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Abstract: Introduction: 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. Aim: 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. Method: 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. Results: 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. Conclusions: 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.

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.

The authors present the history of a 62-year-old man on continuous rivaroxaban therapy who was scheduled for pulmonary vein isolation due to persistent atrial fibrillation. Preoperative transesophageal echocardiography detected the presence of left atrial appendage thrombus. Thrombophilia tests showed that the patient was heterozygous carrier of the methylene-tetrahydrofolate reductase gene mutation. The authors hypothesized that a direct thrombin inhibitor might exert a more appropriate effect against thrombosis in this case and, therefore, a switch to dabigatran was performed. After two months of anticoagulation with the direct thrombin inhibitor and folic acid supplementation the thrombus resolved. The authors underline that thrombus formation may develop in atrial fibrillation even if the patient is adequately treated with rivaroxaban. This case suggests, that methylene-tetrahydrofolate reductase gene mutation may modulate the efficacy of direct Xa factor inhibitors. According to this case history, dabigatran may be an effective therapeutic option in resolving established thrombus. Orv. Hetil., 2016, 157(4), 154–156.

The authors present the history of a 62-year-old man on continuous rivaroxaban therapy who was scheduled for pulmonary vein isolation due to persistent atrial fibrillation. Preoperative transesophageal echocardiography detected the presence of left atrial appendage thrombus. Thrombophilia tests showed that the patient was heterozygous carrier of the methylene-tetrahydrofolate reductase gene mutation. The authors hypothesized that a direct thrombin inhibitor might exert a more appropriate effect against thrombosis in this case and, therefore, a switch to dabigatran was performed. After two months of anticoagulation with the direct thrombin inhibitor and folic acid supplementation the thrombus resolved. The authors underline that thrombus formation may develop in atrial fibrillation even if the patient is adequately treated with rivaroxaban. This case suggests, that methylene-tetrahydrofolate reductase gene mutation may modulate the efficacy of direct Xa factor inhibitors. According to this case history, dabigatran may be an effective therapeutic option in resolving established thrombus.

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.