Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2003;108:1954-1959
Published online before print October 6, 2003, doi: 10.1161/01.CIR.0000091410.19963.9A
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
108/16/1954    most recent
01.CIR.0000091410.19963.9Av1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by van der Burg, A. E. B.
Right arrow Articles by Schalij, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van der Burg, A. E. B.
Right arrow Articles by Schalij, M. J.
Related Collections
Right arrow Nuclear cardiology and PET

(Circulation. 2003;108:1954.)
© 2003 American Heart Association, Inc.


Clinical Investigation and Reports

Impact of Viability, Ischemia, Scar Tissue, and Revascularization on Outcome After Aborted Sudden Death

Alida E. Borger van der Burg, MD; Jeroen J. Bax, MD; Eric Boersma, PhD; Ernest K.J. Pauwels, MD; Ernst E. van der Wall, MD; Martin J. Schalij, MD

From the Department of Cardiology, Leiden University Medical Center, Leiden, and Department of Epidemiology/Statistics (E.B.), Erasmus University Rotterdam, the Netherlands.

Correspondence to Jeroen J. Bax, MD, PhD, Leiden University Medical Center, Albinusdreef 2, 2300 RC Leiden, the Netherlands. E-mail jbax{at}knoware.nl

Received February 24, 2003; de novo received May 21, 2003; revision received July 22, 2003; accepted July 22, 2003.


*    Abstract
up arrowTop
*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Background— Survivors of aborted sudden death attributable to ventricular arrhythmias in the presence of coronary artery disease are at risk for recurrences. The substrate underlying these arrhythmias is not clear, and therefore the relation between ischemia, viability, scar tissue (and revascularization), and the incidence of ventricular arrhythmias (and survival) was studied over up to 3 years.

Methods and Results— One hundred fifty-three survivors of sudden death underwent stress-rest perfusion imaging. Patients with ischemic/viable myocardium (n=73) were revascularized if possible. Final antiarrhythmic therapy was based on the outcome of electrophysiological testing or left ventricular ejection fraction (LVEF). Implantation of a defibrillator was performed in 112 (72%) patients. During 3-year follow-up, 15 cardiac deaths occurred and 42 (29%) patients had recurrent ventricular arrhythmias. Patients with events (death or recurrence) exhibited more often a severely depressed LVEF (<=30%), more extensive scar tissue, and less ischemic/viable myocardium on perfusion imaging and less frequently underwent revascularization. Multivariate analysis identified extensive scar tissue and LVEF <=30% as the only predictors of death/recurrent ventricular arrhythmias.

Conclusions— In patients with aborted sudden death, extensive scar tissue and severely depressed LVEF are the only predictors of death or recurrent ventricular arrhythmias. These patients should be considered for implantation of a defibrillator.


Key Words: ischemia • arrhythmia • death, sudden


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Survivors of cardiac arrest attributable to life-threatening ventricular arrhythmias are at high risk for recurrent arrhythmic events, and managing this patient group is challenging.1,2 Most ventricular arrhythmias are secondary to ischemic heart disease.1,3

However, the exact trigger for ventricular arrhythmias has been a matter of debate.4–6 Ischemia has been recognized as a trigger for ventricular arrhythmias, and studies have demonstrated that revascularization of ischemic territories resulted in a lower inducibility rate of ventricular arrhythmias.4–6 Revascularization also resulted in a reduction of sudden-death rate, and revascularization of hibernating myocardium may also increase electrical stability and thereby prevent arrhythmic death.4–8 There are presently no studies that have specifically addressed this issue. Still, a significant number of patients remained inducible after revascularization, and a sudden death-rate of 13% in revascularized patients was demonstrated.4–7,9,10 Most likely, coexistence of large areas of scar tissue is responsible for triggering ventricular arrhythmias. It is well known that patients with previous infarction and large areas of scar tissue are at higher risk of sudden death, and implantation of a defibrillator may be warranted.11–13

Thus, the relation between ischemia, viability, scar tissue, and revascularization on the one hand and the incidence of ventricular arrhythmias (and sudden death) on the other hand is not clear. Accordingly, we have evaluated the relation between ischemia, viability, scar tissue (evaluated with technetium-99m tetrofosmin single photon emission computed tomography), and revascularization versus recurrent ventricular arrhythmias (and survival) over a follow-up period of a maximum of 3 years.


*    Methods
up arrowTop
up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Patients and Protocol
Consecutive survivors of cardiac arrest attributable to ventricular arrhythmias with significant coronary artery disease (>=50% diameter stenosis in >=1 coronary arteries on coronary angiography) were included. All patients underwent stress-rest perfusion scintigraphy to assess stress-inducible ischemia, viability, scar tissue, and left ventricular ejection fraction (LVEF). In the presence of ischemia/viability on scintigraphy, subsequent revascularization of the stenosed coronary arteries was established by either percutaneous transluminal coronary angioplasty (with subsequent stenting if indicated) or coronary artery bypass grafting. Final antiarrhythmic treatment was based on outcome of electrophysiological testing (after revascularization) as described previously14 or LVEF.11 Therapy included implantation of a defibrillator, catheter ablation of ventricular tachycardia (VT), or antiarrhythmic drugs. Patients with VT or ventricular fibrillation (VF) in the setting of an acute infarction (<48 hours) were excluded.

SPECT Imaging
Data Acquisition
The stress protocol included a symptom-limited treadmill exercise test. ß-blocking agents and calcium channel antagonists were discontinued at least 24 hours before scintigraphy. Test end points were physical exhaustion, dyspnea, angina, significant decrease in blood pressure (>10 mm Hg), or achievement of maximum age-related heart rate. Blood pressure, heart rate, and electrocardiographic findings were monitored during the test. Technetium-99m tetrofosmin (500 MBq) was injected intravenously at peak exercise, which was continued for 1 minute after tracer injection. In patients unable to exercise (n=67), adenosine stress was used. On the second day, resting images were obtained (using 500 MBq technetium-99m tetrofosmin) after the patient’s daily dose of nitrates. The resting studies were acquired using ECG gating, allowing assessment of LVEF.15

Imaging was performed using a triple-head SPECT camera system (GCA 9300/HG, Toshiba Corp) equipped with low-energy general-purpose collimators. A 20% window was used around the 140-keV energy peak of technetium-99m tetrofosmin. A total of 90 projections (step and shoot mode, 35 seconds per projection, imaging time 23 minutes) were obtained over a 360-degree circular orbit. Data were stored in a 64x64, 16-bit matrix. The raw scintigraphic data were reconstructed by filtered back projection using a Butterworth filter (cutoff frequency at 0.17 cycles per pixel, of order 3.5). No attenuation correction was used.

Data Analysis and Tissue Characterization
Additional reconstruction yielded standard long- and short-axis projections perpendicular to the heart axis. Reconstructed slices were 8 mm in all projections. The short-axis slices were displayed in polar map format, adjusted for peak myocardial activity (100%). The myocardium was divided into 17 segments, as recently proposed.16

Segmental tracer activity was expressed as percentage of maximum. Perfusion defects on stress images were considered present when tracer activity was <75% of maximum. When significant fill-in (>10%) of perfusion defects was observed on the resting images, segments were classified as ischemic.17 Segments without fill-in were classified as viable when activity on the resting images was >=50%.18 Ischemic and viable segments were combined and classified as jeopardized myocardium. Segments were classified as scar tissue when tracer activity on the resting images was <50%.18 Myocardial segments were subsequently allocated to the vascular territories according to recent guidelines.16

Patients were scored as having ischemic or viable tissue (jeopardized myocardium) or having scar tissue. Because nearly all patients exhibited some extent of scar tissue, patients were classified as having extensive scar tissue (>1 vascular territory) or small areas of scar tissue (<=1 vascular territories). LVEF was calculated from the gated SPECT images using commercially available automated software.15

Long-Term Follow-Up
Long-term follow-up was assessed by outpatient visits and chart review. Follow-up data were acquired up to a maximum of 3 years. Events included cardiac death (including sudden cardiac death and death attributable to ongoing heart failure) and recurrences of ventricular arrhythmias (documented cardiac arrest, VF/sustained VT). Moreover, in patients who underwent implantable cardioverter defibrillator (ICD) implantation, device discharges (based on VT/VF) were evaluated and included as recurrent ventricular arrhythmias. Only the first event was taken into account for statistical analysis.

Statistical Analysis
Continuous data are presented as median value and corresponding interquartile range (ie, 25th to 75th percentile of the distribution), and dichotomous data are presented as numbers and percentages. Differences between patient subgroups were evaluated by Wilcoxon tests, Kruskal-Wallis tests, and {chi}2 tests, as appropriate. The method of Kaplan-Meier was applied to describe and evaluate the incidence of the primary end point (cardiac death or recurrence) over time, and differences in event rate between patient subgroups were evaluated by log-rank tests. Univariable and multivariable Cox proportional hazards regression analyses were performed to evaluate the relation between age, gender, LVEF, prevalence of jeopardized or scar tissue, and treatment with coronary revascularization and the incidence of death or recurrence during long-term follow-up. All variables that were significant (P<0.05) in the univariable analysis were entered in the multivariable model. The multivariable model also included an interaction term between the prevalence of jeopardized myocardium and treatment with coronary revascularization. P<0.05 was considered significant.


*    Results
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
Study Population
A total of 156 survivors (132 men, mean age 63±10 years) of nonfatal cardiac arrest were included in the study. The presenting arrhythmia was VF in 84 (54%) and VT in 72 (46%). Most (143, 92%) had a previous infarction (>2 months before study entrance). At presentation, 8 (5%) had creatine kinase-MB levels that were slightly elevated (maximum, 38 U/L), possibly indicating minimal myocardial damage.

Based on the inclusion criteria, all patients showed significant coronary artery disease on coronary angiography, and they had on average 2.0±0.8 stenosed coronary arteries. The mean LVEF was 40±19%, and 66 (42%) patients had a LVEF <=30%.

All patients underwent stress-rest perfusion scintigraphy. Jeopardized myocardium was present in 73 (47%) patients, and subsequent revascularization was performed in 44 (60%) patients. Most revascularized patients (27, 61%) underwent coronary artery bypass grafting, whereas the remaining 17 (39%) underwent percutaneous transluminal coronary angioplasty. The decision for revascularization was based on the clinical data, combined with the presence of jeopardized myocardium; 29 (19%) patients with jeopardized myocardium did not undergo revascularization because of comorbidity or poor target vessel quality (not suited for coronary revascularization). Final therapy was based on the outcome of electrophysiological testing or LVEF. Implantation of a defibrillator was performed in 112 (72%) patients. In addition, 21 (13%) patients underwent radiofrequency catheter ablation of VTs, and 81 (52%) patients received antiarrhythmic medication.

Survival and Ventricular Arrhythmias
During a median follow-up period of 26 months (25th to 75th percentile, 6 to 36 months), 15 (10%) patients died; cardiac death occurred in 11 (7%) patients. The cardiac deaths were sudden cardiac death in 1 patient and death attributable to (ongoing) heart failure in 10 (91%) patients.

The 3-year survival rate was 86%. Recurrences of ventricular arrhythmias occurred in 42 (27%) patients. Most of these recurrences (36, 86%) occurred in patients who underwent ICD implantation. A composite end point was reached in 50 patients (42 recurrences, 8 deaths; ie, 7 patients died after a recurrence). Patients with recurrences had comparable QRS duration compared with patients without recurrences (112±84 versus 106±67 ms, NS).

Findings on SPECT
Segments
In the 156 patients, 2652 segments were analyzed. Of these, 748 exhibited a defect on the stress perfusion images. Ischemia was observed in 174 (23%) segments. Of the remaining 574 segments with a fixed defect, 217 (29%) showed >=50% tracer uptake and were classified as viable, whereas 357 (48%) had <50% tracer uptake and were classified as scar tissue.

Patients
Of the 156 patients, 111 (71%) exhibited extensive scar tissue, and 73 (47%) had jeopardized myocardium.

Predictors of Death or Recurrences
Baseline characteristics of patients with and without events (death or recurrences) are shown in the Table. Patients with events had a significantly lower LVEF, more frequently had scar tissue, less frequently had jeopardized myocardium, and less frequently underwent revascularization. Univariable analysis identified these last 4 characteristics as predictors of events (Figures 1 through 4DownDownDown). The event curves of patients with and without revascularization are shown in Figure 1. A significantly higher event rate was observed in patients who did not undergo revascularization (53% versus 15%, P<0.05).


View this table:
[in this window]
[in a new window]
 
Baseline Characteristics of Patients With and Without Events



View larger version (14K):
[in this window]
[in a new window]
 
Figure 1. Three-year event curves according to revascularization treatment. Patients who underwent revascularization (n=44) had a significantly lower event rate compared with patients who were treated medically (n=112).



View larger version (15K):
[in this window]
[in a new window]
 
Figure 2. Three-year event curves according to the presence or absence of extensive scar tissue on SPECT. Patients without extensive scar tissue (n=45) had a significantly lower event rate compared with patients with extensive scar tissue (n=111).



View larger version (16K):
[in this window]
[in a new window]
 
Figure 3. Three-year event curves according to the presence and absence of jeopardized myocardium on SPECT. Patients with jeopardized myocardium (n=73) had a significantly lower event rate compared with the patients without jeopardized myocardium (n=83).



View larger version (14K):
[in this window]
[in a new window]
 
Figure 4. Three-year event curves according to the LVEF; patients with severely depressed LVEF (<=30%, n=66) had a significantly higher event rate compared with patients with LVEF >30% (n=90).

As displayed in Figure 2, the event rate was 54% in the patients with extensive scar tissue compared with 16% (P<0.05) in patients without or with small areas of scar tissue (<=1 vascular territory). Patients with jeopardized myocardium had a significantly lower event rate compared with patients without jeopardized myocardium (30% versus 55%, P<0.05, Figure 3). Finally, patients with severely depressed LVEF (<=30%) had a significantly higher event rate compared with patients with LVEF >30% (59% versus 33%, P<0.05).

Thus, revascularization and the presence of jeopardized myocardium were beneficial on univariable analysis, whereas extensive scar tissue and LVEF <=30% were harmful (Figure 5A, {blacksquare}). The finding that jeopardized myocardium was beneficial was unexpected. However, patients with jeopardized myocardium underwent revascularization when possible. When the patients with jeopardized myocardium only were analyzed according to the treatment, it seemed that the event rate was significantly higher in patients with jeopardized myocardium who did not undergo revascularization (38%) compared with the patients with jeopardized myocardium who underwent revascularization (14%, P<0.05).



View larger version (16K):
[in this window]
[in a new window]
 
Figure 5. Left, Results of univariable ({blacksquare}) and multivariable ({square}) analyses to identify predictors of events (cardiac [heart failure and arrhythmic] death, recurrences). In the univariate model, extensive scar tissue, jeopardized myocardium, revascularization, and LVEF were predictive, whereas in the multivariate model, only LVEF and the presence of extensive scar tissue remained predictive. Right, Results of univariable ({blacksquare}) and multivariable ({square}) analyses to identify predictors of events (arrhythmic death, recurrences). In the univariate model, extensive scar tissue, jeopardized myocardium, revascularization, and LVEF were predictive, whereas in the multivariate model, only LVEF and the presence of extensive scar tissue remained predictive.

Multivariable analysis identified LVEF <=30% (hazard ratio, 2.0; 95% CI, 1.1 to 3.5; P=0.02) and the presence of extensive scar tissue (hazard ratio, 2.4; 95% CI, 1.0 to 5.9; P=0.05) as the only 2 independent predictors of events (Figure 5, left, {square}).

The survival analysis was repeated when only arrhythmic death (and recurrences) were used as the combined end point (and heart failure deaths were excluded); the results of the univariable and multivariable analysis were similar (Figure 5, right) and confirmed that, on multivariable analysis, LVEF <=30% (hazard ratio, 2.4; 95% CI, 1.2 to 4.4; P=0.09) and the presence of extensive scar tissue (hazard ratio, 4.2; 95% CI, 1.3 to 14; P=0.02) were the only 2 independent predictors of events.


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
The present study evaluated, in survivors of out-of-hospital cardiac arrest, the interaction between ischemia, viability, scar tissue, and revascularization on the one hand and survival and recurrences of ventricular arrhythmias on the other hand. The results indicated that, in a multivariable model, extensive scar tissue and LVEF <=30% were the only 2 predictors of events.

Events
Most (91%) cardiac deaths were attributable to heart failure, whereas only 1 sudden cardiac death occurred. However, because 86% of the recurrences occurred in patients who underwent ICD implantation, the likelihood of sudden cardiac death would have been high when patients would not have received an ICD. Previous studies19,20 focusing on ischemia, viability, scar tissue, and long-term survival were not capable of distinguishing between these modes of deaths, but because of the presence of the ICD, the present study is the first to provide information on mode of death in these patients. This is probably also the explanation for the relatively low death rate in the present study compared with earlier studies.19,20 The main question is whether these recurrences were caused by jeopardized myocardium or scar tissue.

Ischemia, Viability, and Scar Tissue Versus Treatment and Prognosis
The beneficial effect of revascularization of ischemic myocardium has been demonstrated in large studies.21,22 Indeed, revascularization of ischemic myocardium resulted in superior survival, as evidenced by the results from the CASS and European Coronary Surgery Study Group.21,22 More recently, focus has shifted toward the importance of viable myocardium.20 Various studies have shown that revascularization of dysfunctional but viable myocardium resulted in improvement of contractile function.23 However, not all patients with viable myocardium exhibited improvement in function after revascularization.8,23 Still, patients with viable myocardium who underwent revascularization had an excellent survival. In contrast, an extremely high event rate was observed in patients with viable myocardium who were treated medically.20 Pooling of the available studies revealed an annual death rate of 16% among patients with substantial viable tissue who did not undergo revascularization.20 Based on these observations, additional benefits of revascularization of viable myocardium were considered. In particular, the prevention of ventricular arrhythmias was considered an explanation for the beneficial effect of revascularization of viable myocardium.8 This issue has not been studied previously and was addressed in the present study. Patients with ischemia or viable myocardium were grouped and referred to as having jeopardized myocardium. To our surprise, patients with jeopardized myocardium had a lower event rate compared with patients without jeopardized myocardium. However, when treatment was considered, it seemed that patients with jeopardized myocardium who underwent revascularization had a low event rate (13%) whereas patients with jeopardized myocardium who were treated medically had a significantly higher event rate (38%). These findings confirm the suggestion that revascularization of jeopardized myocardium is needed to avoid events. It has been suggested previously that jeopardized myocardium may provide an unstable substrate and that revascularization may result in electrical stability.8

Of interest, the presence of extensive scar tissue was another strong predictor of events. Moreover, severely depressed LVEF was also a predictor of events. These 2 parameters are both reflecting the severity of (infarct) damage of the LV. Previous studies have already indicated that scar tissue and depressed LVEF were important predictors of events. Machecourt et al24 performed a long-term follow-up study (33±10 months) in 1926 patients and clearly showed the relation between the extent of defects on thallium-201 imaging and survival. The authors demonstrated that the probability of cardiovascular mortality was 0.24% in patients without perfusion defects, 6% in patients with perfusion defects extending to 3 segments, and 17% in patients with defects extending to >=4 segments (67% of the LV). Recent data by Hachamovitch et al25 also demonstrated an increasing event rate that paralleled the increasing abnormalities on perfusion imaging. In addition, Sharir et al26 have recently emphasized again the strong prognostic value of LVEF (in that study derived from gated SPECT data).

Another finding in the present study was that on multivariable analysis, only LVEF and extensive scar tissue remained predictive. These findings suggest that for long-term risk stratification, viability or ischemia may not be that important. However, in the present study, revascularization and the presence of jeopardized myocardium were interrelated, which makes definitive conclusions difficult. Additional, randomized (to treatment) trials are needed to draw definitive conclusions concerning this issue.

Limitations
Several limitations of the present study need to be addressed. First, although the data were collected in a prospective manner, randomization to treatment (revascularization versus medical therapy) is lacking and future studies (eg, the STICH Trial) may provide additional insight in these complex issues.27 Second, viability and ischemia were grouped as jeopardized myocardium. However, from a pathophysiological point of view it may be difficult to separate these entities exactly, because it is likely that ischemia and viability are parts of a continuum of damage in ischemic heart disease.28 Moreover, from a scintigraphic point of view, it may be difficult to separate these issues exactly, because many segments contain viable myocytes that also suffer from ischemia (segments with tracer uptake >=50% and reversible defects).In addition, 5% of patients presented with minimally elevated creatine kinase-MB levels at the index event. It cannot be ruled out that some viable myocardium progressed to scar tissue and that, at the time of the SPECT study, only scar tissue could be detected. This may have influenced the results in the present study. Finally, assessment of viability with technetium-99m tetrofosmin may slightly underestimate the presence of viable tissue, as demonstrated in direct comparisons with positron emission tomography and F18-fluorodeoxyglucose.29

Clinical Implications and Conclusion
The findings in present study highlight the importance of scintigraphic evaluation of patients with aborted sudden death and coronary artery disease. Gated SPECT imaging allows assessment of ischemia, viability, scar tissue, and LVEF. These aspects are important in the evaluation of these patients. In the presence of jeopardized myocardium, an attempt at revascularization should be made, because revascularization of jeopardized myocardium was associated with a low event rate. In addition, patients with extensive scar tissue and LVEF <=30% are at high risk for recurrences, and ICD implantation may be preferred in these patients. ICD implantation will prevent sudden cardiac death, as illustrated in the present results. Finally, the next step in treatment of these patients will be focusing on treatment options for heart failure, because most (>90%) patients died of ongoing heart failure.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Myerburg RJ, Kessler KM, Estes D, et al. Long-term survival after prehospital cardiac arrest: analysis of outcome during an 8 year study. Circulation. 1984; 70: 538–546.[Abstract/Free Full Text]

2. Waldo AL, Biblo LA, Carlson MD. General evaluation of out of hospital sudden cardiac death survivors. Circulation. 1992; 85: 103–106.

3. De Vreede-Swagemakers JJ, Gorgels AP, Dubois-Arbouw WI, et al. Out-of-hospital cardiac arrest in the 1990’s: a population-based study in the Maastricht area on incidence, characteristics and survival. J Am Coll Cardiol. 1997; 15: 30:1500–1505.

4. Brugada J, Aguinaga L, Mont L, et al. Coronary revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction: effects on the electrophysiologic substrate and outcome. J Am Coll Cardiol. 2001; 37: 529–533.[Abstract/Free Full Text]

5. Manolis AS, Rastegar H, Estes NAM II. Effects of coronary artery bypass grafting on ventricular arrhythmias: results with electrophysiological testing and long-term follow-up. Pacing Clin Electrophysiol. 1993; 16: 984–991.[CrossRef][Medline] [Order article via Infotrieve]

6. Kelly P, Rushkin JN, Vlahakes GJ, et al. Surgical coronary revascularization in survivors of prehospital cardiac arrest: its effect on inducible ventricular arrhythmias and long-term survival. J Am Coll Cardiol. 1990; 15: 267–273.[Abstract]

7. Every NR, Fahrenbruch CE, Hallstrom AP, et al. Influence of coronary bypass surgery on subsequent outcome of patients resuscitated from out of hospital cardiac arrest. J Am Coll Cardiol. 1992; 19: 1435–1439.[Abstract]

8. Bonow RO. The identification of viable myocardium. Circulation. 1996; 94: 2674–2680.[Free Full Text]

9. Natale A, Sra J, Axtell K, et al. Ventricular fibrillation and polymorphic ventricular tachycardia with critical coronary artery stenosis: does bypass surgery suffice? J Cardiovasc Electrophysiol. 1994; 5: 988–994.[Medline] [Order article via Infotrieve]

10. Geelen P, Primo J, Wellens F, et al. Coronary artery bypass grafting and defibrillator implantation in patients with ventricular tachyarrhythmias and ischemic heart disease. Pacing Clin Electrophysiol. 1999; 22: 1132–1139.[CrossRef][Medline] [Order article via Infotrieve]

11. Moss AJ, Zareba W, Hall WJ, et al. The Multicenter Automatic Defibrillator Implantation Trial II Investigators: prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002; 346: 877–883.[Abstract/Free Full Text]

12. The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997; 337: 1576–1583.[Abstract/Free Full Text]

13. Connolly SJ, Gent M, Roberts RS, et al for the CIDS Investigators. Canadian Implantable Defibrillator Study (CIDS): a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation. 2000; 101: 1297–1302.[Abstract/Free Full Text]

14. Borger van der Burg AE, de Groot NMS, van Erven L, et al. Radiofrequency catheter ablation of ventricular tachycardia: a successful approach? J Cardiovasc Electrophysiol. 2002; 13: 417–423.[CrossRef][Medline] [Order article via Infotrieve]

15. Germano G, Berman DS. Quantitative gated SPECT. J Nucl Med. 2001; 42: 528–529.[Free Full Text]

16. Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation. 2002; 105: 539–542.[Free Full Text]

17. Elhendy A, Bax JJ, Poldermans D. Dobutamine stress myocardial perfusion imaging in coronary artery disease. J Nucl Med. 2002; 43: 1634–1646.[Abstract/Free Full Text]

18. Stollfuss JC, Haas F, Matsunari I, et al. 99mTc-tetrofosmin SPECT for prediction of functional recovery defined by MRI in patients with severe left ventricular dysfunction: additional value of gated SPECT. J Nucl Med. 1999; 40: 1824–1831.[Abstract/Free Full Text]

19. Lee KS, Marwick TH, Cook SA, et al. Prognosis of patients with left ventricular dysfunction, with and without viable myocardium after myocardial infarction: relative efficacy of medical therapy and revascularization. Circulation. 1994; 90: 2687–2694.[Abstract/Free Full Text]

20. Allman KC, Shaw LJ, Hachamovitch R, et al. Myocardial viability testing and impact of revascularization on prognosis in patients with coronary artery disease and left ventricular dysfunction: a meta-analysis. J Am Coll Cardiol. 2002; 39: 1151–1158.[Abstract/Free Full Text]

21. European Coronary Surgery Study Group Principal Investigators and their associates long-term results of prospective randomised study of coronary artery bypass surgery in stable angina pectoris. Lancet. 1982; 2: 1173–1180.[Medline] [Order article via Infotrieve]

22. CASS Principal Investigators and their associates. Coronary Artery Surgery Study (CASS): a randomized trial of coronary artery bypass surgery. Survival data. Circulation. 1983; 68: 939–950.[Abstract/Free Full Text]

23. Bax JJ, Wijns W, Cornel JH, et al. Accuracy of currently available techniques for prediction of functional recovery after revascularization in patients with left ventricular dysfunction due to coronary artery disease: comparison of pooled data. J Am Coll Cardiol. 1997; 30: 1451–1460.[Abstract]

24. Machecourt J, Longere P, Fagret D, et al. Prognostic value of thallium-201 single-photon emission computed tomographic myocardial perfusion imaging according to extent of myocardial defect: study in 1,926 patients with follow-up at 33 months. J Am Coll Cardiol. 1994; 23: 1096–1106.[Abstract]

25. Hachamovitch R, Berman DS, Shaw LJ, et al. Incremental prognostic value of myocardial perfusion single photon emission computed tomography for the prediction of cardiac death: differential stratification for risk of cardiac death and myocardial infarction. Circulation. 1998; 97: 535–543.[Abstract/Free Full Text]

26. Sharir T, Berman DS, Lewin HC, et al. Incremental prognostic value of rest-redistribution (201)TI single-photon emission computed tomography. Circulation. 1999; 100: 1964–1970.[Abstract/Free Full Text]

27. Bonow RO. Myocardial viability and prognosis in patients with ischemic left ventricular dysfunction. J Am Coll Cardiol. 2002; 39: 1159–1162.[Free Full Text]

28. Schelbert HR. Measurements of myocardial metabolism in patients with ischemic heart disease. Am J Cardiol. 1998; 82: 61K–67K.[CrossRef][Medline] [Order article via Infotrieve]

29. Matsunari I, Boning G, Ziegler SI, et al. Attenuation-corrected 99mTc-tetrofosmin single-photon emission computed tomography in the detection of viable myocardium: comparison with positron emission tomography using 18F-fluorodeoxyglucose. J Am Coll Cardiol. 1998; 32: 927–935.[Abstract/Free Full Text]




This article has been cited by other articles:


Home page
Eur Heart JHome page
C. J. W. Borleffs, L. van Erven, M. Schotman, E. Boersma, P. Kies, A. E. B. van der Burg, K. Zeppenfeld, M. Bootsma, E. E. van der Wall, J. J. Bax, et al.
Recurrence of ventricular arrhythmias in ischaemic secondary prevention implantable cardioverter defibrillator recipients: long-term follow-up of the Leiden out-of-hospital cardiac arrest study (LOHCAT)
Eur. Heart J., July 1, 2009; 30(13): 1621 - 1626.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
A. M. Gillis
Tincture of Time: When to Implant a Prophylactic Cardioverter-Defibrillator Following Coronary Revascularization?
J. Am. Coll. Cardiol., May 2, 2006; 47(9): 1818 - 1819.
[Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
V. S. Chauhan, E. Downar, K. Nanthakumar, J. D. Parker, H. J. Ross, W. Chan, and P. Picton
Increased ventricular repolarization heterogeneity in patients with ventricular arrhythmia vulnerability and cardiomyopathy: a human in vivo study
Am J Physiol Heart Circ Physiol, January 1, 2006; 290(1): H79 - H86.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
A. Elhendy, S. Chapman, T. R. Porter, and J. Windle
Association of Myocardial Ischemia With Mortality and Implantable Cardioverter-Defibrillator Therapy in Patients With Coronary Artery Disease at Risk of Arrhythmic Death
J. Am. Coll. Cardiol., November 1, 2005; 46(9): 1721 - 1726.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
S. Nazarian, D. A. Bluemke, A. C. Lardo, M. M. Zviman, S. P. Watkins, T. L. Dickfeld, G. R. Meininger, A. Roguin, H. Calkins, G. F. Tomaselli, et al.
Magnetic Resonance Assessment of the Substrate for Inducible Ventricular Tachycardia in Nonischemic Cardiomyopathy
Circulation, November 1, 2005; 112(18): 2821 - 2825.
[Abstract] [Full Text] [PDF]


Home page
Mayo Clin Proc.Home page
T. J. Bunch, S. C. Hammill, and R. D. White
Outcomes After Ventricular Fibrillation Out-of-Hospital Cardiac Arrest: Expanding the Chain of Survival
Mayo Clin. Proc., June 1, 2005; 80(6): 774 - 782.
[Abstract] [PDF]


Home page
J Am Coll CardiolHome page
D. Bello, D. S. Fieno, R. J. Kim, F. S. Pereles, R. Passman, G. Song, A. H. Kadish, and J. J. Goldberger
Infarct morphology identifies patients with substrate for sustained ventricular tachycardia
J. Am. Coll. Cardiol., April 5, 2005; 45(7): 1104 - 1108.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
R. J. Gibbons and P. A. Araoz
The year in cardiac imaging
J. Am. Coll. Cardiol., November 16, 2004; 44(10): 1937 - 1944.
[Full Text] [PDF]


Home page
J Am Coll CardiolHome page
R. Lampert, C. A. McPherson, J. F. Clancy, T. L. Caulin-Glaser, L. E. Rosenfeld, and W. P. Batsford
Gender differences in ventricular arrhythmia recurrence in patients with coronary artery disease and implantable cardioverter-defibrillators
J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2293 - 2299.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
J. M. Canty Jr, G. Suzuki, M. D. Banas, F. Verheyen, M. Borgers, and J. A. Fallavollita
Hibernating Myocardium: Chronically Adapted to Ischemia but Vulnerable to Sudden Death
Circ. Res., April 30, 2004; 94(8): 1142 - 1149.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
108/16/1954    most recent
01.CIR.0000091410.19963.9Av1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by van der Burg, A. E. B.
Right arrow Articles by Schalij, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by van der Burg, A. E. B.
Right arrow Articles by Schalij, M. J.
Related Collections
Right arrow Nuclear cardiology and PET