Programmed ventricular stimulation in survivors of acute myocardial infarction: long-term follow-up

ELSEVIER International Journal of Cardiology 49 (1995) 55-65

Programmed ventricular stimulation in survivors of acute myocardial infarction: long-term follow-up

Beatrice Brembilla-Perrot*a, Arnaud Terrier de la Chaise”, Serge BrianConb, Christine Suty-Seltona, Daniel Beurriera, Noel Martina, Bernard Thiel”,

Pierre Louisa, Nicolas Danchina

%krdiology A-B, CHU of Brabois, 54500 Vandoeuvre, France bEpidemiology medicine university, Nancy, France

Received 7 July 1994; revision received; accepted 21 December 1994

Abstract

The prognostic significance of ventricular tachyarrhythmias induced by programmed ventricular stimulation was evaluated in 492 consecutive survivors of acute myocardial infarction (AMI). Holter monitoring, signal-averaged elec- trocardiogram (ECG) and measurement of left ventricular ejection fraction (EF) were also performed. The protocol used up to 3 extrastimuli. Sustained monomorphic ventricular tachycardia (VT) < 270 beats/min, > 270 beats/min (ventricular flutter) (VFl), and ventricular fibrillation (VF) were induced in 99, 66 and 52 patients, respectively. Long term follow-up (mean 3.7 f 2.2 years) showed that most episodes of VT occurred during the first months following AM1 (n = 14), but some patients (n = 6) could develop VT as late as 4 years after AMI. Sudden death (SD) (n = 22) always occurred during the first year following AMI. Multivariate analysis demonstrated that EF < 30% and induction of a VT c 270 beats/mm were the only predictors for total cardiac death (P c 0.001). EF < 30%, induction of a VT < 270 beats/min and also of VFl (P < 0.05) were predictors for VT and SD: the risk was 4% in patients without inducible VT, 12% in those with inducible VFl, and 21% in those with inducible VT < 270 beats/min. In conclusion, induction of a sustained monomorphic VT c 270 beats/mm or > 270 beats/min is a predictor of arrhythmic events during the first year as well as 4 years after myocardial infarction. However the risk of arrhythmic sudden death decreases after the first year, while the risk of VT persists. Because of the low positive predictive value of programmed stimulation (respectively 21% and 12% for the induction of a sustained VT and VFl), we recommend the indication of programmed stimulation in only the patients with one abnormal non-invasive investigation.

Keywords: Programmed ventricular stimulation; Ventricular tachycardia; Myocardial infarction

1. Introduction

* Corresponding author, Service de cardiologie A, CHU Brabois, 54500 Vandoeuvre, Les Nancy, France.

In recent years, the role of programmed ventricular stimulation for the identification of patients at high risk for sudden cardiac death or spontaneous

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56 B. Brembilla-Perrot et al. /International Journal of Cardiology 49 (1995) 55-65

occurrence of sustained ventricular tachycardia (VT) after acute myocardial infarction (AMI) has been investigated at many institutions [ 1,231. These groups have noted that the ability to induce sustained ventricular tachyarrhythmias in survivors of AM1 lacking spontaneous arrhythmias can define a group at high risk of death or spontaneous VT or fibrillation (VF) in the next 2 years.

This study examined the results of routine electrophysiologic testing in 492 survivors of myocardial infarction who had not experienced spontaneous VT or VF after the first 48 h after infarction. The purpose of the study was to evaluate which duration of follow-up is necessary after myocardial infarction and to define the indications of programmed stimulation after myocardial infarction.

2. Population and methods

2.1. Population The study population consisted of 492 con-

secutive patients admitted between January 1983 and December 1991 because of Q-wave AM1 or for evaluation of the status after AMI. Patients aged c 75 years were systematically enrolled after informed consent. Patients were excluded from the study if they had (1) experienced early recurrence of angina requiring therapy with a @-adrenergic blocker, calcium channel antagonist or coronary artery bypass grafting, (2) experienced spontaneous VT or VF within the first 48 h after infarction, (3) clinical heart failure not controhed by treatment with furosemide, (4) significant noncardiac disease, and (5) received chronic amiodarone treatment. Electrophysiologic testing was performed between 1 and 6 months after infarction (usually 4 to 6 weeks after AMI) in patients who consented; 15 patients refused consent. No study patient received a P-adrenergic blocking drug, digoxin or other antiarrhythmic drug for 7 days before electrophysiologic testing. Patients who received amiodarone were excluded.

2.2. Protocol of study Electrophysiologic testing was performed with

patients in the postabsorptive state under 1% lignocaine local anesthesia. Three electrode

catheters were inserted percutaneously and posi- tioned in the right atrium, right ventricle and for His bundle recording.

Stimulation was performed with a program- mable stimulator (Explorer 2000, Ela medical, Montrouge, France). A constant-current source delivered rectangular impulses, 1.8 ms in duration, at twice diastolic threshold. Recordings were obtained with a 12 channel physiologic recorder (VR12, Hellige GMBH, Freiburg, West Germany) and real-time recordings were obtained with an ink-jet recorder (Siemens-Elema Mingograph, Siemens Medical system, Inc, South Iselin, NJ).

Atria1 pacing was performed at rate increments up to the onset of anterograde atrioventricular nodal Wenckebach block. Ventricular pacing was performed at rate increments up to 200 beats/min. The protocol of programmed stimulation used a single premature ventricular extrastimulus (S2) and double ventricular extrastimuli (S2 and S3), which were introduced during sinus rhythm and during paced cycle lengths (600 and 400 ms), to the right ventricular apex initially, and subsequently at the right ventricular outflow tract. From January 1987, a third extrastimulus was added if a sustained VT flutter or fibrillation was not induced. Triple extrastimuli (S2, S3, S4) were introduced during sinus rhythm and during paced cycle lengths (600 and 400 ms) at the right ventricular outflow tract and the apex.

2.3. End points at electrophysiologic study End points of programmed stimulation included

the completion of either protocol or the induction of flutter (VFl) or VF or VT lasting >30 s or requiring termination because of hemodynamic intolerance. Sustained VT was defined as monomorphic VT with a cycle length > 220 ms and VFl as monomorphic VT with a cycle length 5 220 ms.

2.4. Follow-up and endpoints of the study Follow-up was by telephone contact with

patients and their medical attendants. For the purpose of this study, only documented spontaneous VT, VF and witnessed instantaneous death in the absence of symptoms of ischemia were considered arrhythmic end points. Cardiac deaths, excluding

B. Brembilla-Perrot et al. 1 International Journal of Cardiology 49 (1995) 55-65 51

arrhythmic deaths, were attributed to reinfarction or congestive heart failure. There was no post mor- tem examination.

Each patient was followed for 2 6 months from the data of the index infarction. The mean follow- up was 3.7 years (& 2.2). Between January 1983 and December 1987, the patients did not receive antiarrhythmic drug therapy. Since 1988, antiarrhythmic drug therapy was prescribed in patients who had inducible VT or VF. The antiarrhythmic drug therapy was guided by Holter monitoring (n = 40) or by electrophysiologic study (n = 47). Oral therapy was commenced with a class I drug. If the treatment was not effective, the class I antiarrhythmic drug was replaced by 400 mglday of amiodarone. The detailed protocol and results of the study will be reported in the second part of the study.

During the follow-up, patients routinely received betablockers (50 to 100 mg of atenolol) except if they remained in Killip class III, IV or they had a contra-indication. The incidence of coronary artery angioplasty was 35%.

2.5. Assessments during initial admission In addition to recording age, gender, site of

myocardial infarction, radionuclide left ventricular ejection fraction was measured by technetium 99 m gated blood pool imaging in the left anterior oblique view. Systematic 24 h Holter monitoring was recorded (Anatec, Ela medical).

Signal-averaging was performed in 328 patients without bundle branch block on the same day as programmed stimulation, using the Simson’s method. The first high amplification ECG system was developed by Dr. Osypka (Gmbh), after which the LP 3000 (Cardionics) was used.

We used a bidirectional filter with a high band- pass frequency of 25 Hz. A late potential was defined as a low-amplitude signal ( < 20 pV), in the last 40 ms of the filtered QRS complex or a pro- longed low-amplitude signal (< 40 ,uV) in the ter- minal QRS (>40 ms). A long filtered QRS complex was detined as total filtered QRS duration greater than 120 ms. An abnormal signal- averaged ECG was defined as the presence of a late potential and/or a long filtered QRS.

2.6. Statistical analysis Unless otherwise stated, all values were quoted

as mean values f 1 S.D. Comparisons between groups were made using unpaired Student’s t-test

Table 1 Clinical characteristics of 492 survivors of myocardial infarction with and without inducible ventricular tachycardia at electrophysiologic study

Not inducible Inducible (total)

VT<270 beats/min

VFl VF

n 216 217 99 66 52 Age 51 * 13 57 f 12 56 f 14 56 f 12 54.5 f 11 Sex

M 233 195 81 64 50 F 42 22 18 2 2

Site of MI A 133 106 61 28 17 I 118 120 36 31 33 L 10 s 2 2 1

LVEF (%) 45 * 15 39 zt 14 34* 16 42 f 12 46 f 14 Holter M 73 (26%) 73 (34%) 36 (36%) 21 (32%) 16 (31%)

(grade IV) Late potentials 62/170 (36%) 89/l 58 (56%) 52112 (12%) 23146 (50%) 14140 (35%)

Holter M, Holter monitoring (grade IV = Grade IVa and IVb of Lown); LVEF, left ventricular ejection fraction; n, number of patients; Sex: M, male; F, female; MI, myocardial infarction; Site of MI: A, anterior; I, inferior; L, lateral; VF, ventricular fibrillation; VFl, ventricular flutter; VT, ventricular tachycardia;


and chi-square analysis where appropriate. Step- wise logistic regression analysis was performed to identify the independent variables predictive of inducible VT. Survival curves were calculated using the Kaplan-Meier product-limit method and compared by the generalized Wilcoxon (Breslow) test. Actuarial probabilities of survival of variables for sudden death or arrhythmia recurrence were performed by the method of Cox. A P value < 0.05 was considered significant.

> 230 ms was induced in 99 patients (20%), either by 2 extrastimuli (n = 81) or 3 extrastimuli (n = 18). - VFl was induced in 66 patients (13%), either by 2 extrastimuli (n = 56) or 3 extrastimuli (n = 10). - VF was induced in 52 patients (10.5%), either by 2 extrastimuli in 26 patients or 3 extrastimuli in 26 patients.

3. Results

3.1. Results of electrophysiologic study Programmed stimulation was performed up to 2

extrastimuli in 185 patients and up to 3 extrastimuli in 307 patients. - The stimulation was negative in 275 patients

(56%). - Sustained monomorphic VT with a cycle length

3.2. Clinical characteristics (Table I) Patients with and without inducible ventricular

tachyarrhythmias were comparable in age, gender distribution, site of index infarction, left ventricular ejection fraction (EF) and incidence of grade IVa and IVb of Lown Holter monitoring. The incidence of abnormal signal-averaged ECG was higher (P < 0.05) in patients with inducible ventricular arrhythmias than in patients without inducible arrhythmias. Among patients with inducible arrhythmias, only those with inducible

.+.......+.......+.......+..... 1.0 +P

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P.....P.

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.40 +

.20 +

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+

+

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0.0 40. 80. l*O month S

Fig. 1. Survival curve of patients free of cardiac events after acute myocardial infarction.

B. Brembilla-Perrot et al. /International Journal of Cardiology 49 (1995) 55-65 59

Table 2 Clinical outcome of the total population

Not inducible Inducible VT < 270 VFl VF (total) beats/mm

;T 275 5 217 15 99 12 66 52 (2%) (7%) (12%) 3 (4%) 0

SD 8 (3%) 14 (6%) 9 (9%) 5 (8%) 0 CD 6 (2%) 6 (3%) 5 (5%) 1 (1.5%) 0 Other 3 4 4 0 0

CD, cardiac death; Other: non-cardiac death, transplantation; SD, sudden death; VT, ventricular tachycardia

sustained monomorphic VT < 270 beatslmin had significantly (P < 0.01) more frequent an abnor- ma1 signal-averaged ECG than patients without inducible arrhythmias. The same patients with inducible sustained monomorphic VT c 270 beats/min had a lower EF (P < 0.001) than pa-

tients with inducible VFl or VF. Patients with inducible VF had generally inferior myocardial infarction (P < 0.05).

3.3. Outcome in patients 15 patients were excluded from the analysis

.+.......t.......+.......+.......+.......+.......+... 1.0 +o...............................................=

-2.. -BACCA.A. VF

-BB C. A......A....AA - BB C. A ............

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140

mo Fig. 2. Actuarial probability curves for remaining free of cardiac events in infarct survivors with inducible ventricular tachycardia < 270 beats/mm (VT), inducible ventricular flutter (VFl), inducible ventricular fibrillation (VF) and non-inducible sustained VT, VFI, VF (0).


because they presented with recurrent myocardial infarction (n = 4) or a cardiac surgery was made (n = 11). A further 5 patients had a cardiac transplantation.

Fig. 1 reports the general survival curve. Actu- arial probability of survival and freedom from arrhythmic events were 92% f 2% at 1 year, 89% f 3% at 2 years, and 82% at 5 years.

Table 2 compares the clinical outcome of the general population. During the extended follow- up, there were significantly more electrical ventricular events in patients with inducible sustained monomorphic VT than in patients without inducible VT (Fig. 2). There was also significantly (P < 0.05) more arrhythmic events (VT and sudden death, together) in patients with inducible VFl than in patients without inducible ventricular arrhythmia. Patients with inducible VF had a good prognosis at short and long-term follow-up.

In the total population, the occurrence of sudden cardiac death was noted in the months following AMI (mean 9 f 6). In 3 of these patients, VF was documented.

The occurrence of sustained VT was noted either in the months following myocardial infarction (n = 14) (mean 12 f 6), or at least 4 years after AM1 (mean 5 years) (n = 6). In these last patients, there was neither change in therapy, nor new infarction during the follow-up. In all patients

but 2, the morphology of the spontaneous VT was similar to the morphology of previously induced VT. The rate of the spontaneous tachycardia was slightly slower than the rate of induced tachycardia. Among the 28 patients with inducible ventricular arrhythmias who have presented either a spontaneous sustained VT and/or a cardiac sudden death, the third extrastimulus was required to induce the ventricular arrhythmia in only 3 patients.

3.4. Profile of patients who presented an arrhythmic event or a cardiac death (Table 3)

As others have previously reported [l-4], alive patients had a significantly (P < 0.005) higher left ventricular EF (Fig. 3) and less frequently (P < 0.05) inducible sustained VT or VFl than patients who presented an event. Patients with lower EF and inducible VT were at high risk of arrhythmic events and had also a higher risk of cardiac death unrelated to an arrhythmic event. Lown grade 4A and 4B ventricular ectopic activity on Holter monitoring was found more frequently (P c 0.05) in patients who presented a sudden cardiac death than in all other patients (Fig. 4).

All patients with inducible ventricular flutter, who presented with sudden death, had grade IV ventricular ectopic activity. Patients with inducible

Table 3 Profile of patients who presented an arrhythmic event, ventricular tachycardia (VT) or sudden death (SD) or a cardiac death related to heart failure (CD)

:ge

Sex M F

Site of MI A I

LVEF Holter M Grade IV (%) VT or Vfl at stimulation

("W Late potentials

VT SD CD Alive

20 56 +z 8 60 22 iz 12 64zt 12 16 427 57* 13

19 20 10 374 1 2 2 53

13 17 5 215 7 5 7 212

32 * 13 34* 15 29 iz 8 43.5 f 12 20 64 33 29 74 64 67 30

1006 6114 315 1281289


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.+.......+.......+.......*. 20. 60.

0.0 40.

. . . . . + . . . . . .

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120 140

mo Fig. 3. Actuarial probability curves for remaining free of arrhythmic events in infarct survivors with left ventricular ejection < 0.30 (A), < 0.40 (B)

VFl who developed spontaneous VT had an abnormal signal-averaged ECG.

3.5. Predictors of arrhythmic events and total cardiac mortality

Shown in Table 4 are the univariate predictors of cardiac events during follow-up. These included the location of myocardial infarction (anterior myocardial infarction, P = 0.0017), decreased left ventricular EF < 0.40 (P = O.OOOl), inducible sustained VT (P = 0.0003), and inducible VFl (P = 0.01). The presence of late potentials and grade IVA and IVB ventricular arrhythmias on Holter monitoring did not have a significant prognostic value because of lack of specificity. How- ever, some signal-averaged ECGs of patients who developed an event were missing (Fig. 5).

These variables were then tested with a Stepwise

multivariate Cox model. This model demonstrated that decreased left ventricular EF (<0.40) (P = 0.0001) and inducible VT (P = 0.0000) were the only two multivariate predictors of cardiac events. Decreased left ventricular EF (P = 0.03), inducible VT (P = 0.0002) and inducible VFl (P = 0.048) were three multivariate predictors of arrhythmic events.

The prognostic value of each arrhythmia induction was rather low and is detailed in Table 5. The sensitivity and positive predictive value of the induction of a VT for the prediction of arrhythmic events was similar to that of non-invasive investigations, when two abnormal non-invasive investigations were combined.

3.6. Clinical application The study of the 42 patients who presented with

62 B. Brembilla-Perrot et al. / Internalional Journal of Cardiology 49 (1995) 55-65

.80 +

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.20 +

0.0 +

oonn.nn 00. n......nn...n. 0. nn.....n.........

o.......o. 0.. .O ct......... o....

o.....

. . . , . . . . . N

I Y

+ .+.......+.......+.......+.......+.......+.......+.......+..... 20. 60. 100 140 0.0 40. 80. 120 mo

Fig. 4. Actuarial probability curves for remaining free of cardiac events in infarct survivors with grade IVa, IVb Holter monitoring (Y) and with grade 0, I, II, III (N).

Table 4 Predictors of cardiac events and total cardiac events in survivors of acute myocardial infarction.

Variable Total cardiac Arrhythmic events events (P value) (P value)

Univariate predictors Anterior MI LVEF Grade 4A,4b HM Inducible SVT Inducible VFI LP

0.017 0.2 0.0001 0.01 0.01 0.02 0.0003 0.0001 0.78 0.01 0.14 0.1

Multivariate predictors LVEF Inducible SVT Inducible VFl

o.ooo1 0.016 0.0000 0.0002 0.12 0.023

MI, myocardial infarction; LVEF, left ventricular ejection fraction, HM, Halter monitoring; SVT, sustained ventricular tachycardia; VFI, ventricular flutter; LP, late potentials

spontaneous VT and/or a cardiac sudden death demonstrates that all but one of the patients had an abnormal non-invasive investigation, either a decreased left ventricular EF (< 40%) and/or abnormal signal-averaged ECG and/or grade IVa/IVb ventricular beats on Holter monitoring.

Patients with decreased left ventricular EF and abnormal Holter monitoring were at high risk of sudden death and these patients should be carefully followed during the first year after infarction: 13 of 61 patients with both abnormalities, decreased left ventricular EF (~40%) and grade IVa/IVb ventricular arrhytmias on Holter monitoring died suddenly. The risk of other cardiac events is high (4 cardiac deaths and 2 VT). The risk of sudden death was significantly (P < 0.001) increased in this group compared to the remaining patients (risk of sudden death g/431). Patients with late potentials and decreased left ventricular EF were at high risk of VT: 10 of 67 patients with both ab-


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10. 30. 50. 70. 90. 110 0.0 20. 40. 60. 80. 100 120 mo

Fig. 5. Actuarial probability curves for remaining free of cardiac events in infarct survivors with late potentials (LP) and without LP (0)

Table 5 Diagnosis value of different investigations for the prediction of arrhythmic events (VT and sudden death)

VT < 270 beats/min VT > 270 beats/min VT < and >

270 beats/mm EF < 40%+ ab HM EF < 4O%+LP

21 12

18 26 22

83 87

70 90 83

PPV NPV (W W)

21 95 12 92

18 97 26 98 22 98

VT < 270 beats/min, induction of a VT with a rate < 270 beats/min; VT > 270 beats/min, induction of a ventricular flutter; EF < 40%, decreased left ventricular ejection fraction; ab HM, grade IV ventricular premature beats on Holter monitoring; LP, late potentials. Se, sensitivity; Sp, specificity; PPV, positive predictive value; NPV, negative predictive value.

normalities developed spontaneous VT during the 1 to 4 years after infarction. The risk was significantly increased (P < 0.001) in this group compared to remaining patients (6 of 261 presented VT). The risk of sudden death (5167) was not significantly increased compared to remaining patients without both abnormalies (g/261).

4. Discussion

Since the report of Green [S], the usefulness of programmed ventricular stimulation to identify patients at risk for VT and/or sudden cardiac death after myocardial infarction has been evaluated in several studies [l- 111. The most recent studies [l-4] demonstrated that the induction of a sustained monomorphic VT < 270 beats/min was associated with a high risk of VT and sudden cardiac death. Similar data were found in the pre-


sent study: compared to patients with negative electrophysiologic study, the patients with inducible VT < 270 beats/mm had a risk of VT which increased from 2% to 12% (P < 0.01) and a risk of sudden death which increased from 3% to 9% (P < 0.05).

The importance of the present study is the longer follow-up than in other studies; in previous studies, the follow-up did not exceed 2 years [l-l 11. After a longer follow-up (> 4 years), the patients could develop spontaneous VT. The significance of these tachycardias needs to be discussed, because the substrate of ventricular arrhythmias could have been changed during this long follow-up. However there was no reinfarction or cardiac heart surgery in these patients which could explain a change in arrhythmia substrate.

The second interesting area of the present study is the significance of VFl. In previous studies [1,2,4], the risk of event during follow-up was related to the cycle length of inducible VT: an event during follow-up was more likely if cycle length of VT was 230 ms or more: in the present study the total risk of arrhythmic event was significantly increased in patients with inducible VFl compared to the patients without inducible arrhythmias. Moreover, the incidence of arrhythmic events was smaller in patients with inducible VFl (12%) than in patients without inducible VT < 270 beats/min (4%). The patients with inducible flutter who developed an arrhythmic event had either grade IV ventricular ectopy (n = 7), or a depressed left EF (<30%) or late potentials. The patients with inducible flutter who presented a sudden death had always grade IV ventricular ectopy. Those who developed VT had late potentials. Patients with inducible VFl and EF > 30%, normal holter monitoring and signal-averaged ECG had an excellent prognosis. Therefore, because of its low sensitivity, programmed stimulation could be in- dicated only in the patients with one abnormal non-invasive investigation. Those patients with two abnormal investigations should be more carefully followed and probably treated. The patients with decreased left ventricular EF and abnormal Holter monitoring, at high risk of sudden death during the year following AM1 could require a preventive medical or electrical treat-

ment. The patients with decreased left ventricular EF and late potentials should be followed during at least 4 years to detect spontaneous VT.

Possible limitations of this study need to be discussed: (1) Signal-averaged ECGs were recorded in only 328 patients with narrow QRS com- plexes. This may have limited the predicted value for arrhythmic events in this study; (2) Since 1988, patients with inducible monomorphic VT < or > 270 beats/min were treated using an antiarrhythmic drug. The therapy could have changed the follow-up. However the treatment was controlled. We have not observed proarrhythmic effects with class I antiarrhythmic drugs; (3) The stimulation protocol was changed in 1987 (2 vs. 3 extrastimuli). The use of a third extrastimulus increases the induction of ventricular arrhythmias [6,12-181. In the present study the third extrastimulus was responsible for a significant increase in VF induction from 4% to 15% (P < O.Ol), while the VT induction (< 270 beats/min and > 270 beats/min) was not significantly increased (respectively from 17% to 22% and from 14% to 15%). Among 28 patients who presented an arrhythmic event and who had inducible VT, the VT was induced by 2 extrastimuli in 25 patients; (4) Because the study began in 1983, only 10% of patients received thrombolytic therapy, which could have limited the size of infarction.

In conclusion, we confirm the utility of programmed ventricular stimulation after an AM1 for predicting an arrhythmic event. However, the positive predictive value of inducible sustained monomorphic VT (> 270 beats/min) for the occurrence of an arrhythmic event was low (21%) as in previous studies [l-4]. The risk of arrhythmic events was increased in patients with inducible VFl, but the positive predictive value of the inducible rapid VT for the occurrence of an arrhythmic event was low (12%). Only patients with inducible VFl and with grade IV of Lown ventricular arrhythmias on Holter monitoring or late potentials were at risk of events.

After AMI, the patients could develop arrhythmias in the two first years and also 4 years later. In practice, all arrhythmic events were noted in patients with an abnormal non-invasive investigation. Therefore, because of the low sensitivity of


programmed stimulation we think that programmed stimulation should not be routinely in- dicated, but only in patients with an abnormal investigation either a decreased left ventricular ejection or an abnormal Holter monitoring or signal-averaged ECG.

References

[l] Breithardt G, Borggrefe M, Haerten K. Ventricular late potentials and inducible ventricular tachyarrhythmias as a marker for ventricular tachycardia after myocardial infarction. Eur Heart J 1986; 7 (suppl A): 127-134.

[2] Denniss R, Richards DA, Cody DV, Russell PA, Young AA, Cooper MJ, Ross DL, Uther JB. Prognostic significance of ventricular tachycardia and fibrillation induced at programmed stimulation and delayed potentials detected on the signal-averaged electrocardiograms of survivors of acute myocardial infarction. Circulation 1986; 74: 731-745.

[3] Tesaka Y, Nogami A, Aonuma K, Nitta J, Chun YH, Fujiwara H, Hiraoka M. Prognostic significance of sustained monomorphic ventricular tachycardia induced by programmed ventricular stimulation using up to triple extrastimuli in survivors of acute myocardial infarction. Am J Cardiol 1990; 65: 1057-1063.

[4] Bourke JP, Richards DAB, Ross DL, Wallace EM, MC Guire MA, Uther JB. Routine programmed electrical stimulation in survivors of acute myocardial infarction for prediction of spontaneous ventricular tachyarrhythmias during follow-up: results, optimal stimulation protocol and cost-effective screening. J Am Co11 Cardiol 1991; 18: 780-788.

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[7] Hamer A, Vohra J, Hunt D, Sloman JG. Prediction of sudden death by electrophysiologic studies in high risk patients surviving acute myocardial infarction. Am J Cardiol 1982; 50: 223-229.

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[l l] Roy D, Marchand E, Theroux P, Waters D, Pelletier G, Bourassa M. Programmed ventricular stimulation in survivors of an acute myocardial infarction. Circulation 1985; 72; 487-494.

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[13] Mann DE, Luk JC, GriftIn JC, Herre JM, Limacker MC, Magro SA, Robertson NW, Wyndham CRC. Induction of clinical ventricular tachycardia using programmed stimulation: value of third and fourth extrastimuli. Am J Cardiol 1983; 52: 501-506.

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Programmed ventricular stimulation in survivors of acute myocardial infarction: long-term follow-up

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Transcript of Programmed ventricular stimulation in survivors of acute myocardial infarction: long-term follow-up