Skip to main content

Main menu

  • Home
  • Content
    • Current
    • Ahead of print
    • Past Issues
    • JNM Supplement
    • SNMMI Annual Meeting Abstracts
    • Continuing Education
    • JNM Podcasts
  • Subscriptions
    • Subscribers
    • Institutional and Non-member
    • Rates
    • Journal Claims
    • Corporate & Special Sales
  • Authors
    • Submit to JNM
    • Information for Authors
    • Assignment of Copyright
    • AQARA requirements
  • Info
    • Reviewers
    • Permissions
    • Advertisers
  • About
    • About Us
    • Editorial Board
    • Contact Information
  • More
    • Alerts
    • Feedback
    • Help
    • SNMMI Journals
  • SNMMI
    • JNM
    • JNMT
    • SNMMI Journals
    • SNMMI

User menu

  • Subscribe
  • My alerts
  • Log in
  • My Cart

Search

  • Advanced search
Journal of Nuclear Medicine
  • SNMMI
    • JNM
    • JNMT
    • SNMMI Journals
    • SNMMI
  • Subscribe
  • My alerts
  • Log in
  • My Cart
Journal of Nuclear Medicine

Advanced Search

  • Home
  • Content
    • Current
    • Ahead of print
    • Past Issues
    • JNM Supplement
    • SNMMI Annual Meeting Abstracts
    • Continuing Education
    • JNM Podcasts
  • Subscriptions
    • Subscribers
    • Institutional and Non-member
    • Rates
    • Journal Claims
    • Corporate & Special Sales
  • Authors
    • Submit to JNM
    • Information for Authors
    • Assignment of Copyright
    • AQARA requirements
  • Info
    • Reviewers
    • Permissions
    • Advertisers
  • About
    • About Us
    • Editorial Board
    • Contact Information
  • More
    • Alerts
    • Feedback
    • Help
    • SNMMI Journals
  • View or Listen to JNM Podcast
  • Visit JNM on Facebook
  • Join JNM on LinkedIn
  • Follow JNM on Twitter
  • Subscribe to our RSS feeds
Research ArticleCLINICAL INVESTIGATIONS

Cardiac Efficiency and Oxygen Consumption Measured with 11C-Acetate PET After Long-Term Cardiac Resynchronization Therapy

Oliver Lindner, Jens Sörensen, Jürgen Vogt, Eva Fricke, Detlev Baller, Dieter Horstkotte and Wolfgang Burchert
Journal of Nuclear Medicine March 2006, 47 (3) 378-383;
Oliver Lindner
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Jens Sörensen
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Jürgen Vogt
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Eva Fricke
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Detlev Baller
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Dieter Horstkotte
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Wolfgang Burchert
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

Abstract

Cardiac resynchronization therapy (CRT) is a treatment option in patients with severe heart failure and left bundle-branch block (LBBB). This study evaluated the effects of 4 and 13 mo of CRT on myocardial oxygen consumption (MVO2) and cardiac efficiency as compared with mild heart failure patients without LBBB. Methods: Sixteen patients with severe heart failure and LBBB due to idiopathic cardiomyopathy were studied at baseline and after 4 and after 13 mo of therapy. Thirteen patients with mild heart failure without LBBB served as a comparison group. The clearance rate (k2) of 11C-acetate was measured with PET to assess MVO2. Stroke volume was derived from the dynamic PET data according to the Stewart–Hamilton principle and, furthermore, cardiac efficiency using the work metabolic index. Results: After 4 mo of CRT, stroke volume index (SVI) increased by 50% (P = 0.012) and cardiac efficiency increased by 41% (P < 0.001). Global k2 remained unchanged but regional k2 demonstrated a more homogeneous distribution pattern. The parameters showed no significant changes during therapy. Under CRT, cardiac efficiency, SVI, and the distribution pattern of regional k2 did not differ from mild heart failure patients without LBBB. Conclusion: CRT improves cardiac efficiency for at least 13 mo, as demonstrated by a higher SVI, whereas MVO2 remains unchanged. Cardiac efficiency, SVI, and the MVO2 distribution pattern reach the level of patients with mild heart failure without LBBB. The unfavorable hemodynamic performance in heart failure with LBBB is effectively restored by long-term CRT to the level of an earlier disease state.

  • heart failure
  • bundle-branch block
  • pacing
  • cardiac output

In the early 1990s, cardiac resynchronization therapy (CRT) was originally initiated as a bridging therapy for advanced heart failure patients with left bundle-branch block (LBBB) awaiting heart transplantation (1,2). Various trials demonstrated CRT—predominantly performed as biventricular pacing—to be effective with respect to clinical symptoms, exercise tolerance, quality of life, and patient outcome (3–6). Currently available devices also include a cardioverter–defibrillator function, which provides substantial mortality benefits by preventing sudden cardiac death (7). In the 2002 guideline update for implantation of pacemakers and antiarrhythmic devices, CRT was classified as a class IIA indication with an A level of evidence (8).

CRT studies with PET demonstrated no changes in myocardial oxygen consumption (MVO2) but a more homogeneous distribution pattern of MVO2, myocardial perfusion, and glucose metabolism (9–11). However, no data are currently available on the long-term effects of CRT on cardiac efficiency and MVO2. Previous studies on cardiac efficiency addressed either short-term effects after the onset of CRT (12) or effects after discontinuation of long-term CRT for 2 or 24 h (13,14).

This study was initiated to evaluate the long-term effects of CRT on cardiac efficiency and MVO2. The study should further clarify whether the functional response to CRT is a continuously ongoing process or completed after a certain period. Moreover, the comparison with mild heart failure patients without LBBB—that is, the comparison with an early disease state—served to evaluate the extent of the functional restoration induced by CRT.

MATERIALS AND METHODS

Study Population

Sixteen patients with severe heart failure and LBBB (Table 1), scheduled for CRT, and 13 patients with mild heart failure without LBBB (Table 2) were studied. In all subjects the cause of heart failure was idiopathic cardiomyopathy. A significant stenosis of the coronary arteries (narrowing > 50%) was excluded angiographically. The patients with severe heart failure and LBBB, who were all in New York Heart Association (NYHA) class III, showed a QRS width > 160 ms, a left ventricular ejection fraction ≤ 30%, a left ventricular end-diastolic diameter > 60 mm, and sinus rhythm. At the time of study enrollment they were clinically stable and on individually optimized heart failure medication (amiodarone, n = 2; angiotensin-converting enzyme (ACE) inhibitors, n = 13; angiotensin receptor blockers, n = 3; β-blockers, n = 15; digoxin, n = 13; diuretics, n = 16; and nitrates, n = 2). During the study the heart failure medication was not changed substantially. An adjustment of β-blocker dose to its optimal dosage occurred in 4 patients in whom this level could not be reached before CRT.

View this table:
  • View inline
  • View popup
TABLE 1

Characteristics of Patients with Severe Heart Failure and LBBB

View this table:
  • View inline
  • View popup
TABLE 2

Characteristics of Comparison Group: Patients With Mild Heart Failure Without LBBB

Those 13 patients with mild heart failure without LBBB at an earlier state of disease served as a comparison group. Heart failure was in 7 cases of infective and in 6 cases of unknown origin. The patients showed a QRS width ≤ 120 ms, an average left ventricular end-diastolic diameter of 68 mm, a slightly reduced ejection fraction (47%), and sinus rhythm. The NYHA class ranged from I to III (class I, n = 2; class II, n = 10; class III, n = 1). The medication consisted of amiodarone (n = 2), ACE inhibitors (n = 12), β-blockers (n = 7), digoxin (n = 9), and diuretics (n = 6).

The study protocol was approved by the local Ethics Committee of the Ruhr-University of Bochum, Germany, and the German Federal Office for Radiation Protection. All patients gave their written informed consent.

Biventricular Pacemaker Implantation

Before definite pacemaker implantation all patients had undergone a hemodynamic test in the electrophysiologic laboratory to differentiate responders from nonresponders (15). Only responders with a pulse pressure increase of ≥10% above baseline (85% of the patients screened) were included. The average pulse pressure increase was 15 ± 9 mm Hg. The device implantation was performed as described in detail earlier (16,17).

PET

The PET scans were acquired with an ECAT-951 R or an ECAT EXACT HR+ PET scanner (CTI/Siemens Medical Systems) after a bolus injection of 370 MBq 11C-acetate at rest. In the CRT group, scans were performed before pacemaker implantation (11 ± 15 d), 4 mo (122 ± 32 d), and 13 mo (403 ± 36 d) under CRT.

Blood pressure and heart rate were assessed oscillometrically immediately before the tracer injection. 11C-Acetate was injected as a bolus (<2 s) followed by 20 mL sodium chloride. Data processing was performed using a reversible 1-tissue compartment model (18,19). The modeling procedure resulted in 20-segment parametric polar maps of the acetate clearance (rate constant, k2). The acetate clearance was used as a measure of MVO2 (given in 1/min). To obtain a measure of global MVO2, the acetate clearance rates (k2) of all 20 segments of each measurement were averaged. For regional analysis the segments were assigned to the anterior, lateral, inferior, or septal wall and averaged. Then the coefficient of variation of regional k2 was determined. The apical segments were excluded from regional analysis. Segments outside the field of view of the PET scanner or with a fractional blood volume > 0.50, indicating an incorrect wall detection, were also excluded. In the resynchronization group, 900 of 960 segments were analyzed and in the comparison group 235 of 260 segments were analyzed.

Cardiac output was assessed according to the Stewart–Hamilton principle as described previously in detail (20). In brief, a region of interest was placed in the right ventricular cavity. A time–activity curve was generated and the downslope of the ventricular activity curve fitted to a monoexponential function with forward extrapolation to correct for recirculation (Fig. 1). The equation to determine cardiac output (CO) is:MathEq. 1orMathEq. 2where c(t) is the right ventricular tracer concentration at time t measured with PET and corrected for recirculation. The integral c(t)dt is the area under this curve. Stroke volume index (SVI, in mL/m2) was calculated as cardiac output/heart rate, indexed to body surface area. Cardiac efficiency was determined using the concept of work metabolic index given by:MathEq. 3where SBP is systolic blood pressure, and HR is heart rate.

FIGURE 1. 
  • Download figure
  • Open in new tab
  • Download powerpoint
FIGURE 1. 

Right ventricular activity concentration curve after bolus injection. Dotted line represents monoexponential fit to downslope of activity concentration curve with forward extrapolation to correct for recirculation. Cardiac output is calculated as injected dose divided by area under concentration curve corrected for recirculation.

FIGURE 2. 
  • Download figure
  • Open in new tab
  • Download powerpoint
FIGURE 2. 

Acetate clearance rate k2, a measure of MVO2 rate (A); coefficient of variation of k2 between myocardial walls (B); SVI (C); cardiac efficiency in patients with severe heart failure and LBBB (n = 16) at baseline, after 4 mo, and after 13 mo of CRT (D). Values are mean ± SD. *P < 0.05 vs. 4 mo and 13 mo of CRT. Dotted horizontal line indicates mean value of corresponding parameter of comparison group with mild heart failure patients without LBBB (n = 13) and dashed lines indicate mean ± SD.

Statistical Analysis

Data are given as mean value ± SD. Comparisons of hemodynamic, PET data (k2, coefficient of variation of regional k2, SVI, cardiac efficiency) in the CRT group were performed with ANOVA for repeated measures followed by a post hoc Bonferroni analysis. For comparisons of the measurements in the CRT group with the comparison group, the unpaired 2-tailed t test with a Bonferroni–Holmes correction was used. Comparison of proportions was performed by χ2 analysis. P < 0.05 was considered significant.

RESULTS

Hemodynamic Data

Heart rate, systolic blood pressure, and diastolic blood pressure of the CRT group did not change from baseline to 4 mo of CRT and showed no further changes at the 13-mo measurement point (Table 3). The comparison with the mild heart failure patients revealed that (a) the systolic blood pressure of the CRT patients was lower (P = 0.02) before therapy, that (b) the diastolic blood pressure of the CRT patients was always lower (baseline vs. comparison group, P = 0.004; 4-mo CRT vs. comparison group, P = 0.02; 13-mo CRT vs. comparison group, P = 0.001), and that (c) the heart rate showed no significant differences.

View this table:
  • View inline
  • View popup
TABLE 3

Hemodynamic, MVO2, and Efficiency Data

MVO2 and Coefficient of Variation of Oxygen Consumption

Global k2 did not change significantly under CRT. However, before and after 4 mo of therapy, k2 was lower than that in the comparison group with mild heart failure (P = 0.012 and P = 0.023, respectively), but not after 13 mo of therapy (Table 3; Fig. 2A).

The regional k2 distribution among the myocardial walls, expressed by the coefficient of variation, became more homogeneous under CRT and decreased by up to 41% (baseline vs. 4-mo CRT, P = 0.0002; baseline vs. 13-mo CRT, P = 0.0006). From 4 to 13 mo of therapy no significant changes were observed. The k2 coefficient of variation of the comparison group was similar to those under CRT but lower than that before CRT (P = 0.0014) (Table 3; Fig. 2B).

SVI

The SVI increased by up to 50% with CRT (baseline vs. 4-mo CRT, P = 0.012; baseline vs. 13-mo CRT, P < 0.001). During therapy the SVI showed no significant changes. Before CRT the SVI was lower (P = 0.01) than that in the comparison group but during CRT was similar to that of the comparison group (Table 3; Fig. 2C).

Cardiac Efficiency

Cardiac efficiency increased by up to 41% during CRT (baseline vs. 4-mo CRT, P > 0.001; baseline vs. 13-mo CRT, P < 0.001). Between 4 and 13 mo of CRT, cardiac efficiency showed no significant changes. Before CRT cardiac efficiency was lower than that in the comparison group (P = 0.004). During CRT cardiac efficiency was the same as that of the comparison group (Table 3; Fig. 2D).

DISCUSSION

CRT restores left ventricular synchrony in patients with heart failure and LBBB. The coincidence of heart failure and LBBB depends on the disease state and ranges from 9.7% in NYHA class 0–I, from 32% in NYHA class II, to 53% in NYHA class III (21). Although the underlying cause of heart failure is not treated directly, echocardiography demonstrated a positive impact on left ventricular architecture with remodeling for up to 1-y follow-up (5,22). The objective of the present study was to add functional data for such an observation period.

The results demonstrate a long-term improvement in cardiac efficiency for up to 13-mo follow-up with CRT. This gain is based on a higher SVI without a concomitant increase in oxygen consumption, heart rate, or blood pressure. The efficiency level after 4 mo continued to persist for up to at least 13 mo of therapy and, hence, demonstrates a long-lasting CRT effect. Previous studies with similar issues addressed either short-term effects after the onset of CRT (12) or effects after acute discontinuation of long-term CRT (13,14). After 8–13 mo of CRT, Ukkonen et al. (13) found a 12% and Sundell et al. (14) found a 24% decrease in efficiency when CRT was switched off for 2 or 24 h, respectively. The changes in efficiency demonstrated in the present study are more substantial. There are 3 potential explanations for the observed differences: (i) A different methodologic approach was used to determine stroke volume. The method in the present study has been validated in a pig model versus thermodilution but not in humans with a standard method—for example, echocardiography (20). To reduce a potential systematic bias, only changes but not the absolute values were considered in the comparison with other studies. (ii) The present study applied compartmental modeling for the acetate clearance, whereas Ukkonen et al. and Sundell et al. used exponential curve fitting (indicated as kmono), which underestimates the acetate clearance (23). Considering that kmono and k2 showed merely minimal changes in all efficiency studies, only a minor effect is to be expected with respect to changes of SVI and cardiac efficiency through the different methods. (iii) Ventricular remodeling was likely to occur during the 13-mo observation period of the present study—as indicated by the decrease in LVEDD—but not between the short-term measurements of the cited studies (13,14). Therefore, the remodeling process may have enhanced the direct short-term effect of CRT on cardiac efficiency. Summarizing the results of all efficiency studies, they give rise to the statement that the response to CRT occurs immediately but that it is initially incomplete.

The question that arises from our results is whether CRT is able to induce a regression of disease state. With regard to morphologic studies there is evidence of a reverse remodeling process (22). However, the cited studies with measurements after interruption of long-term CRT reveal that the therapeutic benefit is closely related to the induced electromechanical resynchronization and reversible after cessation of therapy. MVO2, which was reduced in cardiomyopathy (24,25), may serve as an indirect marker for the disease state. Transforming the measured 11C-acetate clearance rates into an absolute MVO2 (26), it amounts to 6.0 ± 0.8 at baseline and at 3 mo, to 6.4 ± 1.2 at 13-mo follow-up for the CRT patients, and to 7.4 ± 1.4 mL/min/100 g for the mild heart failure patients. These data indicate a reduced MVO2 (normal range > 7.6 mL/min/100 g (27)) in the CRT group and no basic regression of the underlying disease during the observation period. Although not statistically different from the earlier measurements, the 13-mo MVO2 shows a trend toward higher values that is underlined by its insignificant difference to the MVO2 of the comparison group. This finding may indicate, therefore, that CRT eventually induces slight changes to the cardiomyopathic process. It is consistent with the hypothesis that dyssynchrony itself contributes to disease pathophysiology (28).

Intraventricular dyssynchrony in LBBB has been characterized with PET as having regional inhomogeneities of perfusion and metabolism. CRT reduces the intraventricular delay and balances regional perfusion and metabolism with a more homogeneous distribution pattern in the left ventricular myocardium (9,11,13,29). As a measure of inhomogeneity, the coefficient of variation of regional k2 (MVO2) significantly decreased with CRT and remained at this level. The finding also suggests, as implied by previous efficiency studies, that the process of pacemaker-induced resynchronization succeeds completely, at least after 4 mo, without any further adaptation.

Considering the improvement of symptoms and NYHA class by CRT, an additional intention of the present study was to evaluate the degree of CRT-induced changes in relation to a comparison group in an earlier state of disease—that is, with mild heart failure without LBBB (3–5). Parameters directly influenced by CRT are both at the 4-mo and the 13-mo follow-up on the level of the comparison group. This finding implies that (a) dyssynchrony is at least one of the leading factors that worsens cardiac function in heart failure patients with LBBB, that (b) dyssynchrony is effectively treatable with CRT, and that (c) CRT induces working conditions similar to that of patients in an earlier state of disease without LBBB.

CONCLUSION

CRT improves cardiac efficiency by a higher SVI without a concomitant increase in metabolic cost, heart rate, or blood pressure over a follow-up interval of 13 mo. MVO2, heart rate, and blood pressure showed no changes within this period. Parameters directly influenced by CRT, comprising the distribution pattern of MVO2, change to the level of a comparison group with mild heart failure but without LBBB. To summarize, the unfavorable hemodynamic performance in heart failure with LBBB is effectively and permanently suspended with CRT, restoring the working condition of an earlier disease state without LBBB.

Acknowledgments

Dr. Vogt has worked as a consultant for Guidant Germany. The other authors have no conflicts of interest with regard to the topic of this article. The funding source had no impact on study design, data collection, data interpretation, or report writing.

References

  1. 1.↵
    Hochleitner M, Hortnagl H, Fridrich L, Gschnitzer F. Long-term efficacy of physiologic dual-chamber pacing in the treatment of end-stage idiopathic dilated cardiomyopathy. Am J Cardiol. 1992;70:1320–1325.
    OpenUrlCrossRefPubMed
  2. 2.↵
    Abraham WT, Hayes DL. Cardiac resynchronization therapy for heart failure. Circulation. 2003;108:2596–2603.
    OpenUrlFREE Full Text
  3. 3.↵
    Abraham WT, Fisher WG, Smith AL, et al. Cardiac resynchronization in chronic heart failure. N Engl J Med. 2002;346:1845–1853.
    OpenUrlCrossRefPubMed
  4. 4.
    Cazeau S, Leclercq C, Lavergne T, et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med. 2001;344:873–880.
    OpenUrlCrossRefPubMed
  5. 5.↵
    Linde C, Leclercq C, Rex S, et al. Long-term benefits of biventricular pacing in congestive heart failure: results from the multisite stimulation in cardiomyopathy (MUSTIC) study. J Am Coll Cardiol. 2002;40:111–118.
    OpenUrlCrossRefPubMed
  6. 6.↵
    Cleland JG, Daubert JC, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005;352:1539–1549.
    OpenUrlCrossRefPubMed
  7. 7.↵
    Ezekowitz JA, Armstrong PW, McAlister FA. Implantable cardioverter defibrillators in primary and secondary prevention: a systematic review of randomized, controlled trials. Ann Intern Med. 2003;138:445–452.
    OpenUrlCrossRefPubMed
  8. 8.↵
    Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article—a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation. 2002;106:2145–2161.
    OpenUrlFREE Full Text
  9. 9.↵
    Lindner O, Vogt J, Kammeier A, et al. Effect of cardiac resynchronization therapy on global and regional oxygen consumption and myocardial blood flow in patients with non-ischaemic and ischaemic cardiomyopathy. Eur Heart J. 2005;26:70–76.
    OpenUrlAbstract/FREE Full Text
  10. 10.
    Knaapen P, van Campen LM, de Cock CC, et al. Effects of cardiac resynchronization therapy on myocardial perfusion reserve. Circulation. 2004;110:646–651.
    OpenUrlAbstract/FREE Full Text
  11. 11.↵
    Nowak B, Sinha AM, Schaefer WM, 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.
    OpenUrlCrossRefPubMed
  12. 12.↵
    Nelson GS, Berger RD, Fetics BJ, 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.
    OpenUrlAbstract/FREE Full Text
  13. 13.↵
    Ukkonen H, Beanlands RS, Burwash IG, et al. Effect of cardiac resynchronization on myocardial efficiency and regional oxidative metabolism. Circulation. 2003;107:28–31.
    OpenUrlAbstract/FREE Full Text
  14. 14.↵
    Sundell J, Engblom E, Koistinen J, et al. The effects of cardiac resynchronization therapy on left ventricular function, myocardial energetics, and metabolic reserve in patients with dilated cardiomyopathy and heart failure. J Am Coll Cardiol. 2004;43:1027–1033.
    OpenUrlCrossRefPubMed
  15. 15.↵
    Auricchio A, Stellbrink C, Butter C, et al. Clinical efficacy of cardiac resynchronization therapy using left ventricular pacing in heart failure patients stratified by severity of ventricular conduction delay. J Am Coll Cardiol. 2003;42:2109–2116.
    OpenUrlCrossRefPubMed
  16. 16.↵
    Stellbrink C, Auricchio A, Butter C, et al. Pacing therapies in congestive heart failure II study. Am J Cardiol. 2000;86:138K–143K.
    OpenUrlCrossRefPubMed
  17. 17.↵
    Vogt J, Krahnefeld O, Lamp B, et al. Electrocardiographic remodeling in patients paced for heart failure. Am J Cardiol. 2000;86:152K–156K.
    OpenUrlCrossRefPubMed
  18. 18.↵
    van den Hoff J, Burchert W, Borner AR, et al. [1-11C]Acetate as a quantitative perfusion tracer in myocardial PET. J Nucl Med. 2001;42:1174–1182.
    OpenUrlAbstract/FREE Full Text
  19. 19.↵
    Wolpers HG, 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.
    OpenUrlAbstract/FREE Full Text
  20. 20.↵
    Sorensen J, Stahle E, Langstrom B, et al. Simple and accurate assessment of forward cardiac output by use of 1-11C-acetate PET verified in a pig model. J Nucl Med. 2003;44:1176–1183.
    OpenUrlAbstract/FREE Full Text
  21. 21.↵
    Stellbrink C, Auricchio A, Diem B, et al. Potential benefit of biventricular pacing in patients with congestive heart failure and ventricular tachyarrhythmia. Am J Cardiol. 1999;83:143D–150D.
    OpenUrlPubMed
  22. 22.↵
    St John Sutton MG, Plappert T, Abraham WT, et al. Effect of cardiac resynchronization therapy on left ventricular size and function in chronic heart failure. Circulation. 2003;107:1985–1990.
    OpenUrlAbstract/FREE Full Text
  23. 23.↵
    Beanlands R, Wolpers HG, Gropler RJ. Quantification of myocardial oxygen consumption using 11C-acetate. In: Schwaiger M, ed. Cardiac Positron Emission Tomography. Boston, MA: Kluwer Academic Publishers; 1995:297–309.
  24. 24.↵
    Henry PD, Eckberg D, Gault JH, Ross JJ. Depressed inotropic state and reduced myocardial oxygen consumption in the human heart. Am J Cardiol. 1973;31:300–306.
    OpenUrlCrossRefPubMed
  25. 25.↵
    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.
    OpenUrlAbstract/FREE Full Text
  26. 26.↵
    Beanlands RS, Bach DS, 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.
    OpenUrlPubMed
  27. 27.↵
    Baller D, Schenk H, Strauer BE, Hellige G. Comparison of myocardial oxygen consumption indices in man. Clin Cardiol. 1980;3:116–122.
    OpenUrlPubMed
  28. 28.↵
    Spragg DD, Leclercq C, Loghmani M, et al. Regional alterations in protein expression in the dyssynchronous failing heart. Circulation. 2003;108:929–932.
    OpenUrlAbstract/FREE Full Text
  29. 29.↵
    Auricchio A, Salo RW. Acute hemodynamic improvement by pacing in patients with severe congestive heart failure. Pacing Clin Electrophysiol. 1997;20:313–324.
    OpenUrlCrossRefPubMed
  • Received for publication October 14, 2005.
  • Accepted for publication December 1, 2005.
PreviousNext
Back to top

In this issue

Journal of Nuclear Medicine: 47 (3)
Journal of Nuclear Medicine
Vol. 47, Issue 3
March 2006
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Index by author
Print
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for your interest in spreading the word on Journal of Nuclear Medicine.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Cardiac Efficiency and Oxygen Consumption Measured with 11C-Acetate PET After Long-Term Cardiac Resynchronization Therapy
(Your Name) has sent you a message from Journal of Nuclear Medicine
(Your Name) thought you would like to see the Journal of Nuclear Medicine web site.
Citation Tools
Cardiac Efficiency and Oxygen Consumption Measured with 11C-Acetate PET After Long-Term Cardiac Resynchronization Therapy
Oliver Lindner, Jens Sörensen, Jürgen Vogt, Eva Fricke, Detlev Baller, Dieter Horstkotte, Wolfgang Burchert
Journal of Nuclear Medicine Mar 2006, 47 (3) 378-383;

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Cardiac Efficiency and Oxygen Consumption Measured with 11C-Acetate PET After Long-Term Cardiac Resynchronization Therapy
Oliver Lindner, Jens Sörensen, Jürgen Vogt, Eva Fricke, Detlev Baller, Dieter Horstkotte, Wolfgang Burchert
Journal of Nuclear Medicine Mar 2006, 47 (3) 378-383;
Twitter logo Facebook logo LinkedIn logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One
Bookmark this article

Jump to section

  • Article
    • Abstract
    • MATERIALS AND METHODS
    • RESULTS
    • DISCUSSION
    • CONCLUSION
    • Acknowledgments
    • References
  • Figures & Data
  • Info & Metrics
  • PDF

Related Articles

  • This Month in JNM
  • PubMed
  • Google Scholar

Cited By...

  • Effects of the Novel Long-Acting GLP-1 Agonist, Albiglutide, on Cardiac Function, Cardiac Metabolism, and Exercise Capacity in Patients With Chronic Heart Failure and Reduced Ejection Fraction
  • Effects of Mitral Valve Surgery on Myocardial Energetics in Patients With Severe Mitral Regurgitation
  • Nuclear Imaging in Cardiac Resynchronization Therapy
  • Metabolic Mechanisms in Heart Failure
  • Myocardial Energetics and Efficiency: Current Status of the Noninvasive Approach
  • Google Scholar

More in this TOC Section

  • Feasibility of Ultra-Low-Activity 18F-FDG PET/CT Imaging Using a Long–Axial-Field-of-View PET/CT System
  • Cardiac Presynaptic Sympathetic Nervous Function Evaluated by Cardiac PET in Patients with Chronotropic Incompetence Without Heart Failure
  • Validation and Evaluation of a Vendor-Provided Head Motion Correction Algorithm on the uMI Panorama PET/CT System
Show more Clinical Investigations

Similar Articles

SNMMI

© 2025 SNMMI

Powered by HighWire