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J Thorac Cardiovasc Surg 2004;127:385-390
© 2004 The American Association for Thoracic Surgery

Surgery for acquired cardiovascular disease

Why do patients with ischemic cardiomyopathy and a substantial amount of viable myocardium not always recover in function after revascularization?

^a Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands
^b Department of Cardiology, University Hospital Brussels, Brussels, Belgium
^c Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands

Received for publication February 28, 2003; revisions received August 7, 2003; accepted for publication August 11, 2003.

^* Address for reprints: Don Poldermans, MD, PhD, Thoraxcenter Room Ba 300, Erasmus Medical Center, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands
poldermans{at}hlkd.azr.nl

	Abstract

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OBJECTIVE: In patients with ischemic cardiomyopathy and a substantial amount of dysfunctional but viable myocardium, myocardial revascularization may improve left ventricular ejection fraction. The aim of this study was to evaluate why not all patients with a substantial amount of viable tissue recover in function after revascularization.

METHODS: A total of 118 consecutive patients with a depressed left ventricular ejection fraction (on average 29% ± 6%) due to chronic coronary artery disease underwent myocardial revascularization. Before revascularization all patients underwent dobutamine stress echocardiography to assess regional dysfunction, left ventricular volumes, and myocardial viability as well as radionuclide ventriculography to determine the left ventricular ejection fraction. Next, 3 to 6 months after revascularization, the left ventricular ejection fraction and regional contractile function were reassessed. Improvement of left ventricular ejection fraction 5% following revascularization was considered clinically significant.

RESULTS: Dobutamine stress echocardiography revealed that 489 (37%) of the 1329 dysfunctional segments were viable. A total of 61 (52%) patients had a substantial amount of viable myocardium (4 viable segments). In these 61 patients the global function was expected to recover 5% after revascularization. However, left ventricular ejection fraction did not improve in 20 (33%) of 61 patients despite the presence of substantial viability. Clinical characteristics and echocardiographic data were comparable between patients with and without improvement. However, patients without improvement had considerably larger end systolic volumes (153 ± 41 mL vs 133 ± 46 mL, P = .007). The likelihood of recovery of global function decreased proportionally with the increase of end systolic volume (P < .001, R = 0.43, n = 61). Receiver operating characteristic curve analysis demonstrated that an end systolic volume 140 mL had the highest sensitivity/specificity to predict the absence of global recovery.

CONCLUSIONS: In patients with ischemic cardiomyopathy not only the amount of dysfunctional but viable myocardium but also the extent of left ventricular remodeling determines the improvement in function following myocardial revascularization. Patients with a high end systolic volume due to left ventricular remodeling have a decreased likelihood of improvement of global function.

It has become clear that approximately 50% of the patients with ischemic cardiomyopathy have a substantial amount of hibernating myocardium.^8,9 Myocardial contractility in this dysfunctional but viable tissue can be restored by myocardial revascularization. In patients with a substantial amount of dysfunctional but viable myocardium, CABG may improve or even normalize LV ejection fraction (LVEF).^10,11 Moreover, revascularization may substantially improve heart failure symptoms and prognosis.^10,11 However, in daily clinical practice not all patients with ischemic LV dysfunction recover in function after revascularization despite the presence of substantial viable myocardium. Currently, the reasons for this absence of improvement after CABG are not clear. Failure of recovery in patients with considerable viable tissue may be related to an increased LV volume due to extensive ventricular remodeling.^12,13 To test this hypothesis, patients with ischemic cardiomyopathy were studied before and 3 to 6 months after myocardial revascularization.

	Methods

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Patient population, study protocol
The study population comprised 118 consecutive patients with a depressed LVEF due to chronic coronary artery disease (confirmed by angiography). All patients were already scheduled for myocardial revascularization based on clinical grounds. Patients were in clinically cardiac stable condition and were studied at least 6 months from previous myocardial infarction. Patients with primary cardiomyopathy, significant valvular heart disease, or an inadequate acoustic window were not included in the study. Patients who died perioperatively or during the follow-up were not included in the study. A total of 5 patients died perioperatively (4 cardiac death, 1 sepsis); these patients had on average 9.8 ± 2.2 dysfunctional segments and 3.8 ± 3.0 dysfunctional but viable segments. In these patients the LVEF was 23% ± 6%, the LV end diastolic volume averaged 191 ± 60 mL, and the LV end systolic volume was 148 ± 41 mL. The decision to perform surgical revascularization was based on clinical grounds and coronary angiography. Coronary artery bypass grafting was performed with use of cardiopulmonary bypass in all patients. All patients were operated on by standard techniques and optimization of perioperative support. All patients underwent isolated CABG procedures and patients having concomitant valve surgery were not included.

The study protocol was as follows. Before myocardial revascularization all patients underwent rest and dobutamine stress echocardiography to assess regional dysfunction, LV volumes, and myocardial viability. Radionuclide ventriculography was used to determine the exact LVEF before and 3 to 6 months after revascularization. Before revascularization and at follow-up a structured clinical interview was performed including assessment of the New York Heart Association (NYHA) functional class. The Hospital Ethics Committee approved the protocol and all patients gave informed consent before the study.

Evaluation of regional function and volumes
All echocardiograms were performed with a Sonos-5500 imaging system (Andover, Mass) with a 1.8-MHz transducer using second harmonic imaging to optimize endocardial border visualization. Four standard views (apical 2- and 4-chamber views and parasternal short- and long-axis views) were digitized on optical disks and also stored on videotape. The end diastolic and end systolic LV volumes were measured using the standard biplane Simpson method.

Assessment of myocardial viability
After baseline echocardiography, dobutamine was administered, starting at a dose of 5 µg/kg body weight per minute for 5 minutes, followed by a 10 µg/kg/min dose for 5 minutes (low-dose). Incremental dobutamine doses of 10 µg/kg/min were then given at 3-minute intervals up to a dose of 40 µg/kg/min; atropine was added if necessary. Test end points were: target heart rate, extensive new wall motion abnormalities, ST-segment depression 2 mm, severe angina, systolic blood pressure fall >40 mm Hg, blood pressure > 240/120 mm Hg, significant (supra)ventricular arrhythmia. The echocardiograms were scored by 2 experienced reviewers using a 16-segment model.¹⁴. Regional wall motion and systolic wall thickening were scored on a 5-point scale: 1 = normal, 2 = mild hypokinetic, 3 = severe hypokinetic, 4 = akinetic, 5 = dyskinetic. Myocardial segments were considered normal if the regional wall motion was normal or mildly hypokinetic. Only dysfunctional segments (severe hypokinesia, akinesia, or dyskinesia at resting echocardiography) were evaluated for myocardial viability. Segments with an improvement, worsening, or a biphasic wall motion response during stress echocardiography were considered viable. Segments with unchanged wall motion were considered nonviable. A patient was classified as viable in the presence of 4 dysfunctional viable segments.^8,10,15

Assessment of LVEF
LVEF was assessed by radionuclide ventriculography before and 3 to 6 months after revascularization. A small field-of-view gamma camera system (Orbiter, Siemens, Erlangen, Germany) was used, oriented in a 45° left anterior oblique position with a 5° to 10° caudal tilt. After injection of technetium Tc 99m-pertechnate–labeled autologous erythrocytes (550 MBq), radionuclide ventriculography was performed at rest with the patient in supine position. LVEF was calculated by standard methods (Odyssey VP, Picker, Cleveland, Ohio). Improvement of LVEF 5% following revascularization was considered clinically significant, as described previously.¹⁰

Statistical analysis
All continuous data were expressed as mean ± SD and percentages were rounded. Statistical analysis was performed with the BMDP statistical software package (BMDP Statistical Software Inc, Los Angeles, Calif). Continuous variables were compared using the Student t test for unpaired samples. Differences between proportions were compared using the chi-square test. Linear regression analysis was used to determine the relation between end systolic volume and change in LVEF. The LV volume that was related to a low likelihood of improvement of LVEF postrevascularization was determined by receiver operating characteristic (ROC) curve analysis. The optimal cutoff value was the number of segments that yielded the highest sum of sensitivity and specificity. Multivariate analysis was performed to identify the relative contributions of ventricular size and viability on the change in LVEF after coronary bypass surgery. Dependent variable was change in LVEF; independent variables were number of viable segments, end systolic volume, and the end diastolic volume.

	Results

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Patient characteristics
The clinical and echocardiographic characteristics of the study population are presented in Table 1. The study group consisted of 118 patients with ischemic cardiomyopathy (95 men, mean age 60 ± 10 years). The majority of the patients had a previous myocardial infarction, and all patients had heart failure symptoms; the NYHA functional class was on average 2.8 ± 1.2. The range of preoperative ejection fraction was 9% to 35%. A total of 73 (62%) patients had angina. A total of 17 (14%) patients had previous coronary artery bypass operations. A total of 3 patients had perioperative myocardial infarctions (by enzymatic criteria). Thirty-eight patients needed inotropic support postoperatively. An intra-aortic balloon pump was placed in 2 patients. Ventricular assist devices were not used.

Myocardial viability and functional outcome
Dobutamine stress echocardiography revealed that 489 (37%) of the dysfunctional segments were viable. Of the 489 dysfunctional but viable segments, 293 segments showed a sustained improvement pattern during dobutamine stimulation and the remaining 196 segments had an ischemic pattern. In the remaining 840 (63%) dysfunctional segments, no myocardial viability was present. A total of 61 patients had a substantial amount of viable myocardium (4 dysfunctional but viable segments). In these 61 patients the global function was expected to recover (improvement of LVEF 5%) after revascularization. However, although 41 (67%) of these patients had an improved LVEF following revascularization, the LVEF did not improve in 20 patients despite the presence of a substantial amount of viable myocardium. A total of 57 patients had <4 viable segments and were considered nonviable.

Comparison of viable patients with and without improvement
The patients with a substantial amount of viability were divided into 2 groups: patients with and patients without improvement in LVEF. Table 2 compares these 2 groups. Clinical characteristics and echocardiographic data were comparable between the 2 groups. However, improvement of global function following revascularization was related to the end systolic volume. Patients without improvement of LVEF had considerably larger end systolic volumes compared with the patients with recovery of global function (153 ± 41 ml vs 133 ± 46 mL, P = .007). Patients with improvement had after revascularization had on average 2.7 ± 0.6 stenosed coronary arteries, and patients without improvement had 2.7 ± 0.5 stenosed vessels (P = .54). Coronary artery target vessels were comparable in patients with and without improvement following revascularization. A total of 4 (7%) of the 61 patients with substantial viability had a decrease 5% in LVEF. This was related to a perioperative myocardial infarction in 3 patients and progression of LV dysfunction in 1 patient.

Of the 57 patients with <4 viable segments, 7 (12%) patients had an improved LVEF after revascularization. These 7 patients all had 3 dysfunctional but viable segments and a preserved end systolic volume (81 ± 8 mL).

End systolic volume versus improvement of LVEF
Figure 1 demonstrates the relation between the end systolic volume and the change in LVEF after revascularization in the patients with a substantial amount of viable myocardium. The likelihood of recovery of global function decreased proportionally with the increase of end systolic volume (P < .001, R = 0.43, n = 61). ROC curve analysis demonstrated that an end systolic volume 140 mL was related to a low likelihood of improvement of LVEF postrevascularization; the C-index was 0.75. This value of 140 mL had the highest sensitivity/specificity (68% and 65%, respectively) to predict the absence of global recovery. Multivariate analysis showed the relative contributions of ventricular size and viability on the LVEF after coronary bypass surgery. Predictors of change in LVEF were number of viable segments, hazard ratio 1.4, 95% confidence interval [1.0-1.8] and end systolic volume (per mL), hazard ratio -0.038, 95% confidence interval [0.010-0.066]. The end diastolic volume was not predictive. The best model to predict LVEF was: LVEF change = 2.15 + 1.4 · number of viable segments - 0.038 · end systolic volume.

View larger version (17K): [in this window] [in a new window]   Figure 1. Scatter plot indicating the relation between the end systolic volume (in mL) and the LVEF change following myocardial revascularization in the 61 patients with a substantial amount of viability (R = 0.43, P < .001).

	Discussion

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Previous studies
The current results are in line with previous observations by Louie and colleagues.¹² In that study 22 patients with ischemic cardiomyopathy underwent myocardial revascularization. In patients with a successful revascularization, the end diastolic dimension was smaller than in patients with failed revascularization (68 ± 3 mm vs 81 ± 4 mm, P < .05). Yamaguchi and colleagues¹³ studied 20 patients with ischemic cardiomyopathy. Patients were divided into 2 groups on the basis of the end systolic volume index. The mean LVEF improved significantly after revascularization in patients with an end systolic volume index < 100 mL/m². However, myocardial viability was not in this study.¹³ In the present study, the preoperative end systolic volume dictated the postoperative LV function, even in patients with a substantial amount of dysfunctional but viable myocardium. This may be caused by an increased wall stress and adverse LV geometry. Restoration of myocardial blood flow may not be capable of reversing myocardial function in these segments. Nevertheless, Kim and colleagues¹⁷ have suggested that patients with ischemic cardiomyopathy and LV dilation should not be excluded from surgical revascularization based on ventricular size alone. Due to revascularization of viable myocardium, the remodeling process may be stopped, resulting in an improved long-term survival, even in the absence of improvement of function. In addition, resection of nonviable scar tissue may also favorably influence survival. Randomized clinical trials, like the Surgical Treatment for IsChemic Heart failure (STICH) trial, are needed to assess the optimal treatment in these patients.¹⁸

Clinical implications
Previous studies have demonstrated that a certain amount of dysfunctional but viable tissue is needed for an improvement of global function following revascularization.^10,11,15 Usually a level of 4 viable segments is advised as a cutoff value to predict improvement of LVEF.^10,15 This cutoff value represents approximately 25% of the LV and can be used to identify patients who may benefit from revascularization.^10,15 The present study confirms the findings from these previous studies. An enlarged end systolic volume prevented global recovery, even in patients with substantial viability. In these patients CABG could be combined with resection of nonviable scar tissue. Traditionally, only dyskinetic regions (cardiac aneurysms) were excised and closed. However, it was recognized that surgical reduction of akinetic regions may reduce wall stress and improve the geometry and LV function in selected patients.^19,20 In patients with a previous anterior infarction, surgical anterior ventricular endocardial restoration is a safe and effective operation to restore geometry and reverse LV remodeling.²⁰ Further studies are needed to determine the value of these additional surgical procedures in patients with a substantial amount of viable tissue.

The present data suggest that improvement may also occur in patients with <4 viable segments. A total of 57 patients had <4 viable segments and were considered nonviable. Interestingly, 7 of the nonviable patients had an improved LVEF after revascularization. This was probably related to the combination of 3 dysfunctional but viable segments and a preserved end systolic volume in these patients. Hence, the cutoff value of 4 viable segments is to some extent arbitrary, because not only myocardial viability but also remodeling and enlargement of the LV should be considered. This may further improve case selection before revascularization procedures in patients with ischemic cardiomyopathy.

Techniques to assess viability
In the present study, dobutamine stress echocardiography was used to assess myocardial viability. Although positron emission tomography may be slightly more accurate for the prediction of functional recovery after revascularization, both techniques provide similar prognostic information and accurately identify high-risk patients who may benefit from revascularization.²¹ In particular, Allman and colleagues²² have demonstrated in a meta-analysis that no significant difference in prognostic value between stress echocardiography and positron emission tomography existed. Recently, magnetic resonance imaging combined with gadolinium-based contrast agents was proposed to evaluate myocardial viability.²³ Importantly, LV volumes and the transmural extent of viable/nonviable myocardium can be determined with the high spatial resolution of magnetic resonance imaging. This may have important clinical implications as the extent of transmural injury is related to functional improvement after revascularization.

Study limitations
Several limitations of this study have to be mentioned. First, during bypass surgery an attempt was made to revascularize all vessels with a significant stenosis; however, angiography was not repeated at follow-up, and therefore graft occlusion may have prevented functional recovery of viable segments. Second, improvement in global function was assessed before and 3 to 6 months after revascularization. A longer follow-up time may be needed for complete recovery of contractile function in all dysfunctional but viable segments.²⁴ Third, beta-blockers and angiotensin-converting enzyme inhibition were used based on clinical grounds. This may have influenced LV function; however, this reflects daily clinical practice. Finally, magnetic resonance imaging may be more accurate than 2-dimensional echocardiography to assess LV volumes.

	Conclusions

Top Abstract Methods Results Discussion Conclusions References

 
In patients with ischemic cardiomyopathy not only the amount of dysfunctional but viable myocardium but also the extent also LV remodeling and enlargement determines the improvement in function following myocardial revascularization. Patients with a high end systolic volume due to LV remodeling have a decreased likelihood of improvement of global function. Additional surgical procedures may be needed to improve LV function in these patients.

	References

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1. Gheorghiade M, Bonow RO. Chronic heart failure in the United States—a manifestation of coronary artery disease. Circulation. 1998;97:282–289[Free Full Text]
   
2. Baker DW, Jones R, Hodges J, Massie BM, Konstam MA, Rose EA. Management of heart failure. III. The role of revascularization in the treatment of patients with moderate or severe left ventricular systolic dysfunction. JAMA. 1994;272:1528–1534[Abstract]
   
3. Zaroff JG, Rosengard BR, Armstrong WF, et al. Consensus conference report: maximizing use of organs recovered from the cadaver donor: cardiac recommendations. Circulation. 2002;106:836–841[Abstract/Free Full Text]
   
4. Elefteriades JA, Tolis G Jr, Levi E, Millis LK, Zaret BL. Coronary artery bypass grafting in severe left ventricular dysfunction: excellent survival with improved ejection fraction and functional state. J Am Coll Cardiol. 1993;22:1411–1417[Abstract]
   
5. Trachiotis GD, Weintraub WS, Johnston TS, Jones EL, Guyton RA, Crave JM. Coronary artery bypass grafting in patients with advanced left ventricular dysfunction. Ann Thorac Surg. 1998;66:1632–1639[Abstract/Free Full Text]
   
6. Cimochowski GE, Harostock MD, Foldes PJ. Minimal operative mortality in patients undergoing coronary artery bypass with significant left ventricular dysfunction by maximization of metabolic and mechanical support. J Thorac Cardiovasc Surg. 1997;113:655–664[Abstract/Free Full Text]
   
7. Mickleborough LL, Maruyama H, Takagi Y, Mohamed S, Sun Z, Ebizaki L. Results of revascularization in patients with severe left ventricular dysfunction. Circulation. 1995;92(Suppl II):II73–79
   
8. Schinkel AFL, Bax JJ, Boersma E, Elhendy A, Roelandt JR, Poldermans D. How many patients with ischemic cardiomyopathy exhibit viable myocardium? Am J Cardiol. 2001;88:561–564[Medline]
   
9. Auerbach MA, Schoder H, Hoh C, et al. Prevalence of myocardial viability as detected by positron emission tomography in patients with ischemic cardiomyopathy. Circulation. 1999;99:2921–2926[Abstract/Free Full Text]
   
10. Bax JJ, Poldermans D, Elhendy A, et al. Improvement of left ventricular ejection fraction, heart failure symptoms and prognosis after revascularization in patients with chronic coronary artery disease and viable myocardium detected by dobutamine stress echocardiography. J Am Coll Cardiol. 1999;34:163–169[Abstract/Free Full Text]
    
11. Di Carli MF, Maddahi J, Rokhsar S, et al. Long-term survival of patients with coronary artery disease and left ventricular dysfunction: implications for the role of myocardial viability assessment in management decisions. J Thorac Cardiovasc Surg. 1998;116:997–1004[Abstract/Free Full Text]
    
12. Louie HW, Laks H, Milgalter E, et al. Ischemic cardiomyopathy. Criteria for coronary revascularization and cardiac transplantation. Circulation. 1991;84:III290–295
    
13. Yamaguchi A, Ino T, Adachi H, Mizuhara A, Murata S, Kamio H. Left ventricular end-systolic volume index in patients with ischemic cardiomyopathy predicts postoperative ventricular function. Ann Thorac Surg. 1995;60:1059–1062[Abstract/Free Full Text]
    
14. Bourdillon PD, Broderick TM, Sawada SG, et al. Regional wall motion index for infarct and non-infarct region after reperfusion in acute myocardial infarction: comparison with global wall motion index. J Am Soc Echocardiogr. 1989;2:398–407[Medline]
    
15. Nagueh SF, Vaduganathan P, Ali N, et al. Identification of hibernating myocardium: comparative accuracy of myocardial contrast echocardiography, rest-redistribution thallium-201 tomography and dobutamine echocardiography. J Am Coll Cardiol. 1997;29:985–993[Abstract]
    
16. Bax JJ, Wijns W, Cornel JH, Visser FC, Boersma E, Fioretti PM. Accuracy of currently available techniques for prediction of functional recovery after revascularization in patients with left ventricular dysfunction due to chronic coronary artery disease: comparison of pooled data. J Am Coll Cardiol. 1997;30:1451–1460[Abstract]
    
17. Kim RW, Ugurlu BS, Tereb DA, Wackers FJ, Tellides G, Elefteriades JA. Effect of left ventricular volume on results of coronary artery bypass grafting. Am J Cardiol. 2000;86:1261–1264[Medline]
    
18. McMurray J, Pfeffer MA. New therapeutic options in congestive heart failure: part I. Circulation. 2002;105:2099–2106[Free Full Text]
    
19. Dor V, Sabatier M, Di Donato M, Montiglio F, Toso A, Maioli M. Efficacy of endoventricular patch plasty in large postinfarction akinetic scar and severe left ventricular dysfunction: comparison with a series of large dyskinetic scars. J Thorac Cardiovasc Surg. 1998;116:50–59[Abstract/Free Full Text]
    
20. Athanasuleas CL, Stanley AW Jr, Buckberg GD, Dor V, Di Donato M, Blackstone EH. Surgical anterior ventricular endocardial restoration (SAVER) in the dilated remodeled ventricle after anterior myocardial infarction. RESTORE group. Reconstructive Endoventricular Surgery, returning Torsion Original Radius Elliptical Shape to the LV. J Am Coll Cardiol. 2001;37:1199–1209[Abstract/Free Full Text]
    
21. Schinkel AFL, Bax JJ, Geleijnse ML, et al. Noninvasive evaluation of ischaemic heart disease: myocardial perfusion imaging or stress echocardiography? Eur Heart J. 2003;24:789–800[Free Full Text]
    
22. Allman KC, Shaw LJ, Hachamovitch R, Udelson JE. 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]
    
23. Kim RJ, Wu E, Rafael A, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med. 2000;343:1445–1453[Abstract/Free Full Text]
    
24. Vanoverschelde JL, Depre C, Gerber BL, et al. Time course of functional recovery after coronary artery bypass graft surgery in patients with chronic left ventricular ischemic dysfunction. Am J Cardiol. 2000;85:1432–1439[Medline]
    

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schinkel, A. F. L. Articles by Bax, J. J. Search for Related Content PubMed PubMed Citation Articles by Schinkel, A. F. L. Articles by Bax, J. J. Related Collections Myocardial infarction