International Elsevier
Journal of Cardiology,
21s
29 (1990) 215-220
CARD10 01149
Prognostic role of inducible ventricular tachycardia in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia Heinz D. G&singer, First
Michael Jung, Ludwig Wagner, Christoph Stain, Peter Siostrzonek, Ilse Schwarzinger and Herbert Miisslacher Department of Medicine,Division of Cardiology. Universi!v of Vtenna. Vienna. Ausma (Received 11 December 1989: revision accepted
15 May 1990)
G&singer HD, Jung M, Wagner
L, Stain C, Siostrzonek P, Schwarzinger I, MBsslacher H. Prognostic role of inducible ventricular tachycardia in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia. Int J Cardiol 1990:29:215-220.
We studied the prognostic relevance of inducible ventricular tachycardia in 32 patients with dilated cardiomyopathy and spontaneous nonsustained asymptomatic ventricular tachycardia. Programmed ventricular stimulation included basic drive cycle lengths of 600, 500, 430, 370, 330 and 300 msec at single, double, and triple extrastimuli. Ventricular tachycardia ( 2 6 beats) was initiated in 7 patients (22%), with sustained monomorphic ventricular tachycardia being seen in 4 of them. During median follow-up of 21 months (13~44), 14 patients died. Sudden cardiac death occurred in two of the seven patients with inducible tachycardia and in only one of the 25 patients in whom it was not possible to induce tachycardia. Although patients with inducible tachycardia did not differ clinically from those in whom tachycardia could not be induced, the projected mean survival time was significantly shorter in those with inducible tachycardia (10 months vs. 32 months, P = 0.04). For late sudden cardiac death, the positive predictive value of inducible tachycardia was 28%. The negative predictive value was %%. We conclude that induction of ventricular tachycardia by programmed stimulation might indicate poorer prognosis in patients with dilated cardiomyopathy. Key words: Dilated cardiomyopathy; Ventricular tachycardia
Sudden
cardiac
Introduction Patients with dilated almost equal proportions
Correspondence
to: H.D.
Medicine, University Vienna. Austria. 0167-5273/90/$03.50
cardiomyopathy die in from sudden, presuma-
G&singer.
M.D.,
of Vienna, Lazarettgasse
1st Dept. of
14. A-1090
0 1990 Elsevier Science Publishers
death:
Programmed
stimulation:
bly arrhythmic, death and from an inexorable decline in cardiac performance [l]. Many studies have reported that measurements of the severity of left ventricular dysfunction can grossly predict early mortality in those with heart failure. The prediction of sudden cardiac death, however, is more difficult. Controversy exists on the predictive value
of spontaneous
tachycardia
in respect
B.V. (Biomedical
Division)
nonsustained
to late sudden
ventricular
cardiac
death
216
[2-41. Furthermore, there is little information on the prognostic value of ventricular tachycardia when induced by programmed ventricular stimulation in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia [5-71. The present study was designed to ascertain the prognostic significance of inducible ventricular tachycardia in dilated cardiomyopathy. Material
and Methods
Patients Between April 1986 and November 1988, 32 consecutive patients with dilated cardiomyopathy and documented asymptomatic non-sustained ventricular tachycardia (2 3 beats) were entered into this prospective study. Informed consent was obtained from all patients. The patients had a mean age of 54 years (19-67), and 30 patients (90%) were males. On admission, 6 patients (19%) presented in functional class II of the categorization of the New York Heart Association, with 7 patients (22%) in class III, and 19 patients (59%) in class IV. Left bundle branch block pattern was present in the surface electrocardiogram in 13 patients (41%), and a right bundle branch block pattern occurred in 3 patients (9%). Sixteen patients had no conduction delay. The diagnosis of dilated cardiomyopathy was based on the echocardiographic finding of a uniformly impaired left ventricular performance, with an ejection fraction of less than 50%. Coronary angiography was performed in 11 patients (34%) to confirm the clinical diagnosis. Patients with a history of myocardial infarction, syncope or symptomatic ventricular tachycardia were excluded from the study. Programmed ventricular stimulation Programmed ventricular stimulation was performed with the patients in the fasting and unsedated state. Patients who were on digitalis were continued on this medication. No patient received antiarrhythmic treatment before the procedure. After insertion of a 4F electrode catheter to the
right ventricular apex, the stimulation procedure was carried out using a programmable impulse generator (Medtronic SP503). The stimuli were 2 msec in duration and at twice the diastolic threshold. The stimulation protocol included basic drives of 600, 500, 430, 370, 330 and 300 msec cycle length. Single, double and triple extrastimuli were coupled to the stimulation trains with stepwise shortening of the coupling interval by 8 ms until the right ventricular effective refractory period was reached. The intertrain pauses were 3 set in duration. During the stimulation procedure, a 12-lead surface electrocardiogram was recorded with a paperspeed of 50 mm/set. The endpoint of the procedure was the initiation of symptomatic ventricular tachycardia. Non-sustained ventricular tachycardia was defined by 6 or more repetitive ventricular responses with a maximal duration of 30 sec. Sustained tachycardia was assumed when the duration of tachycardia was longer than 30 set, or when hemodynamic compromise during the period of tachycardia necessitated immediate termination of the procedure. Hemodynamic
measurements
Right heart catheterization at rest was performed by the use of a Swan-Ganz catheter. The capillary wedge pressure was measured with the patient apnoeic. The cardiac output was obtained by thermodilution and was averaged over 3 subsequent measurements. Medical treatment and follow-up After programmed stimulation, all patients received a therapeutic regimen consisting of digitalis, vasodilators. oral anticoagulants and diuretics in a dosage adjusted to clinical requirements. Antiarrhythmic drugs were not allowed with the exception of two patients with symptomatic atria1 tachycardia. In addition, four patients with inducible and, so far, non-clinical sustained monomorphic ventricular tachycardia received uncontrolled treatment with amiodarone. The patients were followed clinically at intervals of 3 to 6 months. The duration of median follow up was 21 months (13-44). During this
217
period, 14 patients died. Of these deaths, 12 occurred in-hospital with continuous rhythm surveillance. The death of both out-patients who died was witnessed, and autopsy was performed in one of them. Another 2 patients were excluded from further follow-up because of orthotopic heart transplantation. Definitions Sudden cardiac death was defined as an abrupt and fatal disorder of cardiac rhythm in a patient whose cardiac performance, until that moment, had been adequate for sustenance of the peripheral circulation [8]. Death due to heart failure was defined as progressive impairment of cardiac mechanical performance, with some delay before ultimate cessation of the pulse and respiration [S]. Statistical analysis The values are expressed as mean k standard deviation. Survival estimates were obtained by the use of the Kaplan-Meier life table technique. Comparison of the survival curves were made by the use of the log-rank-test (Mantel-Cox, Breslow). Comparison of non-numericals were carried out by the use of the Wilcoxon-rank-sign test. Numericals were compared by one-way analysis of variance. Significance was assumed with a P value less than 0.05.
TABLE
Response to programmed ventricular stimulation Ventricular tachycardia could be induced in 7 patients (22%). Induction of sustained monomorphic ventricular tachycardia was observed in 4 of them. The individual modes of induction, and the characteristics of the tachycardias induced, are listed in Table 1. The remaining patients either had no ventricular response to programmed ventricular stimulation (five patients) or responded with 1 to 5 ventricular beats until completion of the entire stimulation protocol (20 patients). Comparison of patients in whom ventricular tachycardia could or could not be induced There was no significant difference among these groups of patients in respect to age, symptomatic grading, electrocardiographic features, and left ventricular performance (Table 2). Overall survival During the median period of follow-up of 21 months (13-44) 14 deaths (44%) occurred. Nine patients died of progressive heart failure. Three patients died suddenly. Two patients died of other causes. The estimated mean survival time of the
1
Characteristics Pt. No.
Results
of the induced Induction
ventricular
tachycardias.
mode
Ventricular
Drive CL (msec)
(No.)
Extrastimuli
1 2
370 300
3 4 5 6 7
300 330 600 300 370
Follow-up
tachycardia
CL (msec)
Shape
Sustained
2 3
260 250
monom. polym.
+ _
1 2 3 1 3
380 200 210 340 250
monom. polym. monom. monom. monom.
_ _ + + +
Abbreuiations: NO. = number, CL = cycle length, Infection = death due to postoperative pneumonitis,
SCD = sudden cardiac death, HF = death due monom. = monomorphic, polym. = polymorphic.
SCD HF Infection SCD alive alive HF to progressive
heart
failure,
C,,?,,,L,,Tl”E
0
IN DlLATED
SURVIVAL (KAPLAN-MEIER) PATIENTS WITH CARDIOMYOPATHY
1, 0
10
20
30
40
MONTHS
Fig. 1. Cumulative survival curves significantly differ (P = 0.04 Mantel-Cox) in patients with dilated cardiomyopathy with and without inducible ventricular tachycardia.
entire study population was 29 months. Death occurred in 5 of 7 patients in whom it was possible to induce ventricular tachycardia, and in 9 of 25 in whom ventricular tachycardia could not be induced. Patients with inducible tachycardia had a significantly shorter projected mean survival time (10 months) than did the other patients (32 months) (P = 0.04). The Kaplan Meier curves are presented in Fig. 1.
TABLE
Sudden cardiac death and response to programmed ventricular stimulation Sudden cardiac death occurred in 2 of the 7 patients with inducible ventricular tachycardia, but in only one of the 25 patients in whom it was not possible to induce ventricular tachycardia. The latter patient was successfully resuscitated from primary ventricular fibrillation and has been subsequently censored from life table analysis. For the prediction of sudden cardiac death, initiation of ventricular tachycardia by the above stimulation protocol had a sensitivity of 66%. The specificity was 83%. The positive predictive value was 28% while the negative predictive value was 96%. Discussion An increased risk of dying suddenly in patients with dilated cardiomyopathy might affect the decision when to .place a patient on the waiting list for heart transplantation. The present results suggest that initiation of ventricular tachycardia might be helpful in predicting poorer survival, predominantly due to the more frequent occurrence of
2
Clinical and electrocardiographic inducible ventricular tachycardia.
features
and left ventricular
function
in patients
with dilated
With inducible tachycardia (N = 7)
Without inducible tachycardia (N = 25)
59 1 1 5 2 1 4 23 7.5
54 5 6 14 11 2 12 28 7.2
0.17
with and without
P
Patients
Mean age years) NYHA class II III IV LBBB (N) RBBB (N) NO BBB (N) Mean LVEF (W) LVEDD (cm) CI/PCWP (I/min/m2/mm Hg)
cardiomyopathy
(54-66) (14%) (14%) (72%) (29%) (14%) (57%) (18-49) (4.5-8.2) (0.040.35)
0.14
(19-67) (20%) (24%) (56%) (44%) (8%) (48%) (9-49) (5.2-8.6) (0.02-0.6)
NS NS NS NS NS NS NS NS NS NS
Abbreuiurions: LBBB = left bundle branch block; RBBB = right bundle branch block; BBB = bundle branch block; LVEF = left ventricular ejection fraction; LVEDD = left ventricular ejection fraction (%); CI = cardiac index; PCWP = pulmonary capillary wedge pressure.
219
sudden cardiac death. In respect to late sudden cardiac death, however, the positive predictive value of inducible tachycardia is low over a short period of follow up. In contrast, an inability to induce ventricular tachycardia designates patients as having a low risk of dying suddenly. Inducibility of ventricular tachycardia The present study compares to earlier reports showing poor reproduction of clinically documented non-sustained ventricular tachycardia in dilated cardiomyopathy by programmed ventricular stimulation [7]. Of note, the inducibility of non-sustained ventricular tachycardia may depend largely on the aggressiveness of the applied protocol for stimulation, since a pacing protocol limited to basic drive cycle lengths between 600 and 430 msec and double extrastimuli failed completely to reproduce non-sustained ventricular tachycardia in patients with dilated cardiomyopathy and ventricular arrhythmia in grade IV B of Lown [9]. initiation of non-clinical sustained Moreover, monomorphic ventricular tachycardia can be expected in 0 to 30% of patients with impaired left ventricular function and spontaneous non-sustained ventricular tachycardia [6,9,10]. Potential predictive value of inducible tachycardia Preliminary information already exists on the predictive value of the initiation of sustained monomorphic ventricular tachycardia for the late occurrence of this type of tachycardia in dilated cardiomyopathy [5]. In view of the variety of trigger arrhythmias in sudden cardiac death [ll], however, even the initiation of non-sustained monomorphic or polymorphic tachycardia could indicate the potential to develop fatal arrhythmia in selected patients. It is noteworthy that the low positive predictive value of inducible tachycardia reflects inherent limitations, since the initiation of non-clinical tachycardia does not necessarily mean subsequent clinical appearance. Vice versa, programmed ventricular stimulation fails to produce any ventricular tachycardia in a considerable percentage of patients with dilated cardiomyopathy suffering aborted sudden cardiac death [12]. Our
results contrast to prior reports on this issue [13] in respect to a lower incidence of sudden cardiac death and a different predictive role of inducible tachycardia. These discrepancies may, in part, relate to the use of vasodilators which affect survival by improvement of left ventricular function [14]. Furthermore, it is not clear whether the administration of uncontrolled antiarrhythmic drugs. as reported in earlier trials on this issue [13]. prevents or even facilitates the occurrence of fatal arrhythmia in individual patients [12]. Limitations Despite a 44% incidence of death, with continuous electrocardiographic surveillance in most cases, the relatively small number of patients may somewhat limit the results of our study. Another limitation may be that the follow-up period is rather short. References 1 Dunica S, Coumel P. Incidence and mechanisms of sudden cardiac death in patients with left ventricular dysfunction. Heart Failure 1986;1:24&255. 2 Meinertz T, Hofmann T, Kasper W et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. Am J Cardiol 1984;53:902-907. 3 Unverferth DV, Magorien RD. Moeschberger ML, Baker PB, Fetters JK. Leier CV. Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol 1984;54:147-152. 4 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. 5 Das SK. Morady F. DiCarlo L. Baerman J. Krol R. De Buitleir M, Crevey B. Prognostic usefulness of programmed ventricular stimulation in idiopathic dilated cardiomyopathy without symptomatic ventricular arrhythmias. Am J Cardiol 1986;58:998-1000. 6 Poll DS, Marchlinski FE. Buxton AE. Josephson ME. Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy. Am J Cardiol 1986;58:992-997. 7 Gonska BD, Bethge KP. Kreuzer H. Programmed ventricular stimulation in coronary artery disease and dilated cardiomyopathy: influence of the underlying heart disease on the results of electrophysiologic testing. Clin Cardiol 1987:10:294-304. 8 Hinkle LE. Thaler HT. Clinical classification of cardiac death. Circulation 1982;65:457-463. 9 Meinertz T, Treese N, Kasper W et al. Determinants of prognosis in idiopathic dilated cardiomyopathy as de-
220 termined by programmed electrical stimulation. Am J Cardiol 1985;56:337-341. 10 Breithardt G, Borgreffe M, Podczek A. Electrophysiology and pharmacology of asymptomatic nonsustained ventricuJar tachycardia. Clin Progr Electrophysiol Pacing 1986;4:81. 11 Bayes de Luna A, Coumel P, Leclercq JF. Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmia on the basis of data from 157 cases. Am Heart J 1989;117:151-159. 12 Liem LB, Swerdlow CD. Value of electropharmacologic
testing in idiopathic dilated cardiomyopathy and sustained ventricular tachyarrhythmias. Am J Cardiol 1988;62:611616. 13 Bellocci F, Montenero S, Nobile A et al. Usefulness of programmed ventricular stimulation in patients with idiopathic dilated cardiomyopathy and non sustained ventricular tachycardia (abstr.) PACE 1988;11:834. 14 The CONSENSUS Trial Study Group: Effects of enalapril on the mortality in severe congestive heart failure. N Engl J Med 1987;316:1429-1435.
Journal of Cardiology,
21s
29 (1990) 215-220
CARD10 01149
Prognostic role of inducible ventricular tachycardia in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia Heinz D. G&singer, First
Michael Jung, Ludwig Wagner, Christoph Stain, Peter Siostrzonek, Ilse Schwarzinger and Herbert Miisslacher Department of Medicine,Division of Cardiology. Universi!v of Vtenna. Vienna. Ausma (Received 11 December 1989: revision accepted
15 May 1990)
G&singer HD, Jung M, Wagner
L, Stain C, Siostrzonek P, Schwarzinger I, MBsslacher H. Prognostic role of inducible ventricular tachycardia in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia. Int J Cardiol 1990:29:215-220.
We studied the prognostic relevance of inducible ventricular tachycardia in 32 patients with dilated cardiomyopathy and spontaneous nonsustained asymptomatic ventricular tachycardia. Programmed ventricular stimulation included basic drive cycle lengths of 600, 500, 430, 370, 330 and 300 msec at single, double, and triple extrastimuli. Ventricular tachycardia ( 2 6 beats) was initiated in 7 patients (22%), with sustained monomorphic ventricular tachycardia being seen in 4 of them. During median follow-up of 21 months (13~44), 14 patients died. Sudden cardiac death occurred in two of the seven patients with inducible tachycardia and in only one of the 25 patients in whom it was not possible to induce tachycardia. Although patients with inducible tachycardia did not differ clinically from those in whom tachycardia could not be induced, the projected mean survival time was significantly shorter in those with inducible tachycardia (10 months vs. 32 months, P = 0.04). For late sudden cardiac death, the positive predictive value of inducible tachycardia was 28%. The negative predictive value was %%. We conclude that induction of ventricular tachycardia by programmed stimulation might indicate poorer prognosis in patients with dilated cardiomyopathy. Key words: Dilated cardiomyopathy; Ventricular tachycardia
Sudden
cardiac
Introduction Patients with dilated almost equal proportions
Correspondence
to: H.D.
Medicine, University Vienna. Austria. 0167-5273/90/$03.50
cardiomyopathy die in from sudden, presuma-
G&singer.
M.D.,
of Vienna, Lazarettgasse
1st Dept. of
14. A-1090
0 1990 Elsevier Science Publishers
death:
Programmed
stimulation:
bly arrhythmic, death and from an inexorable decline in cardiac performance [l]. Many studies have reported that measurements of the severity of left ventricular dysfunction can grossly predict early mortality in those with heart failure. The prediction of sudden cardiac death, however, is more difficult. Controversy exists on the predictive value
of spontaneous
tachycardia
in respect
B.V. (Biomedical
Division)
nonsustained
to late sudden
ventricular
cardiac
death
216
[2-41. Furthermore, there is little information on the prognostic value of ventricular tachycardia when induced by programmed ventricular stimulation in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia [5-71. The present study was designed to ascertain the prognostic significance of inducible ventricular tachycardia in dilated cardiomyopathy. Material
and Methods
Patients Between April 1986 and November 1988, 32 consecutive patients with dilated cardiomyopathy and documented asymptomatic non-sustained ventricular tachycardia (2 3 beats) were entered into this prospective study. Informed consent was obtained from all patients. The patients had a mean age of 54 years (19-67), and 30 patients (90%) were males. On admission, 6 patients (19%) presented in functional class II of the categorization of the New York Heart Association, with 7 patients (22%) in class III, and 19 patients (59%) in class IV. Left bundle branch block pattern was present in the surface electrocardiogram in 13 patients (41%), and a right bundle branch block pattern occurred in 3 patients (9%). Sixteen patients had no conduction delay. The diagnosis of dilated cardiomyopathy was based on the echocardiographic finding of a uniformly impaired left ventricular performance, with an ejection fraction of less than 50%. Coronary angiography was performed in 11 patients (34%) to confirm the clinical diagnosis. Patients with a history of myocardial infarction, syncope or symptomatic ventricular tachycardia were excluded from the study. Programmed ventricular stimulation Programmed ventricular stimulation was performed with the patients in the fasting and unsedated state. Patients who were on digitalis were continued on this medication. No patient received antiarrhythmic treatment before the procedure. After insertion of a 4F electrode catheter to the
right ventricular apex, the stimulation procedure was carried out using a programmable impulse generator (Medtronic SP503). The stimuli were 2 msec in duration and at twice the diastolic threshold. The stimulation protocol included basic drives of 600, 500, 430, 370, 330 and 300 msec cycle length. Single, double and triple extrastimuli were coupled to the stimulation trains with stepwise shortening of the coupling interval by 8 ms until the right ventricular effective refractory period was reached. The intertrain pauses were 3 set in duration. During the stimulation procedure, a 12-lead surface electrocardiogram was recorded with a paperspeed of 50 mm/set. The endpoint of the procedure was the initiation of symptomatic ventricular tachycardia. Non-sustained ventricular tachycardia was defined by 6 or more repetitive ventricular responses with a maximal duration of 30 sec. Sustained tachycardia was assumed when the duration of tachycardia was longer than 30 set, or when hemodynamic compromise during the period of tachycardia necessitated immediate termination of the procedure. Hemodynamic
measurements
Right heart catheterization at rest was performed by the use of a Swan-Ganz catheter. The capillary wedge pressure was measured with the patient apnoeic. The cardiac output was obtained by thermodilution and was averaged over 3 subsequent measurements. Medical treatment and follow-up After programmed stimulation, all patients received a therapeutic regimen consisting of digitalis, vasodilators. oral anticoagulants and diuretics in a dosage adjusted to clinical requirements. Antiarrhythmic drugs were not allowed with the exception of two patients with symptomatic atria1 tachycardia. In addition, four patients with inducible and, so far, non-clinical sustained monomorphic ventricular tachycardia received uncontrolled treatment with amiodarone. The patients were followed clinically at intervals of 3 to 6 months. The duration of median follow up was 21 months (13-44). During this
217
period, 14 patients died. Of these deaths, 12 occurred in-hospital with continuous rhythm surveillance. The death of both out-patients who died was witnessed, and autopsy was performed in one of them. Another 2 patients were excluded from further follow-up because of orthotopic heart transplantation. Definitions Sudden cardiac death was defined as an abrupt and fatal disorder of cardiac rhythm in a patient whose cardiac performance, until that moment, had been adequate for sustenance of the peripheral circulation [8]. Death due to heart failure was defined as progressive impairment of cardiac mechanical performance, with some delay before ultimate cessation of the pulse and respiration [S]. Statistical analysis The values are expressed as mean k standard deviation. Survival estimates were obtained by the use of the Kaplan-Meier life table technique. Comparison of the survival curves were made by the use of the log-rank-test (Mantel-Cox, Breslow). Comparison of non-numericals were carried out by the use of the Wilcoxon-rank-sign test. Numericals were compared by one-way analysis of variance. Significance was assumed with a P value less than 0.05.
TABLE
Response to programmed ventricular stimulation Ventricular tachycardia could be induced in 7 patients (22%). Induction of sustained monomorphic ventricular tachycardia was observed in 4 of them. The individual modes of induction, and the characteristics of the tachycardias induced, are listed in Table 1. The remaining patients either had no ventricular response to programmed ventricular stimulation (five patients) or responded with 1 to 5 ventricular beats until completion of the entire stimulation protocol (20 patients). Comparison of patients in whom ventricular tachycardia could or could not be induced There was no significant difference among these groups of patients in respect to age, symptomatic grading, electrocardiographic features, and left ventricular performance (Table 2). Overall survival During the median period of follow-up of 21 months (13-44) 14 deaths (44%) occurred. Nine patients died of progressive heart failure. Three patients died suddenly. Two patients died of other causes. The estimated mean survival time of the
1
Characteristics Pt. No.
Results
of the induced Induction
ventricular
tachycardias.
mode
Ventricular
Drive CL (msec)
(No.)
Extrastimuli
1 2
370 300
3 4 5 6 7
300 330 600 300 370
Follow-up
tachycardia
CL (msec)
Shape
Sustained
2 3
260 250
monom. polym.
+ _
1 2 3 1 3
380 200 210 340 250
monom. polym. monom. monom. monom.
_ _ + + +
Abbreuiations: NO. = number, CL = cycle length, Infection = death due to postoperative pneumonitis,
SCD = sudden cardiac death, HF = death due monom. = monomorphic, polym. = polymorphic.
SCD HF Infection SCD alive alive HF to progressive
heart
failure,
C,,?,,,L,,Tl”E
0
IN DlLATED
SURVIVAL (KAPLAN-MEIER) PATIENTS WITH CARDIOMYOPATHY
1, 0
10
20
30
40
MONTHS
Fig. 1. Cumulative survival curves significantly differ (P = 0.04 Mantel-Cox) in patients with dilated cardiomyopathy with and without inducible ventricular tachycardia.
entire study population was 29 months. Death occurred in 5 of 7 patients in whom it was possible to induce ventricular tachycardia, and in 9 of 25 in whom ventricular tachycardia could not be induced. Patients with inducible tachycardia had a significantly shorter projected mean survival time (10 months) than did the other patients (32 months) (P = 0.04). The Kaplan Meier curves are presented in Fig. 1.
TABLE
Sudden cardiac death and response to programmed ventricular stimulation Sudden cardiac death occurred in 2 of the 7 patients with inducible ventricular tachycardia, but in only one of the 25 patients in whom it was not possible to induce ventricular tachycardia. The latter patient was successfully resuscitated from primary ventricular fibrillation and has been subsequently censored from life table analysis. For the prediction of sudden cardiac death, initiation of ventricular tachycardia by the above stimulation protocol had a sensitivity of 66%. The specificity was 83%. The positive predictive value was 28% while the negative predictive value was 96%. Discussion An increased risk of dying suddenly in patients with dilated cardiomyopathy might affect the decision when to .place a patient on the waiting list for heart transplantation. The present results suggest that initiation of ventricular tachycardia might be helpful in predicting poorer survival, predominantly due to the more frequent occurrence of
2
Clinical and electrocardiographic inducible ventricular tachycardia.
features
and left ventricular
function
in patients
with dilated
With inducible tachycardia (N = 7)
Without inducible tachycardia (N = 25)
59 1 1 5 2 1 4 23 7.5
54 5 6 14 11 2 12 28 7.2
0.17
with and without
P
Patients
Mean age years) NYHA class II III IV LBBB (N) RBBB (N) NO BBB (N) Mean LVEF (W) LVEDD (cm) CI/PCWP (I/min/m2/mm Hg)
cardiomyopathy
(54-66) (14%) (14%) (72%) (29%) (14%) (57%) (18-49) (4.5-8.2) (0.040.35)
0.14
(19-67) (20%) (24%) (56%) (44%) (8%) (48%) (9-49) (5.2-8.6) (0.02-0.6)
NS NS NS NS NS NS NS NS NS NS
Abbreuiurions: LBBB = left bundle branch block; RBBB = right bundle branch block; BBB = bundle branch block; LVEF = left ventricular ejection fraction; LVEDD = left ventricular ejection fraction (%); CI = cardiac index; PCWP = pulmonary capillary wedge pressure.
219
sudden cardiac death. In respect to late sudden cardiac death, however, the positive predictive value of inducible tachycardia is low over a short period of follow up. In contrast, an inability to induce ventricular tachycardia designates patients as having a low risk of dying suddenly. Inducibility of ventricular tachycardia The present study compares to earlier reports showing poor reproduction of clinically documented non-sustained ventricular tachycardia in dilated cardiomyopathy by programmed ventricular stimulation [7]. Of note, the inducibility of non-sustained ventricular tachycardia may depend largely on the aggressiveness of the applied protocol for stimulation, since a pacing protocol limited to basic drive cycle lengths between 600 and 430 msec and double extrastimuli failed completely to reproduce non-sustained ventricular tachycardia in patients with dilated cardiomyopathy and ventricular arrhythmia in grade IV B of Lown [9]. initiation of non-clinical sustained Moreover, monomorphic ventricular tachycardia can be expected in 0 to 30% of patients with impaired left ventricular function and spontaneous non-sustained ventricular tachycardia [6,9,10]. Potential predictive value of inducible tachycardia Preliminary information already exists on the predictive value of the initiation of sustained monomorphic ventricular tachycardia for the late occurrence of this type of tachycardia in dilated cardiomyopathy [5]. In view of the variety of trigger arrhythmias in sudden cardiac death [ll], however, even the initiation of non-sustained monomorphic or polymorphic tachycardia could indicate the potential to develop fatal arrhythmia in selected patients. It is noteworthy that the low positive predictive value of inducible tachycardia reflects inherent limitations, since the initiation of non-clinical tachycardia does not necessarily mean subsequent clinical appearance. Vice versa, programmed ventricular stimulation fails to produce any ventricular tachycardia in a considerable percentage of patients with dilated cardiomyopathy suffering aborted sudden cardiac death [12]. Our
results contrast to prior reports on this issue [13] in respect to a lower incidence of sudden cardiac death and a different predictive role of inducible tachycardia. These discrepancies may, in part, relate to the use of vasodilators which affect survival by improvement of left ventricular function [14]. Furthermore, it is not clear whether the administration of uncontrolled antiarrhythmic drugs. as reported in earlier trials on this issue [13]. prevents or even facilitates the occurrence of fatal arrhythmia in individual patients [12]. Limitations Despite a 44% incidence of death, with continuous electrocardiographic surveillance in most cases, the relatively small number of patients may somewhat limit the results of our study. Another limitation may be that the follow-up period is rather short. References 1 Dunica S, Coumel P. Incidence and mechanisms of sudden cardiac death in patients with left ventricular dysfunction. Heart Failure 1986;1:24&255. 2 Meinertz T, Hofmann T, Kasper W et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. Am J Cardiol 1984;53:902-907. 3 Unverferth DV, Magorien RD. Moeschberger ML, Baker PB, Fetters JK. Leier CV. Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol 1984;54:147-152. 4 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. 5 Das SK. Morady F. DiCarlo L. Baerman J. Krol R. De Buitleir M, Crevey B. Prognostic usefulness of programmed ventricular stimulation in idiopathic dilated cardiomyopathy without symptomatic ventricular arrhythmias. Am J Cardiol 1986;58:998-1000. 6 Poll DS, Marchlinski FE. Buxton AE. Josephson ME. Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy. Am J Cardiol 1986;58:992-997. 7 Gonska BD, Bethge KP. Kreuzer H. Programmed ventricular stimulation in coronary artery disease and dilated cardiomyopathy: influence of the underlying heart disease on the results of electrophysiologic testing. Clin Cardiol 1987:10:294-304. 8 Hinkle LE. Thaler HT. Clinical classification of cardiac death. Circulation 1982;65:457-463. 9 Meinertz T, Treese N, Kasper W et al. Determinants of prognosis in idiopathic dilated cardiomyopathy as de-
220 termined by programmed electrical stimulation. Am J Cardiol 1985;56:337-341. 10 Breithardt G, Borgreffe M, Podczek A. Electrophysiology and pharmacology of asymptomatic nonsustained ventricuJar tachycardia. Clin Progr Electrophysiol Pacing 1986;4:81. 11 Bayes de Luna A, Coumel P, Leclercq JF. Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmia on the basis of data from 157 cases. Am Heart J 1989;117:151-159. 12 Liem LB, Swerdlow CD. Value of electropharmacologic
testing in idiopathic dilated cardiomyopathy and sustained ventricular tachyarrhythmias. Am J Cardiol 1988;62:611616. 13 Bellocci F, Montenero S, Nobile A et al. Usefulness of programmed ventricular stimulation in patients with idiopathic dilated cardiomyopathy and non sustained ventricular tachycardia (abstr.) PACE 1988;11:834. 14 The CONSENSUS Trial Study Group: Effects of enalapril on the mortality in severe congestive heart failure. N Engl J Med 1987;316:1429-1435.
