May Fever Trigger Ventricular Fibrillation?

The clinical precipitants of ventricular fibrillation (VF) remain poorly understood. Clinical factors such as hypoxemia, acidosis or electrolyte imbalance, drug-related toxicity, autonomic nervous system disorders as well as viral myocarditis have been proposed to be associated with sudden cardiac death particularly in patients with structural heart disease. However, In the Brugada syndrome, concurrent febrile illness has been reported to unmask the electrocardiographic features of the Brugada syndrome and be associated with an increased propensity for VF. More recently, a febrile illnesses of infectious etiology was associated to polymorphic ventricular tachycardia or VF in patients with normal hearts and without known repolarization abnormality. In this review we detail this phenomenon and its putative mechanisms

Atrial fibrillation and its determinants after radiofrequency ablation of chronic common atrial flutter

Aim. Atrial fibrillation (AFib) is a major clinical issue and its occurrence is the main problem after catheter ablation of atrial flutter. The long-term occurrence of AFib after common atrial flutter ablation is still matter of debate as it may influence the therapeutic approach. So, the aim of our study was to analyze the determinants and the time course of AFib after radiofrequency catheter ablation of chronic common atrial flutter. Methods and Results. 89 consecutive patients (67.5 ± 12.0 yrs) underwent RF ablation of chronic common atrial flutter. 38.2 % had previous history of paroxysmal AFib. 51% had no underlying structural heart disease. Over a mean follow-up of 38 ± 13 months, the occurrence rate of AFib progressively increased up to 32.9% at the end of follow-up. The median occurrence time for AFib was 8 months. AFib occurrence was significantly associated with previous AFib history (P=0.01) but not with the presence of underlying heart disease (P=n.s.). Of particular interest, in our study, AFib never occurred in patients without previous AFib history. Palpitations after chronic common atrial flutter ablation was mostly related to AFib. Conclusion. In conclusion, after chronic common atrial flutter ablation, AFib incidence progressively increased over the follow-up in all patients. Patients with prior AFib history appeared to be a very high risk group. In these patients, closer monitoring is mandatory and the persistent risk of AFib recurrences may justify prolonged anticoagulation policy

Acute Myocarditis Induced by Hepatitis E: An Uncommon Association

International audienceAcute myocarditis is often caused by viral infections. Hepatitis E infection inflicts over 20 million people worldwide each year. Common extra-hepatic manifestations of hepatitis E infection include neurologic, hematologic, and renal sequelae.1 Acute myocarditis, defined by the presence of myocardial inflammatory infiltrates associated with nonischemic myocytic necrosis, is uncommon. Published reports of such cases are limited, and here we present the case of a 45-year-old man with acute myocarditis from hepatitis E infection. This case is the first described in Europe of acute myocarditis associated with hepatitis E infection

New drugs vs. old concepts: A fresh look at antiarrhythmics

International audienceCommon arrhythmias, particularly atrial fibrillation (AF) and ventricular tachycardia/fibrillation (VT/VF) are a major public health concern. Classic antiarrhythmic (AA) drugs for AF are of limited effectiveness, and pose the risk of life-threatening VT/VF. For VT/VF, implantable cardiac defibrillators appear to be the unique, yet unsatisfactory, solution. Very few AA drugs have been successful in the last few decades, due to safety concerns or limited benefits in comparison to existing therapy. The Vaughan-Williams classification (one drug for one molecular target) appears too restrictive in light of current knowledge of molecular and cellular mechanisms. New AA drugs such as atrial-specific and/or multichannel blockers, upstream therapy and anti-remodeling drugs, are emerging. We focus on the cellular mechanisms related to abnormal Na + and Ca 2+ handling in AF, heart failure, and inherited arrhythmias, and on novel strategies aimed at normalizing ionic homeostasis. Drugs that prevent excessive Na + entry (ranolazine) and aberrant diastolic Ca 2+ release via the ryanodine receptor RyR2 (rycals, dantrolene, and flecainide) exhibit very interesting antiarrhythmic properties. These drugs act by normalizing, rather than blocking, channel activity. Ranolazine preferentially blocks abnormal persistent (vs. normal peak) Na + currents, with minimal effects on normal channel function (cell excitability, and conduction). A similar "normalization" concept also applies to RyR2 stabilizers, which only prevent aberrant opening and diastolic Ca 2+ leakage in diseased tissues, with no effect on normal function during systole. The different mechanisms of action of AA drugs may increase the therapeutic options available for the safe treatment of arrhythmias in a wide variety of pathophysiological situations

Generation of catecholaminergic polymorphic ventricular tachycardia patient-specific induced pluripotent stem cell line

International audienc