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Reduced myocardial flow reserve in anatomically normal coronary arteries due to elevated baseline myocardial blood flow in men with old myocardial infarction

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Journal of Nuclear Cardiology Aims and scope

Abstract

Background

Decreased myocardial flow reserve (MFR) in angiographically normal coronary arteries in patients with old myocardial infarction (OMI) has been reported.

Methods and Results

To clarify factors for the reduced MFR in OMI and to compare them with those in angina pectoris (AP), baseline myocardial blood flow (MBF) and MBF during dipyridamole administration were measured with nitrogen 13 ammonia positron emission tomography, after which MFR was calculated for 13 men with AP, 18 men with OMI, and 15 age-matched male control subjects. MFR was compared among the 3 groups in segments perfused by nonstenotic arteries. Baseline MBF in patients with OMI was significantly higher than that in patients with AP and control subjects. MBF during dipyridamole administration in patients with OMI was significantly lower than that in control subjects. MFR in patients with AP was 2.50 ± 0.91 (P < .05 vs control subjects [3.47 ± 1.25]), and that in patients with OMI was 1.83 ± 0.61 (P < .01 vs control and AP groups). Ejection fraction (EF) in patients with OMI was significantly decreased compared with that in patients with AP. However, there was no significant difference in the mean score of the individual risk factors between patients with AP and those with OMI. In the pooled data with AP and OMI, baseline MBF and EF were significant for the reduced MFR.

Conclusions

MFR and EF in patients with OMI were significantly decreased compared with those in patients with AP. Increased baseline MBF and decreased EF were significant factors for the reduced MFR in patients with AP and OMI.

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Correspondence to Ikuo Yokoyama.

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Yonekura, K., Yokoyama, I., Ohtake, T. et al. Reduced myocardial flow reserve in anatomically normal coronary arteries due to elevated baseline myocardial blood flow in men with old myocardial infarction. J Nucl Cardiol 9, 62–67 (2002). https://doi.org/10.1067/mnc.2002.119687

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  • DOI: https://doi.org/10.1067/mnc.2002.119687

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