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INTRODUCTION AND OBJECTIVES Cardiac resynchronization therapy (CRT) is beneficial for selected heart failure (HF) patients, although nonresponse to therapy is still prevalent. We investigated a set of novel biomarkers associated with various pathophysiological pathways of HF. Our purpose was to assess their ability to predict clinical outcomes after CRT. METHODS We studied 136 chronic HF patients undergoing CRT. We measured the plasma levels of fractalkine, pentraxin-3, hepatocyte growth factor (HGF), carbohydrate antigen-125, and matrix metalloproteinase-9 before and 6 months after CRT. The primary endpoint of the study was 5-year all-cause mortality, and we considered the absence of 6-month reverse remodelling (defined as at least a 15% decrease in end-systolic volume) as a secondary endpoint. RESULTS Fifty-eight patients died during the 5-year follow-up period and 66 patients were categorized as nonresponders. In multivariable models, only an increased HGF was an independent predictor of both mortality (HR, 1.35; 95%CI, 1.11-1.64; P=.003; per 1 standard deviation increase) and the absence of reverse remodelling (OR, 1.83; 95%CI, 1.10-3.04; P=.01; per 1 standard deviation increase). Applying HGF to the basic multivariable model of both mortality (net reclassification improvement=0.69; 95%CI, 0.39-0.99; P

Aims There are previous studies on quality of life (QoL) in cardiac resynchronization therapy (CRT) patients; however, there are no data with the short EuroQol-five dimensions (EQ-5D) questionnaire predicting outcomes. We aimed to assess the predictive role of baseline QoL and QoL change at 6 months after CRT with EQ-5D on 5-year mortality and response. Methods and results In our prospective follow-up study, 130 heart failure (HF) patients undergoing CRT were enrolled. Clinical evaluation, echocardiography, and EQ-5D were performed at baseline and at 6 months of follow–up, continued to 5 years. Primary endpoint was all-cause mortality at 5 years. Secondary endpoints were (i) clinical response with at least one class improvement in New York Heart Association without HF hospitalization and (ii) reverse remodelling with 15% reduction in left ventricular end-systolic volume at 6 months. Fifty-four (41.5%) patients died during 5 years, 85 (65.3%) clinical responders were identified, and 63 patients (48.5%) had reverse remodelling. Baseline issues with mobility were associated with lower response [odds ratio (OR) 0.36, 95% confidence interval (CI) 0.16–0.84; P = 0.018]. Lack of reverse remodelling correlated with self-care issues at baseline (OR 0.10, 95% CI 0.01–0.94; P = 0.04). Furthermore, self-care difficulties [hazard ratio (HR) 2.39, 95% CI 1.17–4.86; P = 0.01) or more anxiety (HR 1.51, 95% CI 1.00–2.26; P = 0.04) predicted worse long-term survival. At 6 months, mobility (HR 3.95, 95% CI 1.89–8.20; P

Levels of cardiac necroenzymes, high-sensitive troponin (hsTnT) and creatine kinase muscle-brain (CKMB) increase as a result of a myocardial damage following catheter ablation.To analyze the mid-term alteration of hsTnT and CKMB levels following radiofrequency ablation (RFCA) for atrial fibrillation (AF), atrial flutter (AFlu), AV-nodal reentry tachycardia (AVNRT) and electrophysiological studies (EPS) without ablation.Patients undergoing RFCA for various indications and EPS were consecutively enrolled in our prospective study. Concentrations of hsTnT and CKMB were measured from serial blood samples directly before and after the procedure, 4 and 20 hours later and at 3 months follow-up.Forty-seven patients (10 EPS, 12 AVNRT, 13 AFlu, 12 AF) with mean age of 55 ± 13 were included. hsTnT levels increased significantly in all groups after the procedures, while CKMB changed only in the AF group. hsTnT exceeded the reference value in all patients with ablation and in 80% of patients with EPS 4 hours post-ablation. Peak average hsTnT levels for EPS, AVNRT, AFlu were 24 ± 11, 260 ± 218 and 541 ± 233 ng/L, respectively. The highest hsTnT level was measured in the AF group (799 ± 433 ng/L). We found a positive correlation between hsTnT levels and ablation time after RFCA.The hsTnT levels significantly change after EPS and RFCA, in all patients who underwent ablation, and in 80% of those with EPS had hsTnT positivity in the early post-procedural phase. hsTnT levels depended significantly on the type of the subgroups and correlated with the ablation time. Awareness of those observations is essential to correctly interpret elevated hsTnT levels following RFCA. Orv Hetil. 2019; 160(14): 540-548.Absztrakt: Bevezetés: Ismert, hogy katéteres ablatio által okozott szívizom-károsodás következtében megnő a szívizom-specifikus nekroenzimek koncentrációja. Célkitűzés: A magas érzékenységű troponin T (hsTnT) és a szívizom-specifikus kreatin-kináz (CKMB) szintje középtávú változásának elemzése pitvarfibrilláció (PF), pitvari flutter (PFlu), AV-csomó reentry tachycardia (AVNRT) rádiófrekvenciás katéteres ablatióját követően, illetve elektrofiziológiai vizsgálat után. Módszer: Rádiófrekvenciás ablatión, illetve elektrofiziológiai vizsgálaton átesett betegeket vontunk be konszekutívan prospektív vizsgálatunkba. Sorozatvérmintákból meghatároztuk a hsTnT- és a CKMB-szinteket a procedúra előtt és után közvetlenül, majd 4 és 20 órával és 3 hónappal később. Eredmények: Negyvenhét, 55 ± 13 év átlagéletkorú beteget (10 elektrofiziológiai vizsgálat, 12 AVNRT, 13 PFlu és 12 PF) vontunk be vizsgálatunkba. A hsTnT-szintek minden csoportban szignifikánsan megemelkedtek a beavatkozást követően, a CKMB csak a PF-csoportban változott. A hsTnT-szint négy órával a beavatkozást követően az összes ablatión átesett betegnél és az elektrofiziológiai vizsgálaton átesett betegek 80%-ánál meghaladta a referenciatartományt. A legmagasabb átlagos hsTnT-koncentrációk EFV, AVNRT, PFlu esetén 24 ± 11, 260 ± 218 és 541 ± 233 ng/l-nek bizonyultak. A legmagasabb hsTnT-szint a PF-ablatiós csoportban volt kimutatható 20 órával az ablatio után (799 ± 433 ng/l). Pozitív korrelációt találtunk a rádiófrekvenciás ablatiót követő hsTnT-szint és az ablatio ideje között. Következtetések: A hsTnT alkalmas a rádiófrekvenciás ablatio és az elektrofiziológiai vizsgálat utáni myocardialis necrosis vizsgálatára, az ablatión átesett betegek mindegyikénél; elektrofiziológiai vizsgálat után 80%-ban pozitív a hsTnT. A necrosis mértéke jelentősen függ a beavatkozás típusától, és korrelál az ablatio kiterjedtségével. A fentiekben leírt megfigyelések iránymutatásként szolgálnak a rádiófrekvenciás ablatio utáni hsTnT-szint megfelelő értelmezéséhez. Orv Hetil. 2019; 160(14): 540–548.

Electroanatomical mapping is a useful tool during the ablation of atrial fibrillation. Respiratory movement might influence the mapping accuracy and merging. This study aims to investigate the effect of respiratory gating on the accuracy of magnetic-field-based electroanatomical mapping under spontaneous respiration. Fifty-one consecutive patients (35 male, aged 30–78 years) who underwent left atrial radiofrequency catheter ablation due to atrial fibrillation were included. Electroanatomical mapping was performed with CARTO 3 System under conscious sedation. Respiratory gating was achieved with the AccuResp algorithm (Biosense Webster). Average surface match and maximum distance of the pre-acquired and electroanatomical maps, as well as left atrial volume, were recorded with and without respiratory gating after merging. The average surface match of the electroanatomical map with the left atrial reconstruction was significantly better with respiratory gating than without using the algorithm (3.81 ± 1.09 vs 4.11 ± 1.61 mm, p = 0.0119). It was not dependent of the rhythm during mapping or the image modality used for left atrial reconstruction. The maximal distance between the two maps did not depend on the use of the algorithm (19.81 ± 6.24 mm for gated and 20.87 ± 7.99 mm for non-gated, p = 0.3161). Left atrial volume of the map was significantly lower when using the respiratory compensation module (106.3 ± 31.6 vs 127.0 ± 36.4 ml, p

Aims Data on longer right to left ventricular activation delay (RV-LV AD) predicting clinical outcome after cardiac resynchronization therapy (CRT) by left bundle branch block (LBBB) are limited. We aimed to evaluate the impact of RV-LV AD on N-terminal pro–B-type natriuretic peptide (NT-proBNP), ejection fraction (EF), and clinical outcome in patients implanted with CRT, stratified by LBBB at baseline. Methods and results Heart failure (HF) patients undergoing CRT implantation with EF ≤ 35% and QRS ≥ 120 ms were evaluated based on their RV-LV AD at implantation. Baseline and 6-month clinical parameters, EF, and NT-proBNP values were assessed. The primary endpoint was HF or death, the secondary endpoint was all-cause mortality. A total of 125 patients with CRT were studied, 62% had LBBB. During the median follow-up of 2.2 years, 44 (35%) patients had HF/death, 36 (29%) patients died. Patients with RV-LV AD ≥ 86 ms (lower quartile) had significantly lower risk of HF/death [hazard ratio (HR): 0.44; 95% confidence interval (95% CI): 0.23–0.82; P = 0.001] and all-cause mortality (HR: 0.48; 95% CI: 0.23–1.00; P = 0.05), compared with those with RV-LV AD < 86 ms. Patients with RV-LV AD ≥ 86 ms and LBBB showed the greatest improvement in EF (28–36%; P

Lead dislocations of pacemaker systems are reported in all and even in high-volume centers. Repeated procedures necessitated by lead dislocations are associated with an increased risk of complications. We investigated a minimal invasive method for right atrial and ventricular lead repositioning. The minimal invasive method was applied only when passive fixation leads were implanted. During the minimal invasive procedure, a steerable catheter was advanced through the femoral vein to move the distal end of the lead to the appropriate position. Retrospective data collection was conducted in all patients with minimal invasive and with conventional method, at a single center between September 2006 and December 2012. Forty-five minimal invasive lead repositionings were performed, of which eight were acutely unsuccessful and nine electrodes re-dislocated after the procedure. One hundred two leads were repositioned with opening of the pocket during the same time, including the ones with unsuccessful minimal invasive repositionings. One procedure was acutely unsuccessful in this group and four re-dislocations happened. A significant difference of success rates was noted (66.6% vs. 95.1%, p = 0.001). One complication was observed during the minimal invasive lead repositionings (left ventricular lead microdislodgement). Open-pocket procedures showed different types of complications (pneumothorax, subclavian artery puncture, pericardial effusion, hematoma, fever, device-associated infection which necessitated explantation, atrial lead dislodgement while repositioning the ventricular one, deterioration of renal function). The minimal invasive method as a first alternative is safe and feasible. In those cases when it cannot be carried out successfully, the conventional method is applicable.

Aims There are limited and contradictory data on the effects of CRT with implantable cardioverter defibrillator (CRT-D) on mortality as compared with CRT with pacemaker (CRT-P). Methods and results We evaluated the long-term outcome of patients implanted with a CRT-D or CRT-P device in our high-volume single-centre experience. Data on all-cause mortality were derived from clinic visits and the Hungarian National Healthcare Fund Death Registry. Kaplan–Meier survival analyses and multivariate Cox regression models were used to evaluate all-cause mortality in patients with CRT-D vs. CRT-P, stratified by the aetiology of cardiomyopathy. From 2000 to 2011, 1122 CRT devices, 693 CRT-P (LVEF 28.2 ± 7.4%) and 429 CRT-D (LVEF 27.6 ± 6.4%), were implanted at our centre. During the median follow-up of 28 months, 379 patients died from any cause, 250 patients (36%) with an implanted CRT-P and 129 patients (30%) with an implanted CRT-D. There was no evidence of mortality benefit in patients implanted with a CRT-D compared with a CRT-P in the total cohort [hazard ratio (HR) 0.98, 95% confidence interval (CI) 0.73–1.32, P = 0.884]. In patients with ischaemic cardiomyopathy, CRT-D treatment was associated with a significant 30% risk reduction in all-cause mortality compared with an implanted CRT-P (HR 0.70, 95% CI 0.51–0.97, P = 0.03). In non-ischaemic patients, there was no mortality benefit of CRT-D over CRT-P (HR 0.98, 95% CI 0.73–1.32, P = 0.894, interaction P-value = 0.15). Conclusions In heart failure patients with ischaemic cardiomyopathy, CRT-D was associated with a mortality benefit compared with CRT-P, but no benefit of CRT-D over CRT-P in mortality was observed in non-ischaemic cardiomyopathy.

Treatment of left ventricular electrode dislocation and phrenic nerve stimulation remains an issue in the era of new electrode designs.Safety and efficacy of minimal invasive lead repositioning and pocket opening reposition procedures were evaluated between December 2005 and December 2012 at our center. Minimal invasive method was developed and widely utilized at our center to treat phrenic nerve stimulation. The distally positioned left ventricular lead is looped around by a deflectable catheter in the right atrium introduced from the femoral vein access and then pulled back. Coronary stent implantation was used afterwards for lead stabilization in some patients.42 minimal invasive and 48 electrode repositions with pacemaker pocket opening were performed at 77 patients for left ventricular lead problems. Minimal invasive reposition could be carried out successfully in 69% of (29 patients) cases. Note that in 14.3% of the cases (six patients) minimal invasive procedures were acutely unsuccessful and crossover was necessary. In 16.6% of the cases (seven patients) lead issues were noted later during follow-up. Opening of the pocket could be carried out successfully in 81.2% (39 patients) and was unsuccessful acutely in 6.25% (three patients). Repeated dislocation was noticed, 12.5%, in this group (six patients). Complication during minimal invasive procedures was electrode injury in one case. Pocket openings were associated with several complications: atrial fibrillation, pericardial effusion, fever, hematoma, and right ventricular electrode dislodgement.Minimal invasive procedure-as the first line approach-is safe and feasible for left ventricular electrode repositioning in selected cases.

The chronic inflammation plays an important role in heart failure and complement components might be useful markers of the prognosis. We set out to evaluate their predictive value in the clinical outcomes of patients with cardiac resynchronization therapy (CRT).We determined the complement levels C3, C3a, sC5b-9 and also the N-terminus of the prohormone brain natriuretic peptide (NT-proBNP) of 126 heart failure patients in a prospective, single-center observational study before and 6 months after CRT implantation.CRT reduced the C3a [212.5 (148.2-283.6) vs. 153 (119.8-218.3) ng/mL, p 0.0001] and the sC5b-9 levels [296.9 (234.2-358.8) vs. 255.1 (210.1-319.0) ng/mL, p = 0.0006], but not the total C3 levels [1.43 (1.26-1.61) vs. 1.38 (1.23-1.57) g/L, p = 0.57]. C3a predicted the 5-year mortality of the patients [C3a 165 ng/mL hazard ratio = 4.21 (1.65-10.72), p = 0.003] independent of the NT-proBNP and other factors. After reclassification, we observed a significant net reclassification improvement [NRI = 0.71 (0.43-0.98), p 0.0001] and integrated discrimination improvement [IDI = 0.08 (0.03-0.12), p = 0.0002].In patients with CRT, elevated C3a levels increase the risk of mortality independent of the NT-proBNP levels or other factors. CRT exerts anti-inflammatory effect by reducing the complement activation.

Idiopathic fascicular ventricular tachycardia is an important and not very rare cardiac arrhythmia with specific electrocardiographic features and therapeutic options. Ventricular tachycardia is characterized by relatively narrow QRS complex and right bundle branch block pattern. The QRS axis depends on which fascicle is involved in the re-entry. Left axis deviation is noted with left posterior fascicular tachycardia and right axis deviation with left anterior fascicular tachycardia. A left septal fascicular tachycardia with normal QRS axis is also possible. Idiopathic fascicular tachycardia is usually seen in individuals without structural heart disease. Response to verapamil is an important feature of fascicular tachycardia. In some cases intravenous adenosine may also terminate the arrhythmia. During electrophysiology study, presystolic or diastolic potentials precede the QRS, presumed to originate from the Purkinje fibers. The potentials can be recorded during sinus rhythm and ventricular tachycardia in many patients with fascicular tachycardia. This potential (so-called Purkinje potential) has been used as a guide to catheter ablation. Correct diagnosis of fascicular tachycardia is very important because catheter ablation is very effective in the treatment of this type of ventricular tachycardia. In this review, we describe three patients with idiopathic ventricular tachycardia and their successful catheter ablation, and summarize the actual knowledge of the diagnosis and management of this special ventricular tachycardia.

Prolonged Ca(2+) stimulations often result in a decrease in contractile force of isolated, demembranated human ventricular cardiomyocytes, whereas intact cells are likely to be protected from this deterioration. We hypothesized that cytosolic protein kinase C (PKC) contributes to this protection. Prolonged contracture (10 min) of demembranated human cardiomyocytes at half-maximal Ca(2+) resulted in a 37 +/- 5% reduction of active force (p0.01), whereas no decrease (2 +/- 3% increase) was observed in the presence of the cytosol (reconstituted myocytes). The PKC inhibitors GF 109203X and Gö 6976 (10 micromol/liter) partially antagonized the cytosol-mediated protection (15 +/- 5 and 9 +/- 2% decrease in active force, p0.05). Quantitation of PKC isoform expression revealed the dominance of the Ca(2+)-dependent PKCalpha over PKCdelta and PKCepsilon (189 +/- 31, 7 +/- 3, and 7 +/- 2 ng/mg protein, respectively). Ca(2+) stimulations of reconstituted human cardiomyocytes resulted in the translocation of endogenous PKCalpha, but not PKCbeta1, delta, and epsilon from the cytosol to the contractile system (PKCalpha association: control, 5 +/- 3 arbitrary units; +Ca(2+), 39 +/- 8 arbitrary units; p0.01, EC(50,Ca) = 645 nmol/liter). One of the PKCalpha-binding proteins were identified as the thin filament regulatory protein cardiac troponin I (TnI). Finally, the Ca(2+)-dependent interaction between PKCalpha and TnI was confirmed using purified recombinant proteins (binding without Ca(2+) was only 28 +/- 18% of that with Ca(2+)). Our data suggest that PKCalpha translocates to the contractile system and anchors to TnI in a Ca(2+)-dependent manner in the human heart, contributing to the maintenance of contractile force.

This study is the first pharmacological characterization of the novel chemical entity, ORM-3819 (L-6-{4-[N'-(4-Hydroxi-3-methoxy-2-nitro-benzylidene)-hydrazino]-phenyl}-5-methyl-4,5-dihydro-2H-pyridazin-3-one), focusing primarily on its cardiotonic effects. ORM-3819 binding to cardiac troponin C (cTnC) was confirmed by nuclear magnetic resonance spectroscopy, and a selective inhibition of the phosphodiesterase III (PDE III) isozyme (IC50=3.88±0.3 nM) was revealed during in vitro enzyme assays. The Ca(2+)-sensitizing effect of ORM-3819 was demonstrated in vitro in permeabilized myocyte-sized preparations from left ventricles (LV) of guinea pig hearts (ΔpCa50=0.12±0.01; EC50=2.88±0.14 µM). ORM-3819 increased the maximal rate of LV pressure development (+dP/dtmax) (EC50=8.9±1.7 nM) and LV systolic pressure (EC50=7.63±1.74 nM) in Langendorff-perfused guinea pig hearts. Intravenous administration of ORM-3819 increased LV+dP/dtmax (EC50=0.13±0.05 µM/kg) and improved the rate of LV pressure decrease (-dP/dtmax); (EC50=0.03±0.02 µM/kg) in healthy guinea pigs. In an in vivo dog model of myocardial stunning, ORM-3819 restored the depressed LV+dP/dtmax and improved % segmental shortening (%SS) in the ischemic area (to 18.8±3), which was reduced after the ischaemia-reperfusion insult (from 24.1±2.1 to 11.0±2.4). Our data demonstrate ORM-3819 as a potent positive inotropic agent exerting its cardiotonic effect by a cTnC-dependent Ca(2+)-sensitizing mechanism in combination with the selective inhibition of the PDE III isozyme. This dual mechanism of action results in the concentration-dependent augmentation of the contractile performance under control conditions and in the postischemic failing myocardium.

Introduction: Coronary sinus (CS) leads used for cardiac resynchronization have undergone development in the last years. However, dislocation rate remained high (5–9%). The aim of this study was to investigate the effectiveness and safety of stent implantation in a CS side vein to stabilize the left ventricular lead position after postoperative or intraoperative dislocation of the electrode. Methods and Results: Thirty-six patients (age: 64 ± 9.7 years, 19 primary, 17 ischemic cardiomyopathy, NYHA class III: 30, IV: 6) were treated with stenting. The procedure was performed because of postoperative dislocation in seven patients, while dislocation was observed during the implantation in 29 cases. The electrode was repositioned into the desired position and a bare metal coronary stent was introduced via another guide wire. The stent was deposited at 5- to 15-mm proximal to the tip of the electrode with a pressure of 6 to 14 atmospheres. Control angiography showed no blood flow compromise in any of the side branches or in the coronary sinus. Control echocardiography did not show pericardial effusion due to stenting. During follow-up (11.5 ± 5.5, 2–23 months), left ventricular pacing threshold increased from 2.2 to 5.6 V in one patient, but dislocation was not found by fluoroscopy. Clinically important pacing threshold increase was not detected in the other cases. Impedance measurements did not suggest lead insulation failure. Conclusion: Stent implantation to stabilize the left ventricular lead position seems to be a useful and safe procedure in the treatment of patients with complicated coronary sinus anatomy or lead instability.

Objective.To identify early echocardiographic abnormalities at the time of diagnosis of polymyositis (PM) and dermatomyositis (DM) and follow the echocardiographic findings during the first 3 months of therapy.Methods.We included 30 PM/DM patients (23/7) with a mean age of 42.3 ± 1.6 years and without cardiovascular symptoms. Age-matched healthy patients served as controls. Clinical characteristics were recorded. Traditional echocardiography and tissue Doppler imaging (TDI) were performed to measure systolic [ejection fraction, right ventricular fractional area change (RV FAC), lateral and tricuspid annulus s velocities] and diastolic echocardiographic variables (mitral inflow velocities: E, A; deceleration time: DT; lateral and tricuspid annulus e′, a′ velocities, lateral E/e′).Results.The left and right ventricular systolic dysfunction detected by TDI at the time of the PM/DM diagnosis improved, and characteristic values at the end of the followup period were comparable to those of the controls (lateral s: 10.6 ± 0.2, 8.7 ± 0.4, 9.6 ± 0.3, 11.3 ± 0.2 cm/s; RV FAC: 45.2 ± 2.3, 36.9 ± 1.5, 42.2 ± 1.3, 46.9 ± 1.2%; tricuspid s: 13.3 ± 0.2, 9.5 ± 0.4, 10.3 ± 0.3, 11.6 ± 0.5 cm/s; control, 0, 1, and 3 mos, respectively). Measurements indicated the development of diastolic dysfunction at 3 mos (E/A: 1.4 ± 0.1, 1.29 ± 0.05, 1.03 ± 0.05, 0.92 ± 0.05; DT: 148.6 ± 3.6, 157.3 ± 5.7, 168.3 ± 6.0, 184.3 ± 6.2 ms; lateral e′: 12.8 ± 0.3, 12.1 ± 0.5, 10.2 ± 0.6, 10.8 ± 0.8 cm/s; E/e′: 5.6 ± 0.1, 5.0 ± 0.22, 6.92 ± 0.46, 7.64 ± 0.47; control, 0, 1, and 3 mos, respectively).Conclusion.TDI is a useful method to detect early cardiac abnormalities complementing the conventional echocardiographic measurements. LV and RV systolic dysfunction found in the acute phase significantly improved during the first 3 months of therapy; however, deterioration of diastolic dysfunction was also observed.

Radiofrequency (RF) catheter ablation guided by electroanatomic mapping systems is an effective therapy for atrial fibrillation. However, it may be affected by respiration movements. The aim of this study was to determine the impact of respiratory gating on procedural parameters in patients undergoing catheter ablation of atrial fibrillation (AF).One-hundred forty consecutive patients undergoing pulmonary vein isolation were admitted to study. Respiratory gating module (AccuResp algorithm, Carto3, Biosense Webster) was enabled in 70 patients and disabled in 70 patients during procedures. Successful pulmonary vein isolation and sinus rhythm were obtained in all patients. A significant reduction in total procedure times [median 77, interquartile range (IQR 66-95) min vs median 82 (IQR 72-104) min, p0.05] and fluoroscopy times [median 14 (IQR 9-17) min vs median 16 (IQR 12-22) min, p0.05] were observed in the respiratory gated group. Although ablation times (duration between the first and last ablation) were significantly shorter in respiratory gated group [median 37 (IQR 32-53) min vs median 48 (IQR 39-65) min, p0.05], total RF application durations were not different between two groups [median 1,554 (IQR 1,213-2,196) s vs median 1,802 (IQR 1,344-2,448) s, p = 0.11]. Difference in electroanatomical map reconstruction times was not significant [median 14 (IQR 12-16) min in gated group vs median 13 (IQR 10-18) min in nongated group, p = 0.19].Respiratory gating significantly improves fluoroscopy and ablation times during electroanatomic mapping guided AF ablation. Respiratory gated maps may provide uninterrupted continuous ablation applications. Furthermore, using automatic respiratory gating module does not prolong mapping times.

Both myocardial infarction and ischemic stroke are rare in the young. Yet a 15-year-old male patient suffered a myocardial infarction and later an ischemic stroke despite uninterrupted antiplatelet therapy. His medical history involved the surgical correction of an incomplete atrioventricular canal defect at the age of 13 years. No cardiovascular risk factors other than elevated lipoprotein(a) level could be identified. His antithrombin (AT) activity was decreased and DNA sequence analysis revealed heterozygosity for AT Basel (p.Pro41Leu), a variant with impaired heparin binding. This report supports a possible additional pathophysiological role for AT Basel and elevated lipoprotein(a) level in arterial thrombogenesis.

Aim Failure rate to implant left ventricular (LV) lead transvenously is 4-8% in cardiac resynchronization therapy (CRT) patients. Epicardial lead placement is an alternative method and if not applicable case reports and small series showed the feasibility of endocardial LV lead implantation. Electroanatomical mapping might be a useful tool to guide this procedure. Methods and results Four patients had undergone endocardial LV lead implantation after unsuccessful transvenous implantation or epicardial LV lead dysfunction using the transseptal approach. Electroanatomical mapping was used to mark the location of the transseptal puncture. This location point guided the mapping catheter from the subclavian access and facilitated positioning of the LV lead at the adjacent latest activation area of the left ventricle detected by activation mapping. Endocardial active fixation LV leads were successfully implanted in all patients with stable electrical parameters immediately after implantation and over a mean follow-up of 18.3 months (lead impedance 520 ± 177 vs. 439 ± 119 Ω and pacing threshold 0.8 ± 0.2 V, 0.5 ms vs. 0.6 ± 0.1 V, 0.5 ms, respectively). Patients were maintained on anticoagulation therapy with a target international normalized ratio of 3.5-4.5 and did not show any thromboembolic, haemorrhagic events, or infection. Echocardiography showed significant improvement of LV systolic function with marked improvement of the functional status. Conclusions Electroanatomical mapping is a useful technical tool to guide endocardial LV lead implantation. It helps to identify the location of the transseptal puncture and the use of activation mapping might facilitate location of the optimal lead positions during CRT.

A 29-year-old male was admitted to our outpatient clinic because of palpitation and documented narrow QRS arrhythmia. Based on the ECG, supraventricular tachycardia was diagnosed, electrophysiological examination was indicated and ablation therapy was recommended. During positioning of the catheter the patient developed arrhythmia. On the coronary sinus catheter the activation spread from distal to proximal electrodes, suggesting left atrial origin. During atrial entrainment pacing long return cycle was observed and distal coronary sinus pacing resulted in a 15 ms longer cycle length than the arrhythmia. Therefore, the left atrial origin of the arrhythmia was confirmed and double transseptal puncture was performed. Lasso and irrigated tip catheter were introduced into the left atrium and electroanatomical mapping was performed with CARTO3 system. After electroanatomical mapping the origin of tachycardia was located proximally in the left superior pulmonary vein. Ablation was started at the earliest activation point, where acceleration was observed and the arrhythmia stopped after the first ablation. Pulmonary vein isolation was completed, and bidirectional block could be confirmed. After 30 minutes the arrhythmia was not inducible. During follow-up, Holter-examination was negative and the patient remained asymptomatic. The pulmonary vein tachycardia is a supraventricular arrhythmia that can occur at any age, but the diagnosis based on the ECG is not always simple. Detailed electroanatomical mapping is very important in the diagnosis of this type of arrhythmia, although it can be verified with conventional electrophysiological methods as well. Focal ablation may be a therapeutic option; however, total isolation of pulmonary veins can be more effective. Orv. Hetil., 2011, 152, 1374–1378.

The aim of our investigation was to test the suitability of a novel method for the analysis of the integrity of an explanted pacemaker lead stabilized by a stent. A coronary sinus lead has been explanted 27 months after implantation and has been examined by optical-, confocal-, x-ray-, and scanning electron microscopy. Several surface injuries were found on the insulation. Based on the surface characteristics, it is possible to define and differentiate the source of damages as well as to measure the extent of injuries. Impedance of the explanted lead has also been measured and electronic integrity has been verified.

Aims Phrenic nerve stimulation (PNS), which is often intolerable for the patient, is a known complication of resynchronization therapy. We describe a new, minimal invasive method for treating PNS. Methods and results Untreatable PNS was found in nine cardiac resynchronization therapy patients with distal coronary sinus (CS) lead position 6 ± 6 (0.5–17) months after the implantation. Ablation catheter and Amplatz Left 2 type guiding catheter were introduced into the right atrium via the right femoral vein. Coronary sinus was cannulated with the Amplatz catheter, and on a normal guide wire, a coronary stent was introduced beside the lead into the side branch in seven cases or a bigger stent into the CS in two patients. The ablation catheter was looped around the CS lead in the atrium with bent tip and was drawn backward together with the CS electrode. New lead positions were evaluated with electrophysiological measurements, and the suitable position was stabilized with inflation of the stent. Pericardial effusion was not detected on post-operative echocardiography. After repositioning, suitable pacing parameters were registered (threshold: 1.6 ± 1.1 V; 0.5 ms, impedance: 565 ± 62 ohm). Phrenic nerve stimulation was not found with 7.5 V; 1.5 ms pacing. During follow-up (7.7 ± 4.6 months), stable pacing threshold and impedance values were measured; transient and reprogrammable PNS was present in only one patient. Conclusion Coronary sinus electrode reposition using the femoral approach seems to be a safe and effective procedure, which means smaller burden for the patients compared with the established reposition operation. The technique can be used successfully if the CS lead is in a distal position.

We describe a case of a 56-year-old male patient, who developed refractory dilated cardiomyopathy 5 years after heart transplantation. An atriobiventricular pacemaker was implanted when indication criteria of cardiac resynchronization therapy (CRT) were seen. The intraventricular dyssynchrony was significant before CRT, while synchronous contraction was demonstrated later with the beneficial reverse remodelling of the left ventricle. Resynchronization therapy resulted in significant improvement of the patient's clinical parameters. The success of this therapy points out the possible role of CRT in the treatment of chronic allograft failure after heart transplantation.

We characterized the Ca2+-sensitizing and phosphodiesterase (PDE)-inhibitory potentials of levosimendan and enoximone to assess their contributions to the positive inotropic effects of these drugs. In guinea pig hearts perfused in the working-heart mode, the maximal increase in cardiac output (55%, P

Endothelin-1 (ET-1) is a potent endogenous arrhythmogenic substance. The aim of our study was to investigate the changes of serum ET-1 and big-endothelin levels in patients suffering from spontaneous, incessant ventricular tachyarrhythmias. The 11 consecutive patients' (mean age, 59 +/- 11 years) underlying diseases were ischemic heart disease, valvular heart disease, dilated cardiomyopathy, primary electrical disease, and arrhythmogenic right ventricular dysplasia in five cases, three cases, one case, one case, and one case, respectively. The mean ejection fraction was 39 +/- 14%, New York Heart Association functional status was I, II, and III in two cases, four cases, and five cases, respectively. Ventricular tachycardias (VT) were detected in five patients, ventricular fibrillation (VF) in three patients, and VT + VF in three patients. VTs terminated spontaneously in two cases. Six patients required multiple external cardioversion/defibrillation shocks, while implantable cardioverter defibrillators terminated all sustained arrhythmias successfully in four cases. Blood samples were collected during arrhythmias and 24 hours (control) following the last VT/VF episode. Serum ET-1 and big-endothelin levels were measured with western blot analysis after immunoprecipitation. Serum ET-1 and big-endothelin levels were significantly higher during the last VT/VF compared with the control period (ET-1, 65.8 +/- 26.8 fmol/mL versus 53.9 +/- 22.3 fmol/mL, P < 0.05; big-endothelin, 115.2 +/- 39.3 fmol/mL versus 89.2 +/- 25.1 fmol/mL, P < 0.05). There was a negative correlation between the age and big-endothelin level measured at both times (during VT/VF, r = 0.94, P < 0.05; control, r = 0.91, P < 0.05). In conclusion, serum big-endothelin and ET-1 levels were significantly higher during incessant VT/VF, which can be a cause of multiple arrhythmia recurrence.

If the first surgical intervention for benign euthyroid goiter diseased portion is not totally removed one cannot be certain of the long-term behaviour of the remaining tissue. In one third of these patients there may be a recurrence with new nodules developing, functional disorders or even carcinoma may appear in the remnants. Hormonal activity of the removed tissue can be completely substituted for by levothyroxine. That is why some experienced specialists recommend primarily radical surgery even in benign disease, based on their experience with large number of patients. The authors started performing radical excisions in the past three years. A total of 477 operations were performed between 1st January 2000 and 31st December 2002, 45% were radical: lobectomy, near-total thyroidectomy and bilateral lobectomy. Surgery was carried out according to the standardized morphologically adjusted technique (SMART). Results of these operations are compared to conventional procedures performed in the same period. Complication rate was low with no mortality. There was no significant difference between early results of the two groups. About 2% rate of permanent recurrent laryngeal nerve injury a 3% rate of postoperative tetany (hypocalcaemia) in both groups is acceptable. Based on their initial experiences the authors recommend the radical surgical technique for the experienced surgeons.

The concentration dependences of the Ca(2+)-sensitizing and the phosphodiesterase-inhibitory effects of levosimendan (the (-) enantiomer of [[4-(1,4,5,6-tetrahydro-4-methyl-6-oxo-3-pyridazinyl)phenyl]hydrazono]propanedinitrile) and its active metabolite, OR-1896 (the (-) enantiomer of N-[4-(1,4,5,6-tetrahydro-4-methyl-6-oxo-3-pyridazinyl)phenyl] acetamide), were compared with their positive inotropic effects to reveal their mechanisms of action in guinea pig hearts. In Langendorff-perfused hearts, left ventricular +dP/dt(max) increased by 26+/-4% and 25+/-3% (mean+/-S.E.M.), with EC(50) values of 15+/-2 and 25+/-1 nM for levosimendan and OR-1896, respectively. In permeabilized myocyte-sized preparations, levosimendan and OR-1896 both increased isometric force production via Ca(2+) sensitization (at pCa 6.2), by 51+/-7% and 52+/-6%, with EC(50) values of 8+/-1 and 36+/-7 nM (P

Subclavian artery puncture and dilation with 9 Fr dilator during pacemaker implantation is a rare complication. We present a case, where this complication occurred and the injury was sealed with collagen-based closure device without any complications. Long term follow-up and the control angio-CT revealed no further late vascular complications. Therefore, use of a collagen based closure device for treating accidental iatrogenic subclavian artery injury can be a simple, successful alternative therapy when surgical direct vascular repair is not possible or not available.