Skip Navigation

European Journal of Heart Failure 2005 7(2):225-230; doi:10.1016/j.ejheart.2004.07.003
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Lindner, O.
Right arrow Articles by Burchert, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lindner, O.
Right arrow Articles by Burchert, W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2005 European Society of Cardiology

Global and regional myocardial oxygen consumption and blood flow in severe cardiomyopathy with left bundle branch block

Oliver Lindnera,*, Jürgen Vogtb, Detlev Ballerb, Annett Kammeiera, Peter Wieleppa, Jens Holzingerb, Barbara Lampb, Dieter Horstkotteb and Wolfgang Burcherta

a Institute of Molecular Biophysics, Radiopharmacy and Nuclear Medicine, Heart and Diabetes Center North Rhine-Westphalia Georgstr. 11, D-32545 Bad Oeynhausen, Germany
b Department of Cardiology, Heart and Diabetes Center North Rhine-Westphalia Bad Oeynhausen, Germany

* Corresponding author. Tel.: +49 5731 97 1309; fax.: +49 5731 97 2190. E-mail address: olindner{at}hdz-nrw.de


   Abstract
Top
 Abstract
1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 Acknowledgments
 References
 
Objective: In patients with dilated cardiomyopathy (DCM), left bundle branch block (LBBB) is a common finding. The characteristic feature is an asynchronous septal wall motion and most frequently a delay of the lateral and/or posterior wall segments. With the onset of cardiac resynchronization therapy, there is a focus on the specific pathophysiology of a LBBB. However, quantitative data on regional myocardial oxygen consumption (MVO2) and blood flow (MBF) are missing.

Methods: We studied 31 patients with severe DCM and LBBB (ejection fraction 22.1±7.1%) and 14 patients with mild to moderate DCM without LBBB (ejection fraction 46.7±7.9%). Global and regional MVO2 as well as MBF were determined from a dynamic 11C-acetate positron emission tomography (PET) study.

Results: Global MVO2 and MBF were lower in the DCM group with LBBB than in the control group (P<0.05). Regionally, the LBBB group revealed a higher (P<0.05) MVO2 and MBF in the lateral wall than in the other walls. The control group did not show significant differences between the myocardial walls and demonstrated a smaller variability of the parameters.

Conclusion: DCM patients with LBBB exhibit a more heterogeneous distribution of MVO2 and MBF among the myocardial walls than DCM patients without LBBB. Due to the LBBB associated electromechanical alterations, the highest regional values of MVO2 and MBF are found in the lateral wall.

Key Words: Cardiomyopathy • Conduction system • Oxygen consumption • Blood flow

Received November 24, 2003; Revised February 18, 2004; Accepted July 5, 2004


   1. Introduction
Top
 Abstract
 1. Introduction
2. Material and methods
 3. Results
 4. Discussion
 Acknowledgments
 References
 
Complete left bundle branch block (LBBB) is a common finding in severe dilated cardiomyopathy (DCM) and the strongest predictor of mortality [1]. Furthermore, the magnitude of the intraventricular conduction delay associated with LBBB is one of the most powerful prognostic predictors [2]. The consequences of a LBBB on myocardial contraction and motion have been investigated by echocardiography and recently by the sophisticated tissue Doppler imaging. The characteristic feature has been recognized to be an asynchronous septal wall motion and most frequently a delay of the lateral and/or posterior wall segments [3,4].

Scintigraphically, a LBBB exhibits, with 201Tl, a reversible septal defect and with 99mTc-labelled perfusion markers, a reduced septal uptake both at stress and rest in the absence of coronary artery disease. These imaging patterns have been attributed to asynchrony of the interventricular septum [5–7]. Metabolic imaging with 18F-fluorodeoxyglucose (FDG) also revealed a reduced septal FDG uptake which was decreased in relation to septal 99mTc-MIBI uptake and therefore characterized as "reversed mismatch" [8–11].

The present study was performed to quantitatively characterize global and regional myocardial oxygen consumption (MVO2) as well as blood flow (MBF) by positron emission tomography (PET) in DCM patients with LBBB scheduled for cardiac resynchronization therapy and DCM patients without LBBB.


   2. Material and methods
Top
 Abstract
 1. Introduction
 2. Material and methods
3. Results
 4. Discussion
 Acknowledgments
 References
 
2.1. Study population
A total of 45 patients with DCM, 31 of them with severe DCM and LBBB scheduled for cardiac resynchronization therapy and 14 controls with mild to moderate DCM without LBBB, were studied. The patients had been referred to our center for diagnosis and treatment of DCM and gave their written informed consent to the PET investigation, which conformed with the principles outlined in the Declaration of Helsinki. In all the patients, a significant stenosis of the coronary arteries (narrowing >50%) was excluded angiographically. The patients with DCM and LBBB had a mean QRS width determined from standard ECG analysis >150 ms. The ejection fraction determined echocardiographically or angiographically was <40%. One patient had atrial fibrillation; the others were in sinus rhythm. All patients were in New York Heart Association functional class III.

The 14 DCM patients without LBBB showed a normal QRS width and a slightly reduced ejection fraction. The New York Heart Association functional class ranged from I to III, three patients were in class I, nine in class II and two in class III.

Blood pressure and heart rate were oscillometrically assessed in all patients immediately before the tracer injection. Table 1 provides data of the study groups.


View this table:
[in this window]
[in a new window]

  		Table 1 Patient characteristics and hemodynamics

 
2.2. Positron emission tomography
2.2.1. Data acquisition and reconstruction
The scans were acquired dynamically (10x10 s, 6x100 s, 3x180 s, 4x300 s [sum, 40 min]) with an ECAT-951 R scanner (CTI/Siemens Medical systems; Knoxville, TN) after a bolus injection of 370 MBq 11C-acetate at rest.

Attenuation correction was performed on the basis of a 10-min transmission scan (68Ge/68Ga rod source) before tracer application. Transaxial images were reconstructed with filtered backprojection (Hanning filter, cut-off 0.4) and a 128x128 image matrix. Finally, the images were three-dimensionally smoothed to isotropic resolution.

2.2.2. Image processing
The image data were transformed into dynamic area-conserving polar maps whose pixels represent equal areas of the myocardial wall. This transformation was achieved with an automatic rendering program described in detail elsewhere [12,13]. The arterial input function was automatically determined in the cavum of the left ventricle. Quantification was performed pixel by pixel on dynamic polar maps using a reversible one-tissue-compartment model, which corrects for tracer recirculation, fractional blood volume, limited recovery and spillover activity from left ventricular blood pool to tissue [14]. For the calculation of MBF, an extraction correction of the acetate uptake values was performed. The above-mentioned steps have been described in detail elsewhere [15]. The quantification procedure revealed parametric polar maps for acetate uptake (rate constant K1, a measure of MBF) and acetate clearance (rate constant k2, a measure of MVO2). The polar maps were divided into 20 segments [16], and the average pixel values of each segment were calculated. For global analysis, the average value of all segments was determined. Similarly, regional values were generated for the anterior, lateral, inferior and septal myocardial walls. Segments outside the field of view of the PET scanner and segments with a fractional blood volume >0.50 indicative of an uncorrected wall detection were excluded. A total of 787 segments were analysed. MVO2 (k2) is given as 1/min and MBF in milliliters per minute per gram tissue.

2.2.3. Echocardiography
Resting two-dimensional echocardiography was performed within 2 weeks of the PET study with a 2.5-MHz multifrequency probe in harmonic imaging mode. Wall motion of the septal and the lateral wall was evaluated visually by digital cine loop analysis or—if available—with tissue Doppler imaging in the apical four- and three-chamber views. Left ventricular ejection fraction was calculated by the Simpson rule.

2.2.4. Statistical analysis
Data are reported as mean value±1 standard deviation. The Student t-test for unpaired data comparisons was used to compare parameters between the LBBB and the non-LBBB group. Probability values <0.05 were considered statistically significant. Intragroup differences of MVO2 and MBF between the myocardial walls were analysed with analysis of variance (ANOVA). In case of a significant F-ratio, the Fisher's protected least significant difference (PLSD) was used for pairwise comparisons. The coefficient of variation among the myocardial walls was used as a measure of heterogeneity. Statistical analysis was performed using StatView 5.0 software (SAS Institute, Cary, NC, USA).


   3. Results
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
4. Discussion
 Acknowledgments
 References
 
Data for global MVO2 and MBF in both groups are given in Table 2. The parameters were significantly lower in patients with severe DCM and LBBB than in patients with mild to moderate DCM without LBBB. The ratio of MVO2 and MBF was not different between LBBB and non-LBBB patients (0.159±0.019 and 0.159±0.020, respectively; not significant).


View this table:
[in this window]
[in a new window]

  		Table 2 Global MBF and MVO2 (k2) of cardiomyopathy patients with and without LBBB

 
In DCM patients with LBBB, the ANOVA of the regional MVO2 revealed significant differences between the myocardial walls (Table 3; Fig. 1). In detail, MVO2 was significantly higher in the lateral wall than in the other walls. The interventricular septum exhibited the lowest MVO2. However, this value did not differ significantly from those of the anterior or inferior walls. The septal-to-lateral MVO2 ratio was significantly lower than in non-LBBB group. This group showed no significant differences in MVO2 between the four myocardial walls (Fig. 2).


View this table:
[in this window]
[in a new window]

  		Table 3 Regional MBF and MVO2 (k2) of cardiomyopathy patients with and without LBBB

 


Figure 1
View larger version (20K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 1 Regional MVO2 in cardiomyopathy patients with and without LBBB.

 


Figure 2
View larger version (55K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 2 Anteroseptal and anterolateral view of a parametric 3-D MVO2 (k2) map in dilated cardiomyopathy with LBBB and without LBBB. MVO2 is more homogeneously distributed over the myocardial walls (septal-to-lateral ratio 0.96) in the non-LBBB than in the LBBB patient who exhibits a higher MVO2 in the lateral wall than in the septum (septal-to-lateral ratio 0.83). MVO2 (k2) is given in 1/min.

 
Regional MBF demonstrated a similar distribution as MVO2 (Table 3; Fig. 3). In the DCM group with LBBB, MBF was significantly higher in the lateral wall than in the other walls and lowest in the interventricular septum. In the non-LBBB group, no significant differences were observed among the myocardial walls. The highest regional MBF was measured in the interventricular septum. The septal-to-lateral MBF ratio was significantly lower in the LBBB group than in the non-LBBB group which exhibited a ratio greater than 1.0 due to a high septal flow.


Figure 3
View larger version (58K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 3 Regional MBF in cardiomyopathy patients with and without LBBB.

 
The coefficient of variation among the myocardial walls was 0.11±0.04 for MVO2 and 0.14±0.06 for MBF in the LBBB group on average. In the non-LBBB group, the coefficient of variation was significantly lower for MVO2 (0.07±0.02; P=0.001) and also for MBF (0.09±0.06; P=0.0047).

Echocardiographic data were available for all of the non-LBBB and for 27 of the LBBB patients. The patients in both groups showed diffuse hypokinesia of different degrees. A total of 25 patients (81%) of the LBBB group had an asynchronous septal motion during ventricular ejection, one patient a synchronous septal motion and one patient an akinetic septum. Echocardiographic data were not available for four patients in this group. In the non-LBBB group, a synchronous septal motion was present in 13 patients (93%). A regionally accentuated hypokinetic septal motion was observed in one patient.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
Acknowledgments
 References
 
The present study documents that patients with severe DCM and LBBB exhibit a significantly lower global MVO2 and MBF at rest than patients with mild to moderate DCM without LBBB. The regional analysis reveals a specific and more inhomogenous distribution of MVO2 and MBF among the myocardial walls in DCM patients with LBBB as compared to non-LBBB patients. The study suggests that these findings are predominantly a consequence of the conduction disturbance and not of the LV dysfunction.

With the successful introduction of cardiac resynchronization therapy in patients with advanced DCM and LBBB, there is a new focus on the specific pathophysiology of LBBB. Although several studies characterized global MVO2 and MBF in cardiomyopathy with PET, they failed to discriminate between LBBB and non-LBBB patients [17–21]. Recent studies that focused on regional aspects of LBBB on a semiquantitative or quantitative basis mostly of the septal and the lateral walls included only a small number of patients [22–26]. To our knowledge, the present study is the first one to quantitatively investigate both global and regional MVO2 as well as global and regional MBF in a larger DCM population.

4.1. Characterization of global MVO2 and MBF in DCM patients
The left ventricular myocardium of the investigated DCM patients was characterized by an impaired MVO2 and a reduced MBF. The alterations were more pronounced in severe DCM than in mild to moderate DCM.

Investigations of MVO2 measured as 11C-acetate clearance in DCM have shown a wide variation in data. Beanlands et al. [18,19] described 11C-acetate clearance rates of 0.105±0.027 and 0.064±0.012/min. van den Heuvel et al. presented acetate clearance data of 0.057±0.014/min and Bengel et al. of 0.06±0.015/min [20,21]. Data from both groups in the present study were within this range. Beanlands et al. [18] derived a regression equation from 11C-acetate clearance rates obtained by modelling and direct measurements of MVO2 in DCM patients. Applying this formula to our acetate clearance data, the average MVO2 for the LBBB patients amounts to 5.88±0.76 ml/min/100 g and for the non-LBBB patients to 6.99±1.47 ml/min/100 g. These results are in agreement with invasive investigations in DCM which demonstrated an impaired MVO2 of 6.3±4.0 [27] and 6.6±2.2 ml/min/100 g, respectively [28].

Measurements of MBF in nonischemic DCM have been performed with microspheres [29], with 13N-ammonia [21], or inert gas washout techniques [30,31]. Results showed a depressed MBF of 0.45±0.15 [30] and of 0.49±0.17 ml/min/g [29], a normal flow of 0.78±0.17 ml/min/g [31] and a high normal flow of 1.02±0.21 ml/min/g [21]. This great variability was probably due to the different methods used and different states of the disease. In severe DCM, the MBF of the present study was within the lower third of this range and in mild to moderate DCM near the lower normal limit [32]. Since basal MBF and MVO2 increase with age, the different mean ages of the groups can be excluded as a reason for the results [33,34].

4.2. Regional MVO2 and MBF in DCM patients with and without LBBB
Compared to the DCM patients with LBBB, those without LBBB demonstrated a more homogenous distribution of MVO2 and MBF without significant differences between the myocardial walls. Echocardiography accordingly showed a synchronous contraction of the septal and the lateral walls.

The regional findings in the LBBB group reflect the delayed conduction and the asynchronous contraction of the septal and lateral walls as demonstrated by echocardiography. In LBBB, the lateral wall represents the site of latest activation and contraction [35]. Its contraction is therefore overlapped by the contraction of the earlier activated myocardial walls that has increased intraventricular pressure and distensed the lateral wall [36]. Thus, regional wall stress becomes highest in the lateral segments. Consequently, the lateral wall has been shown to exhibit the highest MVO2 and also the highest MBF because both parameters are closely linked [37,38]. MVO2 and MBF of the earlier activated walls are lower due to a lower wall stress during their contraction. These regional differences account for the significantly higher variability of MVO2 and MBF among the myocardial walls and for the smaller septal-to-lateral ratios as compared to the non-LBBB group.

The delayed contraction of the lateral wall overlaps with the relaxation of the septum and distenses the interventricular wall [36]. As a consequence, diastolic septal wall stress increases [39]. However, in the present study MVO2 and MBF tend to be lowest in the septal wall. We suppose that the paradoxical septal contraction and a reduced ejection fraction are—despite an elevated wall stress—the main reason for the low septal MVO2 and MBF [40].

An important question that arises despite these explanations is whether the described regional distribution of MVO2 and MBF is caused by the LBBB or only represents a typical sign of severe DCM. In studies of DCM patients predominantly without LBBB, 26 patients with moderate DCM (24 without LBBB, 2 with LBBB, EF 36±10%) and 4 patients with severe DCM (3 without LBBB, 1 with LBBB, EF 21±5%) revealed no significant regional differences in MBF [29,41]. Together with our results, these studies suggest that regional differences and substantial inhomogeneities of MBF and MVO2 are not induced by the state of DCM but by LBBB. Another aspect that underlines this statement is given by cardiac resynchronization therapy. The rationale is to reduce the LBBB associated intraventricular dyssynchrony in DCM patients by synchronous biventricular pacing. Correspondingly, PET investigations revealed that regional inhomogeneities of glucose metabolism, MVO2 and MBF were balanced [22–26].

Furthermore, we assume that the septal-to-lateral ratio and the coefficient of variation may be a noninvasive method to verify acute and long-term success of cardiac resynchronization therapy in the future.


   Acknowledgments
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 Acknowledgments
References
 
The authors thank Dr. Ansgar Steland (Faculty of Mathematics, Ruhr-University Bochum, Germany) for his advice concerning the statistical analysis, Nikola Bogunovic for the echocardiographic analysis, Martina Spickeneder, Heike Wittemeyer, Heidi Soesanto and Ines Haubrock for their excellent technical assistance and Astrid Kohlstädt-Klapper and Dr. Eva Lindner for revising the manuscript.


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

  1. Unverferth D.V., Magorien R.D., Moeschberger M.L., et al. Factors influencing the one-year mortality of dilated cardiomyopathy. Am. J. Cardiol. (1984) 54:147–152.[CrossRef][Web of Science][Medline]
  2. Shamim W., Francis D.P., Yousufuddin M., et al. Intraventricular conduction delay: a prognostic marker in chronic heart failure. Int. J. Cardiol. (1999) 70:171–178.[CrossRef][Web of Science][Medline]
  3. Hultgren H.N., Craige E., Fujii J., Nakamura T., Bilisoly J. Left bundle branch block and mechanical events of the cardiac cycle. Am. J. Cardiol. (1983) 52:755–762.[CrossRef][Web of Science][Medline]
  4. Ansalone G., Giannantoni P., Ricci R., et al. Doppler myocardial imaging to evaluate the effectiveness of pacing sites in patients receiving biventricular pacing. J. Am. Coll. Cardiol. (2002) 39:489–499.[Abstract/Free Full Text]
  5. Burns R.J., Galligan L., Wright L.M., et al. Improved specificity of myocardial thallium-201 single-photon emission computed tomography in patients with left bundle branch block by dipyridamole. Am. J. Cardiol. (1991) 68:504–508.[CrossRef][Web of Science][Medline]
  6. Burns R.J. Septal metabolic mismatch in LBBB. J. Nucl. Med. (1996) 37:1918–1919.[Free Full Text]
  7. Hirzel H.O., Senn M., Nuesch K., et al. Thallium-201 scintigraphy in complete left bundle branch block. Am. J. Cardiol. (1984) 53:764–769.[CrossRef][Web of Science][Medline]
  8. Altehoefer C., vom Dahl J., Buell U. Septal glucose metabolism in patients with coronary artery disease and left bundle-branch block. Coron. Artery Dis. (1993) 4:569–572.[Web of Science][Medline]
  9. Altehoefer C., vom Dahl J., Bares R., Stocklin G.L., Bull U. Metabolic mismatch of septal beta-oxidation and glucose utilization in left bundle branch block assessed with PET. J. Nucl. Med. (1995) 36:2056–2059.[Abstract/Free Full Text]
  10. Zanco P., Chierichetti F., Fini A., Cargnel S., Ferlin G. Myocardial perfusion, glucose utilization and oxidative metabolism in a patient with left bundle branch block, prior myocardial infarction and diabetes. J. Nucl. Med. (1998) 39:261–263.[Abstract/Free Full Text]
  11. Zanco P., Desideri A., Mobilia G., et al. Effects of left bundle branch block on myocardial FDG PET in patients without significant coronary artery stenoses. J. Nucl. Med. (2000) 41:973–977.[Abstract/Free Full Text]
  12. van den Hoff J., Burchert W., Wolpers H.G., Meyer G.J., Hundeshagen H. Visualization and quantification of three-dimensional myocardial wall motion with PET. Eur. J. Nucl. Med. (1996) 23:1235. (abstract).
  13. van den Hoff J., Burchert W. Functional polar maps and 3D visualisation. In: Cardiological Nuclear Medicine—Hör G., Krause B.J., Tillmanns H.H., eds. (1997) Landsberg, Germany: Ecomed Verlag. 192–204. (in German).
  14. Wolpers H.G., Burchert W., van den Hoff J., et al. Assessment of myocardial viability by use of 11C-acetate and positron emission tomography. Threshold criteria of reversible dysfunction. Circulation (1997) 95:1417–1424.[Abstract/Free Full Text]
  15. van den Hoff J., Burchert W., Borner A.R., et al. [1-(11)C]Acetate as a quantitative perfusion tracer in myocardial PET. J. Nucl. Med. (2001) 42:1174–1182.[Abstract/Free Full Text]
  16. Imaging guidelines for nuclear cardiology procedures: part 2. American Society of Nuclear Cardiology. J. Nucl. Cardiol. (1999) 6:G47–G84.[CrossRef][Medline]
  17. Bach D.S., Beanlands R.S., Schwaiger M., Armstrong W.F. Heterogeneity of ventricular function and myocardial oxidative metabolism in nonischemic dilated cardiomyopathy. J. Am. Coll. Cardiol. (1995) 25:1258–1262.[Abstract]
  18. Beanlands R.S., Bach D.S., Raylman R., et al. Acute effects of dobutamine on myocardial oxygen consumption and cardiac efficiency measured using carbon-11 acetate kinetics in patients with dilated cardiomyopathy. J. Am. Coll. Cardiol. (1993) 22:1389–1398.[Abstract]
  19. Beanlands R.S., Armstrong W.F., Hicks R.J., et al. The effects of afterload reduction on myocardial carbon 11-labeled acetate kinetics and noninvasively estimated mechanical efficiency in patients with dilated cardiomyopathy. J. Nucl. Cardiol. (1994) 1:3–16.[Web of Science][Medline]
  20. Bengel F.M., Permanetter B., Ungerer M., Nekolla S., Schwaiger M. Non-invasive estimation of myocardial efficiency using positron emission tomography and carbon-11 acetate–comparison between the normal and failing human heart. Eur. J. Nucl. Med. (2000) 27:319–326.[CrossRef][Web of Science][Medline]
  21. van den Heuvel A.F., van Veldhuisen D.J., van der Wall E.E., et al. Regional myocardial blood flow reserve impairment and metabolic changes suggesting myocardial ischemia in patients with idiopathic dilated cardiomyopathy. J. Am. Coll. Cardiol. (2000) 35:19–28.[Abstract/Free Full Text]
  22. Neri G., Zanco P., Buchberger R. Myocardial perfusion and metabolic changes induced by biventricular pacing in dilated cardiomyopathy and left bundle branch block: description of a case evaluated by positron emission tomography. Ital. Heart J. (2001) 2:472–474.[Medline]
  23. Neri G., Zanco P., Bertaglia E., et al. Myocardial perfusion and metabolic changes induced by conventional right and biventricular pacing in dilated cardiomyopathy evaluated by positron emission tomography. Ital. Heart J. (2002) 3:637–642.[Medline]
  24. Neri G., Zanco P., Zanon F., Buchberger R. Effect of biventricular pacing on metabolism and perfusion in patients affected by dilated cardiomyopathy and left bundle branch block: evaluation by positron emission tomography. Europace (2003) 5:111–115.[Abstract/Free Full Text]
  25. Nowak B., Sinha A.M., Schaefer W.M., et al. Cardiac resynchronization therapy homogenizes myocardial glucose metabolism and perfusion in dilated cardiomyopathy and left bundle branch block. J. Am. Coll. Cardiol. (2003) 41:1523–1528.[Abstract/Free Full Text]
  26. Ukkonen H., Beanlands R.S., Burwash I.G., et al. Effect of cardiac resynchronization on myocardial efficiency and regional oxidative metabolism. Circulation (2003) 107:28–31.[Abstract/Free Full Text]
  27. Henry P.D., Eckberg D., Gault J.H., Ross J. Jr. Depressed inotropic state and reduced myocardial oxygen consumption in the human heart. Am. J. Cardiol. (1973) 31:300–306.[CrossRef][Web of Science][Medline]
  28. Pasternac A., Noble J., Streulens Y., et al. Pathophysiology of chest pain in patients with cardiomyopathies and normal coronary arteries. Circulation (1982) 65:778–789.[Abstract/Free Full Text]
  29. Parodi O., De Maria R., Oltrona L., et al. Myocardial blood flow distribution in patients with ischemic heart disease or dilated cardiomyopathy undergoing heart transplantation. Circulation (1993) 88:509–522.[Abstract/Free Full Text]
  30. Weiss M.B., Ellis K., Sciacca R.R., et al. Myocardial blood flow in congestive and hypertrophic cardiomyopathy: relationship to peak wall stress and mean velocity of circumferential fiber shortening. Circulation (1976) 54:484–494.[Abstract/Free Full Text]
  31. Opherk D., Schwarz F., Mall G., et al. Coronary dilatory capacity in idiopathic dilated cardiomyopathy: analysis of 16 patients. Am. J. Cardiol. (1983) 51:1657–1662.[CrossRef][Web of Science][Medline]
  32. Uren N.G., Melin J.A., De Bruyne B., et al. Relation between myocardial blood flow and the severity of coronary-artery stenosis. N. Engl. J. Med. (1994) 330:1782–1788.[Abstract/Free Full Text]
  33. Uren N.G., Camici P.G., Melin J.A., et al. Effect of aging on myocardial perfusion reserve. J. Nucl. Med. (1995) 36:2032–2036.[Abstract/Free Full Text]
  34. Kates A.M., Herrero P., Dence C., et al. Impact of aging on substrate metabolism by the human heart. J. Am. Coll. Cardiol. (2003) 41:293–299.[Abstract/Free Full Text]
  35. Rosenbush S.W., Ruggie N., Turner D.A., et al. Sequence and timing of ventricular wall motion in patients with bundle branch block. Assessment by radionuclide cineangiography. Circulation (1982) 66:1113–1119.[Abstract/Free Full Text]
  36. Nelson G.S., Berger R.D., Fetics B.J., et al. Left ventricular or biventricular pacing improves cardiac function at diminished energy cost in patients with dilated cardiomyopathy and left bundle-branch block. Circulation (2000) 102:3053–3059.[Abstract/Free Full Text]
  37. Baller D., Wolpers H.G., Hoeft A., et al. Increase of myocardial oxygen consumption due to active diastolic wall tension. Basic Res. Cardiol. (1984) 79:176–185.[CrossRef][Web of Science][Medline]
  38. Eckenhoff J.E., Hafkenschiel J.H., Landmesser C.M. Cardiac oxygen metabolism and control of the coronary circulation. Am. J. Physiol. (1947) 149:634–649.[Free Full Text]
  39. Ono S., Nohara R., Kambara H., Okuda K., Kawai C. Regional myocardial perfusion and glucose metabolism in experimental left bundle branch block. Circulation (1992) 85:1125–1131.[Abstract/Free Full Text]
  40. Grines C.L., Bashore T.M., Boudoulas H., et al. Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony. Circulation (1989) 79:845–853.[Abstract/Free Full Text]
  41. Shikama N., Himi T., Yoshida K., et al. Prognostic utility of myocardial blood flow assessed by N-13 ammonia positron emission tomography in patients with idiopathic dilated cardiomyopathy. Am. J. Cardiol. (1999) 84:434–439.[CrossRef][Web of Science][Medline]

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 JNMHome page
R. A. Tio, A. Dabeshlim, H.-M. J. Siebelink, J. de Sutter, H. L. Hillege, C. J. Zeebregts, R. A.J.O. Dierckx, D. J. van Veldhuisen, F. Zijlstra, and R. H.J.A. Slart
Comparison Between the Prognostic Value of Left Ventricular Function and Myocardial Perfusion Reserve in Patients with Ischemic Heart Disease
J. Nucl. Med., February 1, 2009; 50(2): 214 - 219.
[Abstract] [Full Text] [PDF]

Home page
 Eur J Heart FailHome page
C. Valzania, F. Gadler, R. Winter, F. Braunschweig, L.-A. Brodin, P. Gudmundsson, G. Boriani, and M. J. Eriksson
Effects of cardiac resynchronization therapy on coronary blood flow: Evaluation by transthoracic Doppler echocardiography
Eur J Heart Fail, May 1, 2008; 10(5): 514 - 520.
[Abstract] [Full Text] [PDF]

Home page
 JNMHome page
K. Thompson, G. Saab, D. Birnie, B. J.W. Chow, H. Ukkonen, K. Ananthasubramaniam, R. A. deKemp, L. Garrard, T. D. Ruddy, J. N. DaSilva, et al.
Is Septal Glucose Metabolism Altered in Patients with Left Bundle Branch Block and Ischemic Cardiomyopathy?
J. Nucl. Med., November 1, 2006; 47(11): 1763 - 1768.
[Abstract] [Full Text] [PDF]

Home page
 Eur Heart JHome page
E. Donal, C. Leclercq, C. Linde, and J.-C. Daubert
Effects of cardiac resynchronization therapy on disease progression in chronic heart failure
Eur. Heart J., May 1, 2006; 27(9): 1018 - 1025.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. C. P. Kerckhoffs, O. P. Faris, P. H. M. Bovendeerd, F. W. Prinzen, K. Smits, E. R. McVeigh, and T. Arts
Electromechanics of paced left ventricle simulated by straightforward mathematical model: comparison with experiments
Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1889 - H1897.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
R. J. Gibbons and P. A. Araoz
The Year in Cardiac Imaging
J. Am. Coll. Cardiol., August 2, 2005; 46(3): 542 - 551.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Lindner, O.
Right arrow Articles by Burchert, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lindner, O.
Right arrow Articles by Burchert, W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?