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J Am Coll Cardiol, 2001; 37:1901-1907
© 2001 by the American College of Cardiology Foundation
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CLINICAL STUDY: ELECTROPHYSIOLOGY

Value of programmed ventricular stimulation for prophylactic internal cardioverter-defibrillator implantation in postinfarction patients preselected by noninvasive risk stratifiers

Claus Schmitt, MDa, Petra Barthel, MDa,b, Gjin Ndrepepa, MDa,b, J.ürgen Schreieck, MDa,b, Andreas Plewan, MDa,b, A. Schömig, MDa,b and Georg Schmidt, MDa,b

a Deutsches Herzzentrum München, Munich, Germany
b 1. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany

Manuscript received August 17, 2000; revised manuscript received December 28, 2000, accepted February 15, 2001.

Reprint requests and correspondence: Dr. Claus Schmitt, Deutsches Herzzentrum München, Lazarettstrasse 36, D-80636 München, Germany
schmitt{at}dhm.mhn.de


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES

The aim of this prospective study was to evaluate the role of programmed ventricular stimulation (PVS) after noninvasive risk stratification to identify a subgroup of acute myocardial infarction (AMI) survivors considered at risk for ventricular arrhythmias and whether these patients could benefit from internal cardioverter-defibrillators (ICDs).

BACKGROUND

The predictive value of noninvasive and invasive risk stratifiers after AMI has been questioned. The question of whether the group of patients with inducible monomorphic ventricular tachycardia (VT) after AMI could profit from ICD implantation is unanswered.

METHODS

A consecutive series of 1,436 AMI survivors was screened noninvasively by Holter monitoring, heart rate variability, ventricular late potentials, and ejection fraction. A subgroup of 248 patients (17.3%) were identified as high-risk patients and scheduled for PVS. Due to the study design, 54 patients >75 years were excluded; thus, 194 patients were eligible for PVS. Triple extrastimuli at two paced cycle lengths (600 ms and 400 ms) were applied.

RESULTS

In a subgroup of 98 (51%) high-risk patients, PVS was performed; 21 patients had an abnormal response, and in 20 patients an ICD was implanted. During a mean follow-up of 607 days the arrhythmic event rate (sudden cardiac death, symptomatic VT, cardiac arrest) was 33% with a positive electrophysiological test versus 2.6% (p < 0.0001) with a negative electrophysiological test. A subgroup of 96 high-risk patients declined electrophysiological study. In this nonconsent group, cardiac mortality (combined sudden and nonsudden) was significantly higher (log-rank chi-square 9.38, p = 0.0022, relative risk 4.7, 1.6 to 13.9) compared to the group guided by electrophysiological testing and consecutive ICD implantation.

CONCLUSIONS

After a two-step risk stratification, PVS is helpful in selecting a subgroup of AMI survivors without spontaneous ventricular arrhythmias who benefit from prophylactic ICD implantation.

Abbreviations and Acronyms
  AMI = acute myocardial infarction
  ECG = electrocardiogram, electrocardiographic
  ICD = internal cardioverter-defibrillator
  PVS = programmed ventricular stimulation
  RR = relative risk
  VF = ventricular fibrillation
  VT = ventricular tachycardia

Several studies, using both noninvasive and invasive screening tests, have identified a relatively large number of risk factors that predict the future occurrence of arrhythmic events after acute myocardial infarction (AMI) (1–12). Still, it is difficult to detect with a sufficient sensitivity, specificity and predictive power the subgroup of AMI survivors bound for future development of ventricular tachycardia (VT) or ventricular

fibrillation (VF) in the postdischarge period. Most studies have demonstrated that programmed ventricular stimulation (PVS) represents a strong marker of subsequent occurrence of life-threatening ventricular tachyarrhythmias (11–16). However, a large-scale or routine use of PVS as a risk stratifier in survivors of an AMI has been restricted mostly by its low predictive value (12). The disappointing results with class I (17,18) and more recently class III antiarrhythmic drugs (19–21) in survivors of an AMI have further questioned the value of prophylactic antiarrhythmic treatment in these patients. The recently proposed two-step strategy in risk stratification of AMI survivors using noninvasive and invasive tests (22,23) and the encouraging results with internal cardioverter-defibrillators (ICDs) (24–27) have paved the way for a realistic evaluation of the indications and the value of PVS for arrhythmic risk stratification after AMI.

Therefore, we addressed the question of whether PVS could be used to identify with a sufficient predictive value a subgroup of AMI survivors without spontaneous sustained ventricular arrhythmias, previously identified as high-risk patients by noninvasive screening tests, who are prone to future development of life-threatening ventricular arrhythmias and whether this group of patients could profit from ICD therapy.


   Methods
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 Methods
Results
 Discussion
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Patient population.   A total of 1,436 patients with a confirmed diagnosis of AMI were enrolled into a prospective risk-stratification study between December 1994 and December 1999 at our hospital. Myocardial infarction was diagnosed according to clinical, electrocardiographic (ECG), and enzymatic criteria. All patients underwent coronary angiography, and >90% of patients had a coronary intervention (coronary angioplasty and/or stenting or thrombolysis). In cases involving the narrowing of other (noninfarct-related) arteries of >70%, concomitant angioplasty and/or stenting was performed the second week after the acute event. Patients underwent a noninvasive risk-stratification protocol that included measurement of left ventricular ejection fraction, ventricular ectopy, and heart rate variability in 24-h Holter ECG and detection of ventricular late potentials by signal-averaged ECG before discharge. Normal values for signal-averaged ECG (with 40-Hz high-pass filtering) were considered: the root-mean-square voltage of the terminal 40 ms of the signal-averaged complex >25 µV, duration of the low amplitude signals (<40 µV) in the terminal 40 ms of the QRS complex ≤40 ms, and duration of total filtered QRS complex ≤115 ms. An abnormal signal-averaged ECG was defined as abnormal values of one or more variables. In patients with bundle branch block (22 patients) and prior implanted pacemaker (1 patient), the signal-averaged ECG was not performed.

Of the total patient population, 248 (17.3%) were identified as high-risk patients by this protocol and were scheduled to undergo a PVS for further risk assessment and possible ICD implantation. Table 1 shows the noninvasive scoring system. Patients with a risk score ≥3 were considered high-risk and were advised to undergo invasive risk stratification by PVS. Twenty-six patients in the entire study population developed spontaneous monomorphic VT in the subacute stage of their AMI (>24 h). Patients with spontaneous monomorphic VT underwent electrophysiological study and ICD implantation but are not included in the study.


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  		Table 1 Noninvasive Risk Assessment

 
Electrophysiological study.   An electrophysiological study was performed the third week (median 18 days) after the acute event. After written informed consent was obtained, patients underwent PVS in the postabsorptive state while receiving no antiarrhythmic drugs for a period of time >5 plasma half-lives. Electrode catheters were inserted percutaneously from the femoral groin and positioned in the heart under fluoroscopic guidance at the atrioventricular junction for His bundle recording and at the right ventricular apex. Electrical stimulation of the heart was performed using an external stimulator (UHS20, Biotronik, Berlin, Germany) that produced rectangular impulses 2 ms in duration at twice the diastolic threshold. Bipolar intracardiac electrograms and 12-lead surface ECGs were simultaneously acquired (BARD Labsystem, Lowell, Massachusetts). Intracardiac electrograms were amplified, digitized at 1000 Hz, filtered (30 to 500 Hz), and recorded into an optical disk.

Stimulation protocol.   Stimulation protocol consisted of triple extrastimuli (S2S3S4) delivered at two paced cycle lengths (S1S1 600 ms and 400 ms) at the right ventricular apex. Extrastimuli were applied after eight-beat drive trains with a 3-s interdrive pause. Ventricular extrastimuli were introduced beginning late in diastole and moved progressively earlier in 10-ms steps until either ventricular refractoriness or a coupling interval of 180 ms was reached. The second (S3) and the third (S4) extrastimuli were delivered after the S1S2 interval (S1S2 and S2S3 intervals for S4) was fixed 50 ms longer than ventricular refractoriness of S2 and S3, respectively. The protocol is terminated prematurely if a sustained monomorphic VT with a cycle length ≥230 ms, a sustained VT with a cycle length <230 ms, or VF is induced. Only sustained monomorphic VT with a cycle length ≥230 ms was considered as an abnormal response.

The following definitions were employed: 1) sustained monomorphic VT was a VT faster than 100 beats/min with a regular rate and consistent beat-to-beat morphology that lasted more than 30 s or required immediate termination because of hemodynamic collapse; 2) nonsustained VT was a run of six or more nonpaced ventricular beats that terminated spontaneously within 30 s; 3) polymorphic VT was a VT characterized by frequent changes in QRS morphology and/or axis; and 4) VF was considered a ventricular rhythm characterized by totally disorganized activity and no discernible QRS complexes in the surface ECG.

ICD implantation.   The ICDs were implanted under local anesthesia subcutaneously or subpectorally in the left subclavian groove. The VVI-ICDs with antitachycardia pacing capabilities of various manufacturers were used (CPI-Guidant, Medtronic, Intermedics, Ventritex). The cutoff rate for detection of VT and VF was set high (mean cycle length 352 ± 46 ms, mean cycle length 303 ± 31 ms, respectively) to avoid inappropriate activation of the device.

Follow-up.   Follow-up information was obtained at the time of revisits at the ambulatory arrhythmia clinic or by telephone contact with patients and patients’ private physicians. The end points of the follow-up period were death and development of sustained ventricular tachyarrhythmias. Patients with implanted ICDs were seen at one month after discharge and then at three-month intervals throughout the follow-up and whenever they reported palpitations or shocks. During each follow-up visit, patients were examined and devices interrogated to determine spontaneous episodes with RR intervals and stored electrograms and the appropriateness of the delivered therapy. Modes of death were established from written records and by interviewing witnesses and/or attending physicians. Sudden cardiac death was defined as instantaneous, unexpected death, death within 1 h of the onset of symptoms or unexpected death during sleep. Nonsudden cardiac death was considered to be caused by progressive deterioration of the myocardial dysfunction. Deaths related to diseases in other systems were considered noncardiac deaths. For the purpose of calculation of survival statistics, both the occurrence of documented sustained VT or VF (including information from the interrogation of ICD after ICD interventions) and sudden cardiac death were considered as arrhythmic events.

Statistical analysis.   Data are presented as mean ± SD, percentage or range. Continuous variables were compared by using the Mann-Whitney U test. Discrete variables were compared by chi-square test or the Fisher exact test. Survival curves were estimated using the Kaplan-Meier life tables and were compared with a log-rank test. The Cox proportional hazards survival model was used to calculate the relative risk with use of betas (regression coefficients). A p value <0.05 was considered statistically significant.


   Results
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 Methods
 Results
Discussion
 References
 
Of the noninvasively, preselected 248 high-risk patients, 54 were older than age 75. According to the study design, only patients of the high-risk group ≤75 years of age underwent electrophysiological study. Thus, 194 patients (25 patients, 13% with an ejection fraction ≥40%) were eligible for electrophysiological study and possible ICD implantation. In 96 patients (49%) PVS was not performed. The reasons for not performing electrophysiological study included refusal from the patient, refusal from the patient’s private physician, or other reasons.

Comparison of the patients with and without electrophysiological testing.   Programmed ventricular stimulation was performed in 98 patients (51%). Clinical characteristics of the patients who underwent electrophysiological study and those who did not perform the test are given in Table 2. As seen from Table 2, there were no statistically significant differences related to sex, localization of AMI, coronary interventions in the acute stage of AMI, risk factors for coronary artery disease, extension of coronary artery disease, follow-up therapy, degree of noninvasively defined risk (score points), and overall arrhythmic event rates. However, electrophysiologically tested patients were younger, had a higher peak creatine kinase level and a lower incidence of sudden cardiac death and overall cardiac mortality (sudden and nonsudden) as compared with the group in whom the electrophysiological study was not performed.


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  		Table 2 Clinical Characteristics of Patients Who Underwent Electrophysiological Study (EP) Versus Those Who Did Not

 
Results of PVS.   Results of PVS are shown in Table 3. Sustained monomorphic VT was evoked in 21 patients (22%). All other responses were considered as nonspecific. Clinical characteristics of the patients with an abnormal response versus those with a nonspecific response or negative study are depicted in Table 4. Patients with an abnormal response were older and had a significantly higher incidence of arrhythmic events during follow-up. All other clinical characteristics were equally distributed between the two groups. No vascular or thrombotic complications were observed during electrophysiological study. In 20 patients with an abnormal response, ICDs were implanted 5 ± 4 days (median 3 days; interquartile range 2 to 6 days) after the electrophysiological study.


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  		Table 3 Results of Electrophysiological Study

 

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  		Table 4 Clinical Characteristics of Patients With a Positive and Negative Electrophysiological (EP) Study

 
Follow-up data.   Patients were followed for 607 ± 424 days (up to 1,717 days). During the follow-up period there were altogether 24 deaths (12%). Of these, 21 deaths were of cardiac origin, whereas 3 deaths were of noncardiac origin. Of the cardiac deaths, 10 were sudden cardiac deaths (1 death in the group with a negative electrophysiological study and 9 deaths in the group not tested electrophysiologically). Eleven deaths were nonsudden (3 deaths in the group with electrophysiological study and 8 deaths in the group not tested electrophysiologically). Thus, sudden cardiac death (1% vs. 9%, p = 0.009) and overall cardiac mortality (4% vs. 18%, p = 0.002) were significantly higher in the group not tested electrophysiologically as compared to the group that underwent electrophysiological study and ICD implantation in cases of an abnormal response. Three deaths of noncardiac origin occurred in the group not tested electrophysiologically.

Predictive value of PVS and intervention of ICD.   In 7 of 21 patients with an implanted ICD (33%), the ICD interventions as shock discharge (4 patients), antitachycardia pacing (2 patients), or both (1 patient) were recorded. Analysis of stored electrograms revealed that detected arrhythmia at the time of ICD intervention was monomorphic VT (6 patients) and polymorphic VT (1 patient). Arrhythmic event rate (sustained ventricular arrhythmias causing ICD intervention plus sudden cardiac death) was significantly higher in the group with a positive electrophysiological test plus ICD implantation as compared with the group with a negative electrophysiological test (33% vs. 2.6%, p < 0.0001). Patients who suffered an arrhythmic event had a lower ejection fraction than those who did not experience such events (24.5 ± 6.9% vs. 33.2 ± 7.6%, p < 0.001). No arrhythmic events occurred in the 26 patients with a nonspecific response after PVS.

Survival analysis and relative risk estimation.   The Kaplan-Meier survivorship curves for arrhythmic events in patients with a positive electrophysiological test plus ICD implantation and the patients with a negative electrophysiological test are presented in Figure 1A. It can be seen from the survivorship curves that significant differences existed in the incidence of arrhythmic events in patients with a positive test versus those with a negative test (log-rank chi-square 18, p < 0.0001) and that the majority of events occurred during the first year of follow-up. Relative risk (RR) was 13.8 (2.9 to 66.3). Figure 1B shows the Kaplan-Meier survivorship curve for cardiac mortality (combined sudden and nonsudden) in the group that underwent electrophysiological testing and ICD implantation (patients with a positive test) versus the group that was not tested electrophysiologically. Again, significant differences were seen in the cardiac mortality rates between the two groups (log-rank chi-square 9.38, p = 0.0022, RR 4.7 [1.6 to 13.9]), with the majority of deaths occurring in the first year of follow-up. Survivorship analysis showed that the risk score had an inverse relationship with arrhythmia-free interval (Fig. 2).



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  		Figure 1 (A) Kaplan-Meier curve for arrhythmic events in patients with a negative electrophysiological test versus patients with a positive electrophysiological test plus internal cardioverter-defibrillator (ICD) implantation. (B) Kaplan-Meier survivorship curve for cardiac mortality (combined sudden and nonsudden) in the group that underwent electrophysiological testing plus ICD implantation versus the group of patients not tested electrophysiologically (no-consent group). PVS = programmed ventricular stimulation.

 


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  		Figure 2 Kaplan-Meier survivorship curve for arrhythmic events in patients with different risk scores. LVEF = left ventricular ejection fraction.

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
The use of PVS after AMI.   The mortality rate in the first year after AMI is about 10%, and there is a continuing mortality in the subsequent years of 4% per annum (28). It has been estimated that the majority of these deaths are caused by ventricular tachyarrhythmias (29). Based on the assumption that PVS tests the ability of a potential arrhythmogenic substrate to maintain the sustained reentrant excitation, this technique has been used in numerous studies for arrhythmic risk stratification after AMI. However, conflicting results regarding the predictive power (30–33), debate over whether comparable information can be taken from a combination of noninvasive tests (34,35), low predictive value (11), and the invasive nature associated with potential morbidity (36) have all prevented large-scale use of PVS as a screening tool in patients after AMI. Furthermore, the use of PVS as a screening test after an AMI is marked by such substantial methodological differences that comparison of studies is almost impossible. The current opinion is, however, that PVS prognosticates the subsequent development of life-threatening ventricular arrhythmias after AMI, and it should have a role in clinical practice to screen high-risk patients for arrhythmia development after AMI.

Main findings of our study.   The main findings of our study can be summarized as follows: 1) The combined use of a series of noninvasive tests such as left ventricular ejection fraction, signal-averaged ECG, and Holter monitoring with heart rate variability analysis can effectively preselect a subgroup of patients, among the patients without spontaneous occurrence of VT or VF in the acute phase of AMI, at sufficiently high risk (17% of the total AMI population in this study), to warrant the use of PVS as a risk stratifier. This two-step strategy significantly reduces the number of patients exposed to PVS and to its possible side effects. 2) A positive electrophysiological study had a 33% predictive power to identify patients (7 in 21 patients) that developed VT during follow-up.

In contrast, a negative electrophysiological study identifies a group of patients who have a less than 3% (2 in 77 patients) chance of developing sudden cardiac death in nearly two years after index event. Of note, none of the 26 patients (26%) with inducible fast sustained VT (cycle length <230 ms), polymorphic VT or VF developed life-threatening ventricular arrhythmias during the mean follow-up of almost two years. This corroborates data from an earlier large-scale Australian study in 1,209 AMI survivors undergoing PVS (11). Previous studies (22,37), but not a recent one (23), have reported a significant increase in the positive predictive value using a two-step strategy in the risk-stratification process. Pedretti et al. (22) and Zoni-Berisso et al. (37) reported an increase of positive predictive value from 30% to 65% and from 10% to 66%, respectively.

Conversely, Andresen et al. (23) reported an 18% predictive value after using a two-step strategy for arrhythmic risk stratification after AMI. However, in the Andresen et al. (23) study only two premature beats during PVS were used, thus limiting the sensitivity and predictive value of PVS as already shown by Bourke et al. (11). Overall, differences in the noninvasive tests used, number of extrastimuli, definition of an abnormal response at electrophysiological study, and time of electrophysiological study after AMI could account for the existing differences between our study and their study (23). 3) Survivors of an AMI without spontaneous sustained ventricular arrhythmias, defined as a high-risk group by noninvasive tests and with inducible sustained monomorphic VT, profit from ICD therapy. A significant reduction of sudden cardiac death was observed in the group that was tested electrophysiologically with consecutive ICD implantation in cases of an abnormal response to PVS compared to patients that were not electrophysiologically assessed (1% vs. 9%, p = 0.009).

Before considering this group of patients as suitable candidates for an ICD therapy, we specifically address the aggressiveness of the coronary interventions in the acute phase of AMI. With >90% coronary intervention rate (coronary angioplasty and/or stenting and thrombolysis) our patients could represent a group with the best characterization of arrhythmogenic substrate to date. Concomitantly with dilation and/or stenting of occluded artery, other arteries with narrowings ≥70% were also treated. These revascularization interventions, by restoring coronary blood flow, could have reduced the extent of existing chronic ischemia or the rate of repeated acute ischemic events. That the presence of chronic ischemia could affect the ICD therapy is demonstrated by the results of the CABG-Patch trial (38), which failed to demonstrate benefits of ICD therapy. In addition, results of the CABG-Patch trial—in which patients were screened on the basis of low ventricular ejection fraction and the presence of ventricular late potentials—justify maximal efforts, including invasive screening and interventions to characterize the arrhythmogenic substrate in order to increase the benefits of ICD therapy.

Study limitations.   Although a total of 194 patients were eligible for electrophysiological study, only 98 of them (51%) were assessed with ventricular stimulation. This result was predominantly due to reluctance to undergo this invasive test once its research nature was explained. Additionally, the absence of spontaneous arrhythmias could also have influenced the decision to undergo the test from both patients and patients’ private physicians. Other studies have also reported a reluctance of a large proportion of the patients to undergo electrophysiological study after suffering an AMI (11,34). The patients not studied with ventricular stimulation were similar to the patients that were assessed with ventricular stimulation for most of the characteristics, including ejection fraction, degree of noninvasively defined arrhythmic risk, extension of coronary artery disease, and drug therapy during follow-up. Nevertheless, the nonrandomized nature of our study could not exclude some bias, especially in encouraging the patients to undergo the test. The accuracy of collecting the follow-up information is different in patients with implanted ICD compared to patients without implanted ICD. In patients with implanted ICD, the analysis of arrhythmic events was based on interrogation of ICD. In the patients without ICD, analysis of arrhythmic events was based on traditional definitions. Thus, some nonfatal ventricular arrhythmias could have escaped from documentation in groups without implanted ICD.

Conclusions.   The use of PVS is helpful in selecting a subgroup of AMI survivors without spontaneous occurrence of sustained ventricular arrhythmias, defined as a high-risk group based on noninvasive screening tests that could profit from ICD therapy. A two-step risk-stratification strategy substantially reduces the number of patients who have to undergo PVS. This stratification strategy increases substantially the predictive value of PVS for future development of life-threatening ventricular arrhythmias in survivors of AMI and warrants prophylactic ICD implantation in light of induction of sustained monomorphic VT.


   References
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