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(Circulation. 1997;95:390-394.)
© 1997 American Heart Association, Inc.

Articles

Prediction of Outcome of Patients With Life-Threatening Ventricular Arrhythmias Treated With Automatic Implantable Cardioverter-Defibrillators Using SPECT Perfusion Imaging

Giuseppe Gioia, MD; Bruce Bagheri, MD; Charles D. Gottlieb, MD; David S. Schwartzman, MD; David J. Callans, MD; Frank E. Marchlinski, MD; Jaekyeong Heo, MD; Ami E. Iskandrian, MD

the Division of Cardiology, Department of Medicine, MCP Hahnemann School of Medicine, Allegheny University of the Health Sciences, Philadelphia, Pa.

	Abstract

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Background In the present study, we examined the predictors of outcome of 103 patients with coronary artery disease and left ventricular dysfunction who had life-threatening ventricular arrhythmias and were treated with implantable cardioverter-defibrillators with the use of single-photon emission computed tomography (SPECT).

Methods and Results During a mean follow-up of 29 months, there were 29 cardiac deaths. In comparison with patients who died, survivors had less diabetes mellitus (45% versus 19%, P<.007), higher left ventricular ejection fraction (23±9% versus 27±11%, P=.04), and fewer perfusion defects as determined with stress SPECT (15±5 versus 12±5, P<.004). Most of the perfusion defects were fixed, indicative of scarring; the extent of reversible defects did not differ (2±3 in survivors and 3±4 in nonsurvivors). Multivariate Cox survival analysis identified the number of fixed defects as the only independent predictor of death (²=10, P=.002). There were six deaths among 42 patients (14%) with <8 fixed defects compared with 23 deaths among 61 patients (38%) with 8 defects (P=.005). The 4-year survival was better in patients with <8 segmental fixed defects than in those with 8 fixed defects (80% versus 36%) (²=8, P=.005).

Conclusions The myocardial perfusion pattern is an important determinant of outcome in patients with life-threatening ventricular arrhythmias who are treated with a implantable cardioverter-defibrillator. The extent of scarring separates patients into high- and low-risk groups with a 2.7-fold difference in death rate.

Key Words: arrhythmias • imaging • prognosis • tomography • tachycardia

	Introduction

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Therapy with ICDs has assumed an important role in the treatment of patients with life-threatening ventricular tachyarrhythmias. It is generally accepted that the device reduces the incidence of sudden death.^{1 2 3 4 5 6} Candidates for ICD therapy may also be at risk of dying suddenly from asystole, myocardial infarction, or CHF.^{7 8} Previous studies have addressed the important role of LVEF as a predictor of patient outcome.^{9 10 11} The purpose of the present study was to examine the association between measures of LV function, myocardial perfusion, and clinical evaluation on the one hand and cardiac death on the other hand. Such results may help identify patients who will most likely benefit from device implantation and those in whom such therapy alone may not be sufficient to prevent subsequent death.

	Methods

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Patient Selection
This study included 103 patients with CAD and life-threatening ventricular arrhythmias who were treated with ICDs between May 1987 and May 1995. The demographics are given in Table 1. This group of patients represented 25% of the patients with device implants during the same time period. Of the remaining 314 patients not included in the study, 63 were lost to follow-up, 62 had incomplete data, and 58 had primary cardiomyopathy. A comparison of clinical characteristics of the study patients with those of the remaining 131 patients who had CAD but had no stress myocardial perfusion imaging showed that the two groups were comparable.

View this table: [in this window] [in a new window]   Table 1. Pertinent Data for the Study Group

The diagnosis of CAD was based on abnormal coronary angiogram (95 patients) or Q-wave presence on the ECG (8 patients). The LVEF was measured with radionuclide angiography in 74 patients, with contrast ventriculography in 22 patients, and with two-dimensional echocardiography in 7 patients. Of the 103 patients, 67 had hemodynamically poorly tolerated monomorphic ventricular tachycardia, 29 were survivors of sudden cardiac death, and the remainder had syncope with inducible monomorphic ventricular tachycardia as determined with electrophysiological testing. All patients had electrophysiological studies performed with the use of standard techniques as we described previously.^{12 13} Monomorphic ventricular tachycardia was induced in 73 patients (71%). The ICD was implanted through the use of thoracotomy in 61 patients (59%) and transvenously in 42 patients (41%). In 25 patients, revascularization procedures were also performed at the time of ICD implantation; 19 had coronary artery bypass graft surgery, and 6 had coronary angioplasty. These patients had perfusion imaging performed before ICD implantation. Table 2 is a summary of concomitant drug therapy; the drug assignment was based on the medication taken by the patient on two consecutive follow-up visits.

View this table: [in this window] [in a new window]   Table 2. Pharmacological Therapy in the Study Patients

SPECT Imaging Protocol
The stress modality was exercise in 25 patients and pharmacological (adenosine or dipyridamole) in 78 patients. The SPECT imaging was done with ²⁰¹Tl in 81 patients and with ^99mTc sestamibi in 22 patients. The SPECT images were obtained at 5±9 months from ICD implantation (<6 months in 72 patients and 6 months in 31 patients). The SPECT images were obtained before ICD implantation in 72 patients and after implantation in 31 patients. There were no events between the time of ICD implantation and SPECT imaging. Our methods of stress testing, image acquisition, and analysis have been described in detail.^{14 15 16} Semiquantitative analysis of the images was performed on the basis of 20 segments per patient. Apical, mid, and basal short-axis tomograms were divided into six segments each, and a midventricular vertical long-axis tomogram was used to assess the anteroapical and inferoapical segments. Perfusion defects were subdivided into those that were fixed and those that were reversible. Lung thallium uptake was assessed visually and graded on a scale of 1 (normal) to 3 (severely increased), and LV dilation was assessed as present or absent.

Follow-up information was obtained by telephone interviews with the patients, family members, or treating physicians and from review of medical records and electrophysiology charts. In most patients, we could not determine whether the death was sudden or nonsudden.

Statistical Analysis
All descriptive data are reported as mean±SD. Statistical analysis was done with the Student's t test for continuous variables and the ² test for discrete variables. Nonparametric Wilcoxon rank-sum test was used when indicated.¹⁷ Cox proportional hazards regression analysis was used to identify predictors of survival.^{17 18 19} The following variables were entered in the analysis: age, sex, previous infarction, medications (entered as individual agents), LVEF, number of diseased vessels, diabetes mellitus, presence of ischemia, number of perfusion defects (total, fixed, or reversible), LV dilation, and increased lung thallium uptake. The EF was entered as a continuous variable and dichotomized to 30% or <30%. The number of defects were entered as continuous variables. Survival curves were generated with the Kaplan-Meier method, starting from the day of implantation. Differences between survival curves were assessed using the log-rank method.¹⁷

	Results

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The patients had extensive CAD (2.4±0.8 diseased vessels per patients), elevated LV end-diastolic pressure (23±8 mm Hg), LV dilation with increases in end-diastolic (322±108 mL) and end-systolic (247±104 mL) volumes, and reduced LVEF (26±11%). All patients had abnormal SPECT images; reversible defects were present in 48 patients (47%). There was a mean of 10±6 segments with fixed defects and 2±4 segments with reversible defects (partial or complete). There was LV dilation in 85 patients (83%) and increased lung thallium uptake in 52 of the 81 patients who underwent thallium SPECT (64%).

Comparison Between Survivors and Those Who Died After ICD
During a mean follow-up of 29±20 months (range, 0.2 to 84), there were 29 cardiac deaths (28%), and a minimum of one device discharge was reported by 55 patients (53%). The clinical, angiographic, and radionuclide data for the survivors and for nonsurvivors are given in Table 3. The variables that differed between the survivors and nonsurvivors include the presence of diabetes mellitus (P=.007), the LVEF (P=.04), the number of diseased vessels (P=.04), the total number of abnormal segments (P=.004), and the number of fixed defects (P=.003) (Fig 1). The number of reversible defects, lung thallium uptake, LV dilation, and age were similar for the two groups. Most of the medications were similar for the two groups with the exception of amiodarone therapy (Table 2).

View this table: [in this window] [in a new window]   Table 3. Comparison of Clinical, Angiographic, Hemodynamic, and Radionuclide Data in Patients Who Died and Those Who Survived

View larger version (51K): [in this window] [in a new window]   Figure 1. The SPECT perfusion pattern in survivors and nonsurvivors during the follow-up period. The survivors had less-extensive defects and less-fixed defects.

Predictors of Death
Univariate Cox survival analysis identified the LVEF (²=4.3, P=.04), number of diseased vessels (²=4.0, P=.03), ß-blocker therapy (²=4.0, P=.04), number of abnormal segments (²=7, P=.007), and number of fixed defects (²=10, P=.002) as important predictors of death. The age and sex were not predictors. Multivariate survival analysis showed the number of fixed defects on SPECT to be the only independent predictor of death (²=10, P=.002). There were more deaths in patients with 8 fixed defects than in patients with <8 fixed defects (23 of 61 [38%] versus 6 of 42 [14%], P=.005) (Fig 2). The 4-year survival was 80% in those with <8 fixed defects and 36% in those with 8 defects. There were 11 deaths among 48 patients (23%) with LVEF of 30% and 18 deaths among 55 patients (33%) with LVEF of <30% (P=NS). The 4-year survival was similar in patients with LVEF 30% or <30% (67% versus 55%). The number of fixed defects remained the only independent predictor of death (²=10, P=.002) when the analysis was limited to the 74 patients in whom the LVEF was measured with the use of radionuclide angiography. Although a statistically significant correlation was found between LVEF and number of fixed defects (r=-.57, P=.001), there was considerable scatter around the line of regression, consistent with prior reports.²⁰ The univariate and multivariate predictors of death in the patients who had SPECT within 6 months of ICD implantation or in patients who had SPECT before ICD implantation were similar to those in the entire group of patients.

View larger version (12K): [in this window] [in a new window]   Figure 2. Kaplan-Meier survival curves in patients with <8 fixed defects (representing <40% of the myocardium) and those with 8 defects.

Impact of Revascularization
There was no difference in mortality between patients treated with ICD alone and those treated with combined ICD and revascularization (27% versus 32%, P=NS). The patients who had coronary revascularization were comparable to those who did not in clinical and angiographic data but had more reversible defects (4±4 versus 2±4, P=.02). There was no difference in inducibility of ventricular tachycardia at the time of electrophysiological study between those who had or did not have coronary revascularization (75% versus 75%). Of the 78 patients treated with device therapy alone, 30 patients had evidence of myocardial ischemia on SPECT imaging. There were 10 deaths among the 30 patients (33%) with ischemia and 11 deaths among the 48 patients without ischemia (23%, P=NS). When the combined end points of cardiac death and device discharge were considered, there again was no statistically significant difference between patients with ischemia and those without (63% versus 67%, P=NS). Of the 78 patients with ICD alone, 42 had shocks and 34 did not (we were missing data for 2 patients). Ischemia was detected in 12 patients (29%) with shocks and in 17 patients (50%) without shocks (P=NS). In 43 patients with stored ECGs, ischemia was detected in 9 of 23 patients (39%) with appropriate shocks and in 8 of 20 patients (40%) with no shocks or shocks due to supraventricular tachycardia. There was no correlation between presence and number of reversible segments (0, 2, 3) and presence and number of shocks (0, 1, and 2) (±SD=0.13±0.09).

	Discussion

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The results of this study show a fairly high death rate after ICD implantation in patients with CAD, LV dysfunction, and life-threatening ventricular arrhythmias. The extent of scarring separated the patients into high- and low-risk groups: those with scarring involving 8 segments (or 40% of the myocardium) had a 2.7-fold higher death rate than did those with less scarring (4-year survival, 80% versus 36%) (Fig 2). Although the LVEF was predictive of survival by univariate survival analysis, the 30% cutoff point did not separate patients into high- and low-risk groups. The survival rate at 4 years was 67% in patients with LVEF of 30% and 55% in those with LVEF of <30%. When the results of myocardial perfusion imaging and LVEF were analyzed using a multivariate Cox survival model, the number of fixed defects was the only independent predictor of survival. Previous studies have demonstrated higher mortality in patients with LVEF of <30%: 14% to 43% at 3 years compared with 3% to 15% in patients with LVEF of 30%.^{6 7 8 9 10} Patient selection may account for the differences between our results and those of previous studies. In the study by Kim,⁸ almost 25% of the patients had diseases other than CAD, and the mean LVEF was higher than that in our patients (35% versus 26%). Our series of patients is larger and composed exclusively of patients with CAD, whereas most previous studies included patients with other cardiac diseases.^{9 10} Also, we used cardiac mortality as an outcome, as has recently been recommended,^{21 22 23 24} whereas some studies used projected survival analysis based on the assumption that the first appropriate shock would have resulted in death without the ICD.^{10 11} The limitations of using projected survival analysis as an end point for device efficacy have been recognized.^{23 24} The use of device discharge is criticized because discharges may occur for events other than sustained ventricular tachycardia or fibrillation. Conversely, inclusion of only symptomatic discharges may exclude many events due to ventricular tachycardias in which ICD discharges occur before symptoms develop.

It is generally believed that ICD therapy dramatically reduces sudden death rates. The sudden death rates are extremely low, ranging from 1% to 2% per year. Despite this, total mortality rates are not reduced proportionately.^{25 26 27 28 29} This discrepancy may be due to multiple reasons. As sudden cardiac deaths are prevented by ICD, more patients who would have died suddenly are exposed to other causes of death, such as myocardial infarction or progressive heart failure. This partially cancels the survival benefit of ICDs. Thus, there is a conversion in the mode of death by ICD from sudden to nonsudden without significant prolongation of survival. The patients referred for ICD therapy may also represent a heterogeneous group of patients with a different natural history, and the device would benefit some patients more than others. This is substantiated by the differences in outcome reported in the literature.^{4 5 6 7 27 28 29 30 31 32 33} Some reports^{9 30} have shown a survival as high as 80% at 4 years, whereas others have not shown such good results.⁷ It therefore becomes extremely important to identify prognostic predictors to stratify patients into those with good survival after ICD once the potential for arrhythmic death has been decreased by the device and those who continue to be at risk of death. Our findings suggest an important role of perfusion imaging in risk assessment. The fact that the extent of scarring was more important than LVEF is not surprising because of the effects of remodeling, loading conditions, and, possibly, medications on LVEF. A statistically significant correlation exists between LVEF and extent of scarring, but there is considerable scatter along the regression line. It is possible that other variables may be important, such as LV end-diastolic and end-systolic volumes, as previously reported in patients with CAD.³⁴ Although patients with extensive defects had poor outcome, it is not clear what the outcome would have been without ICD (eg, drug therapy alone) because we did not have a control group. It is conceivable that alternative approaches such as cardiac transplantation³⁵ should be strongly considered in some of these patients, but the limited number of donors detract from the usefulness of this option. In other patients, a more aggressive treatment of congestive heart failure, consideration of the potential risk for asystole, or the need for concomitant amiodarone therapy should be considered.^{35 36 37} In our patients, however, more patients who died were likely to be on amiodarone therapy, probably because they were identified as being more at risk (eg, recurrent device discharges). The role of coronary revascularization in the improvement of LV dysfunction in those with viable hibernating myocardium also must be explored.^{38 39} In our study, ß-blocker therapy was related to improved survival by univariate analysis, which is consistent with other reports.³⁷

Myocardial Ischemia
The presence of ischemia by perfusion imaging was not predictive of subsequent death or total events defined as death and shocks (device discharges). The extent of ischemia was similar in survivors and nonsurvivors. Also, the presence of ischemia in patients with ICD who did not undergo coronary revascularization did not increase the death rate or the number of shocks. These observations support the concept that ischemia does not play a significant role in provoking ventricular tachycardia or death in these patients. A preliminary report by Gradel et al³⁸ also showed that the extent of scarring rather than ischemia correlated with inducibility of sustained ventricular tachycardia on electrophysiological testing. Previous studies showed that coronary revascularization alone is not sufficient to treat survivors of cardiac arrest who had evidence of ischemia.^{39 40 41} In a group of 23 survivors of sudden cardiac death undergoing coronary artery bypass graft surgery and ICD therapy, Daoud et al³⁹ found that 43% of the patients had a mean of 8 shocks during a follow-up interval of 34 months, suggesting that coronary revascularization alone is inadequate for treatment of cardiac arrest survivors. Nevertheless, because of the retrospective nature of our study and the relatively small number of patients, there is insufficient power to conclude that coronary revascularization plays no role in prolonging survival in this patient population.

Study Limitations
This study was retrospective, and the results must be validated prospectively in a different cohort of patients. The use of technetium-labeled perfusion tracers such as sestamibi and tetrofosmin is especially useful because they allow simultaneous assessment of perfusion and function.⁴² It is conceivable that some of the defects, although fixed, may represent viable myocardium, which is predictive of improvement in LVEF after coronary revascularization.³⁶ This issue cannot be readily answered on the basis of this study because the imaging protocols were not uniform during the period of time these patients were studied. It also is not clear whether improvement in LVEF with coronary revascularization (if obtainable) will alter the prognosis in such patients. This issue requires further study.

	Selected Abbreviations and Acronyms

 

CAD = coronary artery disease CHF = congestive heart failure EF = ejection fraction ICD = implantable cardioverter-defibrillator LV = left ventricular SPECT = single-photon emission computed tomography

	Acknowledgments

 
The authors thank Renee Brown for her secretarial support in the preparation of the manuscript.

	Footnotes

 
Reprint requests to Ami E. Iskandrian, MD, William Penn Snyder III Professor of Medicine, Director, Cardiovascular Research Center, Allegheny University of the Health Sciences, MCP Hahnemann School of Medicine, 230 N Broad St, Philadelphia, PA 19102-1192. E-mail iskandrian@allegheny.edu

Presented in part at the 43rd Annual Scientific Sessions of the Society of Nuclear Medicine, Denver, Colo, June 3-6, 1996.

Received July 1, 1996; revision received August 20, 1996; accepted September 4, 1996.

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