International Journal of Cardiology 172 (2014) e513–e515
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Severe coronary artery spasm during radiofrequency ablation for atrial fibrillation☆,☆☆ Keiichi Hishikari a,b,⁎, Taishi Kuwahara a, Atsushi Takahashi a, Mitsuaki Isobe b a b
Cardiovascular Center, Yokosuka Kyosai Hospital, Yokosuka, Japan Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan
a r t i c l e
i n f o
Article history: Received 14 January 2014 Accepted 18 January 2014 Available online 24 January 2014 Keywords: Atrial fibrillation Catheter ablation Complication ST-segment elevation Vasospasm Acetylcholine
Pulmonary vein isolation has become a standard treatment strategy for atrial fibrillation (AF), [1] and is generally considered a safe procedure. However, some serious complications can occur [2]; therefore, attention needs to be paid to potential complications during AF ablation. ST-segment elevations have rarely been reported to occur during transseptal catheterization or left atrial (LA) ablation, and most ST-segment elevations have been reported to be transient, with normal, subsequent coronary arteriography [3]. We report a patient with a severe coronary artery spasm that was resistant to nitrate injection with hemodynamic collapse during LA ablation for AF. A 66-year-old man with drug-resistant, persistent AF was admitted to our institution for radiofrequency (RF) catheter ablation. After obtaining written informed consent, AF catheter ablation was performed. An irrigated ablation catheter, having a 3.5-mm tip (Navistar ThermoCool, Biosense Webster, Diamond Bar, CA, USA), was used, with a RF power of 25–30 W and a cut-off temperature of 45 °C, for 30–60 s at each site. The endpoint of the pulmonary vein isolation ☆ This is an open-access article distributed under the terms of the Creative Commons Attribution–NonCommercial–No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited. ☆☆ Author contributions: Data collection: Taishi Kuwahara, M.D. Data analysis/ interpretation: Atsushi Takahashi M.D., Mitsuaki Isobe* M.D. ⁎ Corresponding author at: Cardiovascular Center, Yokosuka Kyousai Hospital, 1-16, Yonegahama-dori, Yokosuka, Kanagawa, Japan. Tel.: +81 46 822 2710; fax: +81 46 825 2103. E-mail address: [email protected] (K. Hishikari). 0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.01.090
(PVI) was the point at which all pulmonary vein (PV) potentials were eliminated. After isolation of the left-sided PVs, we started RF application at the posteroinferior aspect of the right inferior PV. As was revealed retrospectively, 15 s after beginning the RF delivery, the ST-segment became slightly elevated in the inferior leads of the ECG. This slight change went unnoticed, and the RF delivery was continued for over 60 s at and adjacent to the first ablation point. The ST-segment continued to elevate (Fig. 1, left) until a marked ST-segment elevation was present, and a complete atrioventricular block (Fig. 1, right) developed in conjunction with severe systolic blood pressure hypotension (b50 mm Hg). We stopped RF delivery once the atrioventricular block was noticed. Subsequently, we performed coronary angiography and found that the left coronary artery (LCA) was normal and the right coronary artery (RCA) was totally occluded at its ostium (Fig. 2, left). Supportive therapy, such as noradrenalin injection and right ventricular pacing, was attempted, and nitrate was injected into the coronary artery but the total occlusion was not resolved. Although the coronary artery occlusion was refractory to repeated nitrate injection, the ST-segment elevation gradually improved and normalized 12 min after the start of the STsegment elevation with normal coronary flow through the RCA (Fig. 2, right). We diagnosed this total occlusion of the coronary artery as a coronary artery spasm. Despite ST-segment normalization and the supportive therapy, the systolic blood pressure persisted at b80 mm Hg. Therefore, we decided to end the ablation session. The severe hypotension recovered the next morning, and echocardiography showed normal left ventricular wall motion after the procedure. A month after discharge, the patient was readmitted to for a provocative test with acetylcholine (Ach) in an attempt to confirm a diagnosis of a variant angina pectoris. Ach provocation (50 μg and 100 μg in the LCA, and 25 μg and 50 μg in the RCA) did not induce a spasm in either the LCA or RCA. LA catheter ablation can cause several serious complications, such as atrio-esophageal fistulas, cardiac tamponade, or strokes [2]. However, ST-segment elevations are rarely observed, and most involve transient ST-segment elevations and normal coronary arteries, as demonstrated by coronary angiography performed immediately after the ST-segment elevation [3]. The present patient showed persistent ST-segment elevation due to a severe coronary artery spasm, revealed by subsequent coronary angiography, and the spasm was refractory to the repeated injection of nitrate, leading to hemodynamic collapse. Following an Ach provocation test to elucidate whether this patient had variant angina, we concluded that this patient demonstrated a very rare case of severe coronary artery spasm due to AF catheter ablation.
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K. Hishikari et al. / International Journal of Cardiology 172 (2014) e513–e515
Fig. 1. Left: Twelve-lead electrocardiogram (ECG) with ST-segment elevation in leads II, III, and aVF. Right: Twelve-lead ECG with ST-segment elevation in leads II, III, and aVF and complete atrioventricular block.
Fig. 2. Left: Coronary angiogram showing an occluded proximal right coronary artery and artery shrinkage. Right: Coronary angiogram showing a patent right coronary artery.
The causes of ST-segment elevation other than a spasm may include an air embolism or a thrombotic occlusion [4]. However, we did not exchange catheters before the ST-segment elevation, and the coronary angiography exhibited neither air emboli nor thrombi in the coronary artery. Therefore, a coronary artery spasm likely accounted for the ST-segment elevation in the present case. This patient did not have symptoms of angina, before or after the ablation procedure, and was not taking calcium antagonists or nitrates. Furthermore, a coronary artery spasm was not induced by the Ach provocative test. Okumura reported that the Ach provocation test has a sensitivity and specificity of 89–93% and 100%, respectively, for the induction of coronary artery spasm following intracoronary injection of Ach [5]. The observed results indicated that this patient did not have variant angina, and that the coronary artery spasm that occurred during the LA catheter ablation was from the result of a specific mechanism associated with the LA catheter ablation itself. There are two possible mechanisms for a coronary artery spasm during AF catheter ablation. First, an autonomic nerve activity imbalance may have caused the spasm. The coronary artery spasm occurred during RF delivery to the posteroinferior aspect of the right inferior PV. Epicardial sites in this region are associated with a ganglionated plexus (GP), the so-called right lower GP. Endocardial RF ablation can
affect the epicardial GP through a thermal injury that may cause an imbalance in autonomic nervous activity, frequently stimulating the parasympathetic nerve. Increased parasympathetic nerve activity could, in turn, induce a vasospasm of the coronary artery [6]. Alternatively, the RF energy may have caused direct thermal injury to the coronary artery. The delivery of RF energy adjacent to the coronary artery may cause a coronary artery spasm or occlusion [7]. Since we did not deliver RF energy adjacent to the RCA, we speculate that the mechanism causing the severe coronary artery spasm was most probably an imbalance of autonomic nervous activity caused by RF thermal injury to the GP. We reported a rare case of severe coronary artery spasm occurring during AF catheter ablation, refractory to nitrate injection, and leading to hemodynamic collapse. Supportive therapy and repeated nitrate administration alleviated the spasm, which may have resulted from an autonomic nervous imbalance caused by the application of RF energy. References [1] Raviele A, Natale A, Calkins H, et al. Venice Chart international consensus document on atrial fibrillation ablation: 2011 update. J Cardiovasc Electrophysiol 2012;23:890–923. [2] Cappato R, Calkins H, Chen S-A, et al. Prevalence and causes of fatal outcome in catheter ablation of atrial fibrillation. J Am Coll Cardiol 2009;53:1798–803.
K. Hishikari et al. / International Journal of Cardiology 172 (2014) e513–e515 [3] Le BH, Black JN, Huang SKS. Transient ST-segment elevation during transseptal catheterization for atrial fibrillation ablation. Tex Heart Inst J Tex Heart Inst St Lukes Episcop Hosp Tex Child Hosp 2010;37:717–21. [4] Kuwahara T, Takahashi A, Takahashi Y, et al. Clinical characteristics of massive air embolism complicating left atrial ablation of atrial fibrillation: lessons from five cases. Eur Eur Pacing Arrhythm Card Electrophysiol J Work Groups Card Pacing Arrhythm Card Cell Electrophysiol Eur Soc Cardiol 2012;14:204–8.
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[5] Okumura K, Yasue H, Matsuyama K, et al. Sensitivity and specificity of intracoronary injection of acetylcholine for the induction of coronary artery spasm. J Am Coll Cardiol 1988;12:883–8. [6] Yasue H, Horio Y, Nakamura N, et al. Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm. Circulation 1986;74:955–63. [7] Takahashi Y, Jais P, Hocini M, et al. Acute occlusion of the left circumflex coronary artery during mitral isthmus linear ablation. J Cardiovasc Electrophysiol 2005;16:1104–7.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Severe coronary artery spasm during radiofrequency ablation for atrial fibrillation☆,☆☆ Keiichi Hishikari a,b,⁎, Taishi Kuwahara a, Atsushi Takahashi a, Mitsuaki Isobe b a b
Cardiovascular Center, Yokosuka Kyosai Hospital, Yokosuka, Japan Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan
a r t i c l e
i n f o
Article history: Received 14 January 2014 Accepted 18 January 2014 Available online 24 January 2014 Keywords: Atrial fibrillation Catheter ablation Complication ST-segment elevation Vasospasm Acetylcholine
Pulmonary vein isolation has become a standard treatment strategy for atrial fibrillation (AF), [1] and is generally considered a safe procedure. However, some serious complications can occur [2]; therefore, attention needs to be paid to potential complications during AF ablation. ST-segment elevations have rarely been reported to occur during transseptal catheterization or left atrial (LA) ablation, and most ST-segment elevations have been reported to be transient, with normal, subsequent coronary arteriography [3]. We report a patient with a severe coronary artery spasm that was resistant to nitrate injection with hemodynamic collapse during LA ablation for AF. A 66-year-old man with drug-resistant, persistent AF was admitted to our institution for radiofrequency (RF) catheter ablation. After obtaining written informed consent, AF catheter ablation was performed. An irrigated ablation catheter, having a 3.5-mm tip (Navistar ThermoCool, Biosense Webster, Diamond Bar, CA, USA), was used, with a RF power of 25–30 W and a cut-off temperature of 45 °C, for 30–60 s at each site. The endpoint of the pulmonary vein isolation ☆ This is an open-access article distributed under the terms of the Creative Commons Attribution–NonCommercial–No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited. ☆☆ Author contributions: Data collection: Taishi Kuwahara, M.D. Data analysis/ interpretation: Atsushi Takahashi M.D., Mitsuaki Isobe* M.D. ⁎ Corresponding author at: Cardiovascular Center, Yokosuka Kyousai Hospital, 1-16, Yonegahama-dori, Yokosuka, Kanagawa, Japan. Tel.: +81 46 822 2710; fax: +81 46 825 2103. E-mail address: [email protected] (K. Hishikari). 0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2014.01.090
(PVI) was the point at which all pulmonary vein (PV) potentials were eliminated. After isolation of the left-sided PVs, we started RF application at the posteroinferior aspect of the right inferior PV. As was revealed retrospectively, 15 s after beginning the RF delivery, the ST-segment became slightly elevated in the inferior leads of the ECG. This slight change went unnoticed, and the RF delivery was continued for over 60 s at and adjacent to the first ablation point. The ST-segment continued to elevate (Fig. 1, left) until a marked ST-segment elevation was present, and a complete atrioventricular block (Fig. 1, right) developed in conjunction with severe systolic blood pressure hypotension (b50 mm Hg). We stopped RF delivery once the atrioventricular block was noticed. Subsequently, we performed coronary angiography and found that the left coronary artery (LCA) was normal and the right coronary artery (RCA) was totally occluded at its ostium (Fig. 2, left). Supportive therapy, such as noradrenalin injection and right ventricular pacing, was attempted, and nitrate was injected into the coronary artery but the total occlusion was not resolved. Although the coronary artery occlusion was refractory to repeated nitrate injection, the ST-segment elevation gradually improved and normalized 12 min after the start of the STsegment elevation with normal coronary flow through the RCA (Fig. 2, right). We diagnosed this total occlusion of the coronary artery as a coronary artery spasm. Despite ST-segment normalization and the supportive therapy, the systolic blood pressure persisted at b80 mm Hg. Therefore, we decided to end the ablation session. The severe hypotension recovered the next morning, and echocardiography showed normal left ventricular wall motion after the procedure. A month after discharge, the patient was readmitted to for a provocative test with acetylcholine (Ach) in an attempt to confirm a diagnosis of a variant angina pectoris. Ach provocation (50 μg and 100 μg in the LCA, and 25 μg and 50 μg in the RCA) did not induce a spasm in either the LCA or RCA. LA catheter ablation can cause several serious complications, such as atrio-esophageal fistulas, cardiac tamponade, or strokes [2]. However, ST-segment elevations are rarely observed, and most involve transient ST-segment elevations and normal coronary arteries, as demonstrated by coronary angiography performed immediately after the ST-segment elevation [3]. The present patient showed persistent ST-segment elevation due to a severe coronary artery spasm, revealed by subsequent coronary angiography, and the spasm was refractory to the repeated injection of nitrate, leading to hemodynamic collapse. Following an Ach provocation test to elucidate whether this patient had variant angina, we concluded that this patient demonstrated a very rare case of severe coronary artery spasm due to AF catheter ablation.
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K. Hishikari et al. / International Journal of Cardiology 172 (2014) e513–e515
Fig. 1. Left: Twelve-lead electrocardiogram (ECG) with ST-segment elevation in leads II, III, and aVF. Right: Twelve-lead ECG with ST-segment elevation in leads II, III, and aVF and complete atrioventricular block.
Fig. 2. Left: Coronary angiogram showing an occluded proximal right coronary artery and artery shrinkage. Right: Coronary angiogram showing a patent right coronary artery.
The causes of ST-segment elevation other than a spasm may include an air embolism or a thrombotic occlusion [4]. However, we did not exchange catheters before the ST-segment elevation, and the coronary angiography exhibited neither air emboli nor thrombi in the coronary artery. Therefore, a coronary artery spasm likely accounted for the ST-segment elevation in the present case. This patient did not have symptoms of angina, before or after the ablation procedure, and was not taking calcium antagonists or nitrates. Furthermore, a coronary artery spasm was not induced by the Ach provocative test. Okumura reported that the Ach provocation test has a sensitivity and specificity of 89–93% and 100%, respectively, for the induction of coronary artery spasm following intracoronary injection of Ach [5]. The observed results indicated that this patient did not have variant angina, and that the coronary artery spasm that occurred during the LA catheter ablation was from the result of a specific mechanism associated with the LA catheter ablation itself. There are two possible mechanisms for a coronary artery spasm during AF catheter ablation. First, an autonomic nerve activity imbalance may have caused the spasm. The coronary artery spasm occurred during RF delivery to the posteroinferior aspect of the right inferior PV. Epicardial sites in this region are associated with a ganglionated plexus (GP), the so-called right lower GP. Endocardial RF ablation can
affect the epicardial GP through a thermal injury that may cause an imbalance in autonomic nervous activity, frequently stimulating the parasympathetic nerve. Increased parasympathetic nerve activity could, in turn, induce a vasospasm of the coronary artery [6]. Alternatively, the RF energy may have caused direct thermal injury to the coronary artery. The delivery of RF energy adjacent to the coronary artery may cause a coronary artery spasm or occlusion [7]. Since we did not deliver RF energy adjacent to the RCA, we speculate that the mechanism causing the severe coronary artery spasm was most probably an imbalance of autonomic nervous activity caused by RF thermal injury to the GP. We reported a rare case of severe coronary artery spasm occurring during AF catheter ablation, refractory to nitrate injection, and leading to hemodynamic collapse. Supportive therapy and repeated nitrate administration alleviated the spasm, which may have resulted from an autonomic nervous imbalance caused by the application of RF energy. References [1] Raviele A, Natale A, Calkins H, et al. Venice Chart international consensus document on atrial fibrillation ablation: 2011 update. J Cardiovasc Electrophysiol 2012;23:890–923. [2] Cappato R, Calkins H, Chen S-A, et al. Prevalence and causes of fatal outcome in catheter ablation of atrial fibrillation. J Am Coll Cardiol 2009;53:1798–803.
K. Hishikari et al. / International Journal of Cardiology 172 (2014) e513–e515 [3] Le BH, Black JN, Huang SKS. Transient ST-segment elevation during transseptal catheterization for atrial fibrillation ablation. Tex Heart Inst J Tex Heart Inst St Lukes Episcop Hosp Tex Child Hosp 2010;37:717–21. [4] Kuwahara T, Takahashi A, Takahashi Y, et al. Clinical characteristics of massive air embolism complicating left atrial ablation of atrial fibrillation: lessons from five cases. Eur Eur Pacing Arrhythm Card Electrophysiol J Work Groups Card Pacing Arrhythm Card Cell Electrophysiol Eur Soc Cardiol 2012;14:204–8.
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[5] Okumura K, Yasue H, Matsuyama K, et al. Sensitivity and specificity of intracoronary injection of acetylcholine for the induction of coronary artery spasm. J Am Coll Cardiol 1988;12:883–8. [6] Yasue H, Horio Y, Nakamura N, et al. Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm. Circulation 1986;74:955–63. [7] Takahashi Y, Jais P, Hocini M, et al. Acute occlusion of the left circumflex coronary artery during mitral isthmus linear ablation. J Cardiovasc Electrophysiol 2005;16:1104–7.
