Idiopathic Ventricular Tachycardia and Fihrillation: Incidence, Prognosis, and Therapy JESUS ALMENDRAL, JOSE ORMAETXE, and JUAN L. DELCAN From the Glinical Electrophysiology Laboratory, Gardiology Division, Hospital General Gregorio Maranon, Madrid, Spain
Most patients who develop sustained ventricular tachyarrhythmias have underlying organic heart disease. However, it is well known that in a minority of such patients, no structural or functional abnormality can be demonstrated, except for the presenting arrhythmia. It has been observed that the presence or absence of structural heart disease can affect prognosis in patients with sustained ventricular tachyarrhythmias.^ In cardiac arrest survivors, a depressed left ventricular function was found to be an independent predictor of outcome.^ Therefore, the management of this rather unique patient population, having sustained or even lethal ventricular arrhythmias in the absence of other detectable abnormalities, deserves special consideration. The purpose of this paper is to analyze the available information as to the incidence and prognosis of this patient population according to the presenting arrhythmia, and to suggest guidelines for therapy. Idiopathic Sustained Uniform Ventricular Tachycardia Incidence A minority of patients referred for electrophysiological evaluation, and in whom the final diagnosis is sustained ventricular tachycardia, will have no detectable organic heart disease. For example, in a large series of 516 patients with symptomatic recurrent ventricular tachycardia, 75 (15%) fell into that category.^ In our own series, 12 of 91 patients with recurrent uniform ventricular tachycardia had no detectable organic heart disease. Most of these patients fall into one of two
Address for reprints: Jesiis Almendral, M.D., Servicio de Cardiologia (Planta 5), Hospital Gregorio Maranon, Doctor Esquerdo. 46, 28007-Madrid, Spain.
PAGE, Vol. 15
well-defined syndromes*: (1) repetitive monomorphic right ventricular tachycardia, characterized by a typical QRS morphology (left bundle branch block pattern with an inferior axis), frequent extrasystoles, and runs of nonsustained ventricular tachycardia of the same morphology. The origin is located in the right ventricular outflow tract^'^; (2) idiopathic left ventricular tachycardia with a right bundle block QRS pattern, frequently with a left superior axis in the frontal plane; arrhythmic episodes tend to be less frequent but more prolonged. Its origin is usually located at the left ventricular apex or in the inferior mid-left ventricular septum.''~^° Prognosis Despite a lot of controversy as to the mechanisms of these tachycardias there seems to be general agreement that patients with sustained uniform ventricular tachycardia have little risk of sudden or cardiac death.^'''^° However, occasional instances of sudden death have been reported in these patients.^^ In contrast, syncope does not seem to be rare in these patients, and 7 of our 12 patients had syncope (in the absence of antiarrhythmic drugs) preceding admission for ventricular tachycardia. Recurrence rate can be considerable, and control with antiarrhythmic drugs may be problematic in some of these patients. Patients with repetitive monomorphic ventricular tachycardia tend to respond to beta blockade." Patients with idiopathic left ventricular tachycardia frequently respond to verapamil.^"^ Some patients respond to type I antiarrhythmic agents.^'^ Therapy Since most patients do well on antiarrhythmic agents and their risk for arrhythmic death is small, antiarrhythmic agents seem to be the first choice for this patient population. However, the risk of
April 1992, Part III
627
ALMENDRAL, ET AL.
life-threatening proarrhythmic events seems to be small in patients without organic heart disease^ ^ as opposed to patients after myocardial infarction.^^ A small minority of these patients may be difficult to control with antiarrhythmic agents. In those cases, and in those who do not tolerate antiarrhythmic agents, ablation procedures may be considered. Such procedures have been successful in some of these patients, but they are not uniformly successful.^*'^^ In cases of failure of ablative procedures, implantation of antitachycardia devices can be offered in severely symptomatic patients. Pacing therapy can be of great benefit for those patients without syncope since episodes of sustained ventricular tachycardia usually can be terminated by pacing^" with a small risk of acceleration. However, this risk always exists, and pacing therapy should always include backup defibrillation.
Cardiac Arrest Survivors Incidence Most cardiac arrest survivors have underlying organic heart disease, as do patients with sustained uniform ventricular tachycardia. There is a minority of cardiac arrest survivors in whom no structural heart disease can be detected. Functional abnormalities such as the different forms of the long QT syndrome (eventually intermittent) can be the cause of cardiac arrest in those patients.^" It is well known that ventricular fibrillation (unlike sustained uniform ventricular tachycardia) causing cardiac arrest can occur in structurally and functionally normal hearts in the presence of transient external disturbances such as electrolyte abnormalities, proarrhythmic effects of antiarrhythmic agents, or acute coronary ischemia.^'' Therefore, when no structural or functional abnormalities are detected in a cardiac arrest survivor, the question arises whether the cause of the cardiac arrest was due to a transient factor. Minor structural abnormalities may even be present and difficult to detect." However, although a search for other causes is justified and extremely important, there are cases in which none of those factors can be identified.^^~^^ As
628
summarized in Table I, about 7% of cardiac arrest survivors in different series have no demonstrable structural heart disease or functional abnormalities and no evidence for transient perturbations as the cause of their arrest.^'^-^^ Prognosis Table I summarizes some reported series of cardiac arrest survivors in which there is information on the prognosis of patients without structural heart disease. It is evident that the prognosis of this patient population is not well established since the information available refers to small numbers of patients in all series.^'^^"^^ Moreover, treatment modalities have differed among the studies. However, pooling all studies, the incidence of sudden death or cardiac arrest during follow-up was as high as 21% (Tahle I). It has been observed that ejection fraction was an independent predictor of outcome in a general population of cardiac arrest survivors.^ Since patients without structural heart disease have, by definition, a normal ejection fraction, this relatively high incidence of sudden death of cardiac arrest can be considered unexpected. However, patients with normal ejection fractions in general series of cardiac arrest survivors also included patients with coronary artery disease (CAD) and reversible ischemia whose prognosis has been reported as excellent with antiischemic therapy.^"* It is conceivable that the prognosis of this latter group of patients (if treated with therapy for ischemia) could be better than those without structural heart disease in whom the cause of cardiac arrest remains unknown and therefore untreated. A , sustained ventricular tachyarrhythmia could be induced in about half of the patients with cardiac arrest in the absence of structural heart disease or functional abnormalities (Table I). In a general population of cardiac arrest survivors, inducibility of ventricular tachycardia by programmed electrical stimulation carries a worse prognosis.^'^^'^^ However, whether this also applies for the suhset of patients without structural heart disease is unclear at the present time. In fact, there are reported instances of sudden death^^ or defibrillator discharges preceded by symptoms^^ in noninducible cardiac arrest survivors without structural heart disease.
April 1992, Part III
PAGE, Vol. 15
IDIOPATHIC VENTRICULAR TACHYCARDIA AND FIBRILLATION
Table I. Cardiac Arrest Survivors without Structurai Heart Disease: Incidence and Prognosis in Different Series Reference
No. Pts.
Trappe et al.^ Siebels et al.^^ Wever et al.^^ Poole et al.^^ Belhassen et al.^'^ Benson et al.^^ Wiiber et al.^ Authors Total
6 15 21 12 5 4 8 6 11
15 -. 5 NA 36' 5 18 -
1. SVTA
F/U
4/4 1/15 14/21 4/12 5/5 2/4 NA 3/6 33/67
47 19 32 NA 52 21 NA 25 -
CA/SD 0" 4+ (27%) 6-^+ (29%) NA
o§ 2 (50%) NA 0*** 12/57 (21%)
* Percent of cardiac arrest survivors with no structural heart disease; ** two patients with recurrence of nonfatal ventricular tachycardia; + two of the four had defibrillator shocks with presyncopal symptoms; * * three of the six had defibrillator shocks with (pre)syncopai symptoms; § inducible sustained ventricular tachyarrhythmias were supressed in all five patients with Class lA antiarrhythmic agents; ' the study only refers to young patients (ages 15 to 30); * " one patient had noncardiac death and another patient was lost to follow-up; CA /SD = cardiac arrest or sudden death during follow-up; F/U = mean duration of follow-up in months; I. SVTA = inducible sustained ventricular tachyarrhythmias; NA = not available; No. Pts. = number of patients studied after an episode of cardiac arrest and having no structural heart disease.
Therapy Since neither the etiology nor the triggering mechanisms of cardiac arrest in these patients are known, no etiologic approach is availahle. Antiarrhythmic agents have used with variahle results: two such patients on heta hlockers died suddenly ^^; four other patients died suddenly while on empiric antiarrhythmic agents.^^'^^'^^ In one report, patients with inducihle sustained ventricular tachyarrhythmias during baseline electrophysiolgical study had no sudden death or recurrences on Class IA agents that suppressed inducihle ventricular tachyarrhythmias.^° However, the validity of the study is limited hecause it included only five patients. Catheter ahlation usually is not an option in these patients hecause, if sustained ventricular tachyarrhythmias are inducihle, they are not suitable for mapping hecause of their polymorphic nature or poor tolerance. The implantation of a defihrillator seems to he a reasonahle and promising therapeutic option in these patients. Since recurrences, if they occur at all, usually are infrequent, these patients are good candidates for the
PACE, Vol. 15
defihrillator. The most important drawback of this therapy in this patient population is operative mortality. However, the operative risk of these patients is prohably lower than that of most patients undergoing defibrillator implantation who usually have worse ventricular function and clinical condition. In addition, the recent introduction of nonthoracotomy lead implantation^^ probably decreases the operative risks in this setting. In any event, the spontaneous recurrence of sudden death in these patients exceeds that risk. The question remains if the prognosis of patients with inducihle sustained ventricular tachyarrhythmias suppressed hy antiarrhjrthmic agents can be comparable to that of those with the implantable defibrillator. We feel that since inducible polymorphic ventricular arrhythmias or ventricular fihrillation are not specific responses, they should not be used as a guide for therapy in these patients. On the contrary, inducible sustained uniform ventricular tachycardia, a specific response in the absence of structural heart disease, could be used as a target for drug therapy.
April 1992, Part III
629
ALMENDRAL, ET AL.
References 1. Trappe H, Brugada P, Talajic M, et al. Prognosis of patients with ventricular tachycardia and ventricular fibrillation: Role of underlying etiology. J Am Coll Cardiol 1988; 12:166-174. 2. Wiiber DJ, Garan H, Finkelstein D, et al. Out-ofhospital cardiac arrest. Use of electrophysiologic testing in the prediction of long-term outcome. N Engl J Med 1988; 318:19-24. 3. Zipes DP. Specific arrhythmias: Diagnosis and treatment. In E Braunwald (ed.): Heart Disease. Philadelphia, W.B. Saunders, 1984, pp. 683-743. 4. Marchlinski FE. Ventricular tachycardia: Clinical presentation, course, and therapy. In DP Zipes, J Jalife (eds.): Cardiac Electrophysiology. Philadelphia, W.B. Saunders, 1990, pp. 756-777. 5. Buxton AE, Waxman HL, Marchlinski FE, et al. Right ventricular tachycardia: Clinical and electrophysiologic characteristics. Circulation 1983; 68:917-927. 6. Buxton AE, Marchlinski FE, Doherty JU, et al. Repetitive, monomorphic ventricular tachycardia: Clinical and electrophysiologic characteristics in patients with and without organic heart disease. Am J Cardiol 1984; 54;997-1002. 7. German LD, Packer DL, Bardy GH, et al. Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease. Am J Cardiol 1983; 52:1202-1207. 8. Lin F, Finley D, Rahimtoola SH, et al. Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: A unique clinical entity with specific properties. Am J Cardiol 1983; 52:95-100. 9. Belhassen B, Shapira I, Pelleg A, et al. Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: An ECG-electrophysiologic entity. Am Heart J 1984; 108:1034-1037. 10. Ohe T, Shimomura K, Aihara N, et al. Idiopathic sustained left ventricular tachycardia: Glinical and electrophysiologic characteristics. Girculation 1988; 77:560-568. 11. Deal BJ, Miller SM, Scagliotti D, et al. Ventricular tachycardia in a young population without overt heart disease. Circulation 1986; 73:1111-1118. 12. Pritchett LC, Wilkinson WE. Mortality in patients treated with flecainide and encainide for supraventricular arrhythmias. Am J Cardiol 1991; 67:976-980. 13. The Gardiac Arrhythmia Suppression Trial (GAST) investigators. Preliminary report: Effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989; 321:406-412. 14. Morady F, Kadish AH, DiGarlo L, et al. Long-term
630
15. 16.
17.
18. 19.
20.
21.
22.
23.
24.
25.
26. 27.
results of catheter ablation of idiopathic right ventricular tachycardia. Girculation 1990; 82: 2093-2099. Breithardt G, Borggrefe M, Wichter T. Gatheter ablation of idiopathic right ventricular tachycardia. Girculation 1990; 82:2273-2276. Goumel P, Leclercq JF, Dessertenne F. Torsades de pointes. In ME Josephson, HJJ Wellens (eds.): Tachycardias: Mechanisms Diagnosis, Treatment. Philadelphia, Lea & Febiger, 1984, pp. 325-351. Topp H, Opitz G, Givilibal B,et al. Underestimated role of vasospastic coronary disease in sudden cardiac death? (abstract) Eur Heart J 1991; 12(Suppl):87. Martini B, Nava A, Thiene G, et el. Ventricular fibrillation without apparent heart disease: description of six cases. Am Heart J 1989; 118:1203-1209. Benson DW, Benditt DG, Anderson RW, et al. Gardiac arrest in young, ostensibly healthy patients: Glinical, hemodynamic, and electrophysiologic findings. Am J Gardiol 1983; 52:65-69. Belhassen B, Shapira I, Shoshani D, et al. Idiopathic ventricular fibrillation: Inducibility and beneficial effects of class I antiarrhythmic agents. Girculation 1987;75:809-816. Siebels J, Schneider MAE, Geiger M, et al. Unexpected recurrences in survivors of cardiac arrest without organic heart disease, (abstract) Eur Heart J 1991; 12(Suppl):86. Wever E, Hauer R, Oomen A, et al. Unfavorable outcome in patients with primary electrical disease who survived unexpected cardiac arrest, (abstract) Eur Heart J 1991; 12(Suppl):86. Poole JE, Mathisen T, Kudenchuk PJ, et al. Longterm outcome in patients who survive out of hospital ventricular fibrillation and undergo electrophysiologic studies: evaluation by electrophysiologic subgroups. J Am Goll Gardiol 1990; 16: 657-665. Morady F, DiGarlo L, Winston S, et al. Glinical features and prognosis of patients with out of hospital cardiac arrest and a normal electrophysiologic study. J Am Goll Gardiol 1984; 4:39-44. Freedman RA, Swerdlow GD, Soderholm-Difatte V, et al. Prognostic significance of arrhythmia inducibility or noninducibility at initial electrophysiologic study in survivors of cardiac arrest. Am J Gardiol 1988; 61:578-582. Lemery R, Brugada P, Delia Bella P, et al. Ventricular fibrillation in six adults without overt heart disease. J Am Goll Gardiol 1989;13:911-916. Bardy GH, Allen MD, Mehra R, et al. An effective and adaptable transvenous defibrillation system using the coronary sinus in humans. J Am Goll Gardiol. 1990; 16:887-895.
April 1992, Part III
PAGE, Vol. 15
Most patients who develop sustained ventricular tachyarrhythmias have underlying organic heart disease. However, it is well known that in a minority of such patients, no structural or functional abnormality can be demonstrated, except for the presenting arrhythmia. It has been observed that the presence or absence of structural heart disease can affect prognosis in patients with sustained ventricular tachyarrhythmias.^ In cardiac arrest survivors, a depressed left ventricular function was found to be an independent predictor of outcome.^ Therefore, the management of this rather unique patient population, having sustained or even lethal ventricular arrhythmias in the absence of other detectable abnormalities, deserves special consideration. The purpose of this paper is to analyze the available information as to the incidence and prognosis of this patient population according to the presenting arrhythmia, and to suggest guidelines for therapy. Idiopathic Sustained Uniform Ventricular Tachycardia Incidence A minority of patients referred for electrophysiological evaluation, and in whom the final diagnosis is sustained ventricular tachycardia, will have no detectable organic heart disease. For example, in a large series of 516 patients with symptomatic recurrent ventricular tachycardia, 75 (15%) fell into that category.^ In our own series, 12 of 91 patients with recurrent uniform ventricular tachycardia had no detectable organic heart disease. Most of these patients fall into one of two
Address for reprints: Jesiis Almendral, M.D., Servicio de Cardiologia (Planta 5), Hospital Gregorio Maranon, Doctor Esquerdo. 46, 28007-Madrid, Spain.
PAGE, Vol. 15
well-defined syndromes*: (1) repetitive monomorphic right ventricular tachycardia, characterized by a typical QRS morphology (left bundle branch block pattern with an inferior axis), frequent extrasystoles, and runs of nonsustained ventricular tachycardia of the same morphology. The origin is located in the right ventricular outflow tract^'^; (2) idiopathic left ventricular tachycardia with a right bundle block QRS pattern, frequently with a left superior axis in the frontal plane; arrhythmic episodes tend to be less frequent but more prolonged. Its origin is usually located at the left ventricular apex or in the inferior mid-left ventricular septum.''~^° Prognosis Despite a lot of controversy as to the mechanisms of these tachycardias there seems to be general agreement that patients with sustained uniform ventricular tachycardia have little risk of sudden or cardiac death.^'''^° However, occasional instances of sudden death have been reported in these patients.^^ In contrast, syncope does not seem to be rare in these patients, and 7 of our 12 patients had syncope (in the absence of antiarrhythmic drugs) preceding admission for ventricular tachycardia. Recurrence rate can be considerable, and control with antiarrhythmic drugs may be problematic in some of these patients. Patients with repetitive monomorphic ventricular tachycardia tend to respond to beta blockade." Patients with idiopathic left ventricular tachycardia frequently respond to verapamil.^"^ Some patients respond to type I antiarrhythmic agents.^'^ Therapy Since most patients do well on antiarrhythmic agents and their risk for arrhythmic death is small, antiarrhythmic agents seem to be the first choice for this patient population. However, the risk of
April 1992, Part III
627
ALMENDRAL, ET AL.
life-threatening proarrhythmic events seems to be small in patients without organic heart disease^ ^ as opposed to patients after myocardial infarction.^^ A small minority of these patients may be difficult to control with antiarrhythmic agents. In those cases, and in those who do not tolerate antiarrhythmic agents, ablation procedures may be considered. Such procedures have been successful in some of these patients, but they are not uniformly successful.^*'^^ In cases of failure of ablative procedures, implantation of antitachycardia devices can be offered in severely symptomatic patients. Pacing therapy can be of great benefit for those patients without syncope since episodes of sustained ventricular tachycardia usually can be terminated by pacing^" with a small risk of acceleration. However, this risk always exists, and pacing therapy should always include backup defibrillation.
Cardiac Arrest Survivors Incidence Most cardiac arrest survivors have underlying organic heart disease, as do patients with sustained uniform ventricular tachycardia. There is a minority of cardiac arrest survivors in whom no structural heart disease can be detected. Functional abnormalities such as the different forms of the long QT syndrome (eventually intermittent) can be the cause of cardiac arrest in those patients.^" It is well known that ventricular fibrillation (unlike sustained uniform ventricular tachycardia) causing cardiac arrest can occur in structurally and functionally normal hearts in the presence of transient external disturbances such as electrolyte abnormalities, proarrhythmic effects of antiarrhythmic agents, or acute coronary ischemia.^'' Therefore, when no structural or functional abnormalities are detected in a cardiac arrest survivor, the question arises whether the cause of the cardiac arrest was due to a transient factor. Minor structural abnormalities may even be present and difficult to detect." However, although a search for other causes is justified and extremely important, there are cases in which none of those factors can be identified.^^~^^ As
628
summarized in Table I, about 7% of cardiac arrest survivors in different series have no demonstrable structural heart disease or functional abnormalities and no evidence for transient perturbations as the cause of their arrest.^'^-^^ Prognosis Table I summarizes some reported series of cardiac arrest survivors in which there is information on the prognosis of patients without structural heart disease. It is evident that the prognosis of this patient population is not well established since the information available refers to small numbers of patients in all series.^'^^"^^ Moreover, treatment modalities have differed among the studies. However, pooling all studies, the incidence of sudden death or cardiac arrest during follow-up was as high as 21% (Tahle I). It has been observed that ejection fraction was an independent predictor of outcome in a general population of cardiac arrest survivors.^ Since patients without structural heart disease have, by definition, a normal ejection fraction, this relatively high incidence of sudden death of cardiac arrest can be considered unexpected. However, patients with normal ejection fractions in general series of cardiac arrest survivors also included patients with coronary artery disease (CAD) and reversible ischemia whose prognosis has been reported as excellent with antiischemic therapy.^"* It is conceivable that the prognosis of this latter group of patients (if treated with therapy for ischemia) could be better than those without structural heart disease in whom the cause of cardiac arrest remains unknown and therefore untreated. A , sustained ventricular tachyarrhythmia could be induced in about half of the patients with cardiac arrest in the absence of structural heart disease or functional abnormalities (Table I). In a general population of cardiac arrest survivors, inducibility of ventricular tachycardia by programmed electrical stimulation carries a worse prognosis.^'^^'^^ However, whether this also applies for the suhset of patients without structural heart disease is unclear at the present time. In fact, there are reported instances of sudden death^^ or defibrillator discharges preceded by symptoms^^ in noninducible cardiac arrest survivors without structural heart disease.
April 1992, Part III
PAGE, Vol. 15
IDIOPATHIC VENTRICULAR TACHYCARDIA AND FIBRILLATION
Table I. Cardiac Arrest Survivors without Structurai Heart Disease: Incidence and Prognosis in Different Series Reference
No. Pts.
Trappe et al.^ Siebels et al.^^ Wever et al.^^ Poole et al.^^ Belhassen et al.^'^ Benson et al.^^ Wiiber et al.^ Authors Total
6 15 21 12 5 4 8 6 11
15 -. 5 NA 36' 5 18 -
1. SVTA
F/U
4/4 1/15 14/21 4/12 5/5 2/4 NA 3/6 33/67
47 19 32 NA 52 21 NA 25 -
CA/SD 0" 4+ (27%) 6-^+ (29%) NA
o§ 2 (50%) NA 0*** 12/57 (21%)
* Percent of cardiac arrest survivors with no structural heart disease; ** two patients with recurrence of nonfatal ventricular tachycardia; + two of the four had defibrillator shocks with presyncopal symptoms; * * three of the six had defibrillator shocks with (pre)syncopai symptoms; § inducible sustained ventricular tachyarrhythmias were supressed in all five patients with Class lA antiarrhythmic agents; ' the study only refers to young patients (ages 15 to 30); * " one patient had noncardiac death and another patient was lost to follow-up; CA /SD = cardiac arrest or sudden death during follow-up; F/U = mean duration of follow-up in months; I. SVTA = inducible sustained ventricular tachyarrhythmias; NA = not available; No. Pts. = number of patients studied after an episode of cardiac arrest and having no structural heart disease.
Therapy Since neither the etiology nor the triggering mechanisms of cardiac arrest in these patients are known, no etiologic approach is availahle. Antiarrhythmic agents have used with variahle results: two such patients on heta hlockers died suddenly ^^; four other patients died suddenly while on empiric antiarrhythmic agents.^^'^^'^^ In one report, patients with inducihle sustained ventricular tachyarrhythmias during baseline electrophysiolgical study had no sudden death or recurrences on Class IA agents that suppressed inducihle ventricular tachyarrhythmias.^° However, the validity of the study is limited hecause it included only five patients. Catheter ahlation usually is not an option in these patients hecause, if sustained ventricular tachyarrhythmias are inducihle, they are not suitable for mapping hecause of their polymorphic nature or poor tolerance. The implantation of a defihrillator seems to he a reasonahle and promising therapeutic option in these patients. Since recurrences, if they occur at all, usually are infrequent, these patients are good candidates for the
PACE, Vol. 15
defihrillator. The most important drawback of this therapy in this patient population is operative mortality. However, the operative risk of these patients is prohably lower than that of most patients undergoing defibrillator implantation who usually have worse ventricular function and clinical condition. In addition, the recent introduction of nonthoracotomy lead implantation^^ probably decreases the operative risks in this setting. In any event, the spontaneous recurrence of sudden death in these patients exceeds that risk. The question remains if the prognosis of patients with inducihle sustained ventricular tachyarrhythmias suppressed hy antiarrhjrthmic agents can be comparable to that of those with the implantable defibrillator. We feel that since inducible polymorphic ventricular arrhythmias or ventricular fihrillation are not specific responses, they should not be used as a guide for therapy in these patients. On the contrary, inducible sustained uniform ventricular tachycardia, a specific response in the absence of structural heart disease, could be used as a target for drug therapy.
April 1992, Part III
629
ALMENDRAL, ET AL.
References 1. Trappe H, Brugada P, Talajic M, et al. Prognosis of patients with ventricular tachycardia and ventricular fibrillation: Role of underlying etiology. J Am Coll Cardiol 1988; 12:166-174. 2. Wiiber DJ, Garan H, Finkelstein D, et al. Out-ofhospital cardiac arrest. Use of electrophysiologic testing in the prediction of long-term outcome. N Engl J Med 1988; 318:19-24. 3. Zipes DP. Specific arrhythmias: Diagnosis and treatment. In E Braunwald (ed.): Heart Disease. Philadelphia, W.B. Saunders, 1984, pp. 683-743. 4. Marchlinski FE. Ventricular tachycardia: Clinical presentation, course, and therapy. In DP Zipes, J Jalife (eds.): Cardiac Electrophysiology. Philadelphia, W.B. Saunders, 1990, pp. 756-777. 5. Buxton AE, Waxman HL, Marchlinski FE, et al. Right ventricular tachycardia: Clinical and electrophysiologic characteristics. Circulation 1983; 68:917-927. 6. Buxton AE, Marchlinski FE, Doherty JU, et al. Repetitive, monomorphic ventricular tachycardia: Clinical and electrophysiologic characteristics in patients with and without organic heart disease. Am J Cardiol 1984; 54;997-1002. 7. German LD, Packer DL, Bardy GH, et al. Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease. Am J Cardiol 1983; 52:1202-1207. 8. Lin F, Finley D, Rahimtoola SH, et al. Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: A unique clinical entity with specific properties. Am J Cardiol 1983; 52:95-100. 9. Belhassen B, Shapira I, Pelleg A, et al. Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: An ECG-electrophysiologic entity. Am Heart J 1984; 108:1034-1037. 10. Ohe T, Shimomura K, Aihara N, et al. Idiopathic sustained left ventricular tachycardia: Glinical and electrophysiologic characteristics. Girculation 1988; 77:560-568. 11. Deal BJ, Miller SM, Scagliotti D, et al. Ventricular tachycardia in a young population without overt heart disease. Circulation 1986; 73:1111-1118. 12. Pritchett LC, Wilkinson WE. Mortality in patients treated with flecainide and encainide for supraventricular arrhythmias. Am J Cardiol 1991; 67:976-980. 13. The Gardiac Arrhythmia Suppression Trial (GAST) investigators. Preliminary report: Effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989; 321:406-412. 14. Morady F, Kadish AH, DiGarlo L, et al. Long-term
630
15. 16.
17.
18. 19.
20.
21.
22.
23.
24.
25.
26. 27.
results of catheter ablation of idiopathic right ventricular tachycardia. Girculation 1990; 82: 2093-2099. Breithardt G, Borggrefe M, Wichter T. Gatheter ablation of idiopathic right ventricular tachycardia. Girculation 1990; 82:2273-2276. Goumel P, Leclercq JF, Dessertenne F. Torsades de pointes. In ME Josephson, HJJ Wellens (eds.): Tachycardias: Mechanisms Diagnosis, Treatment. Philadelphia, Lea & Febiger, 1984, pp. 325-351. Topp H, Opitz G, Givilibal B,et al. Underestimated role of vasospastic coronary disease in sudden cardiac death? (abstract) Eur Heart J 1991; 12(Suppl):87. Martini B, Nava A, Thiene G, et el. Ventricular fibrillation without apparent heart disease: description of six cases. Am Heart J 1989; 118:1203-1209. Benson DW, Benditt DG, Anderson RW, et al. Gardiac arrest in young, ostensibly healthy patients: Glinical, hemodynamic, and electrophysiologic findings. Am J Gardiol 1983; 52:65-69. Belhassen B, Shapira I, Shoshani D, et al. Idiopathic ventricular fibrillation: Inducibility and beneficial effects of class I antiarrhythmic agents. Girculation 1987;75:809-816. Siebels J, Schneider MAE, Geiger M, et al. Unexpected recurrences in survivors of cardiac arrest without organic heart disease, (abstract) Eur Heart J 1991; 12(Suppl):86. Wever E, Hauer R, Oomen A, et al. Unfavorable outcome in patients with primary electrical disease who survived unexpected cardiac arrest, (abstract) Eur Heart J 1991; 12(Suppl):86. Poole JE, Mathisen T, Kudenchuk PJ, et al. Longterm outcome in patients who survive out of hospital ventricular fibrillation and undergo electrophysiologic studies: evaluation by electrophysiologic subgroups. J Am Goll Gardiol 1990; 16: 657-665. Morady F, DiGarlo L, Winston S, et al. Glinical features and prognosis of patients with out of hospital cardiac arrest and a normal electrophysiologic study. J Am Goll Gardiol 1984; 4:39-44. Freedman RA, Swerdlow GD, Soderholm-Difatte V, et al. Prognostic significance of arrhythmia inducibility or noninducibility at initial electrophysiologic study in survivors of cardiac arrest. Am J Gardiol 1988; 61:578-582. Lemery R, Brugada P, Delia Bella P, et al. Ventricular fibrillation in six adults without overt heart disease. J Am Goll Gardiol 1989;13:911-916. Bardy GH, Allen MD, Mehra R, et al. An effective and adaptable transvenous defibrillation system using the coronary sinus in humans. J Am Goll Gardiol. 1990; 16:887-895.
April 1992, Part III
PAGE, Vol. 15
