Inhibition of atrial fibrillation by low-level vagus nerve stimulation: the role of the nitric oxide signaling pathway

Purpose

We examined the role of the phosphatidylinositol-3 kinase (PI3K)/nitric oxide (NO) signaling pathway in low-level vagus nerve stimulation (LLVNS)-mediated inhibition of atrial fibrillation (AF).

Methods

In 17 pentobarbital anesthetized dogs, bilateral thoracotomies allowed the attachment of electrode catheters to the superior and inferior pulmonary veins and atrial appendages. Rapid atrial pacing (RAP) was maintained for 6 h. Each hour, programmed stimulation was used to determine the window of vulnerability (WOV), a measure of AF inducibility, at all sites. During the last 3 h, RAP was overlapped with right LLVNS (50 % below that which slows the sinus rate). In group 1 (n?=?7), LLVNS was the only intervention, whereas in groups 2 (n?=?6) and 3 (n?=?4), the NO synthase inhibitor N ^G-nitro-l-arginine methyl ester (l-NAME) and the PI3K inhibitor wortmannin, respectively, were injected in the right-sided ganglionated plexi (GP) during the last 3 h. The duration of acetylcholine-induced AF was determined at baseline and at 6 h. Voltage–sinus rate curves were constructed to assess GP function.

Results

LLVNS significantly decreased the acetylcholine-induced AF duration by 8.2?±?0.9 min (p?<?0.0001). Both l-NAME and wortmannin abrogated this effect. The cumulative WOV (the sum of the individual WOVs) decreased toward baseline with LLVNS (p?<?0.0001). l-NAME and wortmannin blunted this effect during the fifth (l-NAME only, p?<?0.05) and the sixth hour (l-NAME and wortmannin, p?<?0.05). LLVNS suppressed the ability of GP stimulation to slow the sinus rate, whereas l-NAME and wortmannin abolished this effect.

Conclusion

The anti-arrhythmic effects of LLVNS involve the PI3K/NO signaling pathway.     

自主神经干预对心房恢复性质的影响

目的 研究心脏自主神经干预对心房恢复性质的影响.方法 正常成年杂种犬10只,开胸后将多极电生理导管缝置于肺静脉、左右心耳和左右心房处,应用Ag-AgCl电极记录标测部位单相动作电位,在基础状态和颈部迷走神经刺激条件下构建标测部位恢复曲线,分别对标测部位进行快速电刺激,记录心房颤动（房颤）诱发时的起搏周长和持续时间.心脏自主神经节（GP）消融后重复上述步骤.结果 GP消融前迷走神经刺激同基础状态相比显著缩短动作电位时限（APD）,降低恢复曲线最大斜率（Smax）,抑制APD电交替,但房颤容易发生（P＜0.05）.GP消融后,APD较消融前显著延长,恢复曲线Smax增大,APD电交替提前,但房颤不易诱发（P＜0.05）;GP消融后迷走神经刺激效应明显减弱.GP消融前迷走神经刺激能显著增加APD恢复曲线Smax离散度（0.5±0.2对0.3±0.1,P＜0.05）,而GP消融能显著降低APD恢复曲线Smax离散度（0.2±0.1对0.3±0.1,P＜0.05）.结论 恢复曲线的斜率并不能完全解释房颤的诱发和维持,心房APD电交替可能对房颤的诱发并无预测作用,恢复性质的离散可能是诱发房颤的重要因素.     

Dofetilide Promotes Repolarization Abnormalities in Perfused Guinea-pig Heart

Purpose

Dofetilide is class III antiarrhythmic agent which prolongs cardiac action potential duration because of selective inhibition of I _Kr, the rapid component of the delayed rectifier K⁺ current. Although clinical studies reported on proarrhythmic risk associated with dofetilide treatment, the contributing electrophysiological mechanisms remain poorly understood. This study was designed to determine if dofetilide-induced proarrhythmia may be attributed to abnormalities in ventricular repolarization and refractoriness.

Methods

The monophasic action potential duration and effective refractory periods (ERP) were assessed at distinct epicardial and endocardial sites along with volume-conducted ECG recordings in isolated, perfused guinea-pig heart preparations.

Results

Dofetilide was found to produce the reverse rate-dependent prolongation of ventricular repolarization, increased the steepness of action potential duration rate adaptation, and amplified transepicardial variability in electrical restitution kinetics. Dofetilide also prolonged the T peak-to-end interval on ECG, and elicited a greater prolongation of endocardial than epicardial ERP, thereby increasing transmural dispersion of refractoriness. At epicardium, dofetilide prolonged action potential duration to a greater extent than ERP, thus extending the critical interval for ventricular re-excitation. This change was associated with triangulation of epicardial action potential because of greater dofetilide-induced prolonging effect at 90?% than 30?% repolarization. Premature ectopic beats and spontaneous short-lasting episodes of monomorphic ventricular tachycardia were observed in 44?% of dofetilide-treated heart preparations.

Conclusions

Proarrhythmic potential of dofetilide in guinea-pig heart is attributed to steepened electrical restitution, increased transepicardial variability in electrical restitution kinetics, amplified transmural dispersion of refractoriness, increased critical interval for ventricular re-excitation, and triangulation of epicardial action potential.     

Reverse atrial electrical remodelling induced by continuous positive airway pressure in patients with severe obstructive sleep apnoea

Background

Obstructive sleep apnoea (OSA) is associated with cardiovascular morbidity and mortality, including atrial arrhythmias. Continuous positive airway pressure (CPAP) is the gold standard treatment for OSA; its impact on atrial electrical remodelling has not been fully investigated. Signal-averaged p-wave (SAPW) duration is an accepted marker for atrial electrical remodelling.

Objective

The objective of this study is to determine whether CPAP induces reverse atrial electrical remodelling in patients with severe OSA.

Methods

Consecutive patients attending the Sleep Disorder Clinic at Kingston General Hospital underwent full polysomnography. OSA-negative controls and severe OSA were defined as apnoea–hypopnea index (AHI)?<?5 events/hour and AHI?≥?30 events/hour, respectively. SAPW duration was determined at baseline and after 4–6 weeks of CPAP in severe OSA patients or without intervention controls.

Results

Nineteen severe OSA patients and 10 controls were included in the analysis. Mean AHI and minimum oxygen saturation were 41.4?±?10.1 events/hour and 80.5?±?6.5 % in severe OSA patients and 2.8?±?1.2 events/hour and 91.4?±?2.1 % in controls. At baseline, severe OSA patients had a greater SAPW duration than controls (131.9?±?10.4 vs 122.8?±?10.5 ms; p?=?0.02). After CPAP, there was a significant reduction of SAPW duration in severe OSA patients (131.9?±?10.4 to 126.2?±?8.8 ms; p?<?0.001), while SAPW duration did not change after 4–6 weeks in controls.

Conclusion

CPAP induced reverse atrial electrical remodelling in patients with severe OSA as represented by a significant reduction in SAPW duration.     

Left atrial reverse remodeling and prevention of progression of atrial fibrillation with atrial resynchronization device therapy utilizing dual-site right atrial pacing in patients with atrial fibrillation refractory to antiarrhythmic drugs or catheter ablation

Introduction

Dual-site right atrial pacing (DAP) produces electrical atrial resynchronization but its long-term effect on the atrial mechanical function in patients with refractory atrial fibrillation (AF) has not been studied.

Methods

Drug-refractory paroxysmal (PAF) and persistent AF (PRAF) patients previously implanted with a dual-site right atrial pacemaker (DAP) with minimal ventricular pacing modes (AAIR or DDDR mode with long AV delay) were studied. Echocardiographic structural (left atrial diameter [LAD] and left ventricular [LV] end diastolic diameter [EDD], end systolic diameter [ESD]) and functional (ejection fraction [EF]) parameters were serially assessed prior to, after medium-term (n?=?39) and long-term (n?=?34) exposure to DAP.

Results

During medium-term follow-up (n?=?4.5 months), there was improvement in left atrial function. Mean peak A wave flow velocity increased with DAP as compared to baseline (75?±?19 vs. 63?±?23 cm/s, p?=?0.003). The long-term impact of DAP was studied with baseline findings being compared with last follow-up data with a mean interval of 37?±?25 (range 7–145) months. Mean LAD declined from 45?±?5 mm at baseline to 42?±?7 mm (p?=?0.003). Mean LVEF was unchanged from 52?±?9 % at baseline and 54?±?6 % at last follow-up (p?=?0.3). There was no significant change in LV dimensions with mean LVEDD being 51?±?6 mm at baseline and 53?±?5 mm at last follow-up (p?=?0.3). Mean LVESD also remained unchanged from 35?±?6 mm at baseline to 33?±?6 mm at last follow-up (p?=?0.47). During long-term follow-up, 30 patients (89 %) remained in sinus or atrial paced rhythm as assessed by device diagnostics at 3 years.

Conclusions

DAP can achieve long-term atrial reverse remodeling and preserve LV systolic function. DAP when added to antiarrhythmic drug (AAD) and/or catheter ablation (ABL) maintains long-term rhythm control and prevents AF progression in elderly refractory AF patients. Reverse remodeling with DAP may contribute to long-term rhythm control.     

Effects of ganglionated plexi ablation on ventricular electrophysiological properties in normal hearts and after acute myocardial ischemia

Background

Ganglionated plexi (GP) ablation has been shown to play an important role in atrial fibrillation (AF) initiation and maintenance. Also, GP ablation increases chances for prevention of AF recurrence. This study investigated the effects of GP ablation on ventricular electrophysiological properties in normal dog hearts and after acute myocardial ischemia (AMI).

Methods

Fifty anesthetized dogs were assigned into normal heart group (n = 16) and AMI heart group (n = 34). Ventricular dynamic restitution, effective refractory period (ERP), electrical alternans and ventricular fibrillation threshold (VFT) were measured before and after GP ablation in the normal heart group. In the AMI heart group, the incidence of ventricular arrhythmias and VFT were determined.

Results

In the normal heart group, GP ablation significantly prolonged ERP, facilitated electrical alternans but did not increase ERP dispersion, the slope of restitution curves and its spatial dispersion. Also, GP ablation did not cause significant change of VFT. In the AMI heart group, the incidence of ventricular arrhythmias after GP ablation was significantly higher than that in the control group or the GP plus stellate ganglion (SG) ablation group (P < 0.05). Spontaneous VF occurred in 8/12, 1/10 and 2/12 dogs in the GP ablation group, the GP plus SG ablation group and the control group, respectively (P < 0.05). VFT in the GP ablation group showed a decreased trend though a significant difference was not achieved compared with the control or the GP plus SG ablation group.

Conclusions

GP ablation increases the risk of ventricular arrhythmias in the AMI heart compared to the normal heart.     

Protective effect of metoprolol on arrhythmia and heart rate variability in healthy people with 24 hours of sleep deprivation

Purpose

Sleep deprivation, which is a strong stressor, can greatly affect the cardiovascular system of rescue workers. This study aimed to investigate the effect of 24-h sleep deprivation on heart rate variability (HRV) in young healthy people and the protective effect of metoprolol on arrhythmia.

Methods

Sixty young, healthy subjects (6 women and 54 men), aged 25?±?4.5 years, were enrolled in this study. All participants received 24-h continuous ambulatory electrocardiogram monitoring. Arrhythmia, time, and frequency domain parameters were analyzed in subjects at the following three stages: normal sleep stage, sleep deprivation stage, and metoprolol treatment before sleep deprivation stage.

Results

After 24-h sleep deprivation, the high frequency (HF) of HRV was significantly decreased (p?<?0.05), low frequency (LF) was remarkably increased (p?<?0.05), and LF/HF was significantly increased compared with those in normal sleep (p?<?0.05). Some subjects presented with mild palpitation due to premature atrial complexes and premature ventricular complexes. At the metoprolol treatment stage, compared with the sleep deprivation stage, LF and LF/HF were significantly reduced, HF of HRV was elevated (p?<?0.05), and the total amount of premature atrial and ventricular complexes was decreased.

Conclusion

The underlying mechanism of arrhythmia and HRV alteration after 24-h sleep deprivation could be attributable to lower vagal activity and elevated sympathetic activity. Metoprolol improves the change in autonomic nervous system activity after 24-h sleep deprivation, which may be responsible for its protective role on arrhythmia in healthy subjects undergoing sleep deprivation.     

Improvement of left ventricular diastolic function and left atrial reverse remodeling after catheter ablation of premature ventricular complexes

Aims

Catheter ablation of premature ventricular complexes (PVC) improves left ventricular (LV) systolic performance in certain patients; however, the effect on diastolic function and left atrial (LA) remodeling is unclear. We assessed the effects of catheter ablation of PVCs on parameters of LV diastolic function and LA remodeling.

Methods

Forty-seven patients (age 65?±?10 years, 46 men) who underwent catheter ablation for symptomatic PVCs were evaluated using two-dimensional echocardiography before and 6?±?2 months after ablation. The measured diastolic indices included mitral inflow parameters (E wave, A wave, E/A ratio, and deceleration time (DT)), mitral lateral annulus early diastolic velocity (Ea), and E/Ea ratio. The LA volume was measured using modified biplane Simpson's method. We also compared the changes in the left atrial volumes and left atrial volume index (LAVI) after PVC ablation.

Results

After catheter ablation of PVCs, the mean LV ejection fraction (EF) increased significantly (49.9?±?10.3 vs. 42.8?±?11.8, p?<?0.01). Significant improvement was also seen in A wave velocity (71.3?±?17.1 vs. 59.5?±?15.1 cm/s, p?=?0.039), E/A ratio (1.42?±?0.6 vs. 1.07?±?0.5 ml, p?=?0.034), Ea (8.9?±?3.9 vs. 6.8?±?2.9 cm/s, p?=?0.04), and E/Ea ratio (15.4?±?5.8 vs. 10.6?±?3.4, p?=?0.027), whereas mitral E and DT did not show significant change. LAVI decreased significantly after ablation (44.4?±?14.8 vs. 36.7?±?12.5, p?<?0.001). Significant improvement in LAVI was also seen in patients with normal baseline LVEF (p?=?0.04).

Conclusion

Catheter ablation of PVCs improved LV diastolic function and resulted in left atrial reverse remodeling.     

Electrocardiographic P wave changes after thoracoscopic pulmonary vein isolation for atrial fibrillation

Background

Changes in P wave duration (PWD) and P wave area (PWA) have been described following catheter ablation for atrial fibrillation (AF). We hypothesize that video-assisted thoracoscopic pulmonary vein isolation (VATS-PVI) for AF results in decrease of PWD, PWA and P wave dispersion, which may resemble reverse electrical remodeling of the atrium after restoration of sinus rhythm.

Methods

VATS-PVI consisted of PVI and ganglionic plexus ablation in 29 patients (mean age, 59?±?7 years; 23 males; 17 paroxysmal AF) and additional left atrial lesions in patients with persistent AF. PWD and PWA were measured in ECG lead II, aVF and V2 of ECGs during sinus rhythm before, directly after, and 6 months postprocedure. P wave dispersion was derived from the 12 lead ECG.

Results

Prior to VATS-PVI, PWD did not correlate with left atrial size and no difference in left atrial size was found between patients with paroxysmal or persistent AF (p?=?0.27). Following VATS-PVI, PWD initially prolonged in all patients from 115?±?4.6 ms to 131?±?3.6 ms (p?<?0.01) but shortened to 99?±?3.2 ms after 6 months (p?<?0.01). PWA was 5.60?±?0.32 mV*ms at baseline, 6.44?±?0.32 mV*ms post-VATS-PVI (P?=?NS), and 5.40?±?0.28 mV*ms after 6 months (p?=?NS vs. baseline, p?<?0.05 vs. post-VATS-PVI). P wave dispersion decreased in the persistent AF group from baseline 67?±?3.3 to 64?±?2.5 ms post-VATS-PVI (p?=?0.30) and to 61?±?3.4 ms after 6 months (p?<?0.05).

Conclusions

PWD increases significantly directly after successful VATS-PVI in both groups. There was significant decrease in PWD after 6 months. Similarly, P wave dispersion decreased in the persistent group. These changes suggest an immediate procedure related effect, but the later changes may represent reverse electrical atrial remodeling following cessation of AF.     

Effect of isoprenaline chronic stimulation on APD restitution and ventricular arrhythmogenesis

BackgroundIsoprenaline (ISO) acts through β-adrenergic receptors to increase the intracellular Ca²⁺, which has effects on action potential duration (APD) restitution and arrhythmogenesis. Thus, we investigated the effect of chronic stimulation with isoprenaline on APD restitution and ventricular tachyarrhythmias (VA) in the rabbit heart.Methods and resultsRabbits were randomly selected to receive an injection of isoprenaline (ISO group) or an equal volume of 0.9% saline (CTL group). The S₁–S₂ protocol (n = 15) and S₁ dynamic pacing (n = 15) were performed to construct APD restitution and to induce APD alternans or arrhythmia in 10 sites of Langendorff-perfused hearts. Compared with the same sites in the control group, long-term ISO administration (7 days) shortened the APD₉₀ and the effective refractory period (ERP), and greatly increased the spatial dispersion of APD and ERP (p < 0.01). Compared to CTL group, the APD restitution curves were significantly changed (p < 0.01) and showed increased spacial dispersion of maximal slope (S_max) among each site in the ISO group (p < 0.05). In induction of VA and APD alternans, the threshold of VA and alternans was both decreased in each site of the ISO group.ConclusionChronic stimulation with ISO facilitated VA, possibly through the increased spatial dispersion of APD restitution.     

Piceatannol facilitates conduction block and ventricular fibrillation induction in ischemia-reperfused rabbit hearts with pacing-induced heart failure

Background

Piceatannol, a hydroxystilbene natural product, has been reported to exert antiarrhythmic action via I_Na inhibition and slow I_Na inactivation in ischemia-reperfused (IR) rat hearts. The present study aimed to clarify the proarrhythmic property of piceatannol during regional IR injury in failing rabbit hearts.

Methods

Heart failure (HF) was induced by rapid right ventricular pacing for 4 weeks. The IR model was created by coronary artery ligation for 30 min, followed by reperfusion for 15 min in vivo. Simultaneous voltage and intracellular Ca^2 + (Ca_i) optical mapping was then performed in isolated Langendorff-perfused hearts (n = 11 in each HF and control group). Action potential duration (APD) restitution, arrhythmogenic alternans and VF inducibility were evaluated by a dynamic pacing protocol. Conduction velocity was measured along lines across the IR and non-IR zones during pacing. Piceatannol (10 μM) was administered after baseline studies.

Results

In the HF group, piceatannol decreased conduction velocity, induced rate-dependent regional inhomogeneity of conduction delay and wavelength shortening, slowed Ca_i decay, and facilitated arrhythmogenic alternans instead of APD prolongation to increase VF inducibility. In the control group, the proarrhythmic effects of piceatannol on APD restitution, arrhythmogenic alternans and conduction delay were offset by its antiarrhythmic effects (APD and wavelength prolongation), resulting in a neutral effect on VF inducibility.

Conclusions

Piceatannol (10 μM) is proarrhythmic in failing rabbit hearts with regional IR injury. The increased VF inducibility by piceatannol in HF suggests that its undesirable effects are more pronounced than its benefits in failing hearts.     

Bifocal right ventricular pacing: an alternative way to achieve resynchronization when left ventricular lead insertion is unsuccessful

Purpose

To explore the effects on atrial and ventricular function of restoring sinus rhythm (SR) after epicardial cryoablation and closure of the left atrial appendage (LAA) in patients with mitral valve disease and atrial fibrillation (AF) undergoing surgery.

Methods

Sixty-five patients with permanent AF were randomized to mitral valve surgery combined with left atrial epicardial cryoablation and LAA closure (ABL group, n?=?30) or to mitral valve surgery alone (control group, n?=?35). Two-dimensional and Doppler echocardiography were performed before and 6?months after surgery.

Results

At 6?months, 73% of the patients in the ABL group and 46% of the controls were in SR. Patients in SR at 6?months had a reduction in their left ventricular diastolic diameter while the left ventricular ejection fraction was unchanged. In patients remaining in AF, the left ventricular ejection fraction was lower than at baseline. The left atrial diastolic volume was reduced after surgery, more in patients with SR than AF. In patients in SR, the peak velocity during the atrial contraction and the reservoir function were lower in the ABL group than in the control group.

Conclusions

In patients in SR, signs of atrial dysfunction were observed in the ABL but not the control group. Atrial dysfunction may have existed before surgery, but the difference between the groups implies that the cryoablation procedure and/or closure of the LAA might have contributed.     

Cardiac conduction disturbances and differential effects on atrial and ventricular electrophysiological properties in desmin deficient mice

Purpose

Desmin mutations in humans cause desmin-related cardiomyopathy, resulting in heart failure, atrial and ventricular arrhythmias, and sudden cardiac death. The intermediate filament desmin is strongly expressed in striated muscle cells and in Purkinje fibers of the ventricular conduction system. The aim of the present study was to characterize electrophysiological cardiac properties in a desmin-deficient mouse model.

Methods

The impact of desmin deficiency on cardiac electrophysiological characteristics was examined in the present study. In vivo electrophysiological studies were carried out in 29 adult desmin deficient (Des^?/?) and 19 wild-type (Des^+/+) mice. Additionally, epicardial activation mapping was performed in Langendorff-perfused hearts.

Results

Intracardiac electrograms showed no significant differences in AV, AH, and HV intervals. Functional testing revealed equal AV-nodal refractory periods, sinus-node recovery times, and Wenckebach points. However, compared to the wild-type situation, Des^?/? mice were found to have a significantly reduced atrial (23.6?±?10.3 ms vs. 31.8?±?12.5 ms; p?=?0.045), but prolonged ventricular refractory period (33.0?±?8.7 ms vs. 26.7?±?6.5 ms; p?=?0.009). The probability of induction of atrial fibrillation was significantly higher in Des^?/? mice (Des^?/?: 38% vs. Des^+/+: 27%; p?=?0.0255), while ventricular tachycardias significantly were reduced (Des^?/?: 7% vs. Des^+/+: 21%; p?<?0.0001). Epicardial activation mapping showed slowing of conduction in the ventricles of Des^?/? mice.

Conclusions

Des^?/? mice exhibit reduced atrial but prolonged ventricular refractory periods and ventricular conduction slowing, accompanied by enhanced inducibility of atrial fibrillation and diminished susceptibility to ventricular arrhythmias. Desmin deficiency does not result in electrophysiological changes present in human desminopathies, suggesting that functional alterations rather than loss of desmin cause the cardiac alterations in these patients.     

Catheter ablation for atrial fibrillation results in greater improvement in cardiac function in patients with low versus normal left ventricular ejection fraction

Purpose

It is still unknown whether left ventricular ejection fraction (LVEF) might affect the magnitude of improvement after atrial fibrillation (AF) ablation on cardiac function in persistent or longstanding persistent AF (CAF) patients.

Method

We performed echocardiography in 35 patients with CAF before and after catheter ablation (CA). Patients were stratified by LVEF into two groups prior to CA—normal LVEF (≥50 % LVEF, N group, n?=?24) and a low LVEF group (<50 % LVEF, L group, n?=?11). Patients were followed at 1 month, 3 months, 6 months, 1 year, and 2 years after ablation.

Results

After 15.8?±?7.4 months follow-up, the L group showed greater improvement in LVEF and left atrial ejection fraction (LAEF; N group vs L group: LVEF difference (%), 5?±8 vs 20±?13, p?<?0.01; LAEF difference (%), 11?±?12 vs 21?±?10, p?<?0.05). LA maximal volume and E/e′ showed the same tendency after ablation, although the extent of improvement was not statistically significant. Both groups showed almost the same time course of improvement up to 2 years, although the L group showed earlier recovery in LVEF.

Conclusion

The greater improvement in several cardiac functions was seen in patients with greater LV dysfunction, after the CA for CAF.     

Specialty Use Among Patients With Treated Hypertension in a Patient-Centered Medical Home

BACKGROUND

Little is known about how delivery of primary care in the patient-centered medical home (PCMH) influences outpatient specialty care use.

OBJECTIVE

To describe changes in outpatient specialty use among patients with treated hypertension during and after PCMH practice transformation.

DESIGN

One-group, 48-month interrupted time series across baseline, PCMH implementation and post-implementation periods.

PATIENTS

Adults aged 18–85 years with treated hypertension.

INTERVENTION

System-wide PCMH redesign implemented across 26 clinics in an integrated health care delivery system, beginning in January 2009.

MAIN MEASURES

Resource Utilization Band variables from the Adjusted Clinical Groups case mix software characterized overall morbidity burden (low, medium, high). Negative binomial regression models described adjusted annual differences in total specialty care visits. Poisson regression models described adjusted annual differences in any use (yes/no) of selected medical and surgical specialties.

KEY RESULTS

Compared to baseline, the study population averaged 7 % fewer adjusted specialty visits during implementation (P?<?0.001) and 4 % fewer adjusted specialty visits in the first post-implementation year (P?=?0.02). Patients were 12 % less likely to have any cardiology visits during implementation and 13 % less likely during the first post-implementation year (P?<?0.001). In interaction analysis, patients with low morbidity had at least 27 % fewer specialty visits during each of 3 years following baseline (P?<?0.001); medium morbidity patients had 9 % fewer specialty visits during implementation (P?<?0.001) and 5 % fewer specialty visits during the first post-implementation year (P?=?0.007); high morbidity patients had 3 % (P?=?0.05) and 5 % (P?=?0.009) higher specialty use during the first and second post-implementation years, respectively.

CONCLUSIONS

Results suggest that more comprehensive primary care in this PCMH redesign enabled primary care teams to deliver more hypertension care, and that many needs of low morbidity patients were within the scope of primary care practice. New approaches to care coordination between primary care teams and specialists should prioritize high morbidity, clinically complex patients.     

Post-ablation prolongation of atrioventricular nodal refractory period is correlated with long-term success of cryoablation for atrioventricular nodal reentrant tachycardia in the case of the persistence of a residual jump

Purpose

A residual slow pathway after successful cryoablation for atrioventricular nodal reentrant tachycardia (AVNRT) is correlated with a higher recurrence rate. We described determinants of recurrence in subjects with a residual jump.

Methods

We analyzed the data of subjects with acute successful slow pathway cryoablation for AVNRT using a 6-mm-tip cryocatheter. Success was defined as AVNRT non-inducibility. Patients with no baseline elicitable jump, no inducible AVNRT, and transient first atrioventricular (AV) block at the last site were excluded.

Results

From 371 patients who underwent cryoablation from May 2002 to March 2011, 303 fulfilled the entry criteria (mean age, 41?±?16; 222 women). Baseline AV nodal effective refractory period (ERP) was 272?±?57?ms, postprocedural 331?±?64 (P?P?=?0.01). In patients with a jump, only ?? AV nodal ERP was correlated with recurrence (37?±?41 vs. 68?±?47?ms; P?30?ms (P?Conclusions Suppression of slow pathway conduction is the optimal endpoint for AVNRT cryoablation. A residual jump can be tolerated if AV nodal ERP postcryoablation is prolonged >30?ms.     

Increase in pulmonary arterial pressure after atrial fibrillation ablation: incidence and associated findings

Purpose

The stiff left atrial (LA) syndrome is defined as pulmonary hypertension (PH) secondary to reduced LA compliance and has recently been shown to be one cause of PH after atrial fibrillation (AF) ablation. We aimed to determine the incidence of an increase in pulmonary arterial (PA) pressure post-ablation and examine the clinical and echocardiographic associations.

Methods

Patients who underwent AF ablation between 1999 and 2011 were included if they had both an echocardiogram pre-ablation and 3 months post-ablation. Patients were then separated into two groups with the increased PA pressure group defined as patients with >10 mmHg increase in right ventricular systolic pressure (RVSP) post-ablation and a post-ablation RVSP >35 mmHg.

Results

Of the 499 patients meeting the study criteria, 41 (8.2 %) had an increase in RVSP >10 mmHg and RVSP >35 mmHg post-ablation. On echocardiogram, the two groups had similar E/A and E/e’ ratios pre-ablation. However, post-ablation, the increased PA pressure group had higher E/A (2.12 vs. 1.49, p?<?0.01) and E/e’ (14.7 vs. 11.2, p?<?0.01) ratios. LA expansion index values were lower in the increased PA pressure group pre-ablation (51 vs. 92 %, p?<?0.01), but not significantly different post-ablation (82 vs. 88 %, p?=?0.44).

Conclusions

Around 8 % of patients develop an increase in estimated PA pressure after AF ablation. Echocardiographic parameters suggest that patients who develop increased PA pressure are developing (or unmasking) left ventricular diastolic dysfunction.     

Omega-3 Polyunsaturated Fatty Acids Increase Plasma Adiponectin to Leptin Ratio in Stable Coronary Artery Disease

Background

Growing evidence suggests a cardioprotective role of omega-3 polyunsaturated fatty acids (PUFA). However, the exact mechanisms underlying the effects of omega-3 PUFA in humans have not yet been fully clarified.

Purpose

We sought to evaluate omega-3 PUFA-mediated effects on adipokines in patients with stable coronary artery disease (CAD) undergoing elective percutaneous coronary intervention (PCI).

Methods

We conducted a prospective, double-blind, placebo-controlled, randomized study, in which adiponectin, leptin and resistin were determined at baseline, 3–5 days and 30 days during administration of omega-3 PUFA 1 g/day (n?=?20) or placebo (n?=?28).

Results

As compared to controls administration of omega-3 PUFA resulted in increase of adiponectin by 13.4 % (P?<?0.0001), reduction of leptin by 22 % (P?<?0.0001) and increase of adiponectin to leptin (A/L) ratio by 45.5 % (P?<?0.0001) at 30 days, but not at 3–5 days. Compared with placebo adiponectin was 12.7 % higher (P?=?0.0042), leptin was 16.7 % lower (P?<?0.0001) and A/L ratio was 33.3 % higher (P?<?0.0001) in the omega-3 PUFA group at 30 days. Resistin decreased similarly in both groups after 1 month, without intergroup differences (P?=?0.32). The multivariate model showed that the independent predictors of changes in adiponectin at 1 month (P?<?0.001) were: omega-3 PUFA treatment, baseline platelet count, total cholesterol and those in leptin (P?<?0.0001) were: omega-3 PUFA treatment and waist circumference. Independent predictors of A/L ratio changes (P?<?0.0001) were: assigned treatment, current smoking and hyperlipidemia.

Conclusions

In high risk stable coronary patients after PCI omega-3 PUFA supplementation improves adipokine profile in circulating blood. This might be a novel, favourable mechanism of omega-3 PUFA action.     

Anteroseptal basal right ventricular entrainment is simple and superior to apical entrainment in identifying mechanism of supraventricular tachycardia

Background

Differentiation between atrioventricular nodal reentry tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) can be sometimes challenging. Apical right ventricular (RV) entrainment can help in differentiation; however, it has some fallacies. We thought to compare the accuracy of anteroseptal basal RV entrainment to RV apical entrainment in identifying the mechanism of supraventricular tachycardia (SVT).

Methods

Forty-two consecutive patients with SVT who underwent catheter ablation were prospectively studied. Apical RV entrainment was performed initially followed by basal entrainment from the anteroseptal basal RV avoiding His or atrial capture. Postpacing interval (PPI), PPI–tachycardia cycle length (TCL), corrected PPI-TCL, and stimulus–atrial minus ventricular–atrial (VA) intervals were measured.

Results

Entrainment was achieved from both sites of RV in 34 patients (ten men; mean age 42?±?15 years), 20 with typical AVNRT, 1 with atypical AVNRT, and 13 with AVRT (eight left sided, four right sided, and one septal accessory pathways). PPI-TCL, corrected PPI (cPPI)-TCL, and stimulus–atrial–VA intervals were significantly longer with basal entrainment in AVNRT (171?±?30 vs. 153?±?22 ms (p?=?0.003), 148?±?21 vs. 131?±?20 ms (p?=?0.002), and 145?±?17 vs. 136?±?15 ms (p?=?0.005), respectively). Receiver-operating characteristic curves showed higher AUC for the above parameters with basal entrainment compared to apical entrainment. Cutoff values of basal PPI-TCL of >110 ms and cPPI-TCL of >95 ms had better sensitivities (100 % for both vs. 95 and 90 %, respectively, for apical values) and specificities (85 and 92 % vs. 77 and 92 %, respectively) for diagnosis of AVNRT.

Conclusion

Basal RV entrainment from the anteroseptal basal RV is a simple maneuver that is superior to apical ventricular entrainment in identifying the mechanism of SVT.     

N-terminal pro-B-type natriuretic peptide level at long-term follow-up after atrial fibrillation ablation: a marker of reverse atrial remodelling and successful ablation

Aims

We investigated the relationship between arrhythmia burden, left atrial volume (LAV) and N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) at baseline and after long-term follow-up of atrial fibrillation (AF) ablation.

Methods

We studied 38 patients (23 paroxysmal, 6 women, mean age 56?±?11) scheduled for AF ablation. LAV was calculated on the basis of computed tomography images at baseline and long-term follow-up, and arrhythmia burden was graded from self-reported frequency and duration of AF episodes.

Results

After a mean period of 22?±?5?months, 28/38 patients (11/15 persistent) were free from AF recurrence. At baseline there were no differences in mean LAV (125 vs. 130?cm³, p?=?0.7) or median NT-pro-BNP (33.5 vs. 29.5?pmol/L, p?=?0.9) between patients whose ablation had been successful or otherwise. At long-term follow-up, there was a marked decrease in LAV (105 vs. 134?cm³, p?p?r?=?0.71, p?r?=?0.57, p?r?=?0.47, p?r?=?0.52, p?25% of baseline value had a specificity of 0.89 and a sensitivity of 0.6 (receiver operator characteristics, accuracy 0.82) for ablation success.

Conclusions

NT-pro-BNP correlates with LAV and arrhythmia burden in AF patients and both NT-pro-BNP and LAV decrease significantly after successful ablation. A decrease in NT-pro-BNP of >25% from the baseline value could be useful as a marker of ablation success.