Exchange proteins directly activated by cAMP mediate cardiac repolarization and arrhythmogenesis during chronic heart failure.

Most sudden cardiac death in chronic heart failure (CHF) is caused by malignant ventricular arrhythmia (VA); however, the molecular mechanism remains unclear. This study aims to explore the effect of exchange proteins directly activated by cAMP (Epac) on VA in CHF and the potential molecular mechanism. Transaortic constriction was performed to prepare CHF guinea pigs. Epac activation model was obtained with 8-pCPT administration. Programmed electrical stimulation (PES) was performed to detect effective refractory period (ERP) or induce VA. Isolated adult cardiomyocytes were treated with 8-pCPT and (or) the Epac inhibitor. Cellular electrophysiology was examined by whole-cell patch clamp. With Epac activation, corrected QT duration was lengthened by 12.6%. The 8-pCPT increased action potential duration (APD) (APD50: 236.9 ± 18.07 ms vs. 328.8 ± 11.27 ms, p < 0.05; APD90: 264.6 ± 18.22 ms vs. 388.6 ± 6.47 ms, p < 0.05) and decreased rapid delayed rectifier potassium (IKr) current (tail current density: 1.1 ± 0.08 pA/pF vs. 0.7 ± 0.03 pA/pF, p < 0.05). PES induced more malignant arrhythmias in the 8-pCPT group than in the control group (3/4 vs. 0/8, p < 0.05). The selective Epac1 inhibitor CE3F4 rescued the drop in IKr after 8-pCPT stimulation (tail current density: 0.5 ± 0.02 pA/pF vs. 0.6 ± 0.03 pA/pF, p < 0.05). In conclusion, Epac1 regulates IKr, APD, and ERP in guinea pigs, which could contribute to the proarrhythmic effect of Epac1 in CHF.

Assessment and clinical relevance of the dynamic parameters of ventricular repolarization in patients with grade I left ventricular diastolic dysfunction 1.

Imbalance in ventricular repolarization parameters are related to increased risk of severe arrhythmia and sudden cardiac death. There is limited research regarding markers to detect patients at risk in this early stage. We aimed to assess the influence of grade I left ventricular diastolic dysfunction on repolarization parameters in asymptomatic patients. Ambulatory patients with grade I left ventricular diastolic dysfunction were studied and compared with a control group. We assessed the QT dispersion circadian variation, heart rate variability in the time and frequency domains, and dynamics of QT using a 12-lead Holter. In the diastolic dysfunction group, 8 (30%) patients had QT dispersion > 80 ms. One (3.8%) patient presented premature ventricular complex > 10/h. The comparison between the 2 groups showed that the difference between the standard deviation of normal-to-normal intervals and low frequency power in both groups was statistically significant. We therefore conclude that increased parameters of ventricular repolarization and depressed heart rate variability reflect an imbalance in autonomic responses in patients with grade I left ventricular diastolic dysfunction without cardiovascular symptoms, enabling the identification of patients that are at a higher risk for cardiovascular events.

Altered K+ current profiles underlie cardiac action potential shortening in hyperkalemia and ß-adrenergic stimulation.

Hyperkalemia is known to develop in various conditions including vigorous physical exercise. In the heart, hyperkalemia is associated with action potential (AP) shortening that was attributed to altered gating of K+ channels. However, it remains unknown how hyperkalemia changes the profiles of each K+ current under a cardiac AP. Therefore, we recorded the major K+ currents (inward rectifier K+ current, IK1; rapid and slow delayed rectifier K+ currents, IKr and IKs, respectively) using AP-clamp in rabbit ventricular myocytes. As K+ may accumulate at rapid heart rates during sympathetic stimulation, we also examined the effect of isoproterenol on these K+ currents. We found that IK1 was significantly increased in hyperkalemia, whereas the reduction of driving force for K+ efflux dominated over the altered channel gating in case of IKr and IKs. Overall, the markedly increased IK1 in hyperkalemia overcame the relative decreases of IKr and IKs during AP, resulting in an increased net repolarizing current during AP phase 3. ß-Adrenergic stimulation of IKs also provided further repolarizing power during sympathetic activation, although hyperkalemia limited IKs upregulation. These results indicate that facilitation of IK1 in hyperkalemia and ß-adrenergic stimulation of IKs represent important compensatory mechanisms against AP prolongation and arrhythmia susceptibility.

New approach to molsidomine active metabolites coming from the results of 2 models of experimental cardiology.

Molsidomine is a well-known vasodilatating, antianginal drug. Despite earlier studies with its metabolites (3-morpholino-syndnonimine (SIN-1) and N-nitroso-N-morpholino-amino-acetonitrile (SIN-1A)), which indicated a potential favorable cardioprotective activity, a lot of controversy remains. The aim of our research was to compare molsidomine, SIN-1, SIN-1A, and lidocaine influence on arrhythmias and hemodynamic parameters in 2 experimental models in rats. In the Langendorff heart study, SIN-1A markedly elevated left ventricular systolic pressure, maximum rise and fall of the first pressure derivative, coronary flow, and myocardial oxygen consumption. In addition, SIN-1A more so than SIN-1 significantly lowered creatine kinase release. The antiarrhythmic action of SIN-1 was observed, while lidocaine significantly diminished ventricular arrhythmias duration in comparison with the control. In the ischemia-reperfusion-induced arrhythmias model, hypotensive action of molsidomine was observed as well as the reduction in pressure rate product. Molsidomine also prolonged ventricular tachycardia duration. On the other hand, no significant effects on hemodynamic parameters as well as on ventricular arrhythmias were found in any of the SIN-1 and SIN-1A groups. In conclusion, our research suggests a possible direct, cardioprotective action of SIN-1A. It seems worthwhile to further investigate molsidomine derivatives, especially SIN-1A, because of its potential use in invasive cardiology procedures such as percutaneous transluminal coronary angioplasty.

Beat-to-beat variability of cardiac action potential duration: underlying mechanism and clinical implications.

Beat-to-beat variability of cardiac action potential duration (short-term variability, SV) is a common feature of various cardiac preparations, including the human heart. Although it is believed to be one of the best arrhythmia predictors, the underlying mechanisms are not fully understood at present. The magnitude of SV is basically determined by the intensity of cell-to-cell coupling in multicellular preparations and by the duration of the action potential (APD). To compensate for the APD-dependent nature of SV, the concept of relative SV (RSV) has been introduced by normalizing the changes of SV to the concomitant changes in APD. RSV is reduced by ICa, IKr, and IKs while increased by INa, suggesting that ion currents involved in the negative feedback regulation of APD tend to keep RSV at a low level. RSV is also influenced by intracellular calcium concentration and tissue redox potential. The clinical implications of APD variability is discussed in detail.

Risk stratification in patients with heart failure: the value of considering both global longitudinal left ventricular strain and mechanical dispersion.

In previous studies, mechanical dispersion (MD) predicted ventricular arrhythmias independently of left ventricular ejection fraction (LVEF). Moreover, the combination of MD and global longitudinal strain (GLS) increased the prediction of arrhythmic events. We investigated the prognostic value of a new 2-dimensional strain index, GLS/MD, in patients with heart failure (HF). We analyzed 340 consecutive HF outpatients in sinus rhythm. Echocardiography was performed at 1.6 ± 0.4 months after hospital discharge. The end point included sudden cardiac death, ventricular fibrillation, and sustained ventricular tachycardia (SCD/VA). During the follow-up period (36 ± 9 months), SCD/VA occurred in 48 patients (14.1%). A multivariate Cox regression analysis, which included LVEF, early diastolic transmitral / mitral annular velocity ratio (E/E'), GLS, MD, and GLS/MD in the model, revealed that GLS/MD was the best independent predictor of SCD/VA (HR = 3.22, 95% confidence interval = 1.72-6.15, p = 0.03). Separate inclusion of LVEF, systolic mitral annular velocity, E/E', GLS, and MD together with GLS/MD showed that GLS/MD remained the best predictor of SCD/VA (each p < 0.05). The optimal GLS/MD cutoff value to predict SCA/VA was -0.20%/ms (80% sensitivity, 76% specificity). Irrespective of LVEF, free survival was significantly better in patients with GLS/MD ≤ -0.2%/ms (log-rank test, p < 0.001). In conclusion, GLS/MD may improve cardiovascular risk stratification in subjects with HF.

Pathophysiology and prevention of sudden cardiac death.

Sudden cardiac death (SCD) is known to occur in individuals with diverse diseases. Each disease state has a specific etiology and pathophysiology, and is diagnosed and treated differently. Etiologies for SCD include cardiac arrhythmias, coronary artery disease, congenital coronary artery anomalies, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, dilated cardiomyopathy, and aortic valve stenosis. A potential unifying mechanism of SCD in these diseases involves a massive stimulation of the sympathetic nervous system's stress response and the subsequent elevation of circulating catecholamines. The diagnosis of cardiac diseases that contribute to an increased risk for SCD is accomplished by a combination of different techniques including electrocardiography, echocardiography, magnetic resonance imaging, and invasive cardiac catheterization. Several therapies including anti-arrhythmic drugs, ß-blockers, and antiplatelet agents may be used as medical treatment in patients for the prevention of SCD. Invasive therapies including percutaneous angioplasty, coronary artery bypass surgery, and implantable cardioverter-defibrillators are also used in the clinical management of SCD.

CLOCK-BMAL1 regulate the cardiac L-type calcium channel subunit CACNA1C through PI3K-Akt signaling pathway.

The heterodimerized transcription factors CLOCK-BMAL1 regulate the cardiomyocyte circadian rhythms. The L-type calcium currents play important role in the cardiac electrogenesis and arrhythmogenesis. Whether and how the CLOCK-BMAL1 regulate the cardiac L-type calcium channels are yet to be determined. The functions of the L-type calcium channels were evaluated with patch clamping techniques. Recombinant adenoviruses of CLOCK and BMAL1 were used in the expression experiments. We reported that the expressions and functions of CACNA1C (the α-subunit of the L-type calcium channels) showed circadian rhythms, with the peak at zeitgeber time 3 (ZT3). The endocardial action potential durations 90 (APD90) were correspondingly longer at ZT3. The protein levels of the phosphorylated Akt at threonine 308 (pAkt T308) also showed circadian rhythms. Overexpressions of CLOCK-BMAL1 significantly reduced the levels of CACNA1C while increasing the levels of pAkt T308 and pik3r1. Furthermore, the inhibitory effects of CLOCK-BMAL1 on CACNA1C could be abolished by the Akt inhibitor MK2206 or the PDK1 inhibitor GSK2334470. Collectively, our findings suggested that the expressions of the cardiac CACNA1C were under the CLOCK-BMAL1 regulation, probably through the PI3K-Akt signal pathway.

Mechanisms increasing n-3 highly unsaturated fatty acids in the heart.

Due to ambiguous findings on cardiovascular benefits of systemic omega-3 fatty acid therapy, endogenous mechanisms contributing to local organ-specific concentrations of highly unsaturated fatty acids (HUFA) were examined. Using gas chromatography, 43 fatty acids were analyzed in atrial and ventricular myocardium and in pericardial fluid of male Wistar rats. To examine the endogenous fatty acid metabolism, precursors were administered into the pericardial sac. Pro- and anti-inflammatory actions were induced by talc or fenofibrate, respectively. Physical exercise and a sedentary obese state were used for increased beta-oxidation. DHA (22:6n-3) was increased in ventricular when compared with atrial myocardium (9.0 ± 2.1% vs. 4.7 ± 1.0%, p < 0.001). Intrapericardial EPA (20:5n-3) application lead to an increase of the succeeding tetracosapentaenoic acid (24:5n-3) in atrial myocardium, which is a key precursor of DHA. In contrast, proinflammatory stimulation of the n-6 HUFA pathway did not influence the n-3 metabolism. Exercise- and obesity-induced increased beta-oxidation, the finalizing step of DHA synthesis, was associated with increased ventricular DHA concentrations (6.7 ± 1.0% vs. 8.4 ± 1.2%, p < 0.01). It is concluded that the endogenous metabolism contributes markedly to myocardial HUFA concentrations. The findings are supposed to influence the efficacy of oral HUFA treatment and provide a rationale for divergent findings of previous trials on omega-3 therapy.

Functional role of myocardial electrical remodeling in diabetic rabbits.

The objective of the study was to investigate the role of electrical remodeling of the ventricular myocardium in hemodynamic impairment and the development of arrhythmogenic substrate. Experiments were conducted with 11 healthy and 12 diabetic (alloxan model, 4 weeks) rabbits. Left ventricular pressure was monitored and unipolar electrograms were recorded from 64 epicardial leads. Aortic banding was used to provoke arrhythmia. The diabetic rabbits had prolonged QTc, with activation-recovery intervals (surrogates for repolarization durations) being relatively short on the left ventricular base and long on the anterior apical portions of both ventricles (P < 0.05). In the diabetic rabbits, a negative correlation (-0.726 to -0.817) was observed between dP/dt(max), dP/dt(min), and repolarization dispersions. Under conditions of systolic overload (5 min), tachyarrhythmias were equally rare and the QTc and activation-recovery intervals were shortened in both groups (P < 0.05), whereas QRS was prolonged in the diabetic rabbits only. The repolarization shortening was more pronounced on the apex, which led to the development of apicobasal and interventricular end of repolarization gradients in the healthy animals, and to the flattening of the repolarization profile in the diabetic group. Thus, the diabetes-related pattern of ventricular repolarization was associated with inotropic and lusitropic impairment of the cardiac pump function.

[Effects of air pollution on cardiovascular events in cardiac intensive care units]. / Effets de la pollution de l'air sur les évènements cardiovasculaires en unité de soins intensifs cardiologiques.

Many environmental factors influence the occurrence of cardiovascular events. Among these, air pollution is certainly the most harmful, due to its dual composition and effects. Air pollution is both particulate and gaseous, and can vary in concentration and composition according to its source and type of emission. Moreover, clinical effects are not only observed at long-term but also at short-term, following rapid deterioration in air quality. Air pollution must therefore be seen both as a risk factor for atherosclerotic disease, and as a trigger for cardiovascular events. These acute effects are essentially mediated by an increased risk of acute coronary syndromes and heart failure. The effects of air pollution on admissions for ventricular arrhythmias and arterial hypertension are also possible. The cardiotoxicity of pollution is mainly mediated by sympatho-vagal imbalance, by the initiation and amplification of an oxidative, inflammatory and pro-aggregatory cascade, and by endothelial dysfunction and activation of metalloproteinases. Although now well established, the consequences of air pollution on acute cardiovascular events require further investigation. Environmental cardiology is an emerging discipline whose current vision still fails to integrate qualitative aspects, such as the oxidative potential of particulate matter, and the joint effects of multiple environmental exposures.

Focus on malignant ventricular premature contractions.

Premature ventricular contractions (PVCs) are common. Although often benign, they can also be associated with increased morbidity and mortality. The aim of this review was to assess the risk evaluation of PVCs in patients with or without structural heart disease and discuss the management of this arrhythmia. Reports published in English were searched in PubMed with the following search terms: premature ventricular contraction, ectopic ventricular beat, ventricular extrasystole, antiarrhythmic drugs, ablation, ventricular arrhythmia, ventricular tachycardia, ventricular fibrillation and torsade de pointe. This analysis suggests that all patients with frequent PVCs should be assessed for PVC burden, symptom status and the presence of structural heart disease. PVCs in patients with structurally normal hearts was once considered a benign phenomenon. Uncommonly, PVCs may provoke life-threatening arrhythmias. Ventricular fibrillation is the initial mode of malignant rapid ventricular arrhythmias (MRVAs). Patients with malignant PVC and PVC burden >10% are at increased risk of MRVA in case of myocardial infarction and heart failure. MRVA is the primary cause of sudden cardiac death in patients with and without structural heart disease. Therapeutic options include medical therapy and catheter ablation, the latter more effective and potentially curable, particularly in patients with left ventricular dysfunction. The timely recognition and effective treatment of malignant PVCs in symptomatic patients with underling cardiomyopathy are mandatory to initiate early therapies before the occurrence of adverse clinical outcomes and to improve the long-term prognosis.

Prospective evolution of cardiac arrhythmia care: 2030 vision.

Cardiovascular diseases, which are the leading global cause of death, should increase by 40% by 2030, reaching close to 24 million deaths worldwide. Atrial fibrillation is the most common heart rhythm disorder, ahead of conduction disturbances and ventricular arrhythmias. Studies estimate that 7.6 million people aged>65 years in the European Union had atrial fibrillation in 2016, and this figure is predicted to increase by 89% to 14.4 million by 2060. Recent innovations in cardiac arrhythmia care, such as cardiac device miniaturization and smart devices, might revolutionize the future of patient care. Yet, the level of adoption of these breakthroughs will depend on their acceptability by patients and healthcare professionals, and on the pace of transformation of the French healthcare system (encouraged by "Ma Santé 2022"). In this article, we detail the major trends that could impact patients with heart rhythm disorders and their healthcare professionals by 2030. Eight major trends and their associated effects on patient care and healthcare professionals' practices were discussed: technical evolution of cardiac devices; digitalization of the healthcare system, and telecardiology; the rise of smart devices; the rise of "big data" and artificial intelligence; patient empowerment; evolution of healthcare; healthcare transformation with "Ma Santé 2022"; and new funding models. These "multidimensional" changes give us room in this study to outline two scenarios for the evolution of care of patients with heart rhythm disorders in the near future.

Physical activity and aerobic fitness in children with inherited cardiac diseases.

BACKGROUND: Because of sports and exercise restrictions, children with inherited cardiac disease are at risk of physical deconditioning. Guidelines on sports participation in cardiovascular disease have become less restrictive over time, but their real-life application and behavioural impact have seldom been evaluated in children. AIMS: We aimed to evaluate adherence to the 2020 European Society of Cardiology guidelines on sports and exercise in children with inherited cardiac arrhythmia and inherited cardiomyopathy; we also sought to evaluate their aerobic fitness, and the behavioural impact of inherited cardiac diseases on physical activity in children. METHODS: Children aged 6-18 years with inherited cardiomyopathy or inherited cardiac arrhythmia were eligible for this cross-sectional study. Clinical, demographic and qualitative data were analysed. RESULTS: A total of 32 children were included in the study (mean age 12.7±3.5 years). Most children (81.3%) complied with the 2020 European Society of Cardiology guidelines; they were physically active and had good overall aerobic fitness, with a mean peak oxygen uptake (VO2) value of 36.5±8.0mL/kg/min (84.0±17.2% of theoretical value). As a result of personal or parental behaviour, some children at risk of sudden cardiac death did not comply with the recommended upper limit of physical activity intensity, whereas others at low risk did not comply with the lower limit. CONCLUSION: Most children with inherited cardiac arrhythmia or inherited cardiomyopathy complied with current 2020 European Society of Cardiology guidelines on sports cardiology and exercise in cardiovascular disease.

Cardiovascular complications of acromegaly.

Acromegaly is a chronic disease due to growth hormone (GH) and insulin-like growth factor 1 (IGF-1) excess. It is associated with various systemic complications including cardiovascular disease. Arterial hypertension occurs in about 20% to 30% of patients. Its pathogenesis is mainly related to the increase in plasma volume secondary to a sodium retaining actions of GH and IGF-1 in the kidney, but abnormalities in vessel architecture and reactivity participate. Left ventricular hypertrophy and diastolic dysfunctions were frequently reported in echo-based studies and are mostly mild and without clinical consequences. Recent cardiac MRI studies described a much lower frequency of myocardial hypertrophy than echo-based assessments. Progression to systolic dysfunction with congestive heart failure is nowadays very rare. Risk of coronary heart disease and of clinically significant arrythmias does not seem to be increased. Acromegaly-related cardiac valve abnormalities may be related to fibrotic changes and seem to persist after effective treatment of acromegaly. Advances in acromegaly treatment over the last decades significantly diminished the cardiovascular burden of the disease, with the cardiovascular disease anymore being the leading cause of death.

[COVID-19 and arrhythmias]. / COVID-19 et troubles du rythme.

In the pandemic caused by the SARS-CoV2 virus, arrhythmias were not in the foreground. However, the virus seems to affect many organs and the cardiac tropism is now well known. Knowledge in this area is still far from exhaustive, but several series published concerning patients with COVID-19 find a significant proportion of arrhythmias, some of which can potentially lead to a fatal outcome. These rhythm disorders are mainly supraventricular, such as atrial fibrillation (AF) or flutter but also ventricular disorders like ventricular tachycardias (VT) ventricular fibrillation (VF) and more rarely torsades de pointe (TdP). The causes are multiple, due to the multiorgan damage caused by the virus and potential drug interactions. In addition, the question of monitoring rhythm disorders that may emerge in the medium and long term after an infection remains to be explored.

Incidence, clinical features and outcome of Takotsubo syndrome in the intensive care unit.

BACKGROUND: Most diseases encountered in the intensive care unit are associated with major stress that can potentially trigger Takotsubo syndrome. Many severe cardiovascular complications are associated with Takotsubo syndrome, yet little is known about Takotsubo syndrome in the intensive care unit. AIMS: We sought to determine the incidence of Takotsubo syndrome, and to describe its clinical features and outcome in an intensive care unit. METHODS: This prospective single-centre study included all patients admitted consecutively over a 12-month period who had transthoracic echocardiography, electrocardiography and a troponin I assay performed on admission, at 24 and 48hours after admission, and at discharge and in the case of clinical worsening. RESULTS: The incidence of Takotsubo syndrome was 4.6% (13/280 patients) and female sex predominated (69.2%). The median age of the subgroup with Takotsubo syndrome was 64 (56-72) years. Pulmonary disease and sepsis were the most frequent triggers (46.2% and 38.5%, respectively). Median left ventricular ejection fraction was 29.0% (20.0-37.0). Patients with Takotsubo syndrome presented with shock and arrhythmias and needed ventilation more frequently than patients without Takotsubo syndrome (69.2% vs. 36.3%, P=0.035; 46.2% vs. 13.5%, P=0.006; and 92.3% vs. 60.7%, P=0.021), but mortality rates were similar. The median delay to cardiac index recovery, when impaired, was 2.0 (1.0-2.75) days, and that of left ventricular ejection fraction was 12.5 (7-14.75) days. CONCLUSION: Takotsubo syndrome in the intensive care unit is not uncommon and is associated with substantial haemodynamic and respiratory instability. New-onset arrhythmias and respiratory and haemodynamic worsening could arouse suspicion of and prompt screening for Takotsubo syndrome in the intensive care unit.

Risk of thromboembolic complications in adult congenital heart disease: A literature review.

Adult congenital heart disease (ACHD) is a constantly expanding population with challenging issues. Initial medical and surgical treatments are seldom curative, and the majority of patients still experience late sequelae and complications, especially thromboembolic events. These common and potentially life-threating adverse events are probably dramatically underdiagnosed. Better identification and understanding of thromboembolic risk factors are essential to prevent long-term related morbidities. In addition to specific situations associated with a high risk of thromboembolic events (Fontan circulation, cyanotic congenital heart disease), atrial arrhythmia has been recognized as an important risk factor for thromboembolic events in ACHD. Unlike in patients without ACHD, thromboembolic risk stratification scores, such as the CHA2DS2-VASc score, may not be applicable in ACHD. Overall, after a review of the scientific data published so far, it is clear that the complexity of the underlying congenital heart disease represents a major risk factor for thromboembolic events. As a consequence, prophylactic anticoagulation is indicated in patients with complex congenital heart disease and atrial arrhythmia, regardless of the other risk factors, as opposed to simple heart defects. The landscape of ACHD is an ongoing evolving process, and specific thromboembolic risk scores are needed, especially in the setting of simple heart defects; these should be coupled with specific trials or long-term follow-up of multicentre cohorts.

Electrical storm in the early phase of HeartMate® II device implantation: Incidence, risk factors and prognosis.

BACKGROUND: Ventricular arrhythmia is common after left ventricular assist device (LVAD) implantation, especially in the early postoperative phase (<30 days). AIM: To identify the incidence of and risk factors for electrical storm (ES) occurring within 30 days of HeartMate® II implantation. METHODS: We reviewed data from all consecutive patients undergoing HeartMate® II device implantation at our institution from January 2008 to December 2014. Patient demographic data, pharmacotherapies and outcomes were collected. The primary endpoint was occurrence of early ES (within 30 days of surgery), defined as three or more separate episodes of sustained ventricular arrhythmia within a 24-hour interval, requiring appropriate therapy. RESULTS: Forty-three patients (mean age 56.7±11.2 years; 39 men) were included. At HeartMate® II implantation, mean left ventricular ejection fraction was 20±5%, 32 (74.4%) patients had ischaemic cardiomyopathy and 31 (72.1%) were implanted with an indication of bridge to cardiac transplantation. During follow-up, 12 (27.9%) patients experienced early ES after HeartMate® II implantation (median delay 9.1±7.8 days). Early ES was more frequent in larger patients (body surface area 1.99 vs 1.81 m2; P<0.01), tended to be associated with previous sustained ventricular tachycardia (50.0% vs 22.6%; P=0.08), previous implantable cardioverter-defibrillator implantation (66.7% vs 38.7%; P=0.09), discontinuation of long-term beta-blocker therapy (75.0% vs 45.2%; P=0.08), weaning of adrenergic drugs after the third day (66.7% vs 35.5%; P=0.06) and the use of extracorporeal life support (50% vs 22.6%; P=0.079), but was not associated with the cardiomyopathy aetiology or the indication for assistance. Catheter ventricular tachycardia ablation was performed in six (14.0%) patients. Early ES was associated with a significantly higher all-cause mortality rate at the 30th day (33.3% vs 6.5%; P=0.02). CONCLUSION: ES is a common and pejorative feature in the early postoperative period.

[Is it worth delivering Direct-Current Counter shock to critically ill patients with supra-ventricular tachyarrhythmia?] / Vaut-il la peine de délivrer un choc électrique aux patients de réanimation avec tachycardie supra-ventriculaire ?

Supra-ventricular tachyarrhythmia and its treatment have been poorly investigated in ICU patients. AIMS: To evaluate efficacy and safety of cardioversion for supra-ventricular tachyarrhythmia in the intensive care unit (ICU). PATIENTS AND METHODS: Prospective inclusion of all patients who presented supra-ventricular tachyarrhythmias lasting≥30seconds in a single medico-surgical ICU, except cardiac surgery. Anti-arrhythmic drugs and/or direct-current cardioversion were administered on a liberal basis. RESULTS: During the 15-month study period, 108/846 patients (12.8%) experienced supra-ventricular tachyarrhythmias. Anti-arrhythmic drugs were administered in 78 patients (72%); mostly amiodarone (92%), and/or magnesium (23%), resulting in an overall conversion rate of 68%. Direct-current cardioversion was used in 26 patients (24%), (24 patients received drug enhancement by anti-arrhythmic drugs) with an immediate 80.8%-success rate. CONCLUSION: Direct-current cardioversion was associated with sustained conversion to sinus rhythm in 80.8% of ICU patients with supra-ventricular tachyarrhythmias, although most of them had already received drug enhancement.