Updated Survey on Interventional Electrophysiology: 5-Year Follow-Up of Infrastructure, Procedures, and Training Positions in Germany.

OBJECTIVES: This study provides an update and comparison to a 2010 nationwide survey on cardiac electrophysiology (EP), types and numbers of interventional electrophysiological procedures, and training opportunities in 2015. BACKGROUND: In 2010, German cardiology centers performing interventional EP were identified and contacted to provide a survey on cardiac EP. METHODS: German cardiology centers performing interventional EP in 2015 were identified from quality reports and contacted to repeat the 2010 questionnaire. RESULTS: A majority of 131 centers (57%) responded. EP (ablation procedures and device therapy) was mainly part of a cardiology department (89%) and only independent (with its own budget) in 11%. The proportion of female physicians in EP training increased from 26% in 2010 to 38% in 2015. In total, 49,356 catheter ablations (i.e., 81% of reported ablations in 2015) were performed by the responding centers, resulting in a 44% increase compared with 2010 (the median number increased from 180 to 297 per center). Atrial fibrillation (AF) was the most common arrhythmia interventionally treated (47%). At 66% of the centers, (at least) 2 physicians were present during most catheter ablations. A minimum of 50 (75) AF ablations were performed at 80% (70%) of the centers. Pulmonary vein isolation with radiofrequency point-by-point ablation (62%) and cryoablation (33%) were the preferred ablation strategies. About one-third of centers reported surgical AF ablations, with 11 centers (8%) performing stand-alone surgical AF ablations. Only one-third of the responding 131 centers fulfilled all requirements for training center accreditation. CONCLUSIONS: Comparing 2010 with 2015, an increasing number of EP centers and procedures in Germany are registered. In 2015, almost every second ablation was for therapy for AF. Thus, an increasing demand for catheter ablation is likely, but training opportunities are still limited, and most centers do not fulfil recommended requirements for ablation centers.

Low-Level But Not High-Level Baroreceptor Stimulation Inhibits Atrial Fibrillation in a Pig Model of Sleep Apnea.

BACKGROUND: Obstructive sleep apnea (OSA) increases susceptibility to atrial fibrillation (AF) by a combined sympatho-vagal hyperactivation. The purpose of this study was to investigate the effect of autonomic nervous system modulation by low-level baroreceptor stimulation (LL-BRS) compared to high-level BRS (HL-BRS) on atrial arrhythmogenic changes in a pig model of OSA. METHODS AND RESULTS: Sixteen pigs received tracheotomy under general urethane/chloralose anesthesia. Group 1 pigs (n = 8) received LL-BRS (at 80% of that slowing sinus rate) for 3 hours and group 2 pigs (n = 8) received HL-BRS (slowing sinus rate). Changes in atrial effective refractory period (AERP) and AF-inducibility were determined during applied negative thoracic pressure (NTP) for 2 minutes before and at the end of the 3-hour stimulation protocol. Group 1: LL-BRS prolonged AERP from 150 ± 5 to 172 ± 19 milliseconds (P < 0.001). After 3 hours of LL-BRS, NTP-induced AERP-shortening was diminished from -51 ± 10 milliseconds (-34%) to -22 ± 4 milliseconds (-13%) (P < 0.01). AF-inducibility during NTP maneuvers decreased from 90% at baseline to 15% (P < 0.01). Group 2: HL-BRS shortened AERP from 150 ± 17 to 132 ± 8 milliseconds (P = 0.024). After 3 hours of HL-BRS, NTP-induced AERP-shortening was increased from -55 ± 7 milliseconds (-36%) to -72 ± 11 milliseconds (-54%) (P < 0.05) and AF-inducibility was not affected. NTP-induced changes in blood gases and blood pressure were not different between the groups. CONCLUSION: LL-BRS suppressed NTP-induced AERP-shortening and AF-inducibility. By contrast HL-BRS further perpetuated NTP-induced AERP-shortening and increased AF-inducibility. These findings support only the use of LL-BRS as a novel therapeutic modality to treat AF in OSA.

A survey of German centres performing invasive electrophysiology: structure, procedures, and training positions.

AIMS: To provide a nationwide survey (and reference for the future) on cardiac electrophysiologists, types and numbers of invasive electrophysiological procedures, and training opportunities in 2010. METHODS AND RESULTS: German cardiology centres performing invasive electrophysiology were identified from quality reports and contacted to fill a questionnaire. A majority of 122 centres (65%) responded. Electrophysiology (ablation procedures and device therapy) was mainly part of a cardiology department (82%), and only in 9% independent (own budget). In only 58% of the centres, (at least) two physicians were present during catheter ablations. Although in 2010, women represented 59.4% of physicians <35 years old, only 26% of physicians in electrophysiology training were female. In total, 33 420 catheter ablations were performed with a median number of 180 per centre. Atrial fibrillation (AF) was the most common arrhythmia invasively treated (35%). At least 50 AF ablations were performed in 53% of the centres. Of the centres performing AF ablations, consecutive left atrial arrhythmias were treated by catheter ablation only in 75%, and only 44% had in-house surgical backup. Only one-fourth of the 122 centres fulfilled all requirements for training centre accreditation according to the European Heart Rhythm Association and the German Cardiac Society. CONCLUSION: The results indicate a high number of electrophysiology centres and procedures in Germany. Atrial fibrillation was the most common arrhythmia invasively treated. An increasing demand for catheter ablation is likely, but training opportunities are limited. Women are clearly underrepresented. A co-operation of higher and lower volume electrophysiology centres may be necessary for training purposes.

Aldosterone promotes atrial fibrillation.

AIMS: Hyperaldosteronism is associated with an increased prevalence of atrial fibrillation (AF). However, it is unclear whether this is the consequence of altered haemodynamics or a direct aldosterone effect. It was the aim of the study to demonstrate load-independent effects of aldosterone on atrial structure and electrophysiology. METHODS: Osmotic mini-pumps delivering 1.5 µg/h aldosterone were implanted subcutaneously in rats (Aldo). Rats without aldosterone treatment served as controls. After 8 weeks, surface electrocardiogram, the inducibility of AF, and atrial pressures were recorded in vivo. In isolated working hearts, left ventricular function was measured, and conduction in the right atrium (RA) and the left atrium (LA) was mapped epicardially. The atrial effective refractory period (AERP) was determined. Atrial tissue was analysed histologically. RESULTS: Neither systolic nor diastolic ventricular function nor atrial pressures were altered in Aldo rats. All Aldo (11/11) showed inducible atrial arrhythmias vs. two of nine controls (P = 0.03). In Aldo, the P-wave duration and the total RA activation time were longer. Prolongation of local conduction times occurred more often in Aldo, whereas the AERP did not differ between both groups. In Aldo, atrial fibroblasts and interstitial collagen were increased, active matrix metalloproteinase 13 was reduced, and atrial myocytes were hypertrophied. The connexin 43 content was unaltered. CONCLUSIONS: Aldosterone causes a substrate for atrial arrhythmias characterized by atrial fibrosis, myocyte hypertrophy, and conduction disturbances. The described model imputes atrial proarrhythmia directly to aldosterone, since ventricular haemodynamics appeared unaltered in this model. This mechanism may have therapeutical impact for primary and secondary prevention of AF.

Should aldosterone blockade be used beyond current indications in heart failure?

Aldosterone receptor antagonists (ARAs) are becoming important supplementary options in the pharmacologic treatment of congestive heart failure (CHF), and the indication for ARAs continues to grow. Aldosterone is a stimulator of myocardial fibrosis, causing progression of CHF and serving as an important factor in the pathogenesis of diastolic heart failure (ie, heart failure with normal ejection fraction). The beneficial effects of ARAs have already been demonstrated in patients with severe CHF and patients with symptoms of CHF and left ventricular dysfunction early after myocardial infarction. ARAs may also be important in mild to moderate CHF, but current evidence has not been convincing. More is to be expected from the potential role of ARAs in heart failure with normal ejection fraction and perhaps in atrial fibrillation. It is hoped that the results of large randomized clinical trials further elucidate the indications of ARAs beyond current guidelines.

Distinct contractile and molecular differences between two goat models of atrial dysfunction: AV block-induced atrial dilatation and atrial fibrillation.

Atrial dilatation is an independent risk factor for thromboembolism in patients with and without atrial fibrillation (AF). In many patients, atrial dilatation goes along with depressed contractile function of the dilated atria. While some mechanisms causing atrial contractile dysfunction in fibrillating atria have been addressed previously, the cellular and molecular mechanisms of atrial contractile remodeling in dilated atria are unknown. This study characterized in vivo atrial contractile function in a goat model of atrial dilatation and compared it to a goat model of AF. Differences in the underlying mechanisms were elucidated by studying contractile function, electrophysiology and sarcoplasmic reticulum (SR) Ca2+ load in atrial muscle bundles and by analyzing expression and phosphorylation levels of key Ca2+-handling proteins, myofilaments and the expression and activity of their upstream regulators. In 7 chronically instrumented, awake goats atrial contractile dysfunction was monitored during 3 weeks of progressive atrial dilatation after AV-node ablation (AV block goats (AVB)). In open chest experiments atrial work index (AWI) and refractoriness were measured (10 goats with AVB, 5 goats with ten days of AF induced by repetitive atrial burst pacing (AF), 10 controls). Isometric force of contraction (FC), transmembrane action potentials (APs) and rapid cooling contractures (RCC, a measure of SR Ca2+ load) were studied in right atrial muscle bundles. Total and phosphorylated Ca2+-handling and myofilament protein levels were quantified by Western blot. In AVB goats, atrial size increased by 18% (from 26.6+/-4.4 to 31.6+/-5.5 mm, n=7 p<0.01) while atrial fractional shortening (AFS) decreased (from 18.4+/-1.7 to 12.8+/-4.0% at 400 ms, n=7, p<0.01). In open chest experiments, AWI was reduced in AVB and in AF goats compared to controls (at 400 ms: 8.4+/-0.9, n=7, and 3.2+/-1.8, n=5, vs 18.9+/-5.3 mmxmmHg, n=7, respectively, p<0.05 vs control). FC of isolated right atrial muscle bundles was reduced in AVB (n=8) and in AF (n=5) goats compared to controls (n=9) (at 2 Hz: 2.3+/-0.5 and 0.7+/-0.2 vs 5.5+/-1.0 mN/mm2, respectively, p<0.05). APs were shorter in AF, but unchanged in AVB goats. RCCs were reduced in AVB and AF versus control (AVB, 3.4+/-0.5 and AF, 4.1+/-1.4 vs 12.2+/-3.2 mN/mm2, p<0.05). Protein levels of protein kinase A (PKA) phosphorylated phospholamban (PLB) were reduced in AVB (n=8) and AF (n=8) vs control (n=7) by 37.9+/-12.4% and 29.7+/-10.1%, respectively (p<0.01), whereas calmodulin-dependent protein kinase II (CaMKII) phosphorylated ryanodine channels (RyR2) were increased by 166+/-55% in AVB (n=8) and by 146+/-56% in AF (n=8) goats (p<0.01). PKA-phosphorylated myosin-binding protein-C and troponin-I were reduced exclusively in AVB goat atria (by 75+/-10% and 55+/-15%, respectively, n=8, p<0.05). Atrial dilatation developing during slow ventricular rhythm after complete AV block as well as AF-induced remodeling are associated with atrial contractile dysfunction. Both AVB and AF goat atria show decreased SR Ca2+ load, likely caused by PLB dephosphorylation and RYR2 hyperphosphorylation. While shorter APs further compromise contractility in AF goat atria, reduced myofilament phosphorylation may impair contractility in AVB goat atria. Thus, atrial hypocontractility appears to have distinct molecular contributors in different types of atrial remodeling.

Chronic atrial dilation, electrical remodeling, and atrial fibrillation in the goat.

OBJECTIVES: This study was designed to investigate the mutual effects of chronic atrial dilation and electrical remodeling on the characteristics of atrial fibrillation (AF). BACKGROUND: Both electrical remodeling and atrial dilation promote the inducibility and perpetuation of AF. METHODS: In seven goats AF was induced during 48 h by burst pacing, both at baseline and after four weeks of slow idioventricular rhythm (total AV block). Atrial size and refractory period (AERP) were monitored together with the duration and cycle length of AF paroxysms (AFCL). After four weeks of total atrioventricular (AV) block, the conduction in both atria was mapped during AF. Six non-instrumented goats served as controls. RESULTS: At baseline, AF-induced electrical remodeling shortened AERP and AFCL to the same extent (from 185 +/- 9 ms to 149 +/- 14 ms [p < 0.05] and from 154 +/- 11 ms to 121 +/- 5 ms [p < 0.05], respectively). After four weeks of AV block the right atrial diameter had increased by 13.2 +/- 3.0% (p < 0.01). Surprisingly, in dilated atria electrical remodeling still shortened the AERP (from 165 +/- 9 ms to 132 +/- 15 ms [p < 0.05]) but failed to shorten the AFCL (140 +/- 19 ms vs. 139 +/- 11 ms [p = 0.98]). Mapping revealed a higher incidence of intra-atrial conduction delays during AF. Histologic analysis showed no atrial fibrosis but did reveal a positive correlation between the size of atrial myocytes and the incidence of intra-atrial conduction block (r = 0.60, p = 0.03). CONCLUSIONS: In a goat model of chronic atrial dilation, AF-induced electrical remodeling was unchanged. However, AFCL no longer shortened during electrical remodeling. Thus, in dilated atria a wider excitable gap exists during AF, probably caused by intra-atrial conduction defects and a higher contribution of anatomically defined re-entrant circuits.