Novel assessment of temporal variation in fractionated electrograms using histogram analysis of local fractionation interval in patients with persistent atrial fibrillation.

BACKGROUND: The characteristics of atrial electrograms associated with atrial fibrillation (AF) termination are controversial. We investigated the electrogram characteristics that indicate procedural AF termination during continuous complex fractionated electrogram ablation. METHODS AND RESULTS: Fifty-two consecutive patients with persistent AF (47 men; aged 54 ± 9 years), who underwent electrogram-based catheter ablation in the left atrium and coronary sinus after pulmonary vein isolation, were enrolled. The intracardiac bipolar atrial electrogram recordings were characterized by (1) fractionation interval (FI) analysis (>6 seconds), (2) kurtosis (shape of the FI histogram), and (3) skewness (asymmetry of the FI histogram). Sites showing complex, fractionated electrograms (mean FI ≤ 60 ms) were targeted, and AF was terminated in 20 patients (38%) after the pulmonary vein isolation. The conventional complex fractionated electrogram sites (mean ≤ 120 ms) in patients with AF termination exhibited higher median kurtosis (2.69 [interquartile range, 2.03-3.46] versus 2.35 [interquartile range, 1.79-2.48]; P=0.024) and higher complex fractionated electrogram-mean interval (102.7 ± 19.8 versus 87.7 ± 15.0; P=0.008) than patients without AF termination. Furthermore, AF termination sites had higher median kurtosis than targeted sites without AF termination (5.13 [interquartile range, 3.51-6.47] versus 4.18 [interquartile range, 2.91-5.34]; P<0.01) in patients with procedural termination. In addition, patients with AF termination had a higher sinus rhythm maintenance rate after a single procedure than patients without AF termination (log-rank test, P=0.007). CONCLUSIONS: A kurtosis analysis using the FI histogram may be a useful tool in identifying the critical substrate for persistent AF and potential responders to catheter ablation.

Susceptibility genes for coronary heart disease and myocardial infarction.

Coronary heart disease and its main complication, myocardial infarction is leading cause of death worldwide. Over the past years, much progress has been made in the pharmacotherapy of major risk factors like dyslipidemias, diabetes mellitus and hypertension. The targeting of coronary risk factors coupled with advances in the management of coronary artery disease has improved patient survival. However, the incidence of cardiovascular disease is projected to continue to rise and the identification of individuals at risk should improve beyond the traditional models of global risk factor scoring. In the past few years, important progresses have been made in the area of genomics, especially with the completion of the human genome-sequencing Consortium of 2004, proteomics and imaging. This progress will promote a better understanding of cardiovascular risk assessments and disease prediction, thus allowing earlier preventive strategies to prevent and improve cardiovascular outcomes. These genomic advances have improved characterization of disease pathology especially at the molecular level with the discovery and introduction of genetic markers, single nucleotide polymorphisms (SNPs), and haplotype blocks.