Abstract
BackgroundAccelerated clearance of 99mtechnetium-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 11carbon-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 11C-acetate positron emission tomography (PET).MethodsEighteen patients [mean age 69.2 ± 8.7 years, 10 males (56 %)] with reperfused ACS underwent MIBI single-photon emission computed tomography (SPECT), echocardiography, and 11C-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 11C-acetate time-activity curve (kmono).ResultsAmong 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 kmono than group N (0.041 ± 0.009 vs 0.049 ± 0.010, p = 0.02). Group F showed lower kmono than group N (0.039 ± 0.012 vs 0.049 ± 0.010, p = 0.01). However, kmono was similar in group AC and group F (p = 0.99).ConclusionsSegments with accelerated MIBI clearance showed reduced oxidative metabolism in ACS. Loss of MIBI retention may be associated with mitochondrial dysfunction.
Highlights
Accelerated clearance of 99mtechnetium-sestamibi (MIBI) has been observed after reperfusion therapy in patients with acute coronary syndrome (ACS), but the mechanisms have not been fully investigated
11C-acetate positron emission tomography (PET) can non-invasively evaluate myocardial oxidative metabolism [7,8,9,10,11,12] and myocardial blood flow [13, 14]. 11C-acetate clearance is associated with citric acid cycle activity in the mitochondria, in which acetate is converted into acetyl-CoA and metabolized via the action of acetyl-CoA synthetase 2 [15]
Previous studies have suggested an association between accelerated mitochondrial dysfunction is99mTechnetium-sestamibi (MIBI) clearance and mitochondrial dysfunction in dilated and hypertrophic cardiomyopathy based on experimental researches [16]
Summary
Accelerated clearance of 99mtechnetium-sestamibi (MIBI) has been observed after reperfusion therapy in patients with acute coronary syndrome (ACS), but the mechanisms have not been fully investigated. The purpose of this study was to examine the mechanisms of accelerated MIBI clearance in ACS. We compared it to oxidative metabolism estimated using 11C-acetate positron emission tomography (PET). Oxidative metabolism as estimated using 11C-acetate PET can be associated with mitochondrial function. Previous studies have suggested an association between accelerated MIBI clearance and mitochondrial dysfunction in dilated and hypertrophic cardiomyopathy based on experimental researches [16].
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