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Obstructive sleep apnea (OSA) is increasingly recognized as an important risk factor for arrhythmogenesis. Epidemiological and clinical studies have suggested a strong association between OSA and atrial fibrillation (AF). With the increasing global epidemic of obesity, the incidence of OSA is also expected to rise. Various mechanisms mediated through adverse electrical and structural changes have been proposed to explain the increased risk of AF in patients with OSA. Multiple studies have also observed a greater risk of AF recurrence after cardioversion and catheter ablation (CA) in the patients with untreated OSA. The epidemiological and pathophysiological associations between OSA and AF have significant implications on the treatment outcomes of rhythm-control strategies for AF. Adequate screening and optimal management of OSA are of key importance to help improve the clinical outcomes following cardioversion and CA. In this review, we sought to describe the role of various mechanisms by which OSA mediates the pathogenesis of AF and contributes to adverse outcomes following CA.

Notch signaling has previously been shown to play an essential role in regulating cell fate decisions and differentiation during cardiogenesis in many systems including Drosophila, Xenopus, and mammals. We hypothesized that Notch may also be involved in directing the progressive lineage restriction of cardiomyocytes into specialized conduction cells.

The single-procedure efficacy of pulmonary vein isolation (PVI) is less than optimal in patients with persistent atrial fibrillation (AF). Adjunctive techniques have been developed to enhance single-procedure efficacy in these patients. We conducted a study to compare 3 ablation strategies in patients with persistent AF.

Pluripotent stem cells represent one promising source for cellular cardiomyoplasty. In this study, we used cardiac magnetic resonance to examine the ability of highly enriched cardiomyocytes (CMs) derived from murine embryonic stem cells (ESC) to form grafts and improve contractile function of infarcted rat hearts.

With the continued development of genetically engineered mouse models of cardiac disease, further advancement of noninvasive techniques for evaluating cardiac diastolic dysfunction in these models would be valuable. Therefore, we performed comprehensive transmitral and pulmonary venous Doppler echocardiographic studies to devise novel indices of diastolic function in a mouse model with cardiac hypertrophy, which were validated against invasively measured hemodynamic parameters. We examined 10 HopXTgtransgenic mice with diastolic dysfunction and 10 age-matched controls sedated with 1% to 2% isoflurane (male, age 14–18 weeks). These studies revealed that the acceleration time of the transmitral Doppler E-wave was the best Doppler parameter for unmasking LV diastolic dysfunction in HopXTgmice. This is the first study to assess the utility of the acceleration time of the E-wave and pulmonary venous Doppler echocardiography as a primary diagnostic modality for assessing murine diastolic function.

Programmed ventricular stimulation is being performed for the provocation of ventricular arrhythmias in genetically engineered mice. Despite the high level of interest in this area of translational research, little attention has been given to differentiating between selectivity and specificity of induced ventricular tachycardia (VT) in phenotypically normal mice. We aimed to assess factors that may enhance inducibility of VT in wild-type (WT) mice. In vivo intracardiac electrophysiological studies (EPS) were performed in 230 WT mice of 4 strains. An octapolar electrode catheter was inserted into a jugular vein and advanced to the right atrium and ventricle. Baseline ventricular conduction, refractoriness, and arrhythmia inducibility were assessed using programmed electrical stimulation (PES) and burst pacing. We found that nonsustained VT (≥4 beats) was inducible in 68/230 (30%) mice. Duration of VT was 1.6 ± 2.4 s, and the longest episode lasted 24 s. VT inducibility differed by strain and age. Ventricular effective refractory period (VERP) was shorter in mice with inducible VT (44 ± 12 ms) compared with noninducible mice (61 ± 16 ms, P< 0.001). VERP increased with age (P< 0.001), albeit with strain-related variability. We conclude that nonsustained VT in WT mice is reproducibly inducible and common. Genetic background variability may predispose certain strains to a higher incidence of arrhythmia induction. EPS methods impact prevalence and specificity of inducible VT. Increased VT inducibility was seen with shorter coupling intervals and application of tightly coupled extrastimuli techniques. These factors should be carefully considered when analyzing PES and burst pacing data in murine models to minimize false positives and optimize accuracy.