Impact of pulmonary vein isolation on obstructive sleep apnea in patients with atrial fibrillation

Background: Obstructive sleep apnea (OSA) has been identified as associated with the onset and propagation of atrial fibrillation (AF) and predicts recurrences of AF after pulmonary vein isolation (PVI). Vice versa, it has never been investigated whether PVI influences OSA. However, it has been controversial whether a restored atrial function can affect the course of OSA. There­fore, we have assessed whether PVI procedure modulates the prevalence and severity of OSA. Methods and Results: We included 23 individuals with AF that were assigned to undergo PVI into this study. Patients were 65 ± 7 years old, obese (BMI 29.9 ± 5.4 kg/m2), white (100%) and had a normal left ventricular function (LVEF 64 ± 9%). Polygraphic assessment was carried out before and 6 months after PVI. The prevalence of OSA, defined as an apnea-hypopnea index (AHI) ≥ 5 per hour of sleep, was 74% before PVI compared to 70% 6 months after the procedure (p > 0.05). Severity of OSA did not differ (AHI before vs. after: 18 ± 18/h vs. 15 ± 17/h, p > 0.05) as well as further polygraphic parameters did not differ before and after the procedure. Conclusions: Prevalence and severity of OSA are not affected by PVI in patients suffering from AF.

Total beta-adrenoceptor knockout slows conduction and reduces inducible arrhythmias in the mouse heart.

INTRODUCTION: Beta-adrenoceptors (β-AR) play an important role in the neurohumoral regulation of cardiac function. Three β-AR subtypes (β(1), β(2), β(3)) have been described so far. Total deficiency of these adrenoceptors (TKO) results in cardiac hypotrophy and negative inotropy. TKO represents a unique mouse model mimicking total unselective medical β-blocker therapy in men. Electrophysiological characteristics of TKO have not yet been investigated in an animal model. METHODS: In vivo electrophysiological studies using right heart catheterisation were performed in 10 TKO mice and 10 129SV wild type control mice (WT) at the age of 15 weeks. Standard surface ECG, intracardiac and electrophysiological parameters, and arrhythmia inducibility were analyzed. RESULTS: The surface ECG of TKO mice revealed a reduced heart rate (359.2±20.9 bpm vs. 461.1±33.3 bpm; p<0.001), prolonged P wave (17.5±3.0 ms vs. 15.1±1.2 ms; p = 0.019) and PQ time (40.8±2.4 ms vs. 37.3±3.0 ms; p = 0.013) compared to WT. Intracardiac ECG showed a significantly prolonged infra-Hisian conductance (HV-interval: 12.9±1.4 ms vs. 6.8±1.0 ms; p<0.001). Functional testing showed prolonged atrial and ventricular refractory periods in TKO (40.5±15.5 ms vs. 21.3±5.8 ms; p = 0.004; and 41.0±9.7 ms vs. 28.3±6.6 ms; p = 0.004, respectively). In TKO both the probability of induction of atrial fibrillation (12% vs. 24%; p<0.001) and of ventricular tachycardias (0% vs. 26%; p<0.001) were significantly reduced. CONCLUSION: TKO results in significant prolongations of cardiac conduction times and refractory periods. This was accompanied by a highly significant reduction of atrial and ventricular arrhythmias. Our finding confirms the importance of β-AR in arrhythmogenesis and the potential role of unspecific beta-receptor-blockade as therapeutic target

Probability of induction of arrhythmias.

<p>The probability of induction of AF was significantly lower in TKO compared to WT. The probability of induction of VTs was highly significant lower in TKO as in this group not any VTs could be induced during the electrophysiological study. n = 10 for TKO and n = 10 for WT.</p

Induction of atrial fibrillation.

<p>Representative tracings of A: TKO mice and B: WT mice. Atrial burst stimulation close to the refractory period (S1S1: 30 ms) failed to induce atrial fibrillation (AF) in TKO. The same burst led to the induction of an AF episode in WT that terminated spontaneously after 8.7 seconds. Surf: Surface ECG. His: Intracardiac ECG close to His bundle.</p

Induction of ventricular tachycardias.

<p>Representative tracings of A: TKO mice and B: WT mice. Ventricular extrastimulus (VES) pacing close to the ventricular refractory time did not lead to ventricular tachycardias (VTs) in TKO mice (S1S2: 40 ms). In WT a short VT was induced by VES pacing (S1S2: 30 ms). Surf: Surface ECG. His: Intracardiac ECG close to HIS bundle.</p