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Occurrence of de novo sustained monomorphic ventricular tachycardia induced after percutaneous transluminal alcohol septal myocardial ablation for hypertrophic obstructive cardiomyopathy
International Journal of Cardiology 119 (2007) 403 – 407 www.elsevier.com/locate/ijcard
Letter to the Editor
Occurrence of de novo sustained monomorphic ventricular tachycardia induced after percutaneous transluminal alcohol septal myocardial ablation for hypertrophic obstructive cardiomyopathy Yasuhiko Hori, Marehiko Ueda, Takashi Nakayama, Noriko Saegusa, Masae Uehara, Kwangho Lee, Tai Sekine, Masao Daimon, Yoshio Kobayashi, Nobusada Funabashi, Issei Komuro ⁎ Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba City, Chiba 260-8670, Japan Received 11 May 2006; accepted 22 July 2006 Available online 27 October 2006
Abstract We report here a 75-year-old male with hypertrophic obstructive cardiomyopathy of de novo sustained monomorphic ventricular tachycardia (VT) after successful percutaneous transluminal alcohol septal myocardial ablation (PTSMA). In this case history, the necrotic induced by the PTSMA procedure might represent a region of slow conduction that is a circuit of re-entry and therefore stimulation might be spread around. Therefore, the basis of the sustained monomorphic VT was thought to be the presence of a focal necrotic area, itself a complication arising from the PTSMA procedures. In conclusion, the PTSMA procedure may have caused a de novo episode of ventricular arrhythmia. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: De novo sustained monomorphic ventricular tachycardia; Percutaneous transluminal alcohol septal myocardial ablation; Hypertrophic obstructive cardiomyopathy
Percutaneous transluminal alcohol septal myocardial ablation (PTSMA) is appropriate for patients who are refractory to medical treatment for hypertrophic obstructive cardiomyopathy (HOCM) [1–5]. However, abnormalities of conduction system have been reported as common complications of PTSMA [6]. We report here a case of de novo sustained monomorphic ventricular tachycardia (VT) after successful PTSMA. The induction of the sustained VT may be due to a re-entry circuit occurring in the necrotic sites caused by PTSMA procedure. 1. Case Report A 75-year-old male experienced dyspnea with chest pain on effort and had cold sweats at rest 3 months ago. He also ⁎ Corresponding author. E-mail address: [email protected] (I. Komuro). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.07.182
experienced blackouts accompanied with chest pain when going up stairs. Since then, he had often experienced episodes of similar symptoms with loss of consciousness and thus he presented at our hospital. Results of a transthoracic echocardiography were consistent with the features of HOCM, such as thickening of interventricular septum (IVS) 15mm, the presence of systolic anterior motion of the mitral valve, severe mitral regurgitation, and a 30 mm Hg pressure gradient between the outflow tract of the LV and aorta at rest with good LV systolic function. A dobutamineloaded echocardiography showed that the pressure gradient between the outflow tract of the LV and aorta increased up to 109 mm Hg with a decrease of systemic systolic blood pressure and clinical symptoms of chest pain. After the administration of atenolol and cibenzoline, the pressure gradient decreased to 7 mm Hg and his symptoms disappeared. Since, syncope occurred repeatedly, even with medication such as atenolol and cibenzoline, he underwent
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Y. Hori et al. / International Journal of Cardiology 119 (2007) 403–407
Fig. 1. Electrocardiograms before (A) and after (B) percutaneous transluminal alcohol septal myocardial ablation (PTSMA). A. Before PTSMA, one degree atrioventricular block and strain pattern ST decline were observed in the aVL, V5 and, V6 leads. B. After PTSMA, complete right bundle branch block appeared.
PTSMA. Before PTSMA, an electrocardiogram (ECG) revealed normal sinus rhythm, with normal axis deviation and LV hypertrophy pattern (Fig. 1A). The Holter ECG revealed no sustained VT and a coronary angiography revealed normal coronary arteries. The guide wire was first introduced to the 1st septal branch. After balloon inflation and injection of contrast, 3.0 ml of ethanol was injected slowly into the 1st septal branch artery over 3 min (Fig. 2). Echocardiography showed limited brightness in the septal region and complete right bundle branch block (CRBBB) had appeared on the ECG (Fig. 1B).
After PTSMA, he had no trouble and was discharged at 21 days after PTSMA. At 389 days after discharge, he suddenly lost consciousness whilst traveling in the train. Transthoracic echocardiography and an ECG revealed no remarkable changes from ones before discharge. Singleaveraged ECG revealed positive findings of a late potential of the LV, which was not observed before PTSMA (Fig. 3). Since the loss of consciousness may be caused by ventricular arrhythmia, an electrophysiological study was performed. Fractionated potential was present on the Bundle of His on his ECG and ventricular programmed stimulations gave rise
Y. Hori et al. / International Journal of Cardiology 119 (2007) 403–407
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material (350 mgI/dl) (Fig. 5). In the basal IVS, which had shown hypertrophy before the PTSMA, there was an area of low CT contrast in the early phase (arrow Fig. 5A), while abnormal enhancement were observed in the late phase (arrow Fig. 5B), suggesting the presence of a necrotic change. 2. Discussion
Fig. 2. Fluoroscope image from left anterior view. A guide wire (arrow) was introduced to the 1st septal branch before percutaneous transluminal alcohol septal myocardial ablation (PTSMA). After wire access to the 1st septal branch and balloon inflation, contrast injection was performed, 3.0 ml of ethanol was injected slowly into the 1st septal branch artery over 3 min.
to sustained monomorphic VT (Fig. 4). We implanted cardioverter defibrillator in the patient. To evaluate the characteristics of the LV myocardium, enhanced ECG-gated multislice computed tomography (CT) (Light speed ultra 16, General Electrics, WI) was performed at 30 s, and 8 min after the injection of 100 ml of contrast
At present, PTSMA is recognized as an effective treatment for HOCM and the outcomes are as good as surgical septal myectomy [1–4,7,8]. Although the long-term prognosis is uncertain, this therapy is safe and relatively noninvasive. Fatality rates due to complications arising from PTSMA have been reported as approximately 1–2%, which are comparable with those of surgical septal myectomy [5]. However, conduction system abnormalities and ventricular arrhythmias are frequently-observed as complications of the PTSMA procedure. For example, CRBBB can be seen in 45–85% and left bundle branch block in 5–11% during PTSMA procedures [9]. 5–22% subjects revealed an advanced degree of atrioventricular block which required the implantation of a permanent pacemaker and in 2–10% subjects, non-sustained VT occurred. There have been only a few reports of de novo sustained monomorphic VT occurring after successful PTSMA. Our patient received PTSMA for HOCM and his clinical course was first satisfactory without any symptoms. But a new episode of syncope occurred at 410 days after the PTSMA, which might have been due to
Fig. 3. Single-averaged electrocardiogram before (A) and after (B) percutaneous transluminal alcohol septal myocardial ablation (PTSMA). Positive late potential was defined with the modified Gomes' standard in which late potentials were considered positive when both filtered-QRS duration N120 ms (184 ms in this subject after PTSMA) and root-mean-square voltage at the last 40 ms b20 μV (9 μV in this subject after PTSMA). Therefore positive findings of late potential of the ventricle could have occurred only after PTSMA (B), as these were not observed before PTSMA (A).
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Y. Hori et al. / International Journal of Cardiology 119 (2007) 403–407
Fig. 4. In ventricular programmed stimulation (400/240/210/210 ms), sustained monomorphic ventricular tachycardia was induced followed immediately by a fall in blood pressure, and a loss of consciousness.
the existence of sustained VT. PTSMA could cause myocardial infarction (i.e. necrosis) in hypertrophic sites. In this case report, ECG-gated multislice CT was used to evaluate the characteristics of LV myocardium and a necrotic area was represented by an area of low CT contrast in early
phase and abnormal enhancement in late phase [10–13]. In CT, the necrotic area could be clearly observed in basal IVS. Late potentials in single-averaged ECG have been reported to be observed in approximately 70–90% of cases who had VT after myocardial infarction. Similar to this case, the necrotic
Fig. 5. Axial source image of enhanced electrocardiogram-gated multislice computed tomography (CT) (Light speed ultra 16, General Electrics, WI) to evaluate the characteristic of left ventricular myocardium, at 30 s (A) and 8 min (B) after injection of 100 ml of contrast material (350 mgI/dl). In the basal interventricular septum (IVS), which prior to percutaneous transluminal alcohol septal myocardial ablation (PTSMA) had been a hypertrophic site, there was an area of low CT contrast in the early phase (arrow, A), which conversely represented an abnormal enhancement in the late phase (arrow B), suggesting the presence of necrotic change due to PTSMA procedure.
Y. Hori et al. / International Journal of Cardiology 119 (2007) 403–407
area has been reported to represent a region of slow conduction that is a circuit of re-entry, resulting in spread around of stimulation. Therefore, it is highly possible that the basis of the sustained VT is the presence of a focal necrotic area, which probably comes from the PTSMA procedures. In conclusion, the PTSMA procedure may cause a de novo episode of ventricular arrhythmia. References [1] Talreja DR, Nishimura RA, Edwards WD, et al. Alcohol septal ablation versus surgical septal myectomy: comparison of effects on atrioventricular conduction tissue. J Am Coll Cardiol 2004;44:2329–32. [2] Maron MS, Olivotto I, Betocchi S, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med 2003;348:295–303. [3] McKenna WJ, Behr ER. Hypertrophic cardiomyopathy: management, risk stratification, and prevention of sudden death. Heart 2002;87: 169–76. [4] Nagueh SF, Ommen SR, Lakkis NM, et al. Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;38: 1701–6. [5] Gietzen FH, Leuner CJ, Obergassel L, Strunk-Mueller C, Kuhn H. Role of transcoronary ablation of septal hypertrophy in patients with hypertrophic cardiomyopathy, New York Heart Association functional class III or IV, and outflow obstruction only under provocable conditions. Circulation 2002;106:454–9.
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[6] Qin JX, Shiota T, Lever HM, et al. Conduction system abnormalities in patients with obstructive hypertrophic cardiomyopathy following septal reduction interventions. Am J Cardiol 2004;93:171–5. [7] Veselka J, Honek T. Early remodelling of left ventricle and improvement of myocardial performance in patients after percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy. Int J Cardiol 2003;88:27–32. [8] Lee JM, Moon JC, Pennell DJ, Sigwart U, Clague JR. Late recurrence of outflow tract obstruction seven years after septal ablation in hypertrophic cardiomyopathy. Int J Cardiol 2005;100:341–2. [9] Lakkis NM, Nagueh SF, Dunn JK, Killip D, Spencer III WH. Nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy: one-year follow-up. J Am Coll Cardiol 2000;36: 852–5. [10] Funabashi N, Nakagawa K, Komuro I. Partial myocardial fibrosis in hypertrophic cardiomyopathy demonstrated by 18F fluoro-deoxyglucose positron emission tomography and multislice computed tomography. Int J Cardiol 2006;107:284–6. [11] Funabashi N, Komuro I. Focal myocardial fibrosis and edema in acute myocarditis demonstrated by multislice computed tomography. Int J Cardiol 2005;105:346–8. [12] Funabashi N, Yoshida K, Komuro I. Thinned myocardial fibrosis with thrombus in the dilated form of hypertrophic cardiomyopathy demonstrated by multislice computed tomography. Heart 2003;89:858. [13] Funabashi N, Komiyama N, Asano M, Komuro I. Endocardial fibrosis in subacute non-Q wave myocardial infarction demonstrated by multislice computed tomography. Int J Cardiol 2006;109:430–1.
Letter to the Editor
Occurrence of de novo sustained monomorphic ventricular tachycardia induced after percutaneous transluminal alcohol septal myocardial ablation for hypertrophic obstructive cardiomyopathy Yasuhiko Hori, Marehiko Ueda, Takashi Nakayama, Noriko Saegusa, Masae Uehara, Kwangho Lee, Tai Sekine, Masao Daimon, Yoshio Kobayashi, Nobusada Funabashi, Issei Komuro ⁎ Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba City, Chiba 260-8670, Japan Received 11 May 2006; accepted 22 July 2006 Available online 27 October 2006
Abstract We report here a 75-year-old male with hypertrophic obstructive cardiomyopathy of de novo sustained monomorphic ventricular tachycardia (VT) after successful percutaneous transluminal alcohol septal myocardial ablation (PTSMA). In this case history, the necrotic induced by the PTSMA procedure might represent a region of slow conduction that is a circuit of re-entry and therefore stimulation might be spread around. Therefore, the basis of the sustained monomorphic VT was thought to be the presence of a focal necrotic area, itself a complication arising from the PTSMA procedures. In conclusion, the PTSMA procedure may have caused a de novo episode of ventricular arrhythmia. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: De novo sustained monomorphic ventricular tachycardia; Percutaneous transluminal alcohol septal myocardial ablation; Hypertrophic obstructive cardiomyopathy
Percutaneous transluminal alcohol septal myocardial ablation (PTSMA) is appropriate for patients who are refractory to medical treatment for hypertrophic obstructive cardiomyopathy (HOCM) [1–5]. However, abnormalities of conduction system have been reported as common complications of PTSMA [6]. We report here a case of de novo sustained monomorphic ventricular tachycardia (VT) after successful PTSMA. The induction of the sustained VT may be due to a re-entry circuit occurring in the necrotic sites caused by PTSMA procedure. 1. Case Report A 75-year-old male experienced dyspnea with chest pain on effort and had cold sweats at rest 3 months ago. He also ⁎ Corresponding author. E-mail address: [email protected] (I. Komuro). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.07.182
experienced blackouts accompanied with chest pain when going up stairs. Since then, he had often experienced episodes of similar symptoms with loss of consciousness and thus he presented at our hospital. Results of a transthoracic echocardiography were consistent with the features of HOCM, such as thickening of interventricular septum (IVS) 15mm, the presence of systolic anterior motion of the mitral valve, severe mitral regurgitation, and a 30 mm Hg pressure gradient between the outflow tract of the LV and aorta at rest with good LV systolic function. A dobutamineloaded echocardiography showed that the pressure gradient between the outflow tract of the LV and aorta increased up to 109 mm Hg with a decrease of systemic systolic blood pressure and clinical symptoms of chest pain. After the administration of atenolol and cibenzoline, the pressure gradient decreased to 7 mm Hg and his symptoms disappeared. Since, syncope occurred repeatedly, even with medication such as atenolol and cibenzoline, he underwent
404
Y. Hori et al. / International Journal of Cardiology 119 (2007) 403–407
Fig. 1. Electrocardiograms before (A) and after (B) percutaneous transluminal alcohol septal myocardial ablation (PTSMA). A. Before PTSMA, one degree atrioventricular block and strain pattern ST decline were observed in the aVL, V5 and, V6 leads. B. After PTSMA, complete right bundle branch block appeared.
PTSMA. Before PTSMA, an electrocardiogram (ECG) revealed normal sinus rhythm, with normal axis deviation and LV hypertrophy pattern (Fig. 1A). The Holter ECG revealed no sustained VT and a coronary angiography revealed normal coronary arteries. The guide wire was first introduced to the 1st septal branch. After balloon inflation and injection of contrast, 3.0 ml of ethanol was injected slowly into the 1st septal branch artery over 3 min (Fig. 2). Echocardiography showed limited brightness in the septal region and complete right bundle branch block (CRBBB) had appeared on the ECG (Fig. 1B).
After PTSMA, he had no trouble and was discharged at 21 days after PTSMA. At 389 days after discharge, he suddenly lost consciousness whilst traveling in the train. Transthoracic echocardiography and an ECG revealed no remarkable changes from ones before discharge. Singleaveraged ECG revealed positive findings of a late potential of the LV, which was not observed before PTSMA (Fig. 3). Since the loss of consciousness may be caused by ventricular arrhythmia, an electrophysiological study was performed. Fractionated potential was present on the Bundle of His on his ECG and ventricular programmed stimulations gave rise
Y. Hori et al. / International Journal of Cardiology 119 (2007) 403–407
405
material (350 mgI/dl) (Fig. 5). In the basal IVS, which had shown hypertrophy before the PTSMA, there was an area of low CT contrast in the early phase (arrow Fig. 5A), while abnormal enhancement were observed in the late phase (arrow Fig. 5B), suggesting the presence of a necrotic change. 2. Discussion
Fig. 2. Fluoroscope image from left anterior view. A guide wire (arrow) was introduced to the 1st septal branch before percutaneous transluminal alcohol septal myocardial ablation (PTSMA). After wire access to the 1st septal branch and balloon inflation, contrast injection was performed, 3.0 ml of ethanol was injected slowly into the 1st septal branch artery over 3 min.
to sustained monomorphic VT (Fig. 4). We implanted cardioverter defibrillator in the patient. To evaluate the characteristics of the LV myocardium, enhanced ECG-gated multislice computed tomography (CT) (Light speed ultra 16, General Electrics, WI) was performed at 30 s, and 8 min after the injection of 100 ml of contrast
At present, PTSMA is recognized as an effective treatment for HOCM and the outcomes are as good as surgical septal myectomy [1–4,7,8]. Although the long-term prognosis is uncertain, this therapy is safe and relatively noninvasive. Fatality rates due to complications arising from PTSMA have been reported as approximately 1–2%, which are comparable with those of surgical septal myectomy [5]. However, conduction system abnormalities and ventricular arrhythmias are frequently-observed as complications of the PTSMA procedure. For example, CRBBB can be seen in 45–85% and left bundle branch block in 5–11% during PTSMA procedures [9]. 5–22% subjects revealed an advanced degree of atrioventricular block which required the implantation of a permanent pacemaker and in 2–10% subjects, non-sustained VT occurred. There have been only a few reports of de novo sustained monomorphic VT occurring after successful PTSMA. Our patient received PTSMA for HOCM and his clinical course was first satisfactory without any symptoms. But a new episode of syncope occurred at 410 days after the PTSMA, which might have been due to
Fig. 3. Single-averaged electrocardiogram before (A) and after (B) percutaneous transluminal alcohol septal myocardial ablation (PTSMA). Positive late potential was defined with the modified Gomes' standard in which late potentials were considered positive when both filtered-QRS duration N120 ms (184 ms in this subject after PTSMA) and root-mean-square voltage at the last 40 ms b20 μV (9 μV in this subject after PTSMA). Therefore positive findings of late potential of the ventricle could have occurred only after PTSMA (B), as these were not observed before PTSMA (A).
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Y. Hori et al. / International Journal of Cardiology 119 (2007) 403–407
Fig. 4. In ventricular programmed stimulation (400/240/210/210 ms), sustained monomorphic ventricular tachycardia was induced followed immediately by a fall in blood pressure, and a loss of consciousness.
the existence of sustained VT. PTSMA could cause myocardial infarction (i.e. necrosis) in hypertrophic sites. In this case report, ECG-gated multislice CT was used to evaluate the characteristics of LV myocardium and a necrotic area was represented by an area of low CT contrast in early
phase and abnormal enhancement in late phase [10–13]. In CT, the necrotic area could be clearly observed in basal IVS. Late potentials in single-averaged ECG have been reported to be observed in approximately 70–90% of cases who had VT after myocardial infarction. Similar to this case, the necrotic
Fig. 5. Axial source image of enhanced electrocardiogram-gated multislice computed tomography (CT) (Light speed ultra 16, General Electrics, WI) to evaluate the characteristic of left ventricular myocardium, at 30 s (A) and 8 min (B) after injection of 100 ml of contrast material (350 mgI/dl). In the basal interventricular septum (IVS), which prior to percutaneous transluminal alcohol septal myocardial ablation (PTSMA) had been a hypertrophic site, there was an area of low CT contrast in the early phase (arrow, A), which conversely represented an abnormal enhancement in the late phase (arrow B), suggesting the presence of necrotic change due to PTSMA procedure.
Y. Hori et al. / International Journal of Cardiology 119 (2007) 403–407
area has been reported to represent a region of slow conduction that is a circuit of re-entry, resulting in spread around of stimulation. Therefore, it is highly possible that the basis of the sustained VT is the presence of a focal necrotic area, which probably comes from the PTSMA procedures. In conclusion, the PTSMA procedure may cause a de novo episode of ventricular arrhythmia. References [1] Talreja DR, Nishimura RA, Edwards WD, et al. Alcohol septal ablation versus surgical septal myectomy: comparison of effects on atrioventricular conduction tissue. J Am Coll Cardiol 2004;44:2329–32. [2] Maron MS, Olivotto I, Betocchi S, et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med 2003;348:295–303. [3] McKenna WJ, Behr ER. Hypertrophic cardiomyopathy: management, risk stratification, and prevention of sudden death. Heart 2002;87: 169–76. [4] Nagueh SF, Ommen SR, Lakkis NM, et al. Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;38: 1701–6. [5] Gietzen FH, Leuner CJ, Obergassel L, Strunk-Mueller C, Kuhn H. Role of transcoronary ablation of septal hypertrophy in patients with hypertrophic cardiomyopathy, New York Heart Association functional class III or IV, and outflow obstruction only under provocable conditions. Circulation 2002;106:454–9.
407
[6] Qin JX, Shiota T, Lever HM, et al. Conduction system abnormalities in patients with obstructive hypertrophic cardiomyopathy following septal reduction interventions. Am J Cardiol 2004;93:171–5. [7] Veselka J, Honek T. Early remodelling of left ventricle and improvement of myocardial performance in patients after percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy. Int J Cardiol 2003;88:27–32. [8] Lee JM, Moon JC, Pennell DJ, Sigwart U, Clague JR. Late recurrence of outflow tract obstruction seven years after septal ablation in hypertrophic cardiomyopathy. Int J Cardiol 2005;100:341–2. [9] Lakkis NM, Nagueh SF, Dunn JK, Killip D, Spencer III WH. Nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy: one-year follow-up. J Am Coll Cardiol 2000;36: 852–5. [10] Funabashi N, Nakagawa K, Komuro I. Partial myocardial fibrosis in hypertrophic cardiomyopathy demonstrated by 18F fluoro-deoxyglucose positron emission tomography and multislice computed tomography. Int J Cardiol 2006;107:284–6. [11] Funabashi N, Komuro I. Focal myocardial fibrosis and edema in acute myocarditis demonstrated by multislice computed tomography. Int J Cardiol 2005;105:346–8. [12] Funabashi N, Yoshida K, Komuro I. Thinned myocardial fibrosis with thrombus in the dilated form of hypertrophic cardiomyopathy demonstrated by multislice computed tomography. Heart 2003;89:858. [13] Funabashi N, Komiyama N, Asano M, Komuro I. Endocardial fibrosis in subacute non-Q wave myocardial infarction demonstrated by multislice computed tomography. Int J Cardiol 2006;109:430–1.