EJCTS Click here to go to Edwards website
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
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 Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Henrik Arendrup
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kofoed, K. F.
Right arrow Articles by Kelbæk, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kofoed, K. F.
Right arrow Articles by Kelbæk, H.
Related Collections
Right arrow Coronary disease

Eur J Cardiothorac Surg 2002;21:417-423
© 2002 Elsevier Science NL

Prolonged ischemic heart disease and coronary artery bypass — relation to contractile reserve

Klaus F. Kofoeda*, Regitze Bangsgaardb, Steen Carstensena, Jesper H. Svendsena, Peter R. Hansena, Henrik Arendrupc, Birger Hesseb, Henning Kelbæka

a Division of Cardiology, Medical Department B, The Heart Center, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
b Division of Thoracic Surgery, The Heart Center, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
c Department of Clinical Physiology and Nuclear Medicine, The Imaging Center, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

Received 30 August 2001; received in revised form 23 November 2001; accepted 3 December 2001.

* Corresponding author. Cardiovascular PET Research Unit, Section 9201, Medical Department B, The Heart Center, Rigshospitalet, University of Copenhagen, Juliane Mariesvej 24 DK-2100 Copenhagen, Denmark. Tel.: +45-35456704; fax: +45-35456713
e-mail: kkofoed{at}pet.rh.dk


   Abstract
Top
 Abstract
1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Objective: A major effect of coronary artery bypass grafting (CABG) in patients with ischemic heart disease and impaired left ventricular (LV) contractile function is believed to be an improvement in LV function due to recovery of dysfunctional, but viable myocardium. However, recent studies have indicated a time limit for such a recovery. We therefore investigated the extent of viable myocardium in patients with impaired LV function due to ischemic heart disease after a prolonged strategy of medical treatment and its relation to changes in clinical variables after CABG. Methods: Forty-five consecutive patients with a mean duration of ischemic heart symptoms of 9 years and LV ejection fraction (EF) <45% referred for CABG were included and LV extent of viable myocardium was measured preoperatively by glucose metabolism–blood flow positron emission tomography imaging and dobutamine stress echocardiography. Symptoms, exercise-capacity and LV function were evaluated before and 7 months after surgery in event-free survivors. Results: LV extent of myocardial viability was <30% in most patients. In event-free survivors, LVEF decreased from 31±7 to 26±8% 7 months after CABG. The decrease in LVEF was correlated to the LV extent of myocardial metabolism–blood flow reverse mismatch. Most of the patients experienced an improvement in their angina pectoris, heart failure symptoms and exercise capacity after CABG; the overall 3-year survival was 77%. Conclusions: Patients with chronic ischemic heart disease and impairment of LV function, in whom an initial long-standing conservative treatment has been practiced, benefit from CABG, despite a lack of LV functional reserve.

Key Words: Coronary bypass surgery • Left ventricular dysfunction • Myocardial viability


   1. Introduction
Top
 Abstract
 1. Introduction
2. Material and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Coronary artery bypass grafting (CABG) is an effective treatment of patients with ischemic heart disease and reduced left ventricular (LV) contractile function, improving both cardiac symptoms and long-term survival compared with medical treatment [1–3]. The effect of CABG in this patient group is believed to be mediated by a combination of improvement in blood flow to normo- and hypokinetic myocardium supplied by stenosed or occluded coronary arteries and recovery of dysfunctional LV areas [4–6].

Reversibility of the reduced contractile function in areas of viable myocardium was long believed to be a stable condition achieved by myocardial adaptation to a reduced coronary blood supply. However, recent studies have indicated that viability of dysfunctional myocardium can only be maintained for a limited period of time [7,8]. A prolonged conservative strategy of medical treatment of patients with stable ischemic heart disease might consequently lead to deterioration of the viable myocardium and thereby limit the clinical benefit of CABG at this stage of the disease.

Improvement of LV contractile function after CABG may be predicted by positron emission tomography (PET) and dobutamine stress echocardiography [9]. Viable myocardium is mainly characterized by preserved glucose metabolism in hypoperfused myocardium — so-called glucose metabolism–blood flow mismatch — as assessed by the glucose analogue 18F fluorodeoxyglucose (18FDG) and the myocardial blood flow tracer 13N ammonia (13NH3). The clinical significance of a reduced glucose metabolism in areas with normal blood flow — i.e. reverse mismatch — in dysfunctional myocardium remains unknown [10]. Viable myocardium also may be identified by the improvement of contractile function during low dose intravenous infusion of dobutamine.

In this study, we assessed the extent of viable myocardium in patients with ischemic heart disease following a prolonged conservative strategy of medical treatment and evaluated the impact of CABG on the clinical variables and LV function in event-free survivors.


   2. Material and methods
Top
 Abstract
 1. Introduction
 2. Material and methods
3. Results
 4. Discussion
 5. Conclusions
 References
 
2.1. Study population
The study population was a prospectively included series of patients referred for coronary angiography at Rigshospitalet, Copenhagen. Inclusion criteria were: (1) a history of medically treated ischemic heart disease >6 months duration; (2) a left ventricular ejection fraction <45% as measured by radionuclide ventriculography and (3) a clinical indication to perform CABG. Onset of ischemic heart disease was defined as the time of the first acute myocardial infarction or the time of onset of angina pectoris requiring medication. The decision to perform CABG was based on clinical and angiographic criteria according to the recommendations derived from the CASS study [1]. Exclusion criteria were acute myocardial infarction or unstable angina pectoris within 1 month before inclusion and chronic atrial fibrillation. The study was approved by the local ethical committee and all patients gave their written informed consent. Forty-five patients were included in the study. Patient characteristics and angiographic findings are summarized in Table 1.


View this table:
[in this window]
[in a new window]
  		Table 1. Study group (N=45)a

 
2.2. Study protocol
Cardiac symptoms, cardiac medication, bicycle exercise capacity, radionuclide LV function and extent of myocardial viability as determined by PET and dobutamine stress echocardiography (DSE) were recorded within 1 month prior to surgery. Major cardiac events (cardiac death, myocardial infarction, unstable angina pectoris and hospital referral due to episodes of heart failure) were recorded 7 months after CABG. Cardiac symptoms, use of anti-anginal medication and anti-congestive medication, exercise-capacity and global LV function in event-free survivors were reevaluated 7 months after surgery. Long-term cardiac survival was evaluated as a median of 3 years after surgery. Glucose metabolism–blood flow PET images were not available in eight patients due to misalignment of the heart in the scanner (n=4), claustrophobia (n=1) or for logistic reasons (n=3). DSE was not available in seven patients for logistic reasons. One patient died and another patient had an acute myocardial infarction after baseline measurements, but before CABG. Both of these patients were excluded from further analysis. Five event-free patients withdrew from the 7 months post-surgical measurements. Post-CABG exercise capacity could not be determined in one patient for logistic reasons and in another due to new onset of claudication of the legs.

2.3. Symptoms, exercise capacity and use of cardiac drugs
The Canadian Cardiovascular Society and the New York Heart Association classification systems were used to evaluate angina pectoris and heart failure symptoms before and after surgery. Symptom-limited bicycle exercise testing was performed with an initial workload of 25 W with increments of 25 W every 2 min. Standard endpoints were employed together with monitoring of heart rate, blood pressure and continuous 12-lead electrocardiography. Exercise capacity was expressed by metabolic equivalents (Mets) [12]. The use of long acting nitrates, beta-blockers, calcium antagonists (anti-ischemic medication), ACE inhibitors, digoxin and diuretics (anti-congestive medication) were recorded before and after CABG.

2.4. Radionuclide ventriculography
Radionuclide ventriculography was acquired after in vivo labeling of red blood cells with 800 MBq Technetium-99m sodium pertechnetate using a General Electric 300 AC gamma camera. Based on manual delineation of the left ventricular blood pool in end-systole and end-diastole as processed by an experienced blinded observer, the LVEF was calculated as previously described [13].

2.5. Positron emission tomography
Myocardial glucose metabolism–blood flow PET imaging was performed using a General Electric tomograph model ADVANCE. Relative myocardial glucose metabolism was assessed with 18FDG during glucose–insulin clamp [14]. Relative myocardial blood flow was assessed with 13NH3 within 1 day of the 18FDG study. Static attenuation corrected transaxial PET images were reoriented into six short axis slices encompassing the left ventricle. The relative tracer uptake was assessed using circumferential profile analysis and compared to our local reference database of age and gender matched healthy subjects. Myocardial tracer uptake was considered to be reduced when >2 standard deviations below the mean reference value [4]. The following abnormal relative glucose metabolism–blood flow patterns in the LV myocardium were recorded: mismatch (normal 18FDG, reduced 13NH3), match (reduced 18FDG and 13NH3) and reverse mismatch (reduced 18FDG, normal 13NH3). LV extent (%) was calculated using correction factors for the anatomical tapering of the LV radius from the base to the apex [15].

2.6. Dobutamine stress echocardiography
Two-dimensional echocardiographic recordings were obtained in five standard views: apical 2 chamber, apical 4 chamber, parasternal long axis, parasternal short axis at the chorda and mid-papillary level, using commercially available ultrasonic and digitizing equipment (Vingmed CFM 725 and EchoPAC) [16]. Recordings were obtained at rest and at each 3 min stage of dobutamine infusion at rates of 5, 10, 20, 30 and 40 µg/kg/min. Infusion was terminated at the following endpoints: 85% of the age-corrected heart rate, intolerable angina pectoris, obvious stress induced wall motion abnormalities, maximal drug infusion rate or severe side effects (ventricular tachycardia, hypotension, anxiety). Recordings were displayed in a quadscreen format allowing simultaneous and synchronized playback of cineloops in each view obtained at rest and after dobutamine infusion. Using a 16-segment model LV function in each segment was qualitatively evaluated according to the following scoring scale: hyperkinesia=0, normokinesia=1, hypokinesia=2, akinesia=3, dyskinesia=4. Improvement of wall motion score at any stage during DSE of >=1 grade in segments that were hypo- or akinetic at baseline was considered indicative of contractile reserve. The extent of myocardial viability was expressed as the percentage of segments with contractile reserve.

2.7. Coronary artery bypass surgery
CABG was performed during moderate hypothermia (32°C) and cold crystalloid cardioplegia. Median duration of extracorporeal circulation and aortic clamp time were 95 min (range 35–203) and 54 min (range 20–160), respectively. The patients received a median number of 3 (range 2–6) bypass grafts, and arterial conduits were used in all but one lesion in the left anterior descending branch of the left coronary artery. Complete revascularization was performed in all patients except three, in whom the posterior descending branch of the right coronary artery was not graftable. In 80% of the inserted grafts, distal coronary anastomoses were performed on coronary arteries with a luminal diameter >1.5 mm. The average peak creatine kinase MB value was 22 U/l (range 10–55). Early (within 30 days) post-surgical complications were: death 2% (n=1), myocardial infarction 2% (n=1) and transient atrial fibrillation 40% (n=17).

2.8. Statistical analysis
Data are presented by their means and standard deviations unless otherwise stated. Comparison of continuous variables before and after CABG was performed by the paired t-test. Correlations were sought by use of a least-squares regression analysis. Survival curves were constructed using the Kaplan–Meier method. A P value of less than 0.05 was considered statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
4. Discussion
 5. Conclusions
 References
 
3.1. Positron tomography and dobutamine echocardiography findings
The extent of myocardial glucose metabolism–blood flow mismatch and reverse mismatch in addition to dobutamine stress echocardiography findings are shown in Fig. 1 . In more than half of the patients, glucose metabolism–blood flow mismatch was found in less than 10% of the left ventricle, and none of our patients had the mismatch pattern in more than 30% of the left ventricle (Fig. 1, top panel). Very similar findings were recorded by DSE (Fig. 1, bottom panel). In patients with LVEF>=30%, the mean amount of viable myocardium was similar to patient with LVEF below 30% (P=NS). Patients with the longest history of cardiac symptoms had the lowest extent of mismatch (r=-0.37, P=0.01).



View larger version (19K):
[in this window]
[in a new window]
  		Fig. 1. Frequency of glucose metabolism-blood flow patterns and myocardial viability by dobutamine stress echocardiography (DSE) as a function of extent in the left ventricle. Closed bars: mismatch open bars: reverse mismatch hatched bars: myocardial viability by DSE.

 
3.2. Symptoms and cardiac medication after CABG
At 7 months after CABG, five patients had died, one patient had experienced an acute myocardial infarction and two patients had been admitted for hospital treatment of heart failure. Changes in symptoms and use of cardiac medication after CABG in event-free survivors (n=30) are delineated in Table 2. Angina pectoris and functional class improved and the amount of anti-anginal medication taken by the patients decreased. The use of anti-congestive medication was unchanged in most patients. In patients with LVEF <30% improvement in functional class and reduction in anti-congestive medication appeared to be more frequently observed. The average extent of glucose metabolism–blood flow mismatch and DSE viability were similar in patients with and without improvement in angina pectoris and functional class (data not shown).


View this table:
[in this window]
[in a new window]
  		Table 2. Symptoms and cardiac medication after CABGa

 
3.3. Exercise capacity and left ventricular ejection fraction
In event-free survivors, the exercise capacity increased 7 months after surgery (P<0.05, Fig. 2A ). None of the patients had angina pectoris during exercise after CABG, but three patients had silent myocardial ischemia. No relationship was found between extent of glucose metabolism–blood flow mismatch or DSE viability and improvement in exercise capacity after CABG. The mean LVEF decreased from 31 to 26% 7 months after CABG in event-free survivors (Fig. 2B, P<0.0005). In a subgroup of patients with LVEF <30% a similar trend was observed (LVEF 23±4 vs. 20±5%, P=0.058). The change in LVEF after CABG was not correlated with presurgical history of acute myocardial infarction, peak creatine kinase MB value during surgery, duration of extracorporeal circulation or aortic clamp time. Similarly, the change was not related to post-surgical angina pectoris threshold, heart failure symptoms, exercise capacity or the extent of viability by PET or DSE (Fig. 3, top and bottom panels ). The change in LVEF after CABG was inversely correlated to the extent of LV reverse mismatch (Fig. 3, mid panel).



View larger version (19K):
[in this window]
[in a new window]
  		Fig. 2. (A) Exercise capacity and (B) left ventricular ejection fraction before (pre) and 7 months after (post) coronary artery bypass grafting in event-free survivors (n=30). *P<0.05, **P<0.0005. Closed symbols: patients with LVEF >=30% Open symbols: patients with LVEF <30%.

 


View larger version (11K):
[in this window]
[in a new window]
  		Fig. 3. Relationship between the extent of glucose metabolism-blood flow patterns in the left ventricle, myocardial viability by dobutamine stress echocardiography (DSE) and change in left ventricular ejection fraction 7 months after coronary artery bypass grafting. Circles: mismatch. Triangles: reverse mismatch. Diamonds: DSE viability Open symbols: patients with LVEF <30% The relationship for reverse mismatch was y=-0.5x-0.8, r=-0.54, P<0.01.

 
3.4. Long-term survival
During the observation period, 10 patients died from cardiac causes, three from non-cardiac causes, and one patient was referred for heart transplantation and was censored from the survival data. For the 43 patients undergoing CABG, the 3 year cardiac survival was 77%.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
5. Conclusions
 References
 
In this study, we have demonstrated that in patients with ischemic heart disease and impaired LV function following a prolonged strategy of medical treatment, the extent of LV myocardial viability is rather small. In addition, we found that despite an LVEF decrease in event-free survivors, most of the patients experienced relief of angina pectoris and heart failure symptoms and improvement in their exercise capacity 7 months after CABG.

Evaluation of LV extent of myocardial viability before CABG has been performed using a variety of methods including single photon emission computerized tomography (SPECT), PET and dobutamine stress echocardiography [9,14]. The diagnostic value of these different methods is usually high – although the specificity of dobutamine stress echocardiography is probably slightly higher than the other techniques. In the present study, we found that a long-standing conservative treatment strategy was incompatible with the finding of areas of viable myocardium in the left ventricle large enough to induce an increase in LVEF after CABG. By both PET and DSE, the extent of myocardial viability was confined to a fraction <30% of the left ventricle in almost all patients. In a previous study, myocardial viability in at least 25% of the left ventricle was required for CABG to produce an improvement of global LV function [17]. In large unselected patient groups, the number of patients with myocardial viability of this magnitude ranges from 20 to 30% [18,19]. Unfortunately, the duration of medical treatment at the time of viability testing or CABG was not provided in these retrospective reports. We may therefore only speculate that the high frequency of patients with large areas of viable myocardium in these studies is explained by a shorter duration of ischemic heart disease at the time of CABG. Since one of the cornerstones in the treatment strategy of patients with ischemic heart disease is to preserve LV contractile function, evaluation of myocardial viability should apparently not await aggravation of cardiac symptoms. Nevertheless, our results suggest that a substantial clinical benefit may be achieved by CABG even after a prolonged strategy of medical treatment. Despite a post-operative decrease in LVEF in our patients, we found that their cardiac symptoms and exercise capacity improved and the use of anti-anginal medication decreased.

The 3-year cardiac survival for our study group was 77%. Concordantly, the overall 3-year cardiac survival after CABG have been reported to be 75–85% in patients with moderate to severe impairment of LV function [3,20,21]. However, our results are at variance with the assumption that patients with impaired LV function benefit from CABG because of an increase in LVEF. On the other hand, our results correspond to the recent report of Samady et al., who found no relationship between changes in LVEF early after CABG and clinical outcome in patients with impaired LV function [6]. They suggested that additional mechanisms not related to global LV function may be responsible for the beneficial effect of CABG.

The majority of the patients included in our study had glucose metabolism–blood flow mismatch in more than 5% but less than 30% of the left ventricle. Di Carli et al. found that an LV mismatch extent of >18% predicted a significant improvement of functional class after CABG in patients with a wider range (0–74%) of glucose metabolism–blood flow mismatch [4]. In addition, CABG was associated with a substantial improvement in prognosis compared with medical therapy in patients with mismatch in >5% of the left ventricle [3,22]. These reports seem to indicate that revascularization of even small regions of viable myocardium is associated with improvement of symptoms and prognosis, regardless of changes in global LV function. Within the relatively narrow range of mismatch in the left ventricle found in the present study (0–27%), we were not able to demonstrate any relationship between extent of mismatch in the left ventricle and improvement of symptoms or exercise capacity after CABG. Thus, other factors than the extent of myocardial viability may influence the effects of CABG in a patient population like ours. In the current study, myocardial protection during surgery was obtained using cold crystalloid cardioplegia. Recently, Ibrahim and colleagues demonstrated that myocardial protection using blood cardioplegia during surgery in patients with impaired LV function significantly enhanced early post-surgical recovery of LV function when compared to conventional crystalloid cardioplegia [23]. On the other hand, we did not find any significant relationship between the peak creatine kinase leakage during surgery and the post-surgical change in left LV function. Instead, we found a significant correlation between the post-operative decrease in LV function and the extent of glucose metabolism–blood flow reverse mismatch. The decrease in LVEF in patients undergoing CABG, who have relatively large myocardial areas with a normal blood flow, is unexplained, but could reflect a progression of ongoing LV remodeling [24].

4.1. Study limitations
Patency of the coronary artery bypass grafts was not examined in our study and the angiographical extent of coronary revascularization at the time of follow up is therefore unknown. However, virtually all bypass conduits distal to LAD lesions were arterial grafts, the majority of saphenous vein grafts were anastomosed to coronary vessels with a luminal diameter >=1.5 mm and revascularization was complete in all but three patients. None of these patients had angina pectoris after surgery and the average change in their LVEF after CABG was +3%.


   5. Conclusions
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 5. Conclusions
References
 
Previous studies have established that, when dysfunctional but viable myocardium is present, early myocardial revascularization is warranted even in the absence of severe symptoms [22,25]. In this study, we found that when LV function is reduced after a prolonged conservative strategy of medical treatment in patients with ischemic heart disease, areas of dysfunctional but viable myocardium are scarce and improvement of LV function after CABG can rarely be expected. Nevertheless, a substantial symptomatic benefit together with an acceptable long-term cardiac survival was achieved after CABG in these patients.


   Acknowledgments
 
The study was supported by the Danish Heart Foundation, The Research Council of the Rigshospitalet, The Birthe and John Meyer foundation, Novo's Foundation, The Foundation of December 17, 1981, The Foundation of King Christian X, and the Foundation of Mr and Mrs Nyegaard. Drs Søren Holm, Alan Rabøl, Mikael Jensen, Jens Hove and Jacob Freiberg are thanked for their assistance. Technician Helle Jung Larsen is thanked for her excellent assistance.


   References
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 

  1. Alderman E.L., Fisher L.D., Litwin P., Kaiser G.C., Myers W.O., Maynard C., Levine F., Schloss M. Results of coronary artery surgery in patients with poor left ventricular function (CASS). Circulation 1983;68:785-795.[Abstract/Free Full Text]
  2. Varnauskas E. Twelve-year follow-up of survival in the randomized European coronary surgery study. N Engl J Med 1988;319:332-337.[Abstract]
  3. Di Carli M.F., Maddahi J., Rokhsar S., Schelbert H.R., Bianco-Batlles D., Brunken R.C., Fromm B. 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]
  4. Di Carli M.F., Asgarzadie F., Schelbert H.R., Brunken R.C., Laks H., Phelps M.E., Maddahi J. Quantitative relation between myocardial viability and improvement in heart failure symptoms after revascularization in patients with ischemic cardiomyopathy. Circulation 1995;92:3436-3444.[Abstract/Free Full Text]
  5. Pasquet A., Robert A., D'Hondt A.M., Dion R., Melin J.A., Vanoverschelde J.L. Prognostic value of myocardial ischemia and viability in patients with chronic left ventricular ischemic dysfunction. Circulation 1999;100:141-148.[Abstract/Free Full Text]
  6. Samady H., Elefteriades J.A., Abbott B.G., Mattera J.A., McPherson C.A., Wackers F.J. Failure to improve left ventricular function after coronary revascularization for ischemic cardiomyopathy is not associated with worse outcome. Circulation 1999;100:1298-1304.[Abstract/Free Full Text]
  7. Elsasser A., Schlepper M., Klovekorn W.P., Cai W.J., Zimmermann R., Muller K.D., Strasser R., Kostin S., Gagel C., Munkel B., Schaper W., Schaper J. Hibernating myocardium: an incomplete adaptation to ischemia. Circulation 1997;96:2920-2931.[Abstract/Free Full Text]
  8. Beanlands R.S., Hendry P.J., Masters R.G., deKemp R.A., Woodend K., Ruddy T.D. Delay in revascularization is associated with increased mortality rate in patients with severe left ventricular dysfunction and viable myocardium on fluorine 18-fluorodeoxyglucose positron emission tomography imaging. Circulation 1998;98:II51-II56.
  9. Bax J.J., Wijns W., Cornel J.H., Visser F.C., Boersma E., Fioretti P.M. 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]
  10. Schwaiger M., Pirich C. Reverse flow–metabolism mismatch: what does it mean?. J Nucl Med 1999;40:1499-1502.[Free Full Text]
  11. Califf R.M., Phillips H.Rd., Hindman M.C., Mark D.B., Lee K.L., Behar V.S., Johnson R.A., Pryor D.B., Rosati R.A., Wagner G.S. Prognostic value of a coronary artery jeopardy score. J Am Coll Cardiol 1985;5:1055-1063.[Abstract]
  12. strand P.-O., Rodahl K. Textbook of work physiology. New York, NY: McGraw Hill, 1986.
  13. Kelbæk H., Hartling O., Gjørup T., Marving J., Christensen N., Godtfredsen J. Effects of autonomic blockade on cardiac function at rest and during upright exercise in humans. J Appl Physiol 1987;63:554-557.[Abstract/Free Full Text]
  14. Kofoed K.F., Carstensen S., Hesse B., Hove J.D., Holm S., Jensen M., Haunso S., Kelbaek H. Fluorodeoxyglucose uptake in dysfunctional myocardium subtended by an occluded coronary artery. Relation to dobutamine contractile reserve and Sestamibi uptake. Int J Card Imaging 1998;14:97-104.[Medline]
  15. Porenta G., Kuhle W., Czernin J., Ratib O., Brunken R., Phelps M., Schelbert H. Semiquantitative assessment of myocardial viability and perfusion utilizing polar map displays of cardiac PET images. J Nucl Med 1992;33:1623-1631.[Abstract/Free Full Text]
  16. Carstensen S., Ali S., Stensgaard-Hansen F., Toft J., Haunsoe S., Kelbaek H., Saunamaki K. Dobutamine–atropine stress echocardiography in asymptomatic normal individuals: the relativity of stress induced hyperkinesia. Circulation 1995;92:3453-3463.[Abstract/Free Full Text]
  17. Tillisch J., Brunken R., Marshall R., Schwaiger M., Mandelkern M., Phelps M., Schelbert H. Reversibility of cardiac wall-motion abnormalities predicted by positron tomography. N Engl J Med 1986;314:884-888.[Abstract]
  18. Christian T.F., Miller T.D., Hodge D.O., Orszulak T.A., Gibbons R.J. An estimate of the prevalence of reversible left ventricular dysfunction in patients referred for coronary artery bypass surgery. J Nucl Cardiol 1997;4:140-146.[Medline]
  19. Auerbach M.A., Schoder H., Hoh C., Gambhir S.S., Yaghoubi S., Sayre J.W., Silverman D., Phelps M.E., Schelbert H.R., Czernin J. Prevalence of myocardial viability as detected by positron emission tomography in patients with ischemic cardiomyopathy. Circulation 1999;99:2921-2926.[Abstract/Free Full Text]
  20. Mickleborough L.L., Maruyama H., Takagi Y., Mohamed S., Sun Z., Ebisuzaki L. Results of revascularization in patients with severe left ventricular dysfunction. Circulation 1995;92:II73-II79.
  21. Elefteriades J.A., Morales D.L., Gradel C., Tollis G., Jr, Levi E., Zaret B.L. Results of coronary artery bypass grafting by a single surgeon in patients with left ventricular ejection fractions < or =30%. Am J Cardiol 1997;79:1573-1578.[Medline]
  22. Di-Carli M.F., Davidson M., Little R., Khanna S., Mody F.V., Brunken R.C., Czernin J., Rokhsar S., Stevenson L.W., Laks H., Hawkins R., Schelbert H.R., Phelps M.E. Value of metabolic imaging with positron emission tomography for evaluating prognosis in patients with coronary artery disease and left ventricular dysfunction. Am J Cardiol 1994;73:527-533.[Medline]
  23. Ibrahim M.F., Venn G.E., Young C.P., Chambers D.J. A clinical comparative study between crystalloid and blood-based St Thomas' hospital cardioplegic solution. Eur J Cardiothorac Surg 1999;15:75-83.[Abstract/Free Full Text]
  24. Pfeffer M.A., Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation 1990;81:1161-1172.[Abstract/Free Full Text]
  25. Eitzman D., al-Aouar Z., Kanter H.L., vom-Dahl J., Kirsh M., Deeb G.M., Schwaiger M. Clinical outcome of patients with advanced coronary artery disease after viability studies with positron emission tomography. J Am Coll Cardiol 1992;20:559-565.[Abstract]



This article has been cited by other articles:


Home page
 Eur J EchocardiogrHome page
S Carstensen, U Host, K Saunamaki, and H Kelbaek
Quantitative analysis of dobutamine-atropine stress echocardiography
Eur J Echocardiogr, September 1, 2003; 4(3): 169 - 177.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
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 Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Henrik Arendrup
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kofoed, K. F.
Right arrow Articles by Kelbæk, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kofoed, K. F.
Right arrow Articles by Kelbæk, H.
Related Collections
Right arrow Coronary disease

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS