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Impaired myocardial oxidative metabolism in the remote normal region in patients in the chronic phase of myocardial infarction and left ventricular remodeling

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Journal of Nuclear Cardiology Aims and scope

Abstract

Background

Left ventricular (LV) remodeling occurs in the remote normal region in the LVs after myocardial infarction (MI) and is closely involved in heart failure.

Methods

We assessed myocardial oxygen consumption using a clearance rate constant K mono for the time activity curves of 11C-acetate in 15 patients with a prior anterior wall MI, 8 with a prior inferior wall MI, and 10 age-matched normal control subjects. LV end-systolic volume index (ESVI) was determined by echocardiography.

Results

The LVESVI was significantly greater in patients with an anterior and inferior MI than in control subjects. The heart rate systolic pressure product did not differ among the groups. K mono in the remote normal region in patients with an anterior MI was significantly less than that in the corresponding area in control subjects (0.055 ± 0.005 vs 0.065 ± 0.008 min−1, < .001). K mono in the remote normal region in those with an inferior MI was also significantly less compared with controls (0.054 ± 0.007 vs 0.069 ± 0.010 min−1, P < .01).

Conclusion

In patients with a prior MI and LV remodeling, myocardial oxidative metabolism is apparently impaired in the remote normal region where augmented myocardial energy production is needed against the increased end-systolic wall stress caused by LV dilatation.

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Acknowledgments

This work was supported by the Grant-in-Aid for Scientific Research (no. 15591293) from the Japan Society for the Promotion of Science and by the Research Grant for Cardiovascular Diseases (no. 16-C) from the Ministry of Health, Labor and Welfare of Japan.

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Correspondence to Nobuyuki Ohte MD.

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Ohte, N., Narita, H., Iida, A. et al. Impaired myocardial oxidative metabolism in the remote normal region in patients in the chronic phase of myocardial infarction and left ventricular remodeling. J. Nucl. Cardiol. 16, 73–81 (2009). https://doi.org/10.1007/s12350-008-9006-4

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  • DOI: https://doi.org/10.1007/s12350-008-9006-4

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