High-density Mapping Guided Pulmonary Vein Isolation for Treatment of Atrial Fibrillation - Two-year clinical outcome of a single center experience.

Pulmonary vein isolation (PVI) as interventional treatment for atrial fibrillation (AF) aims to eliminate arrhythmogenic triggers from the PVs. Improved signal detection facilitating a more robust electrical isolation might be associated with a better outcome. This retrospective cohort study compared PVI procedures using a novel high-density mapping system (HDM) with improved signal detection vs. age- and sex-matched PVIs using a conventional 3D mapping system (COM). Endpoints comprised freedom from AF and procedural parameters. In total, 108 patients (mean age 63.9 ± 11.2 years, 56.5% male, 50.9% paroxysmal AF) were included (n = 54 patients/group). Our analysis revealed that HDM was not superior regarding freedom from AF (mean follow-up of 494.7 ± 26.2 days), with one- and two-year AF recurrence rates of 38.9%/46.5% (HDM) and 38.9%/42.2% (COM), respectively. HDM was associated with reduction in fluoroscopy times (18.8 ± 10.6 vs. 29.8 ± 13.4 min; p < 0.01) and total radiation dose (866.0 ± 1003.3 vs. 1731.2 ± 1978.4 cGy; p < 0.01) compared to the COM group. HDM was equivalent but not superior to COM with respect to clinical outcome after PVI and resulted in reduced fluoroscopy time and radiation exposure. These results suggest that HDM-guided PVI is effective and safe for AF ablation. Potential benefits in comparison to conventional mapping systems, e.g. arrhythmia recurrence rates, have to be addressed in randomized trials.

[A rest or arrest--asystolic episodes of 7 seconds in a 22-year-old athlete]. / 22-jähriger Sportler mit Sinusarrest und Pausen bis 7 Sekunden.

A 22-year-old athlete with nocturnal asymptomatic episodes of transient sinus arrest/sinoatrial block up to 7.3 s and recurrent inappropriate sinus tachycardias which had been incidentally found during Holter electrocardiography diagnostics is presented. In spite of extensive diagnostic work-up including invasive procedures like coronary angiography and electrophysiological study, no causal etiology was found. Based on the normal findings and the lack of symptoms, we decided not to implant a permanent pacemaker. After 14 months, the patient is still asymptomatic. Howerver, the 24-h Holter electrocardiography shows unchanged frequency of nocturnal transient sinus arrest episodes.

[Genetics of atrial fibrillation: rare mutations, common variants and clinical relevance?]. / Genetik von Vorhofflimmern: seltene Mutationen, häufige Genvarianten und klinische Relevanz?

Atrial fibrillation (AF) is considered the, by far, the most common arrhythmia of man, affecting millions of patients worldwide. The high socio-economic relevance is due to several severe complications and therefore requires profound scientific research in the field of etiology and treatment options. Atrial fibrillation typically occurs in the older patient who often suffers from a number of underlying diseases that act as predisposing factors. That genetics contribute strongly to this rhythm disorder is therefore not evident at a first glance. However, there are a number of investigations that prove familial accumulation for lone AF. Furthermore it is remarkable that many older patients suddenly develop atrial fibrillation without underlying disease, while others remain in sinus rhythm although suffering from a series of risk factors. Considering all this, genetic interference becomes most probable. Therefore in the recent past remarkable endeavours have been ventured to clarify the genetic basis of both lone AF and AF in the context of underlying diseases. For the former, until now four different genetic loci and three disease genes have been identified as causative. Concerning AF in the general population, mainly studies turning the spotlight on single-nucleotide polymorphisms (SNPs) have been applied. It is assumed that SNPs in disease-causing genes are distributed differentially among healthy and diseased individuals. These differences in frequency have been investigated with case-control studies. Up to now six different genes have been found to be associated with AF, including the genes for angiotensin-converting enzyme, angiotensinogen and several cardiac ion channels. Promising new technologies, especially high-throughput SNP genotyping and the genome wide scan for new candidate genes using chip arrays capable of genotyping up to 500 000 SNPs at a time, will multiply the speed to achieve new results. With that the possibility, approaches to optimize existing therapies and to open up new pathways to treat AF.