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Myocardial lipid turnover in dilated cardiomyopathy: A dual in vivo tracer approach

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Journal of Nuclear Cardiology Aims and scope

Abstract

Background

Myocardial lipid metabolism appears abnormal in dilated cardiomyopathy (DCM). A dual-tracer approach with two different fatty acid analogs may allow us to observe such alteration in vivo. 15-(Ortho-123I-phenyl)-pentadecanoic acid (oPPA) and 15-(para-123I-phenyl)-pentadecanoic acid (pPPA) have similar kinetics in circulation, diffusion, and transport. However, pPPA in normal myocardium undergoes β-oxidation and may also be lost from myocardial cells through back-diffusion; oPPA is hardly catabolized and normally retained mainly in the cytosolic lipid pool. Use of both pPPA and oPPA in the dual-tracer approach focuses observation on the turnover of myocardial lipids (with pPPA) that is scaled against loss of fatty acid through back-diffusion into circulation (with oPPA).

Methods and Results

Fifteen patients with idiopathic DCM and five control subjects were given oPPA and pPPA sequentially for dynamic planar scintigraphy. Uptake and elimination rates were determined for both substrates from three myocardial regions per individual; the corresponding six elimination rate constants and the three differences between them were analyzed for significant alterations in patients from control values. At least 66% of the patients had a significant alteration in myocardial lipid turnover in three types of patterns: (1) increased β-oxidation, (2) decreased β-oxidation, and (3) increased back-diffusion, in part associated with decreased β-oxidation. Even with the limited number of patients and control subjects, the pattern of abnormality of lipid turnover in DMC appeared to be consistent individually but heterogeneous in the patient group. Moreover, a highly significant increase in β-oxidation was observed for the posterolateral region of the myocardium compared with the anteroseptal and apical regions in control subjects and patients.

Conclusion

The dual-tracer approach uncovered in vivo that in at least two thirds of the patients with DCM myocardial lipid turnover was significantly altered compared with control values.

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Authors and Affiliations

  1. Institute of Medicine, Research Centre Jülich, Jülich, Germany

    L. E. Feinendegen, M. M. Henrich, J. T. Kuikka, K. H. Thompson, E. G. Vester & B. Strauer

  2. Brookhaven National Laboratory, Upton, New York

    L. E. Feinendegen, M. M. Henrich, J. T. Kuikka, K. H. Thompson, E. G. Vester & B. Strauer

  3. the Department of Nuclear Medicine, University of Ulm, Ulm, Germany

    L. E. Feinendegen, M. M. Henrich, J. T. Kuikka, K. H. Thompson, E. G. Vester & B. Strauer

  4. the Department of Clinical Physiology, Kuopio University Hospital, Kuopio, Finland

    L. E. Feinendegen, M. M. Henrich, J. T. Kuikka, K. H. Thompson, E. G. Vester & B. Strauer

  5. Department of Cardiology, Heinrich-Heine-University of Düsseldorf, Düsseldorf, Germany

    L. E. Feinendegen, M. M. Henrich, J. T. Kuikka, K. H. Thompson, E. G. Vester & B. Strauer

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  1. L. E. Feinendegen
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  2. M. M. Henrich
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  3. J. T. Kuikka
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  4. K. H. Thompson
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  5. E. G. Vester
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  6. B. Strauer
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Feinendegen, L.E., Henrich, M.M., Kuikka, J.T. et al. Myocardial lipid turnover in dilated cardiomyopathy: A dual in vivo tracer approach. J Nucl Cardiol 2, 42–52 (1995). https://doi.org/10.1016/S1071-3581(05)80007-8

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  • DOI: https://doi.org/10.1016/S1071-3581(05)80007-8

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