreasing the incidence of hemorrhagic complications. The guidelines classify interventions according to their benefit and especially their ability to reduce mortality. Organized care systems that improve implementation of guidelines also reduce mortality. Finally, some new therapeutic approaches such as post-conditioning and new therapeutic classes offer encouraging prospects for further reducing the mortality of myocardial infarction.

Nonstructural NSs protein of rift valley fever virus interacts with pericentromeric DNA sequences of the host cell, inducing chromosome cohesion and segregation defects.

Rift Valley fever virus (RVFV) is an emerging, highly pathogenic virus; RVFV infection can lead to encephalitis, retinitis, or fatal hepatitis associated with hemorrhagic fever in humans, as well as death, abortions, and fetal deformities in animals. RVFV nonstructural NSs protein, a major factor of the virulence, forms filamentous structures in the nuclei of infected cells. In order to further understand RVFV pathology, we investigated, by chromatin immunoprecipitation, immunofluorescence, fluorescence in situ hybridization, and confocal microscopy, the capacity of NSs to interact with the host genome. Our results demonstrate that even though cellular DNA is predominantly excluded from NSs filaments, NSs interacts with some specific DNA regions of the host genome such as clusters of pericentromeric gamma-satellite sequence. Targeting of these sequences by NSs was correlated with the induction of chromosome cohesion and segregation defects in RVFV-infected murine, as well as sheep cells. Using recombinant nonpathogenic virus rZHDeltaNSs210-230, expressing a NSs protein deleted of its region of interaction with cellular factor SAP30, we showed that the NSs-SAP30 interaction was essential for NSs to target pericentromeric sequences, as well as for induction of chromosome segregation defects. The effect of RVFV upon the inheritance of genetic information is discussed with respect to the pathology associated with fetal deformities and abortions, highlighting the main role played by cellular cofactor SAP30 on the establishment of NSs interactions with host DNA sequences and RVFV pathogenesis.

[Peroperative myocardial infarction, which treatment at the acute period?]. / Infarctus du myocarde peropératoire, quelle prise en charge à la phase aiguë?

We report the case of a patient who presented, during a hip replacement, a cardiogenic shock following a myocardial infarction. After a successful resuscitation of three cardiac arrests, an intra-aortic balloon pump was inserted, then the patient could have been transferred to the nearest cardiac catheterization laboratory for a percutaneous dilatation of the right coronary artery, allowing the patient to have favourable outcome. Treatment of perioperative myocardial infarction is not really standardized. This case report depicts that in such critical condition, insertion of an intra-aortic balloon pump with early percutaneous angioplasty for acute peroperative myocardial infarction is a valuable option.

Presence and extent of cardiac magnetic resonance microvascular obstruction in reperfused non-ST-elevated myocardial infarction and correlation with infarct size and myocardial enzyme release.

OBJECTIVE: Microvascular obstruction (MO) is a factor of adverse outcome in patients with ST-elevated myocardial infarction (STEMI). We assessed the presence and extent of MO and its relationship with infarct size and left ventricular (LV) functional parameters after acute non-ST-elevated myocardial infarction (NSTEMI). METHODS: Twenty-five patients with first acute NSTEMI underwent a cine and first-pass perfusion cardiac magnetic resonance (CMR) study, with late gadolinium enhancement imaging 72 h after myocardial infarction. RESULTS: MO was detected in 32% of patients, and its extent comprised 0.5-3.1% of the total LV mass (mean 1.9 +/- 1.2%). Patients with MO had a significantly larger infarct size than patients without (14.1 +/- 5.9 vs. 5.3 +/- 4.1% LV mass; p < 0.001). There was no significant difference between both groups for the LV functional parameters and LV ejection fraction (58.5 +/- 6.8 vs. 62.6 +/- 9.6%; p = 0.29). Patients with MO showed a higher troponin I release (570 +/- 364 vs. 148 +/- 103 IU; p = 0.003) and a higher creatine kinase release (29,887 +/- 18,263 vs. 10,287 +/- 5,283 IU; p = 0.007). CONCLUSIONS: In patients with acute NSTEMI, MO has a frequency similar to that observed in patients with STEMI and also correlates with the infarct extent. The prognostic significance on clinical outcome remains to be shown in this specific population.

Acute myocarditis mimicking lateral myocardial infarction.

We report a case of myocarditis mimicking acute lateral myocardial infarction and treated as such initially, which was complicated by ventricular fibrillation a few hours after admission to the intensive care unit. The correct diagnosis was rapidly made using a low-dose delayed-enhanced cardiac multidetector computed tomography scan performed immediately after a normal coronary angiogram, demonstrating typical myocardial late hyperenhancement and good correlation with delayed enhanced magnetic resonance imaging. This case suggests that myocarditis can be accurately diagnosed by delayed-enhanced cardiac multidetector computed tomography in an emergency setting. The other lesson from this case is that patients presenting with severe clinical symptoms, important ECG signs and high myocardial enzyme levels should be closely monitored for at least 72 hours, even when myocardial infarction has been excluded.

[Innovations in emergency management of chest pain with CT angiography]. / Nouveautés dans la prise en charge angioscanographique des douleurs thoraciques dans le cadre de l'urgence.

Recent technological innovations modify the diagnosis opportunities of multislice CT angiography. Emergency chest pain management is therefore optimised and still oriented by clinical presentation. Aortic CT angiography allows the diagnosis and classification of aortic dissection or intramural haematoma. It also shows the extension to aortic thoracoabdominal branches and visceral involvement. Pulmonary embolism diagnosis will be completed by scanographic evaluation of its seriousness. Chest pain caused by pulmonary or digestive diseases will also be documented. A late phase imaging seems useful to diagnose acute myocardial pathology.

WITHDRAWN: Primary angioplasty versus intravenous thrombolysis for acute myocardial infarction.

BACKGROUND: Intravenous thrombolytic therapy is the standard care for patients with acute myocardial infarction, based upon its widespread availability and ability to reduce patient mortality well demonstrated in randomised trials. Despite its proven efficacy, thrombolytic therapy has limitations. Many patients are ineligible for treatment with thrombolytics. Of those given thrombolytic therapy, 10 to 15 percent have persistent occlusion or reocclusion of the infarct-related artery. Consequently, primary angioplasty (primary PTCA) has been advocated as a better treatment of myocardial infarction. OBJECTIVES: To determine whether primary coronary angioplasty is superior to thrombolytic therapy for the treatment of patients with acute myocardial infarction. SEARCH STRATEGY: Electronic search of The Cochrane Library (1998; Issue 2). MEDLINE (to January 1998); references from reviews, trials and previously published meta-analyses; and experts. Date of most recent searches January 1998. SELECTION CRITERIA: All unconfounded, randomised controlled trials comparing primary angioplasty against intravenous thrombolysis in patients with acute myocardial infarction DATA COLLECTION AND ANALYSIS: At least two independent reviewers abstracted data on morbidity and mortality and trial characteristics. The following outcomes were assessed: total mortality at the end of the study, reinfarction, stroke of any type, composite endpoint of death and reinfarction, recurrent ischemia, severe bleeding and coronary artery bypass grafting. MAIN RESULTS: Ten trials including 2573 subjects were identified. Compared to thrombolytic therapy, primary angioplasty was associated with a significant reduction in short-term mortality at the end of the studies (relative reduction in risk RRR = 32% 95%CI = 5%;50%). Similar reductions were observed for the rate of reinfarction (RRR = 52%, 95%CI = 30%;67%), recurrent ischemia (RRR = 54%; 95%CI = 39%,66%) and for the combined criteria death or reinfarction (RRR = 46%; 95%CI=30%;58%). The frequency of strokes of any cause was significantly decreased by 66% (95%CI=28%;84%). No significant difference was observed for the incidence of major bleeding (relative risk RR =1.18, 95%CI = 0.73;1.90) but the confidence interval was large. The superiority of the primary angioplasty over thrombolysis in terms of the composite endpoint (mortality and reinfarction) was less with accelerated t-PA (RR=0.70, 95%CI=0.51;0.97) than with streptokinase (RR=0.30, 95%CI=0.17;0.53). The biggest and most recent trial, Gusto 2B (GUSTO-2B 97), which involved general as well as highly specialised centres, obtained less favorable results. AUTHORS' CONCLUSIONS: This meta-analysis suggests that angioplasty provides a short-term clinical advantage over thrombolysis which may not be sustained. Primary angioplasty when available promptly at experienced centres, may be considered the preferred strategy for myocardial reperfusion. In most situations, however, optimal thrombolytic therapy should still be regarded as an excellent reperfusion strategy.

[Ictero-haemorrhagic leptospirosis with a cardiac presentation in a patient returning from an endemic zone]. / Leptospirose ictéro-hémorragique de presentation cardiaque chez une patiente de retour de zone d'endémie.

On returning from a tropical area, the occurrence of rapidly evolving cardiogenic shock in an infectious context should quickly suggest the diagnosis, for which specific treatment can affect the outcome. The dramatic case of a young female presenting with ictero-haemorrhagic leptospirosis diagnosed post-mortem, demonstrated this pathology with the unusual association of complete atrio-ventricular block and myocarditis in a haemorrhagic context.

[Levosimendan, a revolution in the world of inotropic agents?]. / Le levosimendan, une revolution dans le monde des inotropes?

Levosimendan is the first available drug of a new class of agents called calcium sensitizers. It increases cardiac contractility without increasing myocardial oxygen consumption. This new molecule has no proarrhythmic effects and has anti-ischemic properties. Levosimendan is infused over a 24-hour period and its hemodynamic effects, similar or superior to those of catecholamines, persist during one week. In a selected group of advanced heart failure patients levosimendan was associated with a mortality reduction at 14 days and at 6 months in comparison with dobutamine. In spite of its cost, this new inotropic agent appears very promising and it is expected that it will be widely used.

Primary angioplasty versus intravenous thrombolysis for acute myocardial infarction.

BACKGROUND: Intravenous thrombolytic therapy is the standard care for patients with acute myocardial infarction, based upon its widespread availability and ability to reduce patient mortality well demonstrated in randomised trials. Despite its proven efficacy, thrombolytic therapy has limitations. Many patients are ineligible for treatment with thrombolytics. Of those given thrombolytic therapy, 10 to 15 percent have persistent occlusion or reocclusion of the infarct-related artery. Consequently, primary angioplasty (primary PTCA) has been advocated as a better treatment of myocardial infarction. OBJECTIVES: To determine whether primary coronary angioplasty is superior to thrombolytic therapy for the treatment of patients with acute myocardial infarction. SEARCH STRATEGY: Electronic search of The Cochrane Library (1998; Issue 2). MEDLINE (to January 1998); references from reviews, trials and previously published meta-analyses; and experts. Date of most recent searches January 1998. SELECTION CRITERIA: All unconfounded, randomised controlled trials comparing primary angioplasty against intravenous thrombolysis in patients with acute myocardial infarction DATA COLLECTION AND ANALYSIS: At least two independent reviewers abstracted data on morbidity and mortality and trial characteristics. The following outcomes were assessed: total mortality at the end of the study, reinfarction, stroke of any type, composite endpoint of death and reinfarction, recurrent ischemia, severe bleeding and coronary artery bypass grafting. MAIN RESULTS: Ten trials including 2573 subjects were identified. Compared to thrombolytic therapy, primary angioplasty was associated with a significant reduction in short-term mortality at the end of the studies (relative reduction in risk RRR = 32% 95%CI = 5%;50%). Similar reductions were observed for the rate of reinfarction (RRR = 52%, 95%CI = 30%;67%), recurrent ischemia (RRR = 54%; 95%CI = 39%,66%) and for the combined criteria death or reinfarction (RRR = 46%; 95%CI=30%;58%). The frequency of strokes of any cause was significantly decreased by 66% (95%CI=28%;84%). No significant difference was observed for the incidence of major bleeding (relative risk RR =1.18, 95%CI = 0.73;1.90) but the confidence interval was large. The superiority of the primary angioplasty over thrombolysis in terms of the composite endpoint (mortality and reinfarction) was less with accelerated t-PA (RR=0.70, 95%CI=0.51;0.97) than with streptokinase (RR=0.30, 95%CI=0.17;0.53). The biggest and most recent trial, Gusto 2B (GUSTO-2B 97), which involved general as well as highly specialised centres, obtained less favorable results. REVIEWER'S CONCLUSIONS: This meta-analysis suggests that angioplasty provides a short-term clinical advantage over thrombolysis which may not be sustained. Primary angioplasty when available promptly at experienced centres, may be considered the preferred strategy for myocardial reperfusion. In most situations, however, optimal thrombolytic therapy should still be regarded as an excellent reperfusion strategy.

[Efficacy and safety of low-dose heparin (30 IU/kg) during coronary angioplasty]. / Efficacité et sécurité d'emploi de faibles doses d'héparine (30 UI/kg) en cours d'angioplastie coronaire.

High doses of heparin are recommended during coronary angioplasty although platelet inhibition seems to play a role in the prevention of ischaemic complications. Low dose heparin could reduce the incidence of local complications without increasing that of major coronary events. The authors report the results of a prospective register of coronary angioplasties performed by the femoral approach with a single bolus of 30 IU/Kg of heparin and immediate withdrawal of the 6 French introducer. Only patients with recent infarction or left main stem disease were excluded. All underwent clinical examination and ultrasonic scanning of the puncture site the day after the procedure. Four hundred and eighteen patients were included (mean age: 63.3 +/- 11 years; 79% men; 77% stenting). The average dose of heparin was 2253 +/- 1056 IU; the average procedure time was 25 +/- 16 minutes, and a final activated clotting time was 174 +/- 69 ms. The duration of normal compression was 7.7 +/- 3 min. Eighty-three point five per cent of patients were discharged the day after the procedure with a global cardiovascular complication rate of 2.87%. At 1 month, 1.67% of secondary cardiovascular events was recorded. Ultrasonography of the puncture site was abnormal in 7.6% of patients. Only one serious vascular complication (0.24%) requiring transfusion and surgical repair, was observed. The authors conclude that the use of low dose heparin appears effective and safe in cases without acute myocardial infarction. This protocol allows faster mobilisation and earlier hospital discharge of patients.

Early risk factors in acute type A aortic dissection: is there a predictor of preoperative mortality?

BACKGROUND: To describe the preoperative clinical, echocardiographic and biological findings in patients with acute aortic dissection and attempt to specify high risk factors of preoperative mortality. METHODS: A retrospective, monocentric study of 148 patients admitted for acute type A aortic dissection. All patients underwent a clinical, echocardiographic and biological evaluation on admission. In 75 patients, we measured serum cardiac troponin I (cTnI). RESULTS: In hospital mortality was 25.9% and 15.6% presented with preoperative cardiac circulatory arrest (POCCA). Patients with POCCA were more likely than others to have hypotension (97+/-56 vs 144+/-24 mmHg, p<0.01) or shock (52% vs 3%, p<0.01) on admission. Pericardial effusion (65% vs 35%, p=0.01) and tamponade (61% vs 8%, p<0.01) were also significantly linked to POCCA but not the aortic ascendant diameter. Detection of cTnI was more frequent in patients with POCCA (24% vs 7%, p=0.051) and was found to be a good predictor of in hospital mortality (47% vs 14%, p<0.01). CONCLUSIONS: For patients with acute type A aortic dissection, hypotension or shock on admission, pericardial effusion or tamponade, as well as cTnI detection, were the main predictors for POCCA and imply immediate surgery.

Inhibition of histone deacetylation induces constitutive derepression of the beta interferon promoter and confers antiviral activity.

The induction of alpha/beta interferon (IFN-alpha/beta) genes constitutes one of the first responses of the cell to virus infection. The IFN-beta gene is constitutively repressed in uninfected cells and is transiently activated after virus infection. In this work we demonstrate that histone deacetylation regulates the silent state of the murine IFN-beta gene. Using chromatin immunoprecipitation (ChIP) assays, we show a direct in vivo correlation between the transcriptionally silent state and a state of hypoacetylation of histone H4 on the IFN-beta promoter region. Trichostatin A (TSA), a specific inhibitor of histone deacetylases, induced strong, constitutive derepression of the murine IFN-beta promoter stably integrated into a chromatin context, as well as the hyperacetylation of histone H4, without requiring de novo protein synthesis. We also show in this work that TSA treatment strongly enhances the endogenous IFN level and confers an antiviral state to murine fibroblastic L929 cells. Inhibition of histone deacetylation with TSA protected the cells against the lost of viability induced by vesicular stomatitis virus (VSV) and inhibited VSV multiplication. Using antibodies neutralizing IFN-alpha/beta, we show that the antiviral state induced by TSA is due to TSA-induced IFN production. The demonstration of the predominant role of histone deacetylation during the regulation of the constitutive repressed state of the IFN-beta promoter constitutes an interesting advance on the understanding of the negative regulation of this gene and opens up the possibility of new therapeutic perspectives.

Influence of atrial flutter ablation on right to left inter-atrial conduction.

AIMS: Ablation of the atrial isthmus between the tricuspid annulus and the inferior vena cava changes P-wave morphology during low lateral right atrial pacing. For better understanding of the mechanism of this alteration, the sequence of activation of the inter-atrial septum and the left atrium were compared before and after ablation of the isthmus between the inferior vena cava and the tricuspid annulus. METHODS AND RESULTS: In 13 patients, left atrial mapping was performed using a duodecapolar electrode catheter advanced to the far distal coronary sinus. The inter-atrial septum was mapped using a right atrial duodecapolar electrode catheter. Conduction times were measured during low lateral right atrial pacing from the pacing artefact and during sinus rhythm from the earliest right atrial electrogram to every intra-cardiac electrogram before and after the ablation. During low lateral right atrial pacing, isthmus ablation resulted in a significant delay in every left atrial lead. Changes were maximal at the posterior aspect of the left atrium and minimal at its anterior aspect. No significant change was discernible on the inter-atrial septum. During sinus rhythm, atrial activations remained unchanged. CONCLUSION: Electrocardiographic changes of P-wave morphology result from alteration in the sequence of left atrial activation rather than that of the inter-atrial septum.

[Myocardial infarction and anabolic steroid use. A case report]. / Infarctus du myocarde et prise d'anabolisants. A propos d'un cas.

The potential cardiotoxicity of anabolic steroids is not well known. The authors report the case of a young man who was a top class body builder and who developed severe ischaemic cardiomyopathy presenting with an inferior wall myocardial infarction. The clinical history revealed prolonged and intensive usage of two types of anabolic steroids to be the only risk factor. This cardiotoxicity may be related to several physiopathological mechanisms: accelerated atherogenesis by lipid changes, increased platelet aggregation, coronary spasm or a direct toxic effect on the myocytes. The apparent scarcity of the reported clinical details in the literature is probably an underestimation of the consequences of this usage.