Prediction of atrial fibrillation development and progression:current perspectives

Atrial fibrillation(AF) is the most common arrhythmia in clinical practice. Several conventional and novel predictors of AF development and progression(from paroxysmal to persistent and permanent types) have been reported. The most important predictor of AF progression is possibly the arrhythmia itself. The electrical, mechanical and structural remodeling determines the perpetuation of AF and the progression from paroxysmal to persistent and permanent forms. Common clinical scores such as the hypertension, age ≥ 75 years, transient ischemic attack or stroke, chronic obstructive pulmonary disease, and heart failure and the congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, stroke/transient ischemic attack, vascular disease, age 65-74 years, sex category scores as well as biomarkers related to inflammation may also add important information on this topic. There is now increasing evidence that even in patients with so-called lone or idiopathic AF, the arrhythmia is the manifestation of a structural atrial disease which has recently been defined and described as fibrotic atrial cardiomyopathy. Fibrosis results from a broad range of factors related to AF inducing pathologies such as cell stretch, neurohumoral activation, and oxidative stress. The extent of fibrosis as detected either by late gadolinium enhancement-magnetic resonance imaging or electroanatomic voltage mapping may guide the therapeutic approach based on the arrhythmia substrate. The knowledge of these risk factors may not only delay arrhythmia progression, but also reduce the arrhythmia burden in patients with first detected AF. The present review highlights on the conventional and novel risk factors of development and progression of AF.

Ibutilide and novel indexes of ventricular repolarization in persistent atrial fibrillation patients

AIM: To examine the effect of ibutilide on novel indexes of repolarization in patients with persistent atrial fibrillation (AF). METHODS: We studied consecutive patients scheduled for elective electrical cardioversion. Intravenous ibutilide (1+1mg) was administered before the electrical cardioversion while close electrocardiographic (ECG) monitoring was performed. ECG indexes such as corrected QT interval (QTc), the interval from the peak until the end of T wave (Tpe), and the Tpe/QT ratio were measured before ibutilide infusion and 10 min after the end of infusion. RESULTS: The final study population consisted of 20 patients (mean age: 67.1±9.9 years, 10 men). Six patients were cardioverted pharmacologically and did not proceed to electrical cardioversion. Two patientsdeveloped short non-sustained episodes of torsades de pointes ventricular tachycardia. All but one of the aforementioned ECG indexes increased significantly after ibutilide administration. In specific, the QTc interval increased from 442 ± 29 to 471 ± 37 ms (P=0.037), the Tpe interval in precordial leads from 96 ms (range 80-108 ms) to 101 ms (range 91-119 ms) (P=0.021), the Tpe interval in lead Ⅱ from 79 ms (range 70-88 ms) to 100 ms (range 87-104 ms) (P<0.001), the Tpe/QT ratio in precordial leads from 0.23 ms (range 0.18-0.26 ms) to 0.26 ms (range 0.23-0.28 ms) (P=0.028), and the Tpe interval dispersion from 25 ms (range 23-30 ms) to 35 ms (range 27-39 ms) (P=0.012). However, the Tpe/QT ratio in lead II did not change significantly. CONCLUSION: Ibutilide increases the duration and dispersion of ventricular repolarization. The prognostic value of Tpe and Tpe/QT in the setting of drug-induced proarrhythmia needs further study.

Mechanisms of drug-induced proarrhythmia in clinical practice

Drug-induced proarrhythmia represents a great challenge for those involved in the development of novel pharmaceuticals and in the regulatory bodies for drug approval as well as for the prescribing clinicians.Our understanding of the mechanisms that underlie druginduced proarrhythmia has grown dramatically over the last two decades.A growing number of cardiac and non-cardiac agents have been shown to alter cardiac repolarization predisposing to fatal cardiac arrhythmias such as ventricular tachycardia or ventricular fibrillation and sudden cardiac death.These agents may induce the phenotype of long QT syndrome and less commonly of short QT syndrome and Brugada syndrome(BS).Although,genetic susceptibility underlie drug-induced proarrhythmia in certain cases,current data are limited regarding this topic.The present review surveys the current published literature on the mechanisms and the offending medical agents that predispose to drug-induced long QT syndrome,short QT syndrome and BS.Drug-induced proarrhythmia should be considered as a predictor of sudden cardiac death and should prompt critical re-evaluation of the risks and benefits of the suspicious medication.Survivors of drug-induced proarrhythmia and family members require careful examination and possibly genetic testing for the presence of a channelopathy.Treating physicians are advised to follow the lists of agents implicated in drug-induced proarrhythmia in order to minimize the risk of arrhythmia and sudden cardiac death.

A review on atrioventricular junction ablation and pacing for heart rate control of atrial fibrillation

Atrioventricular junction ablation with permanent pacemaker implantation is a highly effective treatment approach in patients with atrial fibrillation and high ventricular rates resistant to other treatment modalities, especially in the elderly or those with severe comorbidities. Compared with pharmacological therapy alone, the so-called ＂ablate and pace＂ approach offers the potential for more robust control ofven- tricular rate. Atrioventricular junction ablation and pacing strategy is associated with improvement in symptoms, quality of life, and exercise capacity. Given the close relationship between atrial fibrillation and heart failure, there is a particular benefit of such a rate control in patients with atrial fibrillation and reduced systolic fimction. There is increasing evidence that cardiac resynchronization therapy devices may be beneficial in selected populations after atrioventricular junction ablation. The present review article focuses on the current recommendations for atrioventricular junction ablation and pacing for heart rate control in patients with atrial fibrillation. The technique, the optimal implanta- tion time, and the proper device selection after atrioventricular junction ablation are also discussed.