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Erstmals sind Leitlinien fur Sportkardiologie von der European Society of Cardiology (ESC) veroffentlicht worden. Hintergrund ist die Frage nach Empfehlungen zu korperlicher Aktivitat, korperlichem Training sowie Moglichkeiten der Teilnahme an Freizeitsport oder auch Freigabe fur den Leistungssport bei Patienten mit kardiovaskularen Risikofaktoren oder Herzerkrankungen. Die Leitlinien umfassen Empfehlungen fur Patienten mit kardiovaskularen Risikofaktoren, chronischer koronarer Herzerkrankung, chronischer Herzinsuffizienz, Herzklappenerkrankungen, Aortenerkrankungen, Kardiomyopathien, nach Myokarditis und Perikarditis, bei Rhythmusstorungen, Ionenkanalerkrankungen oder kongenitalen Herzerkrankungen. Basis fur die Bewertung der Sport- und Wettkampftauglichkeit sowie der individuellen Empfehlungen zu Belastbarkeit und Training ist die kombinierte kardiologische und sportmedizinische Diagnostik. In der Zusammenschau dieser Ergebnisse und der individuellen medizinischen sowie sportlich-korperlichen Anspruche muss im Sinne des „shared decision making“ eine fundierte Empfehlung gegeben werden. Diese ist nicht immer einfach, weil die Empfehlungen in der ESC Leitlinie Sportkardiologie haufig auf Basis von schwacher wissenschaftlicher Evidenz ausgesprochen werden und sehr durch Erfahrungen und spezifische Erkenntnisse gepragt sind. Deshalb ist eine spezielle Weiterbildung innerhalb der Kardiologie notwendig, welcher durch die Zusatzqualifikation der DGK Rechnung getragen wird.

Purpose The potent, selective phosphodiesterase-9A inhibitor BI 409306 may be beneficial for patients with attenuated psychosis syndrome and could prevent relapse in patients with schizophrenia. Transient BI 409306-dependent increases in heart rate (HR) demonstrated previously necessitated cardiac safety characterisation. We evaluated cardiac effects of BI 409306 in healthy volunteers during rest and exercise. Methods In this double-blind, three-way crossover study, volunteers received placebo, BI 409306 50 mg or 200 mg in randomised order (same treatment on Days 1 [resting] and 3 [exercise]). Cardiopulmonary exercise testing was performed twice post treatment on Day 3 of each period. BI 409306-mediated effects on placebo-corrected change from baseline in resting HR (ΔΔHR) were evaluated based on exposure–response analysis and a random coefficient model. Adverse events (AEs) were recorded. Results Overall, 19/20 volunteers completed. Resting ΔΔHR versus BI 409306 concentration yielded a slope of 0.0029 beats/min/nmol/L. At the geometric mean (gMean) maximum plasma concentration (Cmax) for BI 409306 50 and 200 mg, predicted mean (90% CI) ΔΔHRs were 0.80 (− 0.76, 2.36) and 5.46 (2.44, 8.49) beats/min, respectively. Maximum adjusted mean differences from placebo (90% CI) in resting HR for BI 409306 50 and 200 mg were 3.85 (0.73, 6.97) and 4.93 (1.69, 8.16) beats/min. Maximum differences from placebo in resting HR occurred at/near gMean Cmax and returned to baseline after approximately 4 h. The proportion of volunteers with AEs increased with BI 409306 dose. Conclusion Observed hemodynamic effects following BI 409306 administration were of low amplitude, transient, and followed the pharmacokinetic profile of BI 409306.

To evaluate feasibility of an exercise intervention consisting of high-intensity interval endurance and strength training in breast cancer patients.Twenty-six women with nonmetastatic breast cancer were consecutively assigned to the exercise intervention- (n= 15, mean age 51.9 ± 9.8 years) and the control group (n = 11, mean age 56.9 ± 7.0 years). Cardiopulmonary exercise testing that included lactate sampling, one-repetition maximum tests and a HADS-D questionnaire were used to monitor patients both before and after a supervised six weeks period of either combined high-intensity interval endurance and strength training (intervention group, twice a week) or leisure training (control group).Contrarily to the control group, endurance (mean change of VOOur guided exercise intervention could be used effectively for initiation and improvement of performance capacity and quality of life in breast cancer patients in a relatively short time. This might be especially attractive during medical treatment. Long-term effects have to be evaluated in randomized controlled studies also with a longer follow-up. Implications for Rehabilitation High-intensity interval training allows improvement of aerobic capacity within a comparable short time. Standard leisure training in breast cancer patients is rather suitable for the maintenance of performance capacity and quality of life. Guided high-intensity interval training combined with strength training can be used effectively for the improvement of endurance and strength capacity and also quality of life. After exclusion of contraindications, guided adjuvant high-intensity interval training combined with strength training can be safely used in breast cancer patients.

Atrial fibrillation (AF) is the most common arrhythmia in adult age. Several clinical markers and molecular mechanisms are associated with AF. A large proportion of AF patients experience a reduction of exercise capacity and suffer from dyspnea or early fatigue. The mechanistic link between AF and exercise intolerance is complicated by the fact that AF often occurs in the presence of heart disease like heart failure or valvular dysfunction, which both present with similar symptoms. Exercise can be either protective or a risk factor for AF. This chapter focuses on non-athletes, where exercise has the potential to improve exercise capacity and reduce the burden of AF, mainly by positively affecting risk factors like obesity and hypertension. Sports eligibility and risk of oral anticoagulation are discussed. Specific aspects of exercise testing and training recommendations are explained. Patients with AF can be included in cardiac rehabilitation programs based on their underlying cardiac disease and risk factor profile.

The detection of left ventricular hypertrophy (LVH) is still a common objective of electrocardiography (ECG) in clinical practice. The aim of our study was to evaluate the accuracy of LVH ECG indices in people older than 65 recruited from a population-based cohort (ActiFE-Ulm study). In 432 subjects (mean age 76.2 ± 5.5 years, 51% male), left ventricular mass was echocardiographically determined (Devereux formula) and indexed (LVMI) to body surface area. Several LVH ECG indices (Lewis voltage, Gubner–Ungerleider voltage, Sokolow–Lyon voltage/product, Cornell voltage/product) were calculated with the help of resting ECG data and compared with the echocardiographic assessment. Despite echocardiographic signs of LVH [LVMI > 115 (♂) or >95 g/m2 (♀)] in 47.5% of all subjects, diagnostic performance of all ECG indices was generally low. Magnitude of all LVH-indices was mainly predicted by frontal QRS axis in multivariate linear regression analysis. In comparison with the literature data from younger subjects, average frontal QRS axis turned counterclockwise. Most probably, age-related counterclockwise turn of frontal QRS axis is mainly explanatory for the decreased magnitude of LVH ECG indices and consecutive worse diagnostic performance of these indices in the elderly. ECG indices for detection of LVH have insufficient predictive values in geriatric subjects and should therefore not be used clinically for this purpose. Nevertheless, due to its established relevancy in cardiac risk stratification in this age group, usage of some established ECG indices might keep its significance even in the age of modern cardiac imaging.

The aim of our study was to obtain right ventricular (RV) tissue Doppler imaging (TDI) data in older subjects (n = 95, mean age: 74.5 ± 4.6 years) without evidence of hemodynamically significant structural heart disease recruited from a large population-based cohort (ActiFE-Ulm study). Our data indicate that aging may be accompanied by decreasing RV diastolic function and at most little alterations of RV systolic function. Mean values of all parameters were still within the guideline-suggested reference range with most of them closer to the abnormality thresholds. On an individual basis, respective thresholds were also exceeded in some subjects (almost all parameters

A sexual dimorphism has been reported for the adipo-myokine irisin at rest and in response to exercise. The effects of male and female sex, adiposity, and gonadectomy on irisin secretion have not been investigated before. The objective of this study was to elucidate the effects of sex, adiposity, and gonadectomy in the regulation of irisin secretion as well as PGC-1α/FNDC5 mRNA and protein expression. We hypothesized that a lack of female sex hormones by ovariectomy reduces irisin levels and inhibits skeletal muscle expression of PGC-1α and FNDC5. Circulating irisin was measured in vivo in serum samples of healthy and obese men and women at rest and in response to acute exercise. The effects of gonadectomy on serum irisin, PGC-1α and FNDC5 muscle mRNA, and protein expression were investigated in ovariectomized (OVX) and orchiectomized (ORX) Wistar rats. Serum irisin at rest was not significantly different between men and women (lean or obese). However, in response to acute aerobic exercise, irisin levels increased significantly more in lean women versus men (p ≤ 0.05). In obese individuals, resting irisin concentrations were significantly higher compared to lean subjects (p ≤ 0.001) and the irisin response to acute exercise was blunted. Only the lack of gonadal hormones in OVX but not ORX rats increased serum irisin levels (p ≤ 0.01) and resulted in significantly increased body weight (p ≤ 0.01), adipose tissue content (p ≤ 0.05), muscle FNDC5 mRNA (p ≤ 0.05), and protein (p ≤ 0.01) expression without altering PGC-1α expression. Testosterone treatment in ORX rats leads to increased PGC-1α mRNA content and reduced PGC-1α protein content without affecting FDNC5 expression or serum irisin levels. We show that a sexual dimorphism exists for the acute irisin response to exercise in normal-weight but not in obese subjects. OVX, which is associated with increased adiposity and insulin insensitivity, increases basal FNDC5 expression and serum irisin, without altering PGC-1α expression. This may be an early sign for metabolic disturbances associated with menopause, such as a developing irisin resistance or an attempt of the organism to improve glucose metabolism.

There is an increasing number of patients receiving an ICD due to a hereditary and/or electrical cardiomyopathy [1, 2]. These patients often have the ability to practice competitive sports despite their disease as performance capacity is at most marginally affected. Because of this situation, sports physicians are increasingly confronted with the evaluation of athletes with ICD concerning competitive sports participation. Current guidelines almost invariably prohibit competitive sports participation of ICD patients [3]. However, these recommendations are critically questioned due to their low level of evidence [4]. Here, we present the case of a professional soccer player with hypertrophic cardiomyopathy (HCM) and ICD implanted for primary prevention of sudden cardiac death. Contrary to current recommendations [3, 5, 6], we certified ability for competitive sports participation, whereupon establishment of a close meshed follow-up using Home Monitoring [7] was one important prerequisite for our decision. A 23-year old professional soccer player (third German football league, formerly U21 national team) was introduced by the team doctor due to resting ECG abnormalities. The patient negated any current leading cardiovascular symptoms. However, he reported of three syncopal events within the last 5 years, detailed description rather pointed to a non-cardiac cause. Family history for sudden cardiac death was inconspicuous. Resting ECG showed preterminal T-wave negativity of precordial leads. Ergometry up to 360 W revealed a normal RR-regulation, no arrhythmias, an erection of the negative T-waves and no ECG-alterations suspicious for cardiac ischemia. Echocardiographically, basal septum was mildly hypertrophied (13 mm end-diastolic) with implied apical accentuation. Left ventricular diameter (53 mm end-diastolic), size of the atria, total heart volume (880 ml, respectively, 11.0 ml/kg bodyweight) and left ventricular systolic and diastolic function were normal. Evaluation of right ventricular morphology and function resulted in a slight enlargement and no evidence for impaired systolic function. Because of our findings, we arranged further cardiac imaging. Cardiac MRI revealed an asymmetrical, midventricular to apical septal hypertrophy up to 18 mm (enddiastolic) with an atypical scar within the center consistent to hypertrophic cardiomyopathy (Fig. 1). In the first instance, based on the diagnosis, we did not certify ability for competitive sports participation [5]. Prognosis was estimated to be good due to a hypertrophy \30 mm, normal blood pressure regulation during exercise, negative family history concerning sudden cardiac death and absence of left ventricular outflow tract obstruction [8]. In our opinion, arrhythmia risk seemed to be rather low at this time-point, as additional 7-day Holter ECG showed no abnormalities. For further risk stratification, we recommended the implantation of an event recorder. However, the patient was told to visit an arrhythmia center for a second opinion and thereafter, he should re-visit us to organize further treatment. Our suggested procedure was confirmed by the center. Thereafter, the patient obtained a third opinion in another hospital on his own initiative. In this clinic—unfortunately without contacting us before—an ICD was & Roman Laszlo roman.laszlo@uniklinik-ulm.de

Catheter ablation has become the first line of therapy in patients with symptomatic, recurrent, drug-refractory atrial fibrillation. However, catheter ablation of persistent atrial fibrillation is still a challenge. Various rather complex ablation strategies exist and their results are not very favorable. Therefore, the aim of our study was to evaluate a well-defined reasonable approach to catheter ablation of persistent atrial fibrillation. The strategy consisted of a circumferential pulmonary vein ablation in combination with a potential-guided segmental approach to achieve complete pulmonary vein isolation and a linear lesion at the roof of the left atrium. A total of 43 patients (30 men, 13 women; mean age 55 years (SD ± 9 years)) with symptomatic persistent atrial fibrillation were enrolled in this study. All patients underwent catheter ablation of persistent atrial fibrillation using the above-mentioned approach (with the CARTO or the NAVX system). Additionally, catheter ablation of the mitral isthmus and the right atrial isthmus was performed in selected cases. In all patients, cardiac MRI or multi-detector spiral computed tomography was performed prior to the ablation procedure and a surface rendered model of the left atrium was created. After discharge, patients were scheduled for repeated visits at the arrhythmia clinic at 1, 3, 6, 9, and 12 months after the ablation procedure. The ablation procedure could be performed as planned in all 43 patients. Nine patients had to undergo a repeat ablation procedure, so that a total of 52 procedures were evaluated. An additional linear lesion was created at the mitral isthmus in three patients (7%) during the initial procedure and in one patient (2.3%) during the second procedure. Catheter ablation of the right atrial isthmus was performed in 11 patients (25.6%) during the first procedure and in four additional patients during the redo procedure (9.3%). Twenty-four out of 43 patients (55.8%) experienced an arrhythmia recurrence within the first 3 months after ablation requiring an electrical cardioversion. At 1-year follow-up, analysis of a 7-day Holter monitoring revealed no evidence for an arrhythmia recurrence in 26 of 43 patients (60.5%). In nine of 43 patients (20.9%), only short episodes of paroxysmal atrial fibrillation were documented. In eight patients (18.6%), a recurrence of persistent atrial fibrillation (>48 h) was revealed by the long-term recordings. A duration of persistent atrial fibrillation >3 months was the most powerful predictor for arrhythmia recurrences at 1-year follow-up. A subgroup analysis revealed a markedly higher rate of stable sinus rhythm at 1-year follow-up in patients with a short duration of atrial fibrillation (≤3 months) compared to patients with a longer duration of AF (>3 months) prior to the procedure (72.0% versus 44.4%). There were no major complications. Catheter ablation of persistent atrial fibrillation can be performed safely and effectively using this ablation strategy (especially in patients with short-lasting persistent atrial fibrillation (≤3 months)).

Aims Atrial fibrillation (AF) leads to electrical atrial remodeling including alterations of various ion channels early after arrhythmia onset. The beneficial effects of statins in AF treatment due to their influence on oxidative stress and inflammation are discussed. Our hypothesis was that statins might also alter atrial ion currents and their early tachycardia-induced remodeling. Main methods Effects of an atorvastatin treatment (7 days) on atrial ion currents and their tachycardia-induced alterations were studied in a rabbit model of tachycardia-induced electrical remodeling (rapid atrial pacing (600 min) for 24 and 120 h). Ion currents (L-type calcium channel [I Ca,L ], transient outward current [I to ]) were measured using whole cell patch clamp method and were compared with previous experiments in untreated but also tachypaced animals. Key findings Atorvastatin treatment alone decreased I Ca,L similar to rapid atrial pacing alone, currents were also further reduced by additional atrial tachypacing. I to and its pacing-induced down-regulation after 24 h were not influenced by atorvastatin treatment. However, I to was still reduced after 120 h in atorvastatin-treated animals and did not return to control values as expected. Significance The present study establishes that an atorvastatin treatment can affect atrial ion currents and their tachycardia-induced remodeling in a rabbit model. These results show that—amongst other positive effects on oxidative stress and inflammation—the impact of statins on ion currents and their tachycardia-induced alterations might also play a role in “upstream” treatment of AF with HMG-CoA reductase inhibitors.

Catheter ablation is of growing importance in patients with an ischemic cardiomyopathy and recurrent episodes of ventricular tachyarrhythmias. Most ablation strategies in these patients are based on the detection of areas of scar and border zones to normal myocardium. However, the mapping criteria for identifying these areas have not been validated sufficiently so far. Therefore, we have performed a comparison between electroanatomical bipolar voltage maps obtained during substrate-based VT ablation procedures and [18 F]fluoro-2-deoxyglucose PET studies performed prior to these procedures.Seven patients suffering from severe coronary artery disease and repetitive ventricular tachycardias were enrolled in this study. In all patients, there was a history of myocardial infarction and the left ventricular function was severely impaired. A FDG PET was performed at least 1 day prior to the ablation procedure in all patients. Then, a substrate-based VT ablation procedure was performed using the CARTO system (Biosense Webster, Diamond Bar, CA, USA). Finally, the FDG PET images and the bipolar voltage maps were compared in all patients.The ablation procedures could be performed successfully in all patients and 1-5 monomorphic VTs could be eliminated in each patient. There were no major complications. At 1-year follow-up, five out of seven patients (71.4%) remained free from any arrhythmia recurrence. In all patients, there were extensive areas of scar and adjacent low-voltage areas could be identified in the CARTO bipolar voltage maps. In areas commonly defined as "dense scar" (bipolar voltage amplitude0.5 mV), the mean FDG uptake was 43.1% (SD ±18.2%) indicating predominantly scar tissue. In the so-called low-voltage border zones the mean FDG uptake ranged between 49.5% [(SD ±15.8%);0.5-1 mV] and 60.1% [(SD ±14.8%);1-1.5 mV], thereby indicating the presence of predominantly viable myocardium. In areas with a bipolar voltage amplitude1.5 mV the presence of viable myocardium was confirmed by a mean FDG uptake of approximately 60%.The results of our study demonstrate that there is a significant amount of viable myocardium in the low-voltage border zones of scars frequently targeted as ablation sites. Therefore, RF current delivery in these areas should be restricted to the minimum assumed to be necessary for successful catheter ablation because extensive RF applications might result in a further deterioration of the left ventricular function. Larger studies are needed to validate our results and to develop more reliable criteria for distinguishing areas of scar from viable myocardium in CARTO bipolar voltage maps.

Atrial fibrillation is the most common supraventricular arrhythmia in humans, basic and clinical sciences are still developing. This present review aims to inform non-cardiologists respectively non-electrophysiologists about the most important pathophysiological concepts and their influence on therapeutical principles of atrial fibrillation. Moe's and Allessie's "multiple wavelet" theory is introduced as well as Haissaguerre's concept of ectopic triggering of paroxysmal atrial fibrillation and the most important aspects of atrial remodeling ("atrial fibrillation begets atrial fibrillation" according to Wijffels) during persistence of atrial fibrillation. Impact of these pathophysiological concepts is discussed within the context of medicamentous, surgical and interventional therapy. Concomitantly, limitations of these therapies due to pathophysiological considerations are delineated.

Background: Certain evidence points to a role of inflammation in AF pathophysiology. Thus, antiinflammatory treatment of AF is discussed. Effects of a dexamethasone treatment (7 days) on atrial ion currents (ICa,L, Ito, Isus) and their tachycardia-induced remodeling were studied in a rabbit model. Methods: 6 groups of 4 animals each were built. Rapid atrial pacing (600 min) was performed for 24 and 120 hours with/ without dexamethasone treatment. Ion currents were measured using whole cell patch clamp method. Results: Rapid atrial pacing reduced (ICa,L, Ito was decreased after 24 hours but almost returned to control values after 120 hours. When dexamethasone-treated animals also underwent atrial tachypacing, pacing-induced reduction of ICa,L was still observed after 24 hours and was even augmented after 120 hours compared to untreated but tachypaced animals. Ito was not influenced by dexamethasone alone. In dexamethasone-treated animals, reduction of Ito was not observed after 24 hours but occurred after 120 hours of atrial tachypacing. Isus was neither influenced by rapid atrial pacing nor by dexamethasone. Biophysical properties of all currents were affected neither by rapid atrial pacing nor by dexamethasone. Conclusion: Dexamethasone influenced tachycardia-induced alterations of atrial Ito. Our experiments give evidence that - amongst other anti-inflammatory action – impact of dexamethasone on ion currents and their tachycardia-induced alterations might also play a role in treatment/prevention of AF with steroids.

Background In some patients, above-average alcohol consumption before occurrence of atrial fibrillation (AF) in terms of a "holiday heart syndrome" (HHS) can be determined. There is evidence that long before development of apparent alcohol-induced cardiomyopathy, above-average alcohol consumption generates an arrhythmogenic substrate which abets the onset of AF. Changes of atrial current densities in terms of an electrical remodeling after sustained short-term ethanol infusion in rabbits as a potential part of HHS pathophysiology were examined in this study. Methods Rabbits of the ethanol group (EG) received sustained short-term intravenous alcohol infusion for 120 hours (during infusion period, blood alcohol level did not fall below 158 mg/dl), whereas NaCl 0.9% was infused in the placebo group (PG). Using patch clamp technique in whole-cell mode, atrial current densities were measured and compared between both groups. Results Ethanol infusion did not alter current densities of I(to) [58.7 +/- 5.0 pA/pF (PG, n = 20 cells) vs. 53.9 +/- 5.0 pA/pF (EG, n = 24)], I(sus) [11.3 +/- 1.4 pA/pF (PG, n = 20) vs. 10.2 +/- 1.0 pA/pF (EG, n = 24)], and I(K1) [-1.6 +/- 0.3 pA/pF (PG, n = 17) vs. -2.0 +/- 0.3 pA/pF (EG, n = 22)]. However, alcohol infusion resulted in a remarkable reduction of I(Ca,L) current densities [-28.4 +/- 1.8 pA/pF (PG, n = 20) vs. -15.2 +/- 1.4 pA/pF (EG, n = 22)] and I(Na) [-75.4 +/- 3.6 pA/pF (PG, n = 17) vs. -35.4 +/- 4.4 pA/pF (EG, n = 21)], respectively. Conclusion Sustained short-term ethanol infusion in rabbits alters atrial current densities. HHS might be favored by alcohol-induced atrial electrical remodeling.

Wir berichten von einem Patienten mit ventrikularen Tachyarrhythmien, die wahrend einer manifesten Sepsis nach schwerer Brandverletzung in einen elektrischen Sturm mundeten. Das Oberflachen EKG in der Akutphase zeigte Zeichen von zwei moglichen Ursachen fur diesen lebensbedrohlichen Zustand: 1.) Brugada-Syndrom 2.) kardiale Ischamie. In Angesicht der komplexen klinischen Situation (manifeste Sepsis, Brandverletzungen) differierte unser Behandlungsansatz vom ublichen Management des elektrischen Sturms: unter der primaren Annahme eines fieber-induzierten Brugada-Syndroms initiieren wir eine aggressive Normalisierung der Korpertemperatur anstelle von einer antiadrenergen und antiarrhythmischen Behandlung beziehungsweise einer Koronarangiographie zum Ausschluss einer kardialen Ischamie als Trigger des elektrischen Sturms.

The aim of this study was to assess concurrent validity between activPAL and activPAL3 accelerometers in a sample of 53 community-dwelling older adults ≥ 65 years. Physical activity (PA) was measured simultaneously with activPAL and activPAL3 while performing scripted activities. The level of agreement between both devices was calculated for sitting/lying, standing, and walking. In addition, PA was measured over one week using activPAL to estimate the expected agreement with activPAL3 in real life. Overall agreement between activPAL and activPAL3 was 97%. Compared with activPAL, the largest disagreement was seen for standing, with 5% categorized as walking by activPAL3. For walking and sitting/lying, the disagreement was 2%, respectively. The expected daily differences between activPAL3 and activPAL were +15.0 min (95% CI: 11.3-18.8) for walking and +29.5 min (95% CI: 6.2-52.7) for standing. ActivPAL and activPAL3 showed good agreement in older adults. However, if using these devices interchangeably, observed differences might still bias results.

We investigated the effects of a 7-day verapamil pretreatment (VPT, 7.5 mg/kg bodyweight subcutaneously every 12 h) on ionic currents and molecular mechanisms underlying tachycardia-induced early electrical remodeling after 24-h rapid atrial pacing (RAP, 600 bpm) in rabbit atrium. Animals were divided into four groups (n = 6 each group): control (not paced, no verapamil), paced only, verapamil only and verapamil and paced, respectively. VPT doubled ICa,L [7.0 +/- 0.7 pA/pF (control) vs 14.2 +/- 0.6 pA/pF (verapamil only)]. RAP reduced ICa,L by 48% to 3.6 +/- 0.7 pA/pF (paced only). RAP did not affect ICa,L in verapamil-treated animals and averaged 15.3 +/- 0.2 pA/pF (paced and verapamil). RAP resulted in a significant decrease of the expression of the alpha1c subunit (-24.7%) and the beta2A subunit (-13.3%), respectively. VPT led to a similar alteration of subunit expression as RAP ["control" vs "verapamil only", decrease of alpha1c subunit (-25.4%), but no significant change in beta2A subunit expression]. However, after VPT, further diminishment of alpha1c and beta2A subunit expression after rapid atrial pacing was absent. ("verapamil" vs "verapamil and paced", n = 6 both groups). RAP decreased Ito [-45%, 51.5 +/- 3.9 pA/pF (control) vs 26.8 +/- 1.5 pA/pF (paced only)] and was not influenceable by VPT. IK1 was neither affected by RAP nor verapamil pretreatment. Downregulation of alpha1c and beta2A subunit expression and the resulting decay of ICa,L current densities were prevented by verapamil. However, these effects are abolished by multiple other adverse effects of verapamil on atrial electrophysiology.

Background: Box isolation of the posterior left atrium is one surgical or catheter ablative approach for treating atrial fibrillation (AF). In such cases, incomplete transmurality or recovery of pulmonary vein conduction after the application of various ablative techniques is considered the main reason for the recurrence of postprocedural arrhythmia. The use of solely cut-and-sew box isolation does not have these disadvantages and therefore demonstrates maximum efficacy for this therapeutic approach.Methods: We treated 15 patients with both an indication for open heart surgery and AF (2 paroxysmal, 6 short persistent [12 months] cases) with a solely cut-and-sew box lesion. These patients were then retrospectively followed up over the long term with respect to the end point of freedom of atrial tachyarrhythmias >30 seconds.Results: The median follow-up duration was 42 months (range, 32-84 months). Five (63%) of 8 patients with preoperative paroxysmal or short persistent AF had no arrhythmia recurrence, whereas arrhythmia recurrence was documented in all 7 patients with preoperative long persistent AF.Conclusions: Despite reliable transmural isolation with cut-and-sew lesions, we observed long-term arrhythmia recurrence in patients who had preoperative paroxysmal or short persistent AF, suggesting that therapy approaches that are more complex than box isolation might be needed for selected patients to achieve long-term stable sinus rhythm, despite the initially paroxysmal or short persistent character of the arrhythmia. A high rate of recurrence in patients with severe structural heart disease and preoperative long persistent AF might indicate that, in general, isolation of the left posterior atrium alone is not an adequate therapeutic approach for these patients.

Background and purpose Studies report on the reversal of electrophysiological parameters altered by atrial tachycardia after cessation of the latter. However, there is no data concerning reversal of tachycardia-induced alterations of ion currents. Reverse remodeling of atrial ion currents ( I Ca,L , I to , I sus ) was studied in our rabbit model of tachycardia-induced electrical remodeling. Methods Three groups each with four animals were built. Rapid atrial pacing (600/min) for 5 days was applied in all groups. Thereafter, different time intervals (5, 10, 20 days) were awaited before the patch clamp experiments. Results Similar to I to remodeling in our model, within 20 days after cessation of atrial tachycardia, time course of I to reverse remodeling was also U-shaped. In contrast, there was no significant recovery of I Ca,L which was initially reduced by rapid atrial pacing. Conclusion Relevance of a missing recovery of I Ca,L is likely as this current is closely linked with intracellular calcium handling.

Atrial fibrillation (AF) results in tachycardia-induced ionic remodeling. Pharmacological prevention of tachycardia-induced ionic remodeling not only with "classical" antiarrhythmics but also with drugs which provide a basis for some of the pillars of the so-called "upstream" therapy of AF like corticosteroids or statins has been proposed as a therapeutic strategy. Amongst other ion currents, atrial sodium current I(Na) and its tachycardia-induced alterations play an important role in AF pathophysiology. Thus, effects of a dexamethasone (DT) and atorvastatin treatment (AT) on atrial sodium current I(Na) and its tachycardia-induced remodeling were studied in a rabbit model.9 groups with 4 animals were examined. Atrial pacemaker leads were implanted in all animals. No rapid atrial pacing (600/min) was performed in the control group but for 24 or 120 hours in the respective pacing groups. Instrumentation and pacing did not differ from the respective drug groups but an additional treatment with dexamethasone or atorvastatin (7 days) was performed.Rapid atrial pacing (RAP, 600/min) reduced I(Na) after 24 hours (≈ -50%) with no further reduction after 120 hours. DT reduced I(Na) (≈ -20%), current densities in consecutively tachypaced animals did not differ from those in untreated animals. AT reduced INa similar as RAP, subsequent RAP did not further diminish I(Na).Impact of corticosteroids and statins on INa and its tachycardia-induced alterations also contribute to the mode of action of these substances in upstream treatment of atrial fibrillation.

More and more implantable cardioverter-defibrillators (ICDs) are implanted as primary prevention of sudden cardiac death (SCD). However, major problem in practice is to identify high-risk patients for SCD. Different methods for noninvasive risk stratification do not have a sufficient positive or negative predictive value. Since current approaches lead to implantation of ICDs in a large number of patients who will never suffer an arrhythmic event and simultaneously patients still die of SCD who currently did not seem eligible for primary preventive ICD implantation, there is a need for additional tools for risk stratification. Epidemiological studies point to a hereditary risk of SCD. Different susceptibility of each person concerning arrhythmogenic events might be explained by genetic polymorphisms. By obtaining an individual “pattern” of polymorphisms of genes encoding for proteins which are important in arrhythmogenesis in one patient, risk stratification in primary prevention of SCD might by improved.

Introduction. Tachycardia-induced atrial remodelling (as an equivalent to atrial fibrillation) can be influenced by the renin-angiotensin system. Effects of a seven-day enalapril pre-treatment (EPT, 0.16 mg/kg body weight subcutaneously every 24 h) on ionic currents underlying tachycardia-induced early electrical remodelling after 24 h rapid atrial pacing (RAP, 600 beats/min) in rabbit atrium were studied. Materials and methods. Animals were divided into four groups (n=4 each): control; paced only; enalapril only; and enalapril and paced, respectively. Using patch-clamp technique in whole-cell mode, current densities were measured in isolated atrial myocytes. Results. EPT nearly doubled L-type calcium current (ICa,L, −7.7±0.6 pA/pF [control] vs. f −12.3±1.2 pA/pF [enalapril only]). RAP reduced ICa,L to −3.6±0.7 pA/pF (paced only). Also after EPT, RAP led to a significant downregulation of ICa,L by 39% (−7.5±1.3 pA/pF [paced and enalapril]). RAP decreased transient outward potassium current (Ito, −45%, 51.5±3.9 pA/pF [control] vs. 28.5±4.5 pA/pF [paced only]). EPT did not alter Ito (44.2±8.1 pA/pF [enalapril only]). However, RAP did not affect Ito in enalapril-treated animals and averaged 50.4±9.8 pA/pF (paced and enalapril). Conclusions. In summary, EPT has several effects on ion channels in rabbit atrium: 1) EPT increases ICa,L current density, but cannot prevent its downregulation due to RAP; 2) EPT has no influence on Ito current density, but can prevent its downregulation due to RAP. Although changes of single ion channels must be interpreted in context of the complex atrial electrophysiology as a whole, our results provide a possible explanation of the in vivo observation that angiotensin-converting enzyme inhibition is mainly beneficial on the early electrical remodelling due to the atrial fibrillation-equivalent RAP.

Catheter ablation has become the first line of therapy in patients with symptomatic, recurrent, drug refractory atrial fibrillation. However, catheter ablation of atrial fibrillation is still a challenge. This is partially due to the high degree of variability with regard to the individual anatomy. Nevertheless, 3D imaging systems (CT, MRI) provide detailed information about the individual left atrial and pulmonary vein morphology. A 3D CT or MRI reconstruction of the left atrium can be displayed in the Navx-/Ensite-system in a synchronised way during the ablation procedure, thereby facilitating the intervention. This study summarizes our preliminary experience with different strategies of AF ablation using the Navx-/Ensite-system and a CT-/MRI-guided approach.In a total of 41 patients, cardiac MRI (n = 7) or multi-detector spiral computed tomography (n = 34) was performed prior to an ablation procedure. Catheter ablation was performed for paroxysmal atrial fibrillation in 31 patients and for persistent atrial fibrillation in 10 patients. A 3D MRI or high resolution spiral CT data acquisition was performed and a surface rendered model of the LA was created. This model was displayed in the Navx-/Ensite-system throughout the ablation procedure.Catheter ablation was performed using the Navx-system (n = 38) or the Ensite-system (n = 3). Three strategies were used depending on the type of atrial fibrillation: segmental isolation of the pulmonary veins (facilitated by a 3D real-time visualization of the ablation catheter and a circumferential mapping catheter; group A: 20 patients), linear lesions (group C: 3 patients) and a combined approach (group B; 18 patients). The CT-/MRI-models provided an excellent overview over the pulmonary veins and the left atrial appendage. They revealed a high degree of variability with regard to the individual anatomy (e.g. dimensions of the left atrial appendage, pulmonary vein ostia). The CT scans provided a more detailed reconstruction of the left atrial anatomy than the MRI scans (especially in patients who were in atrial fibrillation at the time of the data acquisition). In some patients, the CT-/MRI-models revealed a very small diameter of some pulmonary veins or side branches close to the ostium (e.g. right inferior pulmonary vein). Therefore, no attempt was made to achieve complete pulmonary vein isolation in some patients. In group A, 16/20 (80%) patients had no arrhythmia recurrence [mean follow-up 359 days (SD +/- 317 days)]. Twelve out of eighteen (67%) patients in group B [mean follow-up 452 days (SD +/- 311 days)] and 2/3 (67%) patients in group C did not experience an arrhythmia recurrence [mean follow-up 1,000 days (SD +/- 34 days)]. There were no major complications.The information derived from 3D CT- or MRI-reconstructions facilitates AF ablations performed with the Navx-/Ensite-mapping system and enhances the safety of these procedures. Furthermore, the availability of an additional impedance-based 3D real-time visualization of the ablation catheter and the circular mapping catheter placed in the pulmonary veins represents a major advantage of the Navx system.

Background: Catheter ablation has become the first line of therapy in patients with symptomatic recurrent, drug-refractory atrial fibrillation (AF). The occurrence of an atrioesophageal fistula is a rare but serious complication after AF-ablation procedures. This risk is even present during segmental pulmonary vein (PV) ablation procedures because the esophagus does frequently have a very close anatomical relationship to the right or left PV ostia. The aim of the present study was to analyze whether the exclusion of areas adjacent to the esophagus does have a significant effect on the success rates after segmental pulmonary vein ablation procedures. Methods: Forty-three consecutive patients with symptomatic paroxysmal AF were enrolled in this study. In all patients, a segmental PV ablation procedure was performed. The procedures were facilitated by a 3D real-time visualization of the circumferential mapping catheter placed in the pulmonary veins using the NavX™ system (St. Jude Medical, St. Paul, MN, USA; open irrigated tip ablation catheter; 43°C; 30 W). In 21 patients, a complete ostial PV isolation was attempted regardless of the anatomical relationship between the ablation sites and the esophagus (group A). In the remaining 22 patients, the esophagus was marked by a stomach tube and areas adjacent to the esophagus were excluded from the ablation procedure (group B). After discharge, patients were scheduled for repeated visits at the arrhythmia clinic at 1, 3, and 6 months after the ablation procedure. Results: The segmental pulmonary vein ablation procedure could be performed as planned in all patients. In group A, all pulmonary veins could be isolated successfully in 14 out of 21 patients (67%). A mean number of 3.7 pulmonary veins (SD ± 0.5 PVs) were isolated per patient. The main reasons for an incomplete PV isolation were: small diameter of the PVs, side branches close to the ostium, or poorly accessible PV ostia. In group B, all PVs could be isolated successfully in only 12 out of 22 patients (55%; P = 0.54). A mean number of 3.2 PVs (SD ± 0.9 PVs) were isolated per patient (P = 0.05). This was mostly due to a close anatomical relationship to the esophagus. The ablation strategy had to be modified in 16/22 patients in group B because of a close anatomical relationship between the left (n = 10) or right (n = 6) PV ostia and the esophagus. After 3 months, the percentage of patients free from an AF recurrence was not significantly different between the two groups (90% vs 95%; P = 0.61). After 6 months, there was no significant difference between the success rates either (81% vs 82%; P = 1.0). There were no major complications in both groups. Conclusions: The exclusion of areas adjacent to the esophagus results in a moderately higher percentage of incompletely isolated PVs. However, it does not have a significant effect on the AF recurrence rate during short-term and mid-term follow-up.

Long-term atrial fibrillation changes in many regulatory and structural processes may result in stabilization of the arrhythmia. There is evidence that decreased amplitude of L-type Ca(2+) current - probably a key mechanism of atrial remodelling -resulting from changes in expression of regulatory proteins is at least jointly responsible.To assess the expressions of protein phosphatases PP1 and PP2A, as well as the effect of verapamil pretreatment (VPT), in the early phases of atrial fibrillation in a rabbit model.FOUR GROUPS, EACH CONSISTING OF SIX ANIMALS, WERE STUDIED: 'not paced, no drug' group; 'paced, no drug' group (rapid atrial pacing [RAP] 600 beats/min for 24 h); 'not paced, verapamil' (NPV) group (duration of VPT was seven days, verapamil 7.5 mg/kg was administered every 12 h); and 'paced, verapamil' (PV) group (pacemaker stimulation after VPT). Protein expression was evaluated by Western blot analysis.RAP resulted in an augmented (32%) PP1 expression (not paced, no drug group versus paced, no drug group). The increase in PP1 expression was prevented with VPT (NPV group versus PV group). Expression of PP2A was not influenced by RAP. However, VPT led to an increase of PP2A expression (16%) after RAP (NPV group versus PV group).Fortified expression of protein phosphatases might be - besides transcriptional downregulation of channel subunits - another important cause of reduced L-type Ca(2+) current after RAP. Blocking L-type Ca(2+) channels with verapamil to prevent tachycardia-induced changes of PP1 expression might be expedient.

Anamnese und klinischer Befund: Ein 71-jahriger Patient stellte sich wegen seit 4 Jahren, trotz Rhythmusprophylaxe mit Flecainid und Bisoprolol, anfallsweise auftretender Palpitationen, Atemnot und Mudigkeit vor. Im durchgefuhrten Langzeit-EKG konnte ein paroxysmales Vorhofflimmern dokumentiert werden. Untersuchungen: Die Ergometrie ergab bei insgesamt hypertensiver Reaktion keinen Hinweis auf eine belastungsinduzierte Koronarinsuffizienz. In der transosophagealen Echokardiographie konnten intrakavitare Thromben ausgeschlossen werden. Diagnose, Therapie und Verlauf: Es wurde die Diagnose eines therapierefraktaren, paroxysmalen Vorhofflimmerns gestellt und eine Pulmonalvenenisolation mit der Cryoballontechnik durchgefuhrt. In der 3-Monats-Nachsorgeuntersuchung konnte im 7-Tage-Holter kein paroxysmales Vorhofflimmern mehr nachgewiesen werden. Folgerung: Im Vergleich zur pharmakologischen Rhythmuskontrolle ist die interventionelle Pulmonalvenenisolation bei Patienten mit paroxysmalem Vorhofflimmern eine effektivere Therapieoption. Die Indikation zur Ablation sollte rechtzeitig erfolgen um ein strukturelles, atriales Remodeling und dadurch Chronifizierung des Vorhofflimmerns zu vermeiden. Die Entwicklung neuer Ablationstechniken tragt zur wesentlichen Vereinfachung der Prozedur und Steigerung des Sicherheitsprofils bei. Sollten sich die vielversprechenden Ergebnisse zur Effektivitat und Sicherheit der Cryoablation in laufenden kontrollierten Studien bestatigen, konnte die Erweiterung der Empfehlung zur Katheterablation als Erstlinientherapie bei Patienten mit paroxysmalen Vorhofflimmern zu erwarten sein.

Electrical cardioversion ist often the treatment of first choice for restoring sinus rhythm in patients with atrial fibrillation. This article reviews the management of patients undergoing electrical cardioversion. As risk of formation of an intra-atrial thrombus formation is low after a short duration of AF (less than 48 h), immediate cardioversion can be performed in these patients (except those with a high risk for thrombembolic events). However, if the AF has lasted for more than 48 hours, patients have to be treated either with anticoagulants for at least three weeks or an atrial thrombus has to be excluded by transesophageal echocardiography. Both options achieve the same short- or long-term success rate for cardioversion. Cardioversion is probably safe even if there are spontaneous echocardiographic contrasts as signs of potential thrombogenic slowing of atrial blood flow, but individual factors of risk/indication have to taken into account. Success rate of cardioversion depends on various patient characteristics as well as on some technical variables, biphasic instead of monophasic shocks being more effective. If there is an early recurrence of AF after initially successful cardioversion, administration of amiodarone (for 4 weeks) increases the success rate of subsequent cardioversion. After successful cardioversion subsequent antiarrhythmic therapy can reduce recurrence of AF. Thrombembolic complications are more frequent within the first few days after cardioversion. Indication for and duration of post-cardioversion anticoagulation depends on individual characteristics (CHADS(2) score) as well as on the duration of the preceding episode of AF.