Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Taiwan Crit. Care Med.2011;12:182-192 Tzu Ming Ou et al. Non-sustained, Symptomatic Ventricular Tachycardia: A case report and literatures review Tzu Ming Ou1, Shih Chung Huang2, Jeng Chuan Shiang1, Yi Chen Wang2 Abstract Non-sustained ventricular tachycardia (NSVT) is commonly seen but poorly understood. Patients with NSVT might be asymptomatic or encountered sudden cardiac death. The prognosis depends on what the concomitant heart disease is. Poor prognosis were found in patient with NSVT during or post exercise; acute myocardial infarction more than 24 hours; chronic ischemic heart disease with left ventricular ejection fraction (LVEF) below 40% with/without inducible sustained ventricular tachycardia in electrophysiology testing; and hypertrophic obstructive cardiomyopathy in the young. Medical therapy including beta-blockers and class III antiarrhythmic agents, while implantable cardiac defibrillators (ICD) and radiofrequency ablation are indicated in certain patients. Here, we report a case that had near syncope and palpitation with NSVT on 24-hours electrocardiography, finally received ablation and antiarrhythmic therapy. No more arrhythmia was found during out patient department follow up. Key Words: Non-sustained ventricular tachycardia (NSVT), Left ventricular ejection fraction (LVEF), Right ventricular outflow tract (RVOT), Implantable cardioveter defibrillator (ICD) Introduction 2-weeks history of epigastric pain, chest tightness, shortness of breath, near syncope, and palpitation. The electrocardiography (Fig. 1) revealed sinus tachycardia and complete right bundle branch block. Initial vital signs showed that the blood pressure was 202/73 mmHg, the pulse rate was 105 beats per minute, the respiratory rate was 18 breaths per minute and the body temperature was 37.2°C. Physical examination revealed mild pale conjunctivae, no jugular vein engorgement, rapidly regular heart beat, no heart murmur, clear breath sound, no legs edema. Laboratory data showed that microcytic anemia, normal cardiac NSVT is usually a benign cause, but it may provoke malignant arrhythmia and then induce sudden cardiac death. The symptoms of NSVT vary from asymptomatic to heart failure. This report describes a 71-year-old woman with NSVT. The symptoms were stabilized after antiarrhythmic agents and electrophysiology study plus ablation. Case Report A 71-year-old woman presented with a Correspondence: Dr. Yi Chen Wang Division of Cardiology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital; No. 2, Zhongzheng 1st Road, Lingya District, Kaohsiung City 80284, Taiwan2 Phone: +886-7-749-4941; E-mail: [email protected] Department of Internal Medicine, Kaohsiung Armed Forces General Hospital1 182 Taiwan Crit. Care Med.2011;12:182-192 Non-sustained, symptomatic ventricular tachycardia enzymes (Hgb: 10.4 gm/dl, Hct.: 30.5%, MCV: 78.2 fl, CK: 35 U/L, CK-MB: 13.4 U/L). Traced her past history, she has had hypertension with medical control (unknown drugs) for 4 years. She also received internal fixation for left femoral fracture 2 years ago. Under the tentative diagnosis of hypertensive emergency, conduction disorder, anemia, peptic ulcer, she was admitted for further management. The upper gastrointestinal panen- doscopy revealed gastric ulcer, duodenal ulcers, and gastroesophageal reflux disease. The 24-hours electrocardiography showed 39 episodes of frequent NSVT (the longest duration was 4 seconds), occasional premature ventricular contractions, and no ischemic change (Fig. 2). The echocardiogram disclosed no hypertrophic or dilated cardiomyopathy and normal left ventricular systolic function. There is no prominent hemodynamic compromise Fig. 1. Electrocardiography revealed sinus tachycardia and complete right bundle branch block. Fig. 2. One episode of NSVT during 24-hours electrocardiography. 183 Taiwan Crit. Care Med.2011;12:182-192 Tzu Ming Ou et al. and syncope, so the patient was monitored at intensive care unit without anti-arrhythmic medication initially. The magnetic resonance imaging of chest (Fig. 5) disclosed no evidence of arrhythmogenic right ventricular dysplasia (ARVD). The coronary angiography disclosed insignificant coronary artery disease (Fig. 3) and the electrophysiology study disclosed right ventricular outflow tract ventricular tachycardia. Radiofrequency catheter ablation with anatomically guided linear ablation of the anterior septum and posterior septum little moving to free wall was performed with a 4-mmtip ablation catheter (Safire, St. Jude Medical, Minnetonka, MN, USA) with the temperature preset at 60°C and radiofrequency pulse duration of 120 seconds (Fig. 4). After discharged, the oral medications included amiodarone 200mg po daily after intravenous loading dose, plus atenolol 25mg po daily and adalat OROS 30mg po daily. Another 24-hour electrocardiographic recording that revealed no more ventricular tachycardia at outpatient department two months later. tive premature ventricular contractions, which may be monomorphic or polymorphic, occurred with rate above 120 beats per minute, lasting less than 30 seconds. Etiology of NSVT The mechanisms of NSVT included: (1) increased automaticity, (2) reentry, and (3) triggered automaticity. Increased automaticity (such as right ventricular outflow tract ventricular tachycardia) is often associated with autonomic tone, ischemia, reperfusion, acidosis, hypokalemia, hypomagnesemia, or cardiotoxic factors.1 It may not have sudden onset or termination. Reentry is usually scar related. NSVT occur after acute myocardial infarction is believed to result from the formation of scar tissue. Monomorphic ventricular tachycardia typically occurs due to reentry or triggered automaticity, while polymorphic ventricular tachycardia is caused by increased automaticity.2 The most common form of right ventricular outflow tract (RVOT) ventricular tachycardia is related to triggered automaticity arising from delayed afterdepolarizations. It is thought to be dependent on intracellular calcium overload and cyclic adenosine monophosphate.3-5 Other causes of triggered automaticity are described in Table 1. Discussion Definition of NSVT NSVT is defined as three or more consecu- (A) (B) Fig. 3. Coronary angiography disclosed insignificant coronary artery disease: (A) Right coronary artery (B) Left anterior descending artery & left circumflex artery. 184 Taiwan Crit. Care Med.2011;12:182-192 Non-sustained, symptomatic ventricular tachycardia Fig. 4. Right ventricular outflow tract ventricular tachycardia was terminated during radiofrequency catheter ablation. Prevalence of NSVT Using 24 to 48 hours electrocardiographic recording, the prevalence in people without symptoms or history of cardiac disease ranged from 0 to 3%,7-11 approximately 20% of patients with hypertrophic cardiomyopathy,12,13 40 to 50% in patients with dilated cardiomyopathy.14-17 The prevalence of NSVT in patients with coronary artery disease depend on the stage of disease. Within the first 24 hours of acute MI, the prevalence ranged from 45 to 75%18-20 and declined as time went on after the event. The SPRINT study showed the incidence of NSVT 48 hours post MI was 3%.21 In the 24-48 hours post infarction, the NSVT is usually due to automaticity or triggered activity; however NSVT is often due to reentry while more than 48 hours post infarction.20,21 The symptoms of NSVT include palpitation, chest distress, pre-syncope, syncope, and heart failure. It is usually asymptomatic but a risk factor for sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac death, especially in patients with high frequency or left ventricular systolic dysfunction. NSVT also may lead to tachycardia-induced cardiomyopathy, Fig. 5. Magnetic resonance imaging of chest disclosed no sufficient evidence of arrhythmogenic right ventricular dysplasia (ARVD). 185 Taiwan Crit. Care Med.2011;12:182-192 Tzu Ming Ou et al. Table 1. The etiologies of NSVT Triggered automaticity6 Early afterdepolarization 1.Drugs (sotalol, N-acetylprocainamide, terfenadine, erythromycin), cesium, barium, low potassium 2.Acquired long-QT syndrome and associated ventricular arrhythmia Increased automaticity Autonomic tone Ischemia Reperfusion Acidosis Hypokalemia Hypomagnesemia Cardiotoxic factors Delay afterdepolarization 1. Gain-of- function mutation in the gene encoding RyR2 2. Catecholaminergic polymorphic ventricular tachycardia Reentry Abnormalities of myocardium or Purkinje fibers (Same as increased automaticity or scar formation post-myocardial infarction) which is reversible. Ventricular tachycardia is the most common manifestation of arrhythmogenic right ventricular dysplasia that is a familial disease causing sudden cardiac death. Idiopathic right ventricular tachycardia commonly presents as non-sustained or repetitive monomorphic ventricular tachycardia. Ventricular tachycardia arising from the RVOT in the absence of structural heart disease is common, accounting up to 10% of all ventricular tachycardias.22 The symptoms of idiopathic RVOT ventricular tachycardia occurred typically between the age of 20 and 40 years, more commonly in women.23 Idiopathic right ventricular tachycardia that is most often arising from the septal region of the right ventricular outflow tract is a benign course. physiology study in risk stratification for arrhythmic death is influenced by the LVEF. Patients with LVEF between 30 % and 40% were suggested for electrophysiology study. In ischemic heart disease with LVEF >40%, the role of electrophysiology study is not yet established. 25 In patients with coronary artery disease, the two and five years rate of sudden death were 18 and 32 percent if not treated in NSVT and induced sustained monomorphic VT.24 Without induced sustained monomorphic VT, the two & five years rate of sudden death were 12 and 24 percent in patients with coronary artery disease and NSVT.26 The ACC/AHA/ESC guidelines suggested electrophysiology testing is reasonable for risk stratification in patients with remote myocardial infarction, NSVT, and LVEF equal to or less than 40% ( Class IIa; Level of Evidence: B).27 Diagnosis of NSVT Diagnosis of NSVT is typically based on the finding of ambulatory 24-hour Holter electrocardiography. It can establish the frequency, duration, and morphology of the NSVT. Echocardiography can provide the left ventricular function and identify other underlying cardiomyopathy. Patients with suspected coronary heart disease may require coronary angiography. Besides, the MUSTT study suggested inducibility of tachyarrhythmia-identified patients whose death was significantly more likely to be arrhythmic.24 The utility of electro- Treatment of NSVT The goals of treatment are prevention of malignant arrhythmia, sudden cardiac death and elimination of symptoms. Treatments included antiarrhythmic medications, implantable cardioveter defibrillator (ICD) and catheter ablation. 1. Anti-arrhythmic medications According to the CAST trial,28 class I antiarrhythmic drugs are not advised due to associated 186 Taiwan Crit. Care Med.2011;12:182-192 Non-sustained, symptomatic ventricular tachycardia with increased mortality in patients with history of myocardial infarction. The safe & effective antiarrhythmic medications are commonly beta-blocker and amiodarone. Beta-blocker can reduce the mortality of patients with ischemic heart disease who both have LVEF below 40% and NSVT. 29 Amiodarone is effective in suppressing ventricular arrhythmias and has a trend toward reduces mortality among those with nonischemic cardiomyopathy, but it cannot reduce the incidence of sudden death or prolong survival among patients with heart failure.30 Another study showed amiodarone is associated with a reduction in the incidence of sudden death in adult HCM patients (including young adults) with NSVT.31 The Canadian Myocardial Infarction Amiodarone Trial (CAMIAT) disclosed that amiodarone reduces the incidence of ventricular fibrillation or arrhythmic death among survivors of acute myocardial infarction with frequent VPCs or NSVT, but no significant reduction in overall mortality was found.32 Amiodarone in combination with beta blockers significantly reduced both arrhythmic and nonarrhythmic cardiac death.32 received ICD implantation. In patients without diminished ejection fraction, further studies will be needed to determine whether those patients would benefit from ICD therapy. The ACC/AHA/HRS 2008 guidelines suggested ICD therapy is indicated in patients with NSVT due to prior myocardial infarction, LVEF less than or equal to 40%, and inducible ventricular fibrillation or sustained ventricular tachycardia at electrophysiological study (Class I; Level of Evidence: B).36 3. Catheter ablation ICD can terminate ventricular tachycardia episodes but does not prevent them. Catheter ablation offers a cure for ventricular tachycardia, which is resistant to antiarrhythmic medications. It can also reduce ICD shock and reversing tachycardia-induced cardiomyopathy. 37 Ablation was recommended in the ACC/AHA/ESC guidelines as useful therapy in patients who are otherwise at low risk for sudden cardiac death and have symptomatic nonsustained monomorphic VT that is drug resistant, who are drug intolerant or who do not wish long-term anti-arrhythmic drugs therapy(Class IIa; Level of Evidence: C).27 The success rate of catheter ablation for ventricular tachycardia ranges from 83%-100%, while recurrence rates from 0%-31% on a variable follow-up period.38-41 Ablation for RVOT ectopy was more likely to fail as opposed to RVOT ventricular tachycardia (sustained or non-sustained).42 The predictors of failed ablation included presence of QRS morphologic variation, wider mean QRS, and taller R wave amplitude in lead II.42 Ablation of ventricular tachycardia is often challenging and lower success rates than ablation of supraventricular tachycardias. The reasons included: (1) large infarct region. (2) Hemodynamically unstable and poorly tolerated. (3) Epicardial or intramural in location. (4) Several reentrant circuits.33 It is controversial that anti-arrhythmic medications needed after successful catheter ablation. Overall, catheter ablation of ventricular tachycardia in the setting of structural heart disease can only be considered an adjunctive therapy, which in general, will require ICD therapy.33 2. Implantable cardioveter defibrillator (ICD) ICD is first-line therapy in patients with ventricular tachycardia who also have structural heart disease with impaired LVEF. It is also superior to medical therapy in primary and secondary prevention of sudden cardiac arrest. In the patients who received ICD implantation as primary prevention of sudden cardiac death, 20% of them would experience at least one ventricular tachycardia episode within 3-5 years after ICD implantation.33 The MUSTT trial disclosed ICD reduced arrhythmic death in patients with asymptomatic NSVT, LVEF≤ 40%, and induced sustained ventricular tachycardia, comparing with no therapy or antiarrhythmic drugs.24,34 The MADIT I study proved the benefit of ICD for improved survival in patient with asymptomatic NSVT and symptomatic ischemic heart disease with LVEF<35%.35 According to the MUSTT and MADIT I results, patients with LVEF below 40%, NSVT, and inducible ventricular tachycardia in electrophysiology study should 187 Taiwan Crit. Care Med.2011;12:182-192 Tzu Ming Ou et al. sudden death43 (see Table 2). In post-myocardial infarction patients with LVEF less than 40%, the risk of sudden death is increased more than fivefold.48, 49 The MUSTT study also disclosed patients with coronary artery disease, left ventricular dysfunction and asymptomatic NSVT in whom sustained ventricular tachycardia can be induced in electrophysiology testing have a higher risk of sudden death or cardiac arrest and higher overall mortality than similar patients without inducible sustained ventricular tachycardia.26 Prognosis of NSVT Spontaneous NSVT in apparently healthy individuals does not imply an adverse prognosis, but long-term follow up is advisable. NSVT in the presence of structural heart disease carries a more serious prognosis than NSVT in the absence of structural heart disease. It is adverse prognostic significance for NSVT attacks during or post exercise, in patient with acute myocardial infarction more than 24 hours, chronic ischemic heart disease with LVEF below 40%, and hypertrophic obstructive cardiomyopathy in the young.43,44 In patients with congestive heart failure, NSVT is an independent marker for increased overall mortality rate and sudden death.45 In adult patients with hypertrophic obstructive cardiomyopathy, NSVT is a sensitive marker for increased risk of sudden death.46 NSVT is an insensitive and nonspecific predictor of sudden death in idiopathic dilated cardiomyopathy patients. 47 However, NSVT in patients with primary ventricular fibrillation, congenital long-QT, Brugada syndrome, arrhythmogenic right ventricular dysplasia, repaired congenital abnormalities, valvular heart disease, hypertension were unknown prognostic significance for Conclusion NSVT is frequently encountered in clinical practice. It may increase the risk for malignant arrhythmia and sudden cardiac death. The prognosis depends on the etiologies. Clinical approach to the patient with NSVT should always be considered what the coexisted heart disease is. In the absence of heart disease, spontaneous NSVT does not carry any adverse prognostic significance. NSVT with adverse prognostic significance were found in patients with some conditions. Treatment to the NSVT included antiarrhythmic medications, Table 2.Prognostic significance of non-sustained ventricular tachycardia with different underlying heart condition.43-49 Adverse prognostic significance 1.NSVT during or post exercise 2.Acute myocardial infarction more than 24 hours 3.Chronic ischemic heart disease with LVEF below 40% with/without inducible sustained ventricular tachycardia in electrophysiology testing 4.Hypertrophic obstructive cardiomyopathy in the young No Adverse prognostic significance Idiopathic dilated cardiomyopathy Unknown prognostic significance 1.Primary ventricular fibrillation 2.Congenital long-QT 3.Brugada syndrome 4.Arrhythmogenic right ventricular dysplasia 5.Repaired congenital abnormalities 6.Valvular heart disease 7.Hypertension 188 Taiwan Crit. Care Med.2011;12:182-192 Non-sustained, symptomatic ventricular tachycardia ICD implantation and catheter ablation. Betablocker and amiodarone are safe and effective anti-arrhythmic medications. ICD implantation is convinced as first line therapy to terminate ventricular tachycardia episode. In patients who have structural heart disease, catheter ablation is recommended as adjunctive therapy if frequent episodes of VT and ICD shocks. Anti-arrhythmic medications therapy after successful catheter ablation is controversial. 11.Takada H, Mikawa T, Murayama M, et al. Range of ventricular ectopic complexes in healthy subjects studied with repeated ambulatory electrocardiographic recording. Am J Cardiol 1989;63:184-186. 12.McKenna WJ, Chetty S, Oakley CM, et al. Arrhythmia in hypertrophic cardiomypathy: Exercise and 48-hour ambulatory electrocardiographic assessment with and without beta adrenergic blocking therapy. Am J Cardiol 1980;45:1-5. 13.Savage DD, Seides SF, Maron BJ, et al. Prevalance of arrhythmias during 24-hour electrocardiographic monitoring and exercise testing in patients with obstructive and nonobstructive cardiomyopathy. Circulation 1979;59:866-875. 14.Huang SK, Messer JV, Denes P. Significance of ventricular tachycardia in idiopathic dilated cardiomyopathy: Observation in 35 patients. Am J Cardiol 1983;51:507-512. 15.Meinertz T, Hofmann T, Kasper W, et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. Am J Cardiol 1984;53:902-907. 16.Neri R, Mestroni L, Salvi A, et al. Arrhythmias in dilated cardiomyopathy. Postgrad Med J 1986;62:593-597. 17.Suyama A, Anan T, Araki H, et al. Prevalance of ventricular tachycardia in patients with different underlying heart disease: A study by Holter ECG monitoring. Am Heart J 1986;112:44-51. 18.Campbell R, Murray A, Julian DG. Ventricular arrthythmias in the first 12 hours of acute myocardial infarction. Br Heart J 1981;46:351-357. 19.de Soyza N, Bennett FA, Murphy ML, et al. The relationship of paroxysmal ventricular tachycardia complicating the acute phase and ventricular arrhythmia during the last hospital phase of myocardial infarction to long-term survival. Am J Med 1978;64:377-381. 20.Heidbüchel H, Tack J, Vanneste L, et al. Significance of arrhythmias during the first 24 hours of acute myocardial infarction treated with alteplase and effect of early administration of a beta-blocker or a bradycardiac agent on their incidence. Circulation 1994;89: 1051-1059. 21.Eldar M, Sievner Z, Goldbourt U, et al. Primary ventricular tachycardia in acute myocardial infarction: clinical characteristics and mortality. The SPRINT Study Group. Ann Intern Med 1992;117:31-36. 22.Joshi S, Wilber DJ. Ablation of idiopathic right ventricular outflow tract tachycardia: current perspectives. J Cardiovasc Electrophysiol 2005;16 Suppl 1:S52-S58. 23.Nakagawa M, Takahashi N, Nobe S, et al. Gender differences in various types of idiopathic ventricular tachycardia. J Cardiovasc Electrophysiol 2002;13: 633-638. 24.Buxton AE, Lee KL, Fisher JD, et al. A randomized References 1.Myerburg RJ, Kessler KM, Castellanos A. Sudden cardiac death: epidemiology, transient risk, and intervention assessment. Ann Intern Med 1993;119:1187-1197. 2.Sheldon SH, Gard JJ, Asirvatham SJ. Premature Ventricular Contractions and Non-sustained Ventricular Tachycardia: Association with Sudden Cardiac Death, Risk Stratification, and Management Strategies. Indian Pacing and Electrophysiology Journal 2010;10(8):357-371. 3.Lerman BB, Stein K, Engelstein ED, et al. Mechanism of repetitive monomorphic ventricular tachycardia. Circulation 1995;92:421-429. 4.Lerman BB, Belardinelli L, West GA, et al. Adenosinesensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activity. Circulation 1986;74:270-280. 5.Lerman BB. Response of nonreentrant catecholaminemediated ventricular tachycardia to endogenous adenosine and acetylcholine. Evidence for myocardial receptor-mediated effects. Circulation 1993;87:382-390. 6.Michael R, Douglas PZ. Braunwald’s heart disease: a textbook of cardiovascular medicine. 9th ed. Philadelphia. Saunders-Elsevier Inc. 2011:672. 7.Califf RM, Mckinnis RA, Burks J, et al. Prognostic implications of ventricular arrhythmias during 24-hour ambulatory monitoring in patients undergoing cardiac catheterization for coronary artery disease. Am J Cardiol 1982;50:23-31. 8.Hinkle LE, Carver ST, Stevens M. The frequency of asymptomatic disturbances of cardiac rhythm and conduction in middle-aged men. Am J Cardiol 1969;24: 629-650. 9.Kantelip JP, Sage E, Duchene-Marullaz P. Findings on ambulatory electrocardiographic monitoring in subjects older than 80 years. Am J Cardiol 1986;57;398-401. 10.Kostis JB, McCrone K, Moreyra AE, et al. Premature ventricular complexes in the absence of identifiable heart disease. Circulation 1981;63:1351-1356. 189 Taiwan Crit. Care Med.2011;12:182-192 Tzu Ming Ou et al. study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med 1999;341:1882-1890. 25.Buxton AE, Lee KL, Hafley GE, et al. Relation of ejection fraction and inducible ventricular tachycardia to mode of death in patients with coronary artery disease: an analysis of patients enrolled in the multicenter unsustained tachycardia trial. Circulation 2002;106: 2466–2472. 26.Buxton AE, Lee KL, DiCarlo L, et al. Electrophysiologic testing to identify patients with coronary artery disease who are at risk for sudden death. Multicenter Unsustained tachycardia Trial Investigators. N Engl J Med 2000;342:1937-1945. 27.Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006;114:e385-e484. 28.William JR, Andrew EE, Joaquin GA, et al. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med 1989;321:406-412. 29.De Ponti R, Ho SY. Mapping of right ventricular outflow tract tachycardia/ectopies: activation mapping versus pace mapping. Heart Rhythm 2008;5:345-347. 30.Singh SN, Fletcher RD, Fisher SG, et al. Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure. N Engl J Med 1995;333:77-82. 31.McKenna WJ, Oakley CM, Krikler DM, et al. Improved survival with amiodarone in patients with hypertrophic cardiomyopathy and ventricular tachycardia. Br Heart J 1985;53:412-416. 32.Cairns JA, Connolly SJ, Roberts R, et al. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators. Lancet 1997;349:675-682. 33.Eckardt L, Breithardt G. Catheter ablation of ventricular tachycardia. From indication to three-dimensional mapping technology. Herz 2009;34:187-196. 34.Buxton AE, Fisher JD, Josephson ME, et al. Prevention of sudden death in patients with coronary artery disease: the Multicenter Unsustained Tachycardia Trial (MUSTT). Prog Cardiovasc Dis 1993;36:215-216. 35.Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med 1996;335:1933-1940. 36.Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation 2008;117;e350-e408. 37.Bogun F, Crawford T, Reich S, et al. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention. Heart Rhythm 2007;4:863-867. 38.Klein LS, Shih HT, Hackett FK, et al. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease. Circulation 1992;85: 1666-1674. 39.Coggins DL, Lee RJ, Sweeney J, et al. Radiofrequency catheter ablation as a cure for idiopathic tachycardia of both left and right ventricular origin. J Am Coll Cardiol 1994;23:1333-1341. 40.O’Connor BK, Case CL, Sokoloski MC, et al. Radiofrequency catheter ablation of right ventricular outflow tachycardia in children and adolescents. J Am Coll Cardiol 1996;27:869-874. 41.Rodriguez LM, Smeets JL, Timmermans C, et al. Predictors for successful ablation of right and leftsided idiopathic ventricular tachycardia. Am J Cardiol 1997;79:309-314. 42.Vestal M, Wen MS, Yeh SJ, et al. Electrocardiographic predictors of failure and recurrence in patients with idiopathic right ventricular outflow tract tachycardia and ectopy who underwent radiofrequency catheter ablation. J Electrocardiol 2003;36:327-332. 43.Katritsis DG, Camm AJ. Nonsustained ventricular tachycardia: where do we stand? Eur Heart J 2004; 25:1093-1099. 44.Monserrat L, Elliott PM, Gimeno JR, et al. Nonsustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients. J Am Coll Cardiol. 2003;42: 190 Taiwan Crit. Care Med.2011;12:182-192 Non-sustained, symptomatic ventricular tachycardia 873-879. 45.Doval HC, Nul DR, Grancelli HO, et al. Nonsustained ventricular tachycardia in severe heart failure. Independent marker of increased mortality due to sudden death. Circulation 1996;94:3198-3203. 46.Maron BJ, Savage DD, Wolfson JK, et al. Prognostic significance of 24 hour ambulatory electrocardiographic monitoring in patients with hypertrophic cardiomyopathy: a prospective study. Am J Cardiol 1981; 48:252-257. 47.Larsen L, Markham J, Haffajee CI. Sudden death in idiopathic dilated cardiomyopathy: role of ventricular arrhythmias. Pacing Clin Electrophysiol 1993;16: 1051-1059. 48.Bigger JT Jr, Fleiss JL, Rolnitzky LM. Prevalence, characteristics and significance of ventricular tachycardia detected by 24-hour continuous electrocardiographic recordings in the late hospital phase of acute myocardial infarction. Am J Cardiol 1986;58:1151-1160. 49.Mukharji J, Rude RE, Poole WK, et al. Risk factors for sudden death after acute myocardial infarction: twoyear follow-up. Am J Cardiol 1984;54:31-36. 191 Taiwan Crit. Care Med.2011;12:182-192 Tzu Ming Ou et al. 非持續性具症狀之心室心搏過速:病例報告及文 獻回顧 1 2 1 2 歐子銘 , 黃世鐘 , 項正川 , 王怡誠 摘要 非持續性心室心搏過速臨床上很常見,但了解的人卻不多。具有非持續 性心室心搏過速的病人輕微者可以無症狀,嚴重者卻有猝死的可能。預後跟 合併的心臟疾病有關。不良的預後常見於運動誘發之非持續性心室心搏過速、 急性心肌梗塞 24 小時過後、慢性缺血性心臟病及左心室射出分率小於 40% 合併有或無於心臟電生理檢查誘發出非持續性心室心搏過速、年輕人之肥厚 性阻塞性心肌病變。藥物治療包含乙型交感神經阻斷劑及 amiodarone,而植 入式心臟整流去顫器及射頻燒灼術適用於某些病人。我們報告一個 71 歲女性 合併有暈厥及心悸的症狀,24 小時心電圖診斷非持續性心室心搏過速。經射 頻燒灼術及藥物治療後病情獲得穩定控制。希望藉由這個病例讓大家更加認 識這個疾病。 關鍵詞:非持續性心室心搏過速,左心室射出分率 聯絡人:王怡誠醫師 802 高雄市苓雅區中正一路 2 號;國軍高雄總醫院心臟內科 2 電話:07-749-4941;E-mail:[email protected] 1 國軍高雄總醫院內科部 192