Heart rhythm : the official journal of the Heart Rhythm Society
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Depending on the ablation strategy, up to 30% to 50% of patients will develop an atrial tachycardia after undergoing radiofrequency catheter ablation of atrial fibrillation. This review discusses the mechanisms, mapping techniques, and catheter ablation of atrial tachycardias that occur after radiofrequency ablation of atrial fibrillation.
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The following briefly reviews features and management of long QT syndrome (LQTS), Brugada Syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), and short QT syndrome (SQTS). LQTS is marked by QT prolongation, syncope and sudden death due to torsades de pointes. Risk stratification is based on age, gender, history of symptoms, QT interval, and genetic subtype of LQTS. ⋯ Treatment modalities include anti-adrenergic therapy and ICD implantation. Congenital SQTS is a relatively recently described disorder characterized by a very short QT interval and by susceptibility to atrial and ventricular fibrillation. ICD implantation is the primary therapy; quinidine may be a useful adjunctive therapy.
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Paroxysmal atrioventricular block (AVB) is a poorly defined clinical entity characterized by abrupt and unexpected change from 1:1 atrioventricular conduction to complete heart block, leading to syncope and potential sudden cardiac death. Although a dangerous condition because of unreliable escape mechanism, proper diagnosis of paroxysmal AVB is often missed and overlooked because of its unfamiliarity, unpredictability, and in some cases, no clear evidence of atrioventricular conduction disease during normal 1:1 conduction.
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Functional characterization of mutations involving the SCN5A-encoded cardiac sodium channel has established the pathogenic mechanisms for type 3 long QT syndrome and type 1 Brugada syndrome and has provided key insights into the physiological importance of essential structure-function domains. ⋯ A severe clinical phenotype characterized by fever-induced monomorphic ventricular tachycardia and QT interval prolongation emerged in a toddler with compound heterozygosity involving SCN5A: R34fs/60, and R1195H. Unexpectedly, the 94-amino-acid fusion peptide derived from the R34fs/60 mutation accentuated the late sodium current of R1195H-containing Na(V)1.5 channels in vitro.
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Repolarization abnormality, especially during bradycardia, might be critical for initiation of ventricular fibrillation (VF) in patients with Brugada syndrome (BrS), but the contribution of the rate-dependent repolarization dynamics to the occurrence of VF is still unknown. ⋯ Loss of rate-dependent QT dynamics may be associated with occurrence of VF in BrS.