Key result
Myocardial segments with accelerated 99mTc-sestamibi clearance showed reduced oxidative metabolism compared to normal segments in patients with acute coronary syndrome.
Why the study?
Is accelerated 99mTc-sestamibi clearance associated with reduced oxidative metabolism in reperfused myocardium of patients with acute coronary syndrome?
Observational (n=18)
No
Is accelerated 99mTc-sestamibi clearance associated with reduced oxidative metabolism in reperfused myocardium of patients with acute coronary syndrome?
Accelerated 99mTc-sestamibi clearance in reperfused myocardium is associated with reduced oxidative metabolism, suggesting mitochondrial dysfunction.
Answers are grounded in this paper and cite their sources.
Suggests mitochondrial dysfunction in reperfused ACS segments; hypothesis-generating and requires prospective validation before clinical adoption.
BACKGROUND: Accelerated clearance of (99m)technetium-sestamibi (MIBI) has been observed after reperfusion therapy in patients with acute coronary syndrome (ACS), but the mechanisms have not been fully investigated. MIBI retention may depend on mitochondrial function. The clearance rate of (11)carbon-acetate reflects such mitochondrial functions as oxidative metabolism. The purpose of this study was to examine the mechanisms of accelerated MIBI clearance in ACS. We therefore compared it to oxidative metabolism estimated using (11)C-acetate positron emission tomography (PET). METHODS: Eighteen patients [mean age 69.2 ± 8.7 years, 10 males (56 %)] with reperfused ACS underwent MIBI single-photon emission computed tomography (SPECT), echocardiography, and (11)C-acetate PET within 3 weeks of the onset of ACS. MIBI images were obtained 30 min and 3 h after MIBI administration. Regional left ventricular (LV) function was evaluated by echocardiography. The measurement of oxidative metabolism was obtained through the mono-exponential fitting of the (11)C-acetate time-activity curve (k mono). RESULTS: Among 95 segments of reperfused myocardium, MIBI SPECT showed 64 normal segments (group N), 14 segments with accelerated MIBI clearance (group AC), and 17 segments with fixed defect (group F). Group AC showed lower k mono than group N (0.041 ± 0.009 vs 0.049 ± 0.010, p = 0.02). Group F showed lower k mono than group N (0.039 ± 0.012 vs 0.049 ± 0.010, p = 0.01). However, k mono was similar in group AC and group F (p = 0.99). CONCLUSIONS: Segments with accelerated MIBI clearance showed reduced oxidative metabolism in ACS. Loss of MIBI retention may be associated with mitochondrial dysfunction.
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Masuda et al. (2016) conducted an observational in Acute coronary syndrome (n=18). 99mTc-sestamibi (MIBI) SPECT and 11C-acetate PET vs. Normal myocardial segments was evaluated on Oxidative metabolism (kmono) (p=0.02). Myocardial segments with accelerated 99mTc-sestamibi clearance showed reduced oxidative metabolism compared to normal segments in patients with acute coronary syndrome.
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