Research

Relation between regional and global systolic function in patients with ischemic cardiomyopathy after β-Blocker therapy or revascularization

TAM Kaandorp¹ , JJ Bax² , SE Bleeker³ , J Doornbos¹ , EP Viergever² , D Poldermans⁴ , EE van der Wall² , A de Roos¹ and HJ Lamb¹

¹  Department of Radiology, Leiden University Medical Center, the Netherlands

²  Department of Cardiology, Leiden University Medical Center, the Netherlands

³  Regional Public Health Laboratory Kennemerland, Haarlem, the Netherlands

⁴  ThoraxCenter Rotterdam, the Netherlands

author email corresponding author email

Journal of Cardiovascular Magnetic Resonance 2010, 12:7doi:10.1186/1532-429X-12-7

The electronic version of this article is the complete one and can be found online at: http://www.jcmr-online.com/content/12/1/7

Received:	28 March 2009
Accepted:	27 January 2010
Published:	27 January 2010

© 2010 Kaandorp et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background

To assess the relationship between improved regional and global myocardial function in patients with ischemic cardiomyopathy in response to β-blocker therapy or revascularization.

Materials and methods

Cardiovascular Magnetic Resonance (CMR) was performed in 32 patients with ischemic cardiomyopathy before and 8 ± 2 months after therapy. Patients were assigned clinically to β-blocker therapy (n = 20) or revascularization (n = 12). CMR at baseline was performed to assess regional and global LV function at rest and under low-dose dobutamine. Wall thickening was analyzed in dysfunctional, adjacent, and remote segments. Follow-up CMR included rest function evaluation.

Results

Augmentation of wall thickening during dobutamine at baseline was similar in dysfunctional, adjacent and remote segments in both patient groups. Therefore, baseline characteristics were similar for both patient groups. In both patient groups resting LV ejection fraction and end-systolic volume improved significantly (p < 0.05) at follow-up. Stepwise multivariate analysis revealed that improvement in global LV ejection fraction in the β-blocker treated patients was significantly related to improved function of remote myocardium (p < 0.05), whereas in the revascularized patients improved function in dysfunctional and adjacent segments was more pronounced (p < 0.05).

Conclusion

In patients with chronic ischemic LV dysfunction, β-Blocker therapy or revascularization resulted in a similar improvement of global systolic LV function. However, after β-blocker therapy, improved global systolic function was mainly related to improved contraction of remote myocardium, whereas after revascularization the dysfunctional and adjacent regions contributed predominantly to the improved global systolic function.

Introduction

Recent estimations reveal that 4.9 million patients suffer from chronic heart failure in the United States, indicating the magnitude of this major health care problem [1]. Ischemic cardiomyopathy is a frequent cause of chronic heart failure. Different treatment options are available for the treatment of ischemic cardiomyopathy, including medical therapy and revascularization.

Beta-blocking agents have shown substantial benefit in patients with various degrees of heart failure [2-4]. The mechanisms by which β-blockers reduce mortality among heart failure patients remain unclear. Heart failure is a complex disease that is characterized by chronic excessive sympathetic nervous system stimulation causing myocardial toxicity and further depression of left ventricular (LV) function [5]. It is suggested that LV function improves after β-blocker therapy as a result of reversal of catecholamine-mediated myocardial toxicity in the partially viable or noninfarcted regions of the LV and possibly by improving function in regions of hibernating myocardium [6]. It has been suggested that dobutamine induced improvement in segmental contraction of dysfunctional myocardium before treatment is related to improved global LV function after medical therapy [7,8]. However, remote myocardium may potentially also contribute to the improvement of LV function after therapy, but this contribution has not yet been evaluated.

The beneficial effect of revascularization of dysfunctional myocardium in patients with ischemic cardiomyopathy has traditionally been measured by its effect on improvement of resting regional and global LV function [9,10]. Revascularization is expected to improve regional function when viable, but jeopardized myocardium is present in an area of dysfunctional myocardium [11]. Furthermore, it has been recognized that LV end-systolic volume predicts long-term outcome to best advantage after revascularization [12].

Cardiovascular magnetic resonance (CMR) is a validated and reliable method to assess global and regional myocardial function in normal and diseased hearts. Functional CMR is well suited to assess resting wall motion [13-17] as well as the response to dobutamine for predicting viability of dysfunctional myocardial segments [18].

We sought to define the contribution of regional myocardial segments to the improvement of global systolic LV function in patients after medical therapy or revascularization. We hypothesized that a differential effect on regional myocardial segments occurs depending on the type of therapy. Systemic medical therapy is expected to have a more global effect on both ischemic, dysfunctional myocardial segments and on non-ischemic, remote myocardium, whereas revascularization will have a more local effect on the ischemic, dysfunctional myocardium depending on the territory of the revascularized vessels.

Therefore, the purpose of the present study was to assess the relationship between improved regional and global myocardial function in patients with ischemic cardiomyopathy in response to β-blocker therapy or revascularization.

Materials and methods

Patient population

Thirty-two patients with chronic ischemic cardiomyopathy and LV ejection fraction (EF) <40% on gated resting Tc-99m-SPECT, were included. All patients were in sinus rhythm. Patients with a recent infarction (<3 months), unstable angina, valvular disease pacemakers and/or intracranial clips were excluded.

Patients were included consecutively. Patients that did not qualify for revascularization were assigned to the β-blocker therapy group. Patients did not qualify for revascularization because: 1. Patients had poor target vessels (small vessels, not amendable for revascularization) 2. Patients had prior existing co-morbidity (e.g. renal failure); 3. Patients refused to undergo revascularization. β-blocker therapy was started at an initial dose of 3.125 mg carvedilol twice daily. Subsequently, carvedilol was titrated at 1-week intervals as tolerated, up to target dose of 25 mg twice daily [19].

β-Blocker treated patients were compared to patients who underwent revascularization. In the revascularization patients, coronary artery bypass surgery was performed in 75% and percutaneous coronary intervention in 25%. Each patient gave informed consent to the study protocol that was approved by the local ethics committee.

CMR acquisition

Patients were studied by CMR before therapy and at 8 ± 2 months after therapy. At baseline, the CMR protocol consisted of a resting cine CMR, Late Gadolinium Enhancement (LGE) and low-dose dobutamine (10 μg/kg/min) cine CMR. Follow-up CMR included rest function evaluation only. The congestive heart failure classification by the New York Heart Association (NYHA) was determined at baseline and follow-up by the patient's cardiologist, who was blinded to the CMR data.

A 1.5-Tesla Gyroscan ACS-NT CMR scanner (Philips Medical Systems, The Netherlands) and a 5 elements cardiac synergy coil were used. Patients were studied in supine position. All images were acquired during breath-holds of approximately 15 seconds and were gated to the vector ECG; blood pressure was monitored continuously during the examination (Millennia, Invivo Research, Orlando Fla, USA). The heart was imaged from apex to base with 10 to 12 imaging levels (dependent on heart size) in short-axis view using a steady-state free-precession sequence. Typical acquisition parameters were: field of view 400 × 400 mm², matrix size 256 × 256, slice thickness 10.00 mm, flip angle 50°, time to echo 1.82 ms and time to repeat 3.65 ms. Temporal resolution was 25-39 ms, depending on heart rate. Geometry settings of rest cine CMR scans were stored and repeated for LGE and low-dose dobutamine stress CMR.

LGE images were acquired approximately 15 minutes after bolus injection of gadopentate dimeglumine (Gadolinium-DTPA, Magnevist, Schering/Berlin, Germany, 0.15 mmol/kg) with an inversion-recovery gradient echo sequence; inversion time was determined using real time planscan. Typical parameters were the following: field of view 400 × 400 mm², matrix size 256 × 256, slice thickness 5.00 mm, slice gap - 5 mm, flip angle 15°, time to echo 1.36 ms and time to repeat 4.53 ms.

For evaluation of myocardial function under pharmacological stress, intravenous dobutamine infusion was started at a rate of 5 μg/kg/min and increased after 5 min to 10 μg/kg/min. Then, after 5 min (at steady state), low-dose dobutamine images were acquired in 2- and 4-chamber and short-axis views. The same parameters were applied as described for rest imaging.

CMR image analysis

Data were analyzed on a remote workstation using MASS software (MASS, Medis, The Netherlands). The endo- and epicardial borders of the end-diastolic and end-systolic frames were manually traced with exclusion of papillary muscles, trabeculae, and epicardial fat [20]. LV end-diastolic and end-systolic volumes were calculated and LVEF was derived.

The amount of infarcted tissue was determined by drawing (manually) regions of interest around the scar tissue. In addition, the percentage of myocardium was calculated that was affected by infarction, relative to the total LV mass. LGE images were scored visually by two experienced observers (blinded to other CMR and clinical data) using a 17-segment model. Each segment was graded on a 5-point scale (segmental scar score) with 0: absence of LGE, 1: LGE of 1-25% of LV wall thickness, 2: LGE extending to 26-50%, 3: LGE extending to 51-75%, and 4: LGE extending to 76-100% of the LV wall thickness [21].

To determine regional wall motion at rest, cine CMR images were visually interpreted by two experienced observers (blinded to other CMR and clinical data) using a 17-segment model. Each segment was assigned a wall motion score using a 5-point scale with 0: normal wall motion, 1: mild hypokinesia, 2: severe hypokinesia, 3: akinesia, and 4: dyskinesia [22]. In the dysfunctional segments at rest (score 1-4), the presence or absence of contractile reserve was based on visual analysis of the difference in myocardial wall motion between CMR acquisitions at rest and during infusion of low-dose dobutamine. An improvement in segmental wall motion score by 1 grade or more was considered indicative of contractile reserve.

Myocardial segments with a visual wall motion score at rest from 1 to 4 were considered as dysfunctional segments. The myocardial segments next to these dysfunctional segments in 3-dimensions, were considered as adjacent segments. The remaining myocardial segments were considered as remote tissue (Figure 1). Wall thickness was then quantified in the above defined three regions: (1) dysfunctional, (2) adjacent, and (3) remote segments, using the centerline method as described before [23]. Wall thickening was calculated based on the difference in wall thickness between end-diastole and end-systole. The change in wall thickening was calculated between baseline and dobutamine stress acquisitions, or between baseline and follow-up acquisitions.

Statistical analysis

Continuous data were expressed as mean ± SD and compared using the Student's t test for (un-) paired data when appropriate. Stepwise multivariate analysis was performed to determine the relation between regional improvement in myocardial function and improvement in global LVEF at follow up. All tests were two-tailed and a P-value < 0.05 was considered statistically significant.

The authors had full access to the data and take responsibility for its integrity. All authors have read and agree to the manuscript as written.

Results

Baseline

Baseline characteristics are summarized in Table 1. The variables listed in Table 1 were not statistically significantly different between patients in the β-blocker and revascularization groups (Table 1). Table 2 summarizes LV dimensions and global systolic function. At baseline, there were no statistically significant differences between both patient groups (Table 2). Table 3 shows scar burden and scar morphology. At baseline, there were no statistically significant differences between both patient groups (Table 3).

The response to low-dose dobutamine at baseline in the dysfunctional, adjacent, and remote myocardial segments is summarized in Figure 2 (left panel). There were no statistically significant differences in wall thickening in any myocardial segment, when comparing the β-blocker and revascularization groups at baseline (Figure 2).

Follow-up after β-blocker or revascularization therapy

Clinical assessment revealed that the NYHA classification changed from 2.3 ± 0.5 at baseline to 1.8 ± 0.6 at follow-up (P < 0.05) in the β-blocker treated patients, and from 2.2 ± 0.5 to 1.5 ± 0.5 in the revascularization patient group (P < 0.05). After β-blocker or revascularization therapy, LV end-diastolic volume did not change significantly in both patient groups while LV end-systolic volume and LVEF improved significantly in both the β-blocker and revascularization groups to the same extent (Table 2).

Comparison of myocardial wall thickening between follow-up and baseline, revealed that in the β-blocker group the remote segments showed the largest improvement (Figure 2, right upper panel). Stepwise multivariate analysis in β-blocker patients revealed that improvement in LVEF after therapy was mainly related to improvement in function of the remote region (y = 2 × Rmt + 1.8, where Rmt = difference in wall thickening at rest in remote tissue between follow-up and baseline, P= 0.002, acceptance value 0.05). In the revascularization patient group, most improvement in myocardial wall thickening between follow-up and baseline was achieved in the dysfunctional segments (Figure 2, right lower panel). Stepwise multivariate analysis in revascularization patients revealed that improvement in LVEF was mainly related to improvement in function of the dysfunctional and adjacent segments (y = 2.6 × Dsf + 1.8 × Adj + 0.6, where Dsf = difference in wall thickening at rest in dysfunctional segments between follow-up and baseline, Adj = difference in wall thickening at rest in adjacent segments between follow-up and baseline, P= 0.001, acceptance value 0.05).

Direct comparison between the β-blocker and revascularization groups concerning the myocardial segments shows a statistically significant difference (P < 0.05) in wall thickening between the dysfunctional and remote segments (Figure 2 right panel, top and bottom). As a consequence, a reversed pattern is observed in the contribution of the dysfunctional and remote myocardial segments to improvement in wall thickening after β-blocker or revascularization therapy. This differential pattern is also illustrated in Figure 3, showing the relative contributions of the myocardial segments to improvement in LVEF after β-blocker or revascularization therapy. In the β-blocker treated patients (Figure 3, top), the remote tissue contributes for 60% to the improvement in LVEF, whereas in the revascularized patients (Figure 3, bottom), the dysfunctional segments contributed for 56% to the improvement in LVEF after therapy.

Discussion

The present study demonstrates the relation between regional and global myocardial function in patients with ischemic cardiomyopathy after β-blocker or revascularization therapy. Following β-blocker therapy, improved global systolic function is mainly related to improved contraction of remote myocardium, whereas after revascularization the dysfunctional and adjacent regions contributed most to the improvement in global systolic function.

Baseline

At baseline, NYHA classification was similar for β-blocker treated and revascularization patients. In addition, global systolic function, the % scar tissue or the number of segments with contractile reserve were similar in both patient groups at baseline. Furthermore, both patient groups showed the same response to low-dose dobutamine at baseline in the dysfunctional, adjacent, and remote myocardial segments. Accordingly, the clinically defined patient groups were comparable at baseline concerning myocardial function.

Follow up after β-blocker or revascularization therapy

Following β-blocker or revascularization therapy, LV systolic function improved significantly, and to a similar extent. Accordingly, the global functional response to therapy was comparable between both patient groups. This finding is consistent with results from previous studies [5,6,9,12,24,25]. Furthermore, improvement in LVEF was accompanied by an improvement in NYHA classification from baseline to follow up, to a similar extent in both patient groups.

Stepwise multivariate analysis in β-blocker patients revealed that improvement in LVEF after therapy was mainly related to improvement in function of the remote myocardium. The present results concerning β-blocker therapy effect on remote tissue are in agreement with previous studies by Reiken et al. Both in a canine model [26] and in a patient study (performed in explanted hearts) [27], the authors showed that β-blockers normalized Ca⁺⁺-channel function in failing myocardium. Remote myocardium in the current study may be regarded as myocardium with relatively preserved myocyte function as compared to adjacent and dysfunctional regions.

However, in remote tissue, myocardial hypertrophy may develop when excessive pressure or volume overload is imposed to sustain the burden of a dysfunctional segment [28]. The remote hypertrophied tissue may appear to contract normally, but could in fact represent "pseudonormalized" myocardium. Therefore, the relatively mildly failing remote myocardium can still show a positive response to restoration of the Ca⁺⁺-channel function by administration of β-blockers, whereas the adjacent and dysfunctional tissue cannot. Furthermore, recent data demonstrated that the effect of β-blocker therapy could be predicted by the increase in LVEF during low-dose dobutamine infusion [29]. Since dobutamine is a β-receptor agonist, it may be able to temporarily mimic sympatic nervous system stimulation, and predict the effect of β-blockers on LVEF. Interestingly, the regional response pattern after β-blocker therapy in the current study (Figure 2, right upper panel) is similar to the regional response to dobutamine in β-blocker treated patients (left upper panel). The latter observation supports the hypothesis that low-dose dobutamine infusion in patients with chronic ischemic LV dysfunction may predict clinical outcome after β-blocker therapy [29].

Stepwise multivariate analysis in revascularization patients revealed that improvement in LVEF was mainly related to improvement in function of the dysfunctional and adjacent myocardial segments. This observation is in agreement with data obtained in previous studies [30,31]. Recovery of hibernating myocardium occurs after successful revascularization [11,32,33]. In the present study, no improvement in wall thickening was noted in the remote region in the revascularization patients. The latter finding may be explained by the fact that only blood flow to dysfunctional and surrounding adjacent tissue is restored. As a result, no short-term improvement in function can be expected in the remote area. An interesting finding in the present study was that adjacent myocardium also contributed significantly to the improvement of global systolic function after revascularization therapy.

Linitations

The number of patients was relatively small and therefore the observations need confirmation in larger cohorts. Myocardial tagging was not performed; this could have provided a more detailed strain assessment across the myocardial segments of interest.

Conclusion

In patients with chronic ischemic LV dysfunction, β-Blocker therapy or revascularization resulted in a similar improvement of global systolic LV function. However, after β-blocker therapy, improved global systolic function was mainly related to improved contraction of remote myocardium, whereas after revascularization the dysfunctional and adjacent regions contributed predominantly to the improved global systolic function.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

TK wrote the manuscript, designed and carried out the study; JB, HL have been involved in writing the article and made substantial contributions to it's conception and design. SB participated in the design of the study and performed the statistical analysis; DP, EV, EvdW and JD have made substantial contributions to acquisition and interpretation of data; AdR conceived of the study, and participated in its design and coordination and helped to draft the manuscript. All authors read and approved the final manuscript.

References

1. American Heart Association: Heart Disease and Stroke Statistics, 2005 Update.

   American Heart Association 2005.

2. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF)

   Lancet 1999 , 353:2001-2007. PubMed Abstract | Publisher Full Text

3. The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial

   Lancet 1999 , 353:9-13. PubMed Abstract | Publisher Full Text

4. Packer M, Coats AJ, Fowler MB, Katus HA, Krum H, Mohacsi P, Rouleau JL, Tendera M, Castaigne A, Roecker EB, Schultz MK, DeMets DL, Carvedilol Prospective Randomized Cumulative Survival Study Group: Effect of carvedilol on survival in severe chronic heart failure.

   N Engl J Med 2001 , 344:1651-1658. PubMed Abstract | Publisher Full Text

5. O'Keefe JH Jr, Magalski A, Stevens TL, Bresnahan DR Jr, Alaswad K, Krueger SK, Bateman TM: Predictors of improvement in left ventricular ejection fraction with carvedilol for congestive heart failure.

   J Nucl Cardiol 2000 , 7:3-7. PubMed Abstract | Publisher Full Text

6. Bello D, Shah DJ, Farah GM, Di Luzio S, Parker M, Johnson MR, Cotts WG, Klocke FJ, Bonow RO, Judd RM, Gheorghiade M, Kim RJ: Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing beta-blocker therapy.

   Circulation 2003 , 108:1945-1953. PubMed Abstract | Publisher Full Text

7. Eichhorn EJ, Grayburn PA, Mayer SA, St John SM, Appleton C, Plehn J, Oh J, Greenberg B, DeMaria A, Frantz R, Krause-Steinrauf H: Myocardial contractile reserve by dobutamine stress echocardiography predicts improvement in ejection fraction with beta-blockade in patients with heart failure: the Beta-Blocker Evaluation of Survival Trial (BEST).

   Circulation 2003 , 108:2336-2341. PubMed Abstract | Publisher Full Text

8. Seghatol FF, Shah DJ, Diluzio S, Bello D, Johnson MR, Cotts WG, O'Donohue JA, Bonow RO, Gheorghiade M, Rigolin VH: Relation between contractile reserve and improvement in left ventricular function with beta-blocker therapy in patients with heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

   Am J Cardiol 2004 , 93:854-859. PubMed Abstract | Publisher Full Text

9. Bax JJ, Poldermans D, Elhendy A, Cornel JH, Boersma E, Rambaldi R, Roelandt JR, Fioretti PM: 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. PubMed Abstract | Publisher Full Text

10. Nagueh SF, Vaduganathan P, Ali N, Blaustein A, Verani MS, Winters WL Jr, Zoghbi WA: 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. PubMed Abstract | Publisher Full Text

11. Rahimtoola SH: From coronary artery disease to heart failure: role of the hibernating myocardium.

    Am J Cardiol 1995 , 75:16E-22E. PubMed Abstract | Publisher Full Text

12. Senior R, Lahiri A, Kaul S: Effect of revascularization on left ventricular remodeling in patients with heart failure from severe chronic ischemic left ventricular dysfunction.

    Am J Cardiol 2001 , 88:624-629. PubMed Abstract | Publisher Full Text

13. Nagel E, Lehmkuhl HB, Bocksch W, Klein C, Vogel U, Frantz E, Ellmer A, Dreysse S, Fleck E: Noninvasive diagnosis of ischemia-induced wall motion abnormalities with the use of high-dose dobutamine stress MRI: comparison with dobutamine stress echocardiography.

    Circulation 1999 , 99:763-770. PubMed Abstract | Publisher Full Text

14. Bogaert JG, Bosmans HT, Rademakers FE, Bellon EP, Herregods MC, Verschakelen JA, Werf F, Marchal GJ: Left ventricular quantification with breath-hold MR imaging: comparison with echocardiography.

    MAGMA 1995 , 3:5-12. PubMed Abstract | Publisher Full Text

15. Katz J, Milliken MC, Stray-Gundersen J, Buja LM, Parkey RW, Mitchell JH, Peshock RM: Estimation of human myocardial mass with MR imaging.

    Radiology 1988 , 169:495-498. PubMed Abstract | Publisher Full Text

16. Pattynama PM, Lamb HJ, Velde EA, Wall EE, de Roos A: Left ventricular measurements with cine and spin-echo MR imaging: a study of reproducibility with variance component analysis.

    Radiology 1993 , 187:261-268. PubMed Abstract | Publisher Full Text

17. Yang PC, Kerr AB, Liu AC, Liang DH, Hardy C, Meyer CH, Macovski A, Pauly JM, Hu BS: New real-time interactive cardiac magnetic resonance imaging system complements echocardiography.

    J Am Coll Cardiol 1998 , 32:2049-2056. PubMed Abstract | Publisher Full Text

18. Wellnhofer E, Olariu A, Klein C, Grafe M, Wahl A, Fleck E, Nagel E: Magnetic resonance low-dose dobutamine test is superior to SCAR quantification for the prediction of functional recovery.

    Circulation 2004 , 109:2172-2174. PubMed Abstract | Publisher Full Text

19. Poole-Wilson PA, Swedberg K, Cleland JG, Di Lenarda A, Hanrath P, Komajda M, Lubsen J, Lutiger B, Metra M, Remme WJ, Torp-Pedersen C, Scherhag A, Skene A, Carvedilol Or Metoprolol European Trial Investigators: Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised controlled trial.

    Lancet 2003 , 362:7-13. PubMed Abstract | Publisher Full Text

20. Lamb HJ, Doornbos J, Velde EA, Kruit MC, Reiber JH, de Roos A: Echo planar MRI of the heart on a standard system: validation of measurements of left ventricular function and mass.

    J Comput Assist Tomogr 1996 , 20:942-949. PubMed Abstract | Publisher Full Text

21. Wu E, Judd RM, Vargas JD, Klocke FJ, Bonow RO, Kim RJ: Visualisation of presence, location, and transmural extent of healed Q-wave and non-Q-wave myocardial infarction.

    Lancet 2001 , 357:21-28. PubMed Abstract | Publisher Full Text

22. Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey WK, Pennell DJ, Rumberger JA, Ryan T, Verani MS, American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging: 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. PubMed Abstract | Publisher Full Text

23. Holman ER, Buller VG, de Roos A, Geest RJ, Baur LH, van der LA, Bruschke AV, Reiber JH, Wall EE: Detection and quantification of dysfunctional myocardium by magnetic resonance imaging. A new three-dimensional method for quantitative wall-thickening analysis.

    Circulation 1997 , 95:924-931. PubMed Abstract | Publisher Full Text

24. Oshinski JN, Han HC, Ku DN, Pettigrew RI: Quantitative prediction of improvement in cardiac function after revascularization with MR imaging and modeling: initial results.

    Radiology 2001 , 221:515-522. PubMed Abstract | Publisher Full Text

25. Baer FM, Theissen P, Schneider CA, Voth E, Sechtem U, Schicha H, Erdmann E: Dobutamine magnetic resonance imaging predicts contractile recovery of chronically dysfunctional myocardium after successful revascularization.

    J Am Coll Cardiol 1998 , 31:1040-1048. PubMed Abstract | Publisher Full Text

26. Reiken S, Gaburjakova M, Gaburjakova J, He KL, Prieto A, Becker E, Yi GH, Wang J, Burkhoff D, Marks AR: beta-adrenergic receptor blockers restore cardiac calcium release channel (ryanodine receptor) structure and function in heart failure.

    Circulation 2001 , 104:2843-2848. PubMed Abstract | Publisher Full Text

27. Reiken S, Wehrens XH, Vest JA, Barbone A, Klotz S, Mancini D, Burkhoff D, Marks AR: Beta-blockers restore calcium release channel function and improve cardiac muscle performance in human heart failure.

    Circulation 2003 , 107:2459-2466. PubMed Abstract | Publisher Full Text

28. Krayenbuehl HP, Hess OM, Schneider J, Turina M: Physiologic or pathologic hypertrophy.

    Eur Heart J 1983 , 4(Suppl A):29-34. PubMed Abstract | Publisher Full Text

29. Kaandorp TA, Lamb HJ, Bax JJ, Boersma E, Viergever EP, Wall EE, de Roos A: Prediction of beneficial effect of beta blocker treatment in severe ischaemic cardiomyopathy: assessment of global left ventricular ejection fraction using dobutamine stress cardiovascular magnetic resonance.

    Heart 2005 , 91:1471-1472. PubMed Abstract | Publisher Full Text | PubMed Central Full Text

30. Baer FM, Voth E, Schneider CA, Theissen P, Schicha H, Sechtem U: Comparison of low-dose dobutamine-gradient-echo magnetic resonance imaging and positron emission tomography with [18F]fluorodeoxyglucose in patients with chronic coronary artery disease. A functional and morphological approach to the detection of residual myocardial viability.

    Circulation 1995 , 91:1006-1015. PubMed Abstract | Publisher Full Text

31. Bax JJ, Cornel JH, Visser FC, Fioretti PM, van Lingen A, Huitink JM, Kamp O, Nijland F, Roelandt JR, Visser CA: Prediction of improvement of contractile function in patients with ischemic ventricular dysfunction after revascularization by fluorine-18 fluorodeoxyglucose single-photon emission computed tomography.

    J Am Coll Cardiol 1997 , 30:377-383. PubMed Abstract | Publisher Full Text

32. Rahimtoola SH: The hibernating myocardium.

    Am Heart J 1989 , 117:211-221. PubMed Abstract | Publisher Full Text

33. Gunning MG, Anagnostopoulos C, Knight CJ, Pepper J, Burman ED, Davies G, Fox KM, Pennell DJ, Ell PJ, Underwood SR: Comparison of 201Tl, 99mTc-tetrofosmin, and dobutamine magnetic resonance imaging for identifying hibernating myocardium.

    Circulation 1998 , 98:1869-1874. PubMed Abstract | Publisher Full Text

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