International Journal of Cardiology 178 (2015) e1–e4
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
A Brugada-like electrocardiogram pattern induced after radiofrequency catheter ablation of atrial fibrillation Chunying Jiang a,⁎, Rui Wang b, Wen Lu a, Bing Han a a b
Department of Cardiology, Xuzhou Central Hospital, Xu Zhou City, China Department of Ultrasound, The Third Affiliated Hospital of Xuzhou Medical Collage, Xu Zhou City, China
a r t i c l e
i n f o
Article history: Received 14 August 2014 Accepted 17 August 2014 Available online 23 August 2014 Keywords: Brugada-like ECG pattern Atrial fibrillation Radiofrequency catheter ablation Iatrogenic injury of myocardium
Radiofrequency catheter ablation (RFCA) of the left atrium (LA) targeting the initiating triggers inside the pulmonary vein (PV) to disconnect PVs has become a very promising and successful treatment in patients with symptomatic and drug refractory atrial fibrillation (AF) of no or minimal structural heart disease [1]. Known complications of RFCA have been defined and investigated, including pulmonary vein stenosis, aortic root and atrial perforation, stroke and pericardial effusion and so on [1,2]. The present report describes one case of ST-segment elevation in electrocardiogram (ECG) monitoring induced after RFCA of AF. The potential underlying mechanisms are discussed. A 43-year-old man with a one-year history of drug-refractory paroxysmal AF was referred to our cardiovascular center for RFCA of the LA. Conventional and tissue Doppler echocardiography revealed normal left ventricular ejection fraction (LVEF) (55%) and LA (35 mm), in which no evidence of thrombus was approved by transesophageal echocardiography (TEE). Coronary heart disease was excluded with 320-row multidetector computed tomography (CT) angiography which has a high concordance with histology when evaluating coronary artery plaque characteristics. Electrocardiogram (ECG) and 99mTcmethoxyisobutylisonitrile (MIBI) single photon emission computed tomography (SPECT) showed normal myocardial perfusion on admission. After the approval from the Local Ethics Committee and informed written consent obtained from the patients, RFCA was performed under local anesthesia by lidocaine. A decapolar catheter was advanced ⁎ Corresponding author at: Department of Cardiology, Xuzhou Central Hospital, Liberation South Road 199, 221003 Xu Zhou City, China. Tel.: +86 51683985061; fax: +86 51683956044. E-mail address: [email protected] (C. Jiang).
http://dx.doi.org/10.1016/j.ijcard.2014.08.111 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
in coronary sinus via left subclavian vein access to the right atrium (RA) and atrial and ventricular electrograms were seen. Two L1-type Swartz sheathes were advanced into the LA through interatrial septum via twice successful transseptal punctures. About 5000 U heparin was infused promptly and followed by 1000 U/h into LA via one sheath to maintain an activated clotting time of 300–400 s. Selective PV venography was administered to identify all PV ostia. The 3.5 mm salineirrigated ablation catheter and decapolar circular mapping catheter were inserted separately into the LA through two long vascular sheaths. After that, a geometry of the LA was reconstructed using the CARTO system (Biosense Webster, Diamond Bar, California, USA). Radiofrequency (RF) energy was delivered to left and right PVs which were identified by venography to form one circular lesion line and the local potential amplitude decreased nearly to baseline. After all, a defibrillator was used to fire an electrical shock to jolt the heart back into a sinus rhythm. The procedure was well tolerated and uneventful. However, regular transthoracic ECG after ablation demonstrated ST-segment elevation greater than 0.05 mV in I avL leads (Fig. 1). J-point and the down-slopping coved ST-segment elevations of 0.1– 0.4 mV were noted in anterior precordial leads with associated T-wave inversions in V1 and flatness in V2 leads suggested a Type-1 Brugada-like ECG pattern. But it has occurred with no symptoms and uneventful during the night after ablation. The following day, blood tests revealed a remarkable increased level of serum troponin I (TnI) 1.95 μg/L, while other parameters such as blood count, blood gas analysis, D-dimer, electrolytes and creatinine were within the normal range. What is more, we recorded the occurrence of ST-segment elevations even higher in I avL, V1–V5 leads which developed incomplete right bundle branch block (RBBB) and ultrasonic cardiogram (UCG) showed normal LVEF and no pericardial effusions. Although the patient presented no symptoms and abnormal physical signs, in view of the ECG dynamic changes and likelihood of silent myocardial infarction (MI), he was transferred to the cardiac catheterization laboratory for a coronary angiogram (CAG) to exclude coronary vessel lesions. CAG performed from radial access showed normal coronary arteries, with no obstructive coronary atherosclerosis. On the third day after ablation, the value of serum TnI declines to 0.85 μg/L. And ECG displayed a normal sinus rhythm and spontaneous reduction in the ST-segment elevation in relevant leads as described before. Although ST-segment elevations and increased values of serum TnI without chest pain made us to focus on acute coronary syndrome
e2
C. Jiang et al. / International Journal of Cardiology 178 (2015) e1–e4
a
b
c
d
e
f
Fig. 1. ST-segment alteration from baseline on admission (a) to elevation in I avL, V1–V5 leads after RFCA of AF immediately (b), and spontaneous reduction gradually in the following day (c), the third day (d) and one week (e) after RFCA, and evolution of ST-elevations to baseline after two weeks follow-up (f). RFCA = radiofrequency catheter ablation; AF = atrial fibrillation.
C. Jiang et al. / International Journal of Cardiology 178 (2015) e1–e4
(ACS) which was excluded late, diagnosis of other complications after RFCA was also considered. Myocardial perfusion SPECT results showed non-segment fixed radioactive defects in anterior wall of left ventricular myocardium (Fig. 2). A pharmacological provocation test for Brugada-like pattern was performed, and ECG revealed Brugada-like phenomenon failed to be induced by intravenous propafenone. When cardiac biomarker TnI assay restored to the normal range, the patient was discharged. Although a further evaluation of electrophysiological test was recommended strongly for possible ventricular arrhythmia detection and risk stratification, he declined. Tracing and follow-up of the patient was performed. There were no embolic and arrhythmic events throughout the patient's follow-up. ECG showed gradual evolution of ST-elevations to baseline and disappearance after two weeks of follow-up. The present report shows a patient undergoing RFCA of AF followed by a strange ECG pattern with the ST-segment and T-wave changes resembled a Brugada-like pattern and subsequently returned toward normal after two weeks. Several major studies suggest that sinus rhythm is better preserved than with antiarrhythmic drugs and the majority of suitable patients who received RFCA of AF have a dramatic improvement in their symptoms and some are completely cured of AF [1]. Many complications during or after the application of RF energy surround PV ostia in the LA have been previously described. The occurrence of life-threatening ST-segment elevation during pulmonary vein isolation may be caused by coronary vessel lesions and spasm. A case of myocardial ischemia prior to any ablation of atrial fibrillation had been reported [3]. The patient complained of severe chest pain during the procedure and a focal occlusion within a distal branch of the 1st diagonal was confirmed by CAG. The authors attributed this effect to coronary occlusion triggered by thromboembolism. Numerous cases have been reported that transient ST-segment elevation during transseptal procedure for RFCA of AF may be an occurrence in patients [4–6]. The authors hypothesize that mechanical manipulation of the intraseptal and left atrial vagal network by the transseptal puncture causes an imbalance in autonomic innervation, which leads to coronary artery spasm followed by ST-segment elevation. A prospective multi-center trial observed four cases of the occurrence of ST-segment elevation in inferior leads greater than 0.2 mV and accompanying left thoracic discomfort among 43 patients who
e3
accepted RFCA of AF. No thrombotic material or air emboli were detected in coronary artery during the selective angiography. Coronary vasospasm caused by manipulations of transseptal puncture had been proposed to explain this phenomenon [6]. In the present case, angiography excluded significant coronary artery stenosis and direct or indirect evidence of air embolism such as slow flow within the coronary arteries. In view of the spontaneous gradually reduction in the ST-segment elevation, a likelihood of coronary vasospasm was not favored. The prompt relief of TnI after ablation of AF led to the hypothesis of myocardium lesion injured by current energy from radiofrequency generator settings. Pericardial effusion complicating RFCA is not rare in patients with AF, and it tends to develop into cardiac tamponade rapidly. An increased incidence of cardiac tamponade response to the complicated manipulations of transseptal procedure had been considered [2]. Cardiac tamponade could be excluded instantaneously by echocardiography. We could not find evidence hinting at pericardial effusion. Brugada syndrome, first described in 1992 by Pedro and Josep Brugada, is a primary electrical disease linked to mutations of the cardiac sodium channel genes of SCN5A that causes syncope and sudden cardiac death resulting from polymorphic ventricular tachycardia or ventricular fibrillation in previously healthy people [7,8]. It is associated with familial tendency and may be mistakenly diagnosed as acute myocardial infarction (AMI) with typical electrocardiography resembling complete RBBB and ST-segment elevation in precordial leads. Intravenous propafenone provocation test is helpful to differentiate Brugada syndrome in patients from acute anterior wall MI and other conditions manifesting with similar changes in ECG. The patient with ECG revealed type-1 Brugada-like phenomenon in the case we presented was a middle-aged male without predisposition and positive family history of syncope or sudden cardiac death. A pharmacological provocation test of intravenous propafenone for Brugada pattern failed to induce typical electrocardiography resembling dynamic ST-segment elevation in this case. The prognostic value of electrophysiological studies for both further confirmation of the diagnosis and determination of treatment strategies in individuals with Brugada syndrome proved to be useful [9]. Be afraid of inducibility of sustained life-threaten ventricular arrhythmias during programmed ventricular stimulation of the heart, the patient declined our suggestion of a further evaluation of electrophysiological test.
Fig. 2. SPECT showed multiple radioactive defects in anterior, inferior and lateral walls of left ventricular myocardium and apical segment in corresponding short-axis (top), vertical longaxis (middle), and horizontal long-axis short axis (bottom) in a 43-year-old man after ablation (b) compared with normal perfusion on admission (a). SPECT = single photon emission computed tomography.
e4
C. Jiang et al. / International Journal of Cardiology 178 (2015) e1–e4
Several medications or conditions including severe hyponatremia, mutation of the SCN5A gene and so on that may cause loss of cardiac sodium channel function in the ventricular epicardium induce ECG findings of ST elevations in precordial leads that resemble the Brugada pattern [8,10]. In the cases we present, we could not detect direct or indirect evidence of drugs or other conditions such as hyperkalemia, severe hyponatremia and so on that may lead to Brugada-like pattern of ECG in individuals. A newly promising study highlighted the risk of myocardial damage complication after pulmonary vein RFCA [11]. Proinflammatory substances of nitric oxide, activated leukocyte cell adhesion molecule and lipoprotein-associated phospholipase released from injured myocardium by radiofrequency catheter ablation may contribute to endothelial dysfunction in left anterior descending (LAD) coronary artery branches' structure confirmed by increased index of microvascular resistance (IMVR) after RFCA. The authors concluded that this mechanism may represent transient diastolic dysfunction and early recurrence of arrhythmia after RFCA. Fixed radioactive defects in ECT myocardial imaging revealed endothelial dysfunction of microvessels in anterior wall of left ventricular myocardium. We, therefore, conclude that a different mechanism may account for this phenomenon. Paralysis of cardiac sodium channel function in result of iatrogenic injury of myocardium caused by current energy from radiofrequency generator settings is favored in this case. It is a pity that IMVR was not assessed after RFCA. Conflict of interest None declared.
References [1] Piccini JP, Sinner MF, Greiner MA, et al. Outcomes of Medicare beneficiaries undergoing catheter ablation for atrial fibrillation. Circulation 2012;126:2200–7. [2] Katritsis GD, Siontis GC, Giazitzoglou E, Fragakis N, Katritsis DG. Complications of transseptal catheterization for different cardiac procedures. Int J Cardiol 2013;168: 5352–4. [3] Michael KA, Redfearn DP, Simpson CS, Baranchuk A. An unusual complication of a pulmonary vein isolation. J Interv Card Electrophysiol 2009;25:203–5. [4] Letsas KP, Pappas LK, Gavrielatos G, Efremidis M, Sideris A, Kardaras F. ST-segment elevation induced during the transseptal procedure for radiofrequency catheter ablation of atrial fibrillation. Int J Cardiol 2007;114:e12–4. [5] Man JP, Lin D, Frankel DS. Transient ST segment elevation and accompanying intracardiac echocardiographic abnormalities of the inferior left ventricular wall during catheter ablation of atrial fibrillation. J Interv Card Electrophysiol 2013;38:51. [6] Risius T, Lewalter T, Luderitz B, et al. Transient ST-segment-elevation during pulmonary vein ablation using circumferential coiled microelectrodes in a prospective multi-centre study. Europace 2006;8:178–81. [7] Brugada J, Boersma L, Abdollah H, Kirchhof C, Allessie M. Echo-wave termination of ventricular tachycardia. A common mechanism of termination of reentrant arrhythmias by various pharmacological interventions. Circulation 1992;85:1879–87. [8] Chen QY, Kirsch GE, Zhang DM, et al. Genetic basis and molecular mechanism for idiopathic: ventricular fibrillation. Nature 1998;392:293–6. [9] Brugada P, Brugada R, Mont L, Rivero M, Geelen P, Brugada J. Natural history of Brugada syndrome: the prognostic value of programmed electrical stimulation of the heart. J Cardiovasc Electrophysiol 2003;14:455–7. [10] Tamene A, Sattiraju S, Wang K, Benditt DG. Brugada-like electrocardiography pattern induced by severe hyponatraemia. Europace 2010;12:905–7. [11] Lim HE, Choi CU, Na JO, et al. Effects of iatrogenic myocardial injury on coronary microvascular function in patients undergoing radiofrequency catheter ablation of atrial fibrillation. Circ Arrhythm Electrophysiol 2013;6:318–26.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
A Brugada-like electrocardiogram pattern induced after radiofrequency catheter ablation of atrial fibrillation Chunying Jiang a,⁎, Rui Wang b, Wen Lu a, Bing Han a a b
Department of Cardiology, Xuzhou Central Hospital, Xu Zhou City, China Department of Ultrasound, The Third Affiliated Hospital of Xuzhou Medical Collage, Xu Zhou City, China
a r t i c l e
i n f o
Article history: Received 14 August 2014 Accepted 17 August 2014 Available online 23 August 2014 Keywords: Brugada-like ECG pattern Atrial fibrillation Radiofrequency catheter ablation Iatrogenic injury of myocardium
Radiofrequency catheter ablation (RFCA) of the left atrium (LA) targeting the initiating triggers inside the pulmonary vein (PV) to disconnect PVs has become a very promising and successful treatment in patients with symptomatic and drug refractory atrial fibrillation (AF) of no or minimal structural heart disease [1]. Known complications of RFCA have been defined and investigated, including pulmonary vein stenosis, aortic root and atrial perforation, stroke and pericardial effusion and so on [1,2]. The present report describes one case of ST-segment elevation in electrocardiogram (ECG) monitoring induced after RFCA of AF. The potential underlying mechanisms are discussed. A 43-year-old man with a one-year history of drug-refractory paroxysmal AF was referred to our cardiovascular center for RFCA of the LA. Conventional and tissue Doppler echocardiography revealed normal left ventricular ejection fraction (LVEF) (55%) and LA (35 mm), in which no evidence of thrombus was approved by transesophageal echocardiography (TEE). Coronary heart disease was excluded with 320-row multidetector computed tomography (CT) angiography which has a high concordance with histology when evaluating coronary artery plaque characteristics. Electrocardiogram (ECG) and 99mTcmethoxyisobutylisonitrile (MIBI) single photon emission computed tomography (SPECT) showed normal myocardial perfusion on admission. After the approval from the Local Ethics Committee and informed written consent obtained from the patients, RFCA was performed under local anesthesia by lidocaine. A decapolar catheter was advanced ⁎ Corresponding author at: Department of Cardiology, Xuzhou Central Hospital, Liberation South Road 199, 221003 Xu Zhou City, China. Tel.: +86 51683985061; fax: +86 51683956044. E-mail address: [email protected] (C. Jiang).
http://dx.doi.org/10.1016/j.ijcard.2014.08.111 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
in coronary sinus via left subclavian vein access to the right atrium (RA) and atrial and ventricular electrograms were seen. Two L1-type Swartz sheathes were advanced into the LA through interatrial septum via twice successful transseptal punctures. About 5000 U heparin was infused promptly and followed by 1000 U/h into LA via one sheath to maintain an activated clotting time of 300–400 s. Selective PV venography was administered to identify all PV ostia. The 3.5 mm salineirrigated ablation catheter and decapolar circular mapping catheter were inserted separately into the LA through two long vascular sheaths. After that, a geometry of the LA was reconstructed using the CARTO system (Biosense Webster, Diamond Bar, California, USA). Radiofrequency (RF) energy was delivered to left and right PVs which were identified by venography to form one circular lesion line and the local potential amplitude decreased nearly to baseline. After all, a defibrillator was used to fire an electrical shock to jolt the heart back into a sinus rhythm. The procedure was well tolerated and uneventful. However, regular transthoracic ECG after ablation demonstrated ST-segment elevation greater than 0.05 mV in I avL leads (Fig. 1). J-point and the down-slopping coved ST-segment elevations of 0.1– 0.4 mV were noted in anterior precordial leads with associated T-wave inversions in V1 and flatness in V2 leads suggested a Type-1 Brugada-like ECG pattern. But it has occurred with no symptoms and uneventful during the night after ablation. The following day, blood tests revealed a remarkable increased level of serum troponin I (TnI) 1.95 μg/L, while other parameters such as blood count, blood gas analysis, D-dimer, electrolytes and creatinine were within the normal range. What is more, we recorded the occurrence of ST-segment elevations even higher in I avL, V1–V5 leads which developed incomplete right bundle branch block (RBBB) and ultrasonic cardiogram (UCG) showed normal LVEF and no pericardial effusions. Although the patient presented no symptoms and abnormal physical signs, in view of the ECG dynamic changes and likelihood of silent myocardial infarction (MI), he was transferred to the cardiac catheterization laboratory for a coronary angiogram (CAG) to exclude coronary vessel lesions. CAG performed from radial access showed normal coronary arteries, with no obstructive coronary atherosclerosis. On the third day after ablation, the value of serum TnI declines to 0.85 μg/L. And ECG displayed a normal sinus rhythm and spontaneous reduction in the ST-segment elevation in relevant leads as described before. Although ST-segment elevations and increased values of serum TnI without chest pain made us to focus on acute coronary syndrome
e2
C. Jiang et al. / International Journal of Cardiology 178 (2015) e1–e4
a
b
c
d
e
f
Fig. 1. ST-segment alteration from baseline on admission (a) to elevation in I avL, V1–V5 leads after RFCA of AF immediately (b), and spontaneous reduction gradually in the following day (c), the third day (d) and one week (e) after RFCA, and evolution of ST-elevations to baseline after two weeks follow-up (f). RFCA = radiofrequency catheter ablation; AF = atrial fibrillation.
C. Jiang et al. / International Journal of Cardiology 178 (2015) e1–e4
(ACS) which was excluded late, diagnosis of other complications after RFCA was also considered. Myocardial perfusion SPECT results showed non-segment fixed radioactive defects in anterior wall of left ventricular myocardium (Fig. 2). A pharmacological provocation test for Brugada-like pattern was performed, and ECG revealed Brugada-like phenomenon failed to be induced by intravenous propafenone. When cardiac biomarker TnI assay restored to the normal range, the patient was discharged. Although a further evaluation of electrophysiological test was recommended strongly for possible ventricular arrhythmia detection and risk stratification, he declined. Tracing and follow-up of the patient was performed. There were no embolic and arrhythmic events throughout the patient's follow-up. ECG showed gradual evolution of ST-elevations to baseline and disappearance after two weeks of follow-up. The present report shows a patient undergoing RFCA of AF followed by a strange ECG pattern with the ST-segment and T-wave changes resembled a Brugada-like pattern and subsequently returned toward normal after two weeks. Several major studies suggest that sinus rhythm is better preserved than with antiarrhythmic drugs and the majority of suitable patients who received RFCA of AF have a dramatic improvement in their symptoms and some are completely cured of AF [1]. Many complications during or after the application of RF energy surround PV ostia in the LA have been previously described. The occurrence of life-threatening ST-segment elevation during pulmonary vein isolation may be caused by coronary vessel lesions and spasm. A case of myocardial ischemia prior to any ablation of atrial fibrillation had been reported [3]. The patient complained of severe chest pain during the procedure and a focal occlusion within a distal branch of the 1st diagonal was confirmed by CAG. The authors attributed this effect to coronary occlusion triggered by thromboembolism. Numerous cases have been reported that transient ST-segment elevation during transseptal procedure for RFCA of AF may be an occurrence in patients [4–6]. The authors hypothesize that mechanical manipulation of the intraseptal and left atrial vagal network by the transseptal puncture causes an imbalance in autonomic innervation, which leads to coronary artery spasm followed by ST-segment elevation. A prospective multi-center trial observed four cases of the occurrence of ST-segment elevation in inferior leads greater than 0.2 mV and accompanying left thoracic discomfort among 43 patients who
e3
accepted RFCA of AF. No thrombotic material or air emboli were detected in coronary artery during the selective angiography. Coronary vasospasm caused by manipulations of transseptal puncture had been proposed to explain this phenomenon [6]. In the present case, angiography excluded significant coronary artery stenosis and direct or indirect evidence of air embolism such as slow flow within the coronary arteries. In view of the spontaneous gradually reduction in the ST-segment elevation, a likelihood of coronary vasospasm was not favored. The prompt relief of TnI after ablation of AF led to the hypothesis of myocardium lesion injured by current energy from radiofrequency generator settings. Pericardial effusion complicating RFCA is not rare in patients with AF, and it tends to develop into cardiac tamponade rapidly. An increased incidence of cardiac tamponade response to the complicated manipulations of transseptal procedure had been considered [2]. Cardiac tamponade could be excluded instantaneously by echocardiography. We could not find evidence hinting at pericardial effusion. Brugada syndrome, first described in 1992 by Pedro and Josep Brugada, is a primary electrical disease linked to mutations of the cardiac sodium channel genes of SCN5A that causes syncope and sudden cardiac death resulting from polymorphic ventricular tachycardia or ventricular fibrillation in previously healthy people [7,8]. It is associated with familial tendency and may be mistakenly diagnosed as acute myocardial infarction (AMI) with typical electrocardiography resembling complete RBBB and ST-segment elevation in precordial leads. Intravenous propafenone provocation test is helpful to differentiate Brugada syndrome in patients from acute anterior wall MI and other conditions manifesting with similar changes in ECG. The patient with ECG revealed type-1 Brugada-like phenomenon in the case we presented was a middle-aged male without predisposition and positive family history of syncope or sudden cardiac death. A pharmacological provocation test of intravenous propafenone for Brugada pattern failed to induce typical electrocardiography resembling dynamic ST-segment elevation in this case. The prognostic value of electrophysiological studies for both further confirmation of the diagnosis and determination of treatment strategies in individuals with Brugada syndrome proved to be useful [9]. Be afraid of inducibility of sustained life-threaten ventricular arrhythmias during programmed ventricular stimulation of the heart, the patient declined our suggestion of a further evaluation of electrophysiological test.
Fig. 2. SPECT showed multiple radioactive defects in anterior, inferior and lateral walls of left ventricular myocardium and apical segment in corresponding short-axis (top), vertical longaxis (middle), and horizontal long-axis short axis (bottom) in a 43-year-old man after ablation (b) compared with normal perfusion on admission (a). SPECT = single photon emission computed tomography.
e4
C. Jiang et al. / International Journal of Cardiology 178 (2015) e1–e4
Several medications or conditions including severe hyponatremia, mutation of the SCN5A gene and so on that may cause loss of cardiac sodium channel function in the ventricular epicardium induce ECG findings of ST elevations in precordial leads that resemble the Brugada pattern [8,10]. In the cases we present, we could not detect direct or indirect evidence of drugs or other conditions such as hyperkalemia, severe hyponatremia and so on that may lead to Brugada-like pattern of ECG in individuals. A newly promising study highlighted the risk of myocardial damage complication after pulmonary vein RFCA [11]. Proinflammatory substances of nitric oxide, activated leukocyte cell adhesion molecule and lipoprotein-associated phospholipase released from injured myocardium by radiofrequency catheter ablation may contribute to endothelial dysfunction in left anterior descending (LAD) coronary artery branches' structure confirmed by increased index of microvascular resistance (IMVR) after RFCA. The authors concluded that this mechanism may represent transient diastolic dysfunction and early recurrence of arrhythmia after RFCA. Fixed radioactive defects in ECT myocardial imaging revealed endothelial dysfunction of microvessels in anterior wall of left ventricular myocardium. We, therefore, conclude that a different mechanism may account for this phenomenon. Paralysis of cardiac sodium channel function in result of iatrogenic injury of myocardium caused by current energy from radiofrequency generator settings is favored in this case. It is a pity that IMVR was not assessed after RFCA. Conflict of interest None declared.
References [1] Piccini JP, Sinner MF, Greiner MA, et al. Outcomes of Medicare beneficiaries undergoing catheter ablation for atrial fibrillation. Circulation 2012;126:2200–7. [2] Katritsis GD, Siontis GC, Giazitzoglou E, Fragakis N, Katritsis DG. Complications of transseptal catheterization for different cardiac procedures. Int J Cardiol 2013;168: 5352–4. [3] Michael KA, Redfearn DP, Simpson CS, Baranchuk A. An unusual complication of a pulmonary vein isolation. J Interv Card Electrophysiol 2009;25:203–5. [4] Letsas KP, Pappas LK, Gavrielatos G, Efremidis M, Sideris A, Kardaras F. ST-segment elevation induced during the transseptal procedure for radiofrequency catheter ablation of atrial fibrillation. Int J Cardiol 2007;114:e12–4. [5] Man JP, Lin D, Frankel DS. Transient ST segment elevation and accompanying intracardiac echocardiographic abnormalities of the inferior left ventricular wall during catheter ablation of atrial fibrillation. J Interv Card Electrophysiol 2013;38:51. [6] Risius T, Lewalter T, Luderitz B, et al. Transient ST-segment-elevation during pulmonary vein ablation using circumferential coiled microelectrodes in a prospective multi-centre study. Europace 2006;8:178–81. [7] Brugada J, Boersma L, Abdollah H, Kirchhof C, Allessie M. Echo-wave termination of ventricular tachycardia. A common mechanism of termination of reentrant arrhythmias by various pharmacological interventions. Circulation 1992;85:1879–87. [8] Chen QY, Kirsch GE, Zhang DM, et al. Genetic basis and molecular mechanism for idiopathic: ventricular fibrillation. Nature 1998;392:293–6. [9] Brugada P, Brugada R, Mont L, Rivero M, Geelen P, Brugada J. Natural history of Brugada syndrome: the prognostic value of programmed electrical stimulation of the heart. J Cardiovasc Electrophysiol 2003;14:455–7. [10] Tamene A, Sattiraju S, Wang K, Benditt DG. Brugada-like electrocardiography pattern induced by severe hyponatraemia. Europace 2010;12:905–7. [11] Lim HE, Choi CU, Na JO, et al. Effects of iatrogenic myocardial injury on coronary microvascular function in patients undergoing radiofrequency catheter ablation of atrial fibrillation. Circ Arrhythm Electrophysiol 2013;6:318–26.
