Ventricular Tachycardia Complicating Alcohol Septal Ablation
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《新英格兰医药杂志》
To the Editor: Percutaneous transluminal septal myocardial ablation is increasingly being used to treat hypertrophic cardiomyopathy. Reported complications have included atrioventricular block, extensive myocardial infarction, and death.1,2 Contrast-enhanced echocardiographic guidance of the procedure may minimize these complications.1,2 Although transient ectopy may occur, it is not known whether percutaneous transluminal septal myocardial ablation increases the long-term incidence of malignant tachyarrhythmias.3
We report the case of a 56-year-old man who had sudden palpitations, lightheadedness, chest pain, and dyspnea. Paramedics arrived within about 10 minutes after the onset of symptoms and found that the patient had a regular, wide-complex tachycardia at a rate of 272 beats per minute (Figure 1). Intravenous lidocaine converted the ventricular tachycardia to sinus rhythm. Sixteen days earlier, the patient had undergone percutaneous transluminal septal myocardial ablation for hypertrophic cardiomyopathy associated with New York Heart Association (NYHA) functional class III dyspnea and a basal subaortic gradient of 70 mm Hg, despite beta-blockade and calcium-channel blockade. The ablation procedure, which was performed with contrast-enhanced echocardiographic guidance, had included two proximal septal perforator vessels that perfused the proximal third of the septum. Coronary angiography had shown no clinically significant stenoses. Immediately after ablation, the subaortic gradient fell from 50 mm Hg to nearly zero. The patient's dyspnea improved to NYHA functional class I. Contrast-enhanced magnetic resonance imaging before and after ablation showed proximal septal akinesis, an ejection fraction of 66 percent, and an infarct that constituted about 10 percent of the left ventricular mass.
Figure 1. Electrocardiographic Recording at the Time of Presentation.
There is rapid, monomorphic ventricular tachycardia. The interval shown at the top of the recording is 1 second. The original tracing was lightly traced in ink by hand to enhance its clarity in reproduction. HR denotes heart rate.
At the time of his presentation with ventricular tachycardia, the patient had decreased his dose of oral atenolol to 12.5 mg per day and had stopped taking his calcium-channel blocker. The electrocardiogram showed Q waves and residual ST-segment elevation in leads V1, V2, and V3. The troponin level peaked at 2.9 ng per milliliter (normal value, <0.5). Rapid, nonsustained ventricular tachycardia recurred when lidocaine was discontinued, and amiodarone loading was begun, but the patient ultimately underwent implantation of a single-chamber defibrillator. His condition has subsequently been clinically stable, without firing of the defibrillator and with the use of low-dose beta-blockade, for 14 months.
Because the five 24-hour Holter recordings obtained during the preceding six years had shown only minimal ectopy, we believe that the ventricular tachycardia was probably a complication of the percutaneous transluminal septal myocardial ablation, rather than of the underlying hypertrophic cardiomyopathy. It may have been the result of the ablation of two septal branches,4 although the infarct size was comparable to that described in a recent report.5 We conclude that late, sustained monomorphic ventricular tachycardia may complicate alcohol septal ablation and that this risk should be considered when patients are selected for this treatment strategy.
Chester M. Boltwood, Jr., M.D.
Walter Chien, M.D.
Valley Heart Associates Medical Group
Modesto, CA 95350
chester@vhamg.com
Thomas Ports, M.D.
Moffitt Hospital
San Francisco, CA 94143
References
Seggewiss H. Current status of alcohol septal ablation for patients with hypertrophic cardiomyopathy. Curr Cardiol Rep 2001;3:160-166.
Kimmelstiel CD, Maron BJ. Role of percutaneous septal ablation in hypertrophic obstructive cardiomyopathy. Circulation 2004;109:452-456.
Crawford FA III, Killip D, Franklin J, Spencer WH III, Gold MR. Implantable cardioverter-defibrillators for primary prevention of sudden cardiac death in patients with hypertrophic obstructive cardiomyopathy after alcohol septal ablation. Circulation 2003;108:Suppl IV:IV-386.
Singh M, Edwards WD, Holmes DR Jr, Tajil AJ, Nishimura RA. Anatomy of the first septal perforating artery: a study with implications for ablation therapy for hypertrophic cardiomyopathy. Mayo Clin Proc 2001;76:799-802.
van Dockum WG, ten Cate FJ, Ten Berg JM, et al. Myocardial infarction after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: evaluation by contrast-enhanced magnetic resonance imaging. J Am Coll Cardiol 2004;43:27-34.
We report the case of a 56-year-old man who had sudden palpitations, lightheadedness, chest pain, and dyspnea. Paramedics arrived within about 10 minutes after the onset of symptoms and found that the patient had a regular, wide-complex tachycardia at a rate of 272 beats per minute (Figure 1). Intravenous lidocaine converted the ventricular tachycardia to sinus rhythm. Sixteen days earlier, the patient had undergone percutaneous transluminal septal myocardial ablation for hypertrophic cardiomyopathy associated with New York Heart Association (NYHA) functional class III dyspnea and a basal subaortic gradient of 70 mm Hg, despite beta-blockade and calcium-channel blockade. The ablation procedure, which was performed with contrast-enhanced echocardiographic guidance, had included two proximal septal perforator vessels that perfused the proximal third of the septum. Coronary angiography had shown no clinically significant stenoses. Immediately after ablation, the subaortic gradient fell from 50 mm Hg to nearly zero. The patient's dyspnea improved to NYHA functional class I. Contrast-enhanced magnetic resonance imaging before and after ablation showed proximal septal akinesis, an ejection fraction of 66 percent, and an infarct that constituted about 10 percent of the left ventricular mass.
Figure 1. Electrocardiographic Recording at the Time of Presentation.
There is rapid, monomorphic ventricular tachycardia. The interval shown at the top of the recording is 1 second. The original tracing was lightly traced in ink by hand to enhance its clarity in reproduction. HR denotes heart rate.
At the time of his presentation with ventricular tachycardia, the patient had decreased his dose of oral atenolol to 12.5 mg per day and had stopped taking his calcium-channel blocker. The electrocardiogram showed Q waves and residual ST-segment elevation in leads V1, V2, and V3. The troponin level peaked at 2.9 ng per milliliter (normal value, <0.5). Rapid, nonsustained ventricular tachycardia recurred when lidocaine was discontinued, and amiodarone loading was begun, but the patient ultimately underwent implantation of a single-chamber defibrillator. His condition has subsequently been clinically stable, without firing of the defibrillator and with the use of low-dose beta-blockade, for 14 months.
Because the five 24-hour Holter recordings obtained during the preceding six years had shown only minimal ectopy, we believe that the ventricular tachycardia was probably a complication of the percutaneous transluminal septal myocardial ablation, rather than of the underlying hypertrophic cardiomyopathy. It may have been the result of the ablation of two septal branches,4 although the infarct size was comparable to that described in a recent report.5 We conclude that late, sustained monomorphic ventricular tachycardia may complicate alcohol septal ablation and that this risk should be considered when patients are selected for this treatment strategy.
Chester M. Boltwood, Jr., M.D.
Walter Chien, M.D.
Valley Heart Associates Medical Group
Modesto, CA 95350
chester@vhamg.com
Thomas Ports, M.D.
Moffitt Hospital
San Francisco, CA 94143
References
Seggewiss H. Current status of alcohol septal ablation for patients with hypertrophic cardiomyopathy. Curr Cardiol Rep 2001;3:160-166.
Kimmelstiel CD, Maron BJ. Role of percutaneous septal ablation in hypertrophic obstructive cardiomyopathy. Circulation 2004;109:452-456.
Crawford FA III, Killip D, Franklin J, Spencer WH III, Gold MR. Implantable cardioverter-defibrillators for primary prevention of sudden cardiac death in patients with hypertrophic obstructive cardiomyopathy after alcohol septal ablation. Circulation 2003;108:Suppl IV:IV-386.
Singh M, Edwards WD, Holmes DR Jr, Tajil AJ, Nishimura RA. Anatomy of the first septal perforating artery: a study with implications for ablation therapy for hypertrophic cardiomyopathy. Mayo Clin Proc 2001;76:799-802.
van Dockum WG, ten Cate FJ, Ten Berg JM, et al. Myocardial infarction after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: evaluation by contrast-enhanced magnetic resonance imaging. J Am Coll Cardiol 2004;43:27-34.