[Anticoagulation after heart valve replacement]. / Antikoagulation nach Herzklappenersatz.

In patients after mechanical heart valve replacement anticoagulation is required for the prevention of thrombotic and thromboembolic events. In this setting oral anticoagulation can only be performed with vitamin K antagonists (VKA), while currently all available non-vitamin K dependent oral anticoagulants (NOAC) are contraindicated in patients with mechanical heart valve replacement. This review deals with anticoagulation in patients with mechanical heart valve replacement as well as coagulation inhibition after bioprosthetic or percutaneous valve replacement. In addition, recommendations are given for antithrombotic medication in patients with mechanical heart valve replacement in various clinical scenarios.

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.

[AV-reentrant tachycardia and Wolff-Parkinson-White syndrome : Diagnosis and treatment]. / AV-Reentry-Tachykardie und Wolff-Parkinson-White-Syndrom : Diagnostik und Therapie.

The AV-reentrant tachycardia (AVRT) is a supraventricular tachycardia with an incidence of 1-3/1000. The pathophysiological basis is an accessory atrioventricular pathway (AP). Patients with AVRT typically present with palpitations, an on-off characteristic, anxiety, dyspnea, and polyuria. This type of tachycardia may often be terminated by vagal maneuvers. Although the clinical presentation of AVRT is quite similar to AV-nodal reentrant tachycardias, the correct diagnosis is often facilitated by analyzing a standard 12-lead ECG at normal heart rate showing ventricular preexcitation. Curative catheter ablation of the AP represents the therapy of choice in symptomatic patients. This article is the fourth part of a series written to improve the professional education of young electrophysiologists. It explains pathophysiology, symptoms, and electrophysiological findings of an invasive EP study. It focusses on mapping and ablation of accessory pathways.

[Implantable loop recorders of the Reveal family (Medtronic)]. / Implantierbare Loop-Rekorder der Reveal-Familie (Fa. Medtronic).

This review explains the implantable loop recorders Medtronic Reveal XT and Medtronic Reveal LINQ. Technical specifications of the two devices are described in great detail. Additional tips for implantation as well as device programming are given including specific considerations of follow-up.

[Typical atrial flutter: Diagnosis and therapy]. / Typisches Vorhofflattern: Diagnostik und Therapie.

Typical, cavotricuspid-dependent atrial flutter is the most common atrial macroreentry tachycardia. The incidence of atrial flutter (typical and atypical forms) is age-dependent with 5/100,000 in patients less than 50 years and approximately 600/100,000 in subjects > 80 years of age. Concomitant heart failure or pulmonary disease further increases the risk of typical atrial flutter.Patients with atrial flutter may present with symptoms of palpitations, reduced exercise capacity, chest pain, or dyspnea. The risk of thromboembolism is probably similar to atrial fibrillation; therefore, the same antithrombotic prophylaxis is required in atrial flutter patients. Acutely symptomatic cases may be subjected to cardioversion or pharmacologic rate control to relieve symptoms. Catheter ablation of the cavotricuspid isthmus represents the primary choice in long-term therapy, associated with high procedural success (> 97 %) and low complication rates (0.5 %).This article represents the third part of a manuscript series designed to improve professional education in the field of cardiac electrophysiology. Mechanistic and clinical characteristics as well as management of isthmus-dependent atrial flutter are described in detail. Electrophysiological findings and catheter ablation of the arrhythmia are highlighted.

Safety of symptom-limited exercise testing in a big cohort of a modern ICD population.

BACKGROUND: Exercise may predispose to ventricular arrhythmias especially in patients with congestive heart failure. As therapy with implanted cardioverter-defibrillators (ICDs) has become standard medical care, there is an emerging number of exercise tests that need to be performed in patients with ICDs. In contrast, little is known about the safety of symptom-limited exercise testing in these patients. METHODS AND RESULTS: 400 ICD patients performed symptom-limited exercise treadmill testing. 200 patients performed a ramp protocol with an initial workload of 0 W increased by 15 W every minute. Another 200 ICD patients did a slightly modified ramp protocol with again an initial workload of 0 W but with an increased capacity of 15 W every 2 min. The study population consists mainly of patients with ischemic (63%) and non-ischemic (34%) heart disease. Atrial fibrillation was present in 16% of the subjects. The mean ejection fraction was 28 ± 8, and 78% of the patients had an ejection fraction below 30%. In this cohort of patients, no sustained ventricular arrhythmias and no deaths occurred during or after exercise testing. No inappropriate shock delivery was observed. The modified ramp protocol resulted in a prolonged exercise time with equal exercise capacity but does not result in an enhanced susceptibility for ventricular arrhythmias. CONCLUSIONS: Symptom-limited exercise treadmill testing in heart failure patients with ICDs is a safe procedure. The use of a ramp protocol is sufficient in terms of safety and is easy to perform in general practice. The exercise duration in heart failure patients with ICDs does not predict serious adverse events.

[AV nodal reentrant tachycardia. Diagnosis and therapy]. / AV-Knoten-Reentrytachykardie. Diagnostik und Therapie.

The AV nodal reentrant tachycardia (AVNRT) is one of the most common arrhythmias encountered in clinical practice. It is characterized by a constant heart rate and an on/off phenomenon. The clinical symptoms may include palpitations, anxiety, polyuria, and dyspnea. Typically, tachycardia may be disrupted by vagal maneuvers in many patients. First-line treatment of symptomatic AVNRT is radiofrequency ablation. The present article deals with the characteristics, differential diagnosis and treatment of AVNRT in the EP lab. It is the second part of a series of manuscripts which may facilitate further education in the specific field of electrophysiology.

Bacteriology of aspiration pneumonia in patients with acute coma.

Loss of protective airway reflexes in patients with acute coma puts these patients at risk of aspiration pneumonia complicating the course of the primary disease. Available data vary considerably with regard to bacteriology, role of anaerobic bacteria, and antibiotic treatment. Our objective was to research the bacteriology of aspiration pneumonia in acute coma patients who were not pre-treated with antibiotics or hospitalized within 30 days prior to the event. We prospectively analyzed 127 patient records from adult patients admitted, intubated and ventilated to a tertiary medical intensive care unit with acute coma. Bacteriology and antibiotic resistance testing from tracheal aspirate sampled within 24 h after admission, blood cultures, ICU scores (APACHE II, SOFA), hematology, and clinical chemistry were assessed. Patients were followed up until death or hospital discharge. The majority of patients with acute coma suffered from acute cardiovascular disorders, predominantly myocardial infarction, followed by poisonings, and coma of unknown cause. In a majority of our patients, microaspiration resulted in overt infection. Most frequently S. aureus, H. influenzae, and S. pneumoniae were isolated. Anaerobic bacteria (Bacteroides spec., Fusobacteria, Prevotella spec.) were isolated from tracheal aspirate in a minority of patients, and predominantly as part of a mixed infection. Antibiotic monotherapy with a 2nd generation cephalosporin, or a 3rd generation gyrase inhibitor, was most effective in our patients regardless of the presence of anaerobic bacteria.

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.

Occurrence of phrenic nerve stimulation in cardiac resynchronization therapy patients: the role of left ventricular lead type and placement site.

AIMS: Unwanted phrenic nerve stimulation (PNS) has been reported in ∼1 in 4 patients undergoing left ventricular (LV) pacing. The occurrence of PNS over mid-term follow-up and the significance of PNS are less certain. METHODS AND RESULTS: Data from 1307 patients enrolled in pre-market studies of LV leads manufactured by Medtronic (models 4193 and 4195 unipolar, 4194, 4196, 4296, and 4396 bipolar) were pooled. Left ventricular lead location was recorded at implant using a common classification scheme. Phrenic nerve stimulation symptoms were either spontaneously reported or identified at scheduled follow-up visits. A PNS-related complication was defined as PNS resulting in invasive intervention or the termination of LV pacing. Average follow-up was 14.9 months (range 0.0-46.6). Phrenic nerve stimulation symptoms occurred in 169 patients (12.9%). Phrenic nerve stimulation-related complications occurred in 21 of 1307 patients (1.6%); 16 of 738 (2.2%) in the unipolar lead studies, and 5 of 569 (0.9%) in the bipolar lead studies (P = 0.08). Phrenic nerve stimulation was more frequent at middle-lateral/posterior, and apical LV sites (139/1010) vs. basal-posterior/lateral/anterior, and middle-anterior sites (20/297; P= 0.01). As compared with an anterior LV lead position, a lateral LV pacing site was associated with over a four-fold higher risk of PNS (P= 0.005) and an apical LV pacing site was associated with over six-fold higher risk of PNS (P= 0.001). CONCLUSION: Phrenic nerve stimulation occurred in 13% of patients undergoing LV lead placement and was more common at mid-lateral/posterior, and LV apical sites. Most cases (123/139; 88%) of PNS were mitigated via electrical reprogramming, without the need for invasive intervention.

Suppression of persistent atrial fibrillation by genetic knockdown of caspase 3: a pre-clinical pilot study.

AIMS: Atrial fibrillation (AF) is linked to cardiomyocyte apoptosis, leading to atrial remodelling and reduction in electrical conduction velocity. We hypothesized that genetic suppression of an apoptotic key enzyme, caspase 3, would prevent the development of persistent AF by reducing apoptosis which may serve as an arrhythmogenic substrate. METHODS AND RESULTS: Atrial fibrillation was induced in domestic pigs by atrial burst pacing via an implanted cardiac pacemaker. Study animals were then assigned to receive either Ad-siRNA-Cas3 gene therapy to inactivate caspase 3 or green fluorescent protein (Ad-GFP) as a control. Adenoviruses were applied using a hybrid technique employing right and left atrial virus injection followed by epicardial electroporation to increase expression of plasmid DNA. In pigs treated with Ad-siRNA-Cas3, the onset of AF was suppressed or significantly delayed compared with controls (10.3 ± 1.2 days vs. 6.0 ± 1.6 days; P= 0.04). Electrical mapping revealed prolonged atrial conduction in the control group that was prevented by Ad-siRNA-Cas3 gene therapy. On the molecular level, Ad-siRNA-Cas3 application resulted in down-regulation of caspase 3 expression and suppression of apoptotic activity. CONCLUSION: Knockdown of caspase 3 by atrial Ad-siRNA-Cas3 gene transfer suppresses or delays the onset of persistent AF by reduction in apoptosis and prevention of intra-atrial conduction delay in a porcine model. These results highlight the significance of apoptosis in the pathophysiology of AF and demonstrate short-term efficacy of gene therapy for suppression of AF.

Atrioventricular delay programming in cardiac resynchronization therapy devices: fixed or adaptive? A randomized monocenter trial.

INTRODUCTION: Cardiac resynchronization therapy devices are routinely programmed on fixed atrioventricular delays (AVD) under resting conditions based on echocardiographic techniques. Whether this AVD also ensures optimal exercise hemodynamics, is unclear. METHODS: In order to compare fixed-AVD with rate-adaptive AVD, 100 patients with cardiac resynchronization therapy systems and sinus rhythm were randomized to fixed-AVD or adaptive-AVD. The patients then underwent bicycle ergometry with noninvasive hemodynamic monitoring. At rest and at peak exercise, stroke volume, cardiac output, and cardiac index were determined using "electrical velocimetry." RESULTS: There were no significant differences in clinical characteristics and baseline hemodynamic parameters between fixed or adaptive AVD. In patients randomized to adaptive AVD, a trend towards higher stroke volume, cardiac output, and cardiac index at peak exercise was encountered. CONCLUSIONS: Based on the trend towards better exercise hemodynamics demonstrated by this pilot study, a randomized follow-up study with clinical end points appears to be justified to clarify this issue.

Genetic suppression of Gαs protein provides rate control in atrial fibrillation.

Gene therapy-based modulation of atrioventricular (AV) conduction by overexpression of a constitutively active inhibitory Gα(i) protein effectively reduced heart rates in atrial fibrillation (AF). However, catecholamine stimulation caused an excessive increase in ventricular rate. We hypothesized that modest genetic suppression of a stimulatory G protein in the AV node would allow persistent rate control in acute AF and would prevent undesired heart rate acceleration during ß-adrenergic activation. Atrial fibrillation was induced in 12 pigs by atrial burst pacing via an implanted cardiac pacemaker. Study animals were then assigned to receive either Ad-siRNA-Gα(s) gene therapy to inactivate Gα(s) protein or Ad-ß-gal as control. Gα(s) protein inactivation resulted in a 20 % heart rate reduction (P < 0.01). AH and HV intervals were prolonged by 37 ms (P < 0.001) and 28 ms (P < 0.001), respectively, demonstrating atrioventricular conduction delay. Impairment of left ventricular ejection fraction (LVEF) during AF was attenuated by Gα(s) suppression (LVEF 49 %) compared with controls (LVEF 34 %; P = 0.03). Isoproterenol application accelerated ventricular heart rate from 233 to 281 bpm (P < 0.001) in control animals but did not significantly affect pigs treated with Ad-siRNA-Gα(s) (192 vs. 216 bpm; P = 0.19). In conclusion, genetic inhibition of Gα(s) protein in the AV node reduced heart rate and prevented AF-associated reduction of cardiac function in a porcine model. Rate control by gene therapy may provide an alternative to current pharmacological treatment of AF.

Genetic suppression of atrial fibrillation using a dominant-negative ether-a-go-go-related gene mutant.

BACKGROUND: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. Gene therapy-dependent modulation of atrial electrophysiology may provide a more specific alternative to pharmacological and ablative treatment strategies. OBJECTIVE: We hypothesized that genetic inactivation of atrial repolarizing ether-a-go-go-related gene (ERG) K(+) currents using a dominant-negative mutant would provide rhythm control in AF. METHODS: Ten domestic swine underwent pacemaker implantation and were subjected to atrial burst pacing to induce persistent AF. Animals were then randomized to receive either AdCERG-G627S to suppress ERG/I(Kr) currents or green fluorescent protein (AdGFP) as control. Adenoviruses were applied using a novel hybrid technique combining atrial virus injection and epicardial electroporation to increase transgene expression. RESULTS: In pigs treated with AdCERG-G627S, the onset of persistent AF was prevented (n = 2) or significantly delayed compared with AdGFP controls (12 ± 2.1 vs. 6.2 ± 1.3 days; P < .001) during 14-day follow-up. Effective refractory periods were prolonged in the AdCERG-G627S group compared with AdGFP animals (221.5 ± 4.7 ms vs. 197.0 ± 4.7 ms; P < .006). Impairment of left ventricular ejection fraction (LVEF) during AF was prevented by AdCERG-G627S application (LVEF(CERG-G627S) = 62.1% ± 4.0% vs. LVEF(GFP) = 30.3% ± 9.1%; P < .001). CONCLUSION: Inhibition of ERG function using atrial AdCERG-G627S gene transfer suppresses or delays the onset of persistent AF by prolongation of atrial refractoriness in a porcine model. Targeted gene therapy represents an alternative to pharmacological or ablative treatment of AF.

Clinical feasibility study for detection of myocardial oedema by a cine SSFP sequence in comparison to a conventional T2-weighted sequence.

BACKGROUND: Cardiovascular magnetic resonance (CMR) T2-imaging is oedema-sensitive and can detect increased myocardial water content to potentially distinguish acute from chronic myocardial infarction (AMI/CMI). Currently applied conventional black-blood T2-weighted-turbo-spin-echo (T2-BB-TSE)-sequences cause various artefacts which limit their image quality and possibly hamper their interpretation. Image contrast of conventional cine steady-state free precession (SSFP)-sequences partly consists of T2 oedema-sensitive information. We therefore sought to prospectively evaluate SSFP cine-imaging to detect myocardial oedema and differentiate AMI from CMI. METHODS: We examined 60 patients with AMI, 30 patients with CMI and 30 healthy volunteers using a 1.5 Tesla-MR whole body scanner. In a blinded fashion, myocardial oedema was assessed with T2-BB-TSE and SSFP-sequences, late gadolinium contrast-enhanced (LGE) CMR images being deemed as the standard reference for identification of infarcted myocardium. Assessment of presence of CMR detectable myocardial oedema was performed visually and quantitatively. P < 0.05 was considered statistically significant. RESULTS: The contrast-to-noise ratio (CNR) in AMI patients was significantly higher (SSFP-STEMI and SSFP-NSTEMI: 19 ± 12 and 20 ± 14; T2-BB-TSE STEMI and T2-BB-TSE-NSTEMI: 33 ± 16 and 31 ± 13) than in CMI for both MR-sequences (SSFP-STEMI and NSTEMI: 3.5 ± 1.5 and T2-BB-TSE:9.3 ± 9.6, p for all <0.001). By visual analysis, SSFP images achieved a sensitivity of 96%, a specificity of 87%, positive and negative predictive values of 95 and 92% when compared to the existence of gadolinium contrast-enhanced scar imaging. Similarly, for T2-BB-TSE, sensitivity and specificity were 93 and 83% with positive and negative predictive values of 92 and 90%. Inter-observer variability was 0.90 for SSFP and 0.83 for T2-BB-TSE images. CONCLUSION: A standard clinical SSFP sequence is not inferior to T2-BB-TSE for the detection of myocardial oedema and can be used to reliably distinguish AMI from CMI. Especially in patients with insufficient T2-BB-TSE image quality, the SSFP sequence may be an alternative for the detection of myocardial oedema.

Connexin 43 gene therapy prevents persistent atrial fibrillation in a porcine model.

AIMS: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, and effective treatment of AF still remains an unmet medical need. AF is associated with atrial conduction disturbances caused by electrical and/or structural remodelling. We hypothesized that AF suppresses expression of the gap junction protein connexin (Cx) 43 and that Cx43 gene transfer to both atria would prevent persistent AF. The first aim of this study was to assess whether AF is associated with connexin remodelling in a porcine model. A strategy to suppress persistent AF by gene therapy was then developed and evaluated in vivo. METHODS AND RESULTS: AF was induced in domestic pigs via atrial burst pacing, causing a 62.4% reduction in atrial Cx43 protein. Adenoviruses encoding for Cx43 (AdCx43) or green fluorescent protein (AdGFP) were injected into both atria, followed by epicardial electroporation to enhance transgene expression. Combining direct injection of adenoviruses with electroporation achieved GFP reporter gene expression in ∼50% of atrial cells in vivo. AdCx43-treated animals exhibited a 2.5-fold increase in atrial Cx43 protein content and did not develop persistent AF during the observation period of 14 days. In contrast, control animals developed persistent AF within 7.4 ± 0.5 days. Rapid ventricular heart rates during AF led to deterioration of cardiac function in control pigs but not in pigs treated with AdCx43. CONCLUSION: Our results highlight the contribution of Cx43 to the pathophysiology of AF and demonstrate the viability of gene therapy for prevention of atrial arrhythmias.

Asymptomatic pulmonary vein stenosis after cryoballoon catheter ablation of paroxysmal atrial fibrillation.

Pulmonary vein (PV) isolation is an effective treatment option for symptomatic atrial fibrillation. PV stenosis is a well-recognized complication of radiofrequency energy application but has not been observed following cryoballoon ablation. Here, we report a case of asymptomatic PV stenosis associated with cryoballoon PV isolation, illustrating a risk that should be considered when applying this technique.

There is no transmural heterogeneity in an index of action potential duration in the canine left ventricle.

BACKGROUND: Transmural heterogeneity in ventricular repolarization demonstrated in vitro has been difficult to confirm in vivo. Whether this discrepancy reflects a physiological phenomenon or a methodological problem remains a vivid matter of debate despite a plethora of experimental work. Therefore, we have measured the relevant electrophysiological parameters first in vivo and repeated these in the same heart and at identical sites in vitro. Methodological issues were tackled by using both unipolar and bipolar recordings. Physiological issues were explored by measuring both local and functional electrophysiological parameters. METHODS: In 10 healthy dogs, 2 high-resolution needle electrodes were inserted into the left ventricle. Effective refractory periods (ERP) as well as activation recovery intervals (ARI) were determined at each electrode along both needles at basic cycle lengths (BCL) of 850 and 300 ms, respectively. After excision of the heart, ERP and ARI measurements were repeated in the arterially perfused wedge preparations. RESULTS: First, we observed that ERPs and ARIs were significantly shorter in vivo than in vitro. Mean ERPs and ARIs of all muscle layers were relatively uniform throughout the ventricular wall in vivo. The transition from the in vivo to the in vitro preparation was associated with a significant albeit small increase of mean ARIs in the subendocardium, whereas interlayer differences in mean ERPs did not reach statistical significance as in vivo. CONCLUSION: In the intact canine left ventricular wall, a more or less homogeneous distribution in transmural ERP and ARI is present.

The basic pacing rate in CRT patients: the higher the better?

BACKGROUND: To maximize the hemodynamic benefit of cardiac resynchronization therapy (CRT), echocardiographic AV interval optimization is routinely performed, complemented by VV interval optimization especially in non-responders. Programming of the basic pacing rate, however, is largely empirical in these patients. Therefore, the present study aimed to systematically evaluate the impact of basic pacing rate on hemodynamic parameters in CRT patients with sinus bradycardia. METHODS AND RESULTS: We included 70 consecutive patients with moderate to severe heart failure, LV ejection fraction 120 ms combined with echocardiographic evidence of ventricular dyssynchrony. All patients were on optimal heart failure medication, with CRT-ICD devices implanted at least 6 months before inclusion into the study. All patients were in sinus rhythm with a spontaneous heart rate <40 bpm. In all patients, cardiac output (CO) and stroke volume (SV) were determined using electrical velocimetry (EV) (Aesculon, Osypka Medical, Berlin, Germany). EV provides a new algorithm to calculate CO based on variations in thoracic electrical bioimpedance, which has been recently validated. Hemodynamic measurements were performed at four different pacing rates ranging from 40 to 70 bpm. A stepwise increase in CO was encountered with increasing heart rates, reaching statistical significance when comparing 70 with 40 bpm. SV remained unchanged throughout all pacing rates. CONCLUSIONS: In the range between 40 and 70 bpm, an increase in basic pacing rate enhances CO without reducing SV. According to this pilot study, a basic pacing rate between 60 and 70 bpm would appear reasonable.

Effect of cardiac resynchronization therapy on conversion of persistent atrial fibrillation to sinus rhythm.

BACKGROUND: Spontaneous conversion of persistent atrial fibrillation to sinus rhythm (SR) has anecdotally been reported following cardiac resynchronisation therapy. OBJECTIVE: This monocenter observational study was designed to estimate the incidence of spontaneous conversion of persistent atrial fibrillation to SR in consecutive patients implanted with a cardiac resynchronisation device. METHODS AND RESULTS: A total of 46 patients with persistent atrial fibrillation (> or =4 weeks pre-implant), left bundle branch block (QRS > 130 ms), left ventricular ejection fraction <0.35 and NYHA III or IV heart failure were implanted with a cardiac resynchronisation pacemaker or defibrillator and followed for at least 6 months between 6/2000 to 12/2006. During 22 +/- 9 (7-34) months of follow-up, eight out of 46 patients (17%) converted to SR. Spontaneous conversion was encountered in seven cases, whereas one patient converted due to an ICD shock delivered for ventricular tachycardia; in the latter patient, previous ICD shocks had not converted atrial fibrillation. The time interval from device implantation to conversion was 12 +/- 11 (3-31) months. In patients converting to SR, the duration of atrial fibrillation before device implantation was significantly shorter than in patients remaining in atrial fibrillation (15 +/- 13 vs. 53 +/- 58 months, P = 0.001). Echocardiographic parameters such as left ventricular ejection fraction, left ventricular end-diastolic diameter, left atrial diameter did not differ significantly between converting and non-converting patients. However, patients converting to SR showed a significant reduction in systolic pulmonary artery pressure on CRT vs. before CRT (45 +/- 13 vs. 29 +/- 5 mmHg, P = 0.008). CONCLUSIONS: This pilot study suggests that CRT favors spontaneous conversion of persistent AF to SR in a minority of patients. If confirmed by larger clinical studies, atrial lead implantation would be encouraged in these patients, in order to provide AV synchronous pacing in case of spontaneous conversion or successful cardioversion to SR on cardiac resynchronisation therapy.