TY - JOUR
T1 - Accelerated 99mTc-sestamibi clearance associated with mitochondrial dysfunction and regional left ventricular dysfunction in reperfused myocardium in patients with acute coronary syndrome
AU - Masuda, Atsuro
AU - Yoshinaga, Keiichiro
AU - Naya, Masanao
AU - Manabe, Osamu
AU - Yamada, Satoshi
AU - Iwano, Hiroyuki
AU - Okada, Tatsuya
AU - Katoh, Chietsugu
AU - Takeishi, Yasuchika
AU - Tsutsui, Hiroyuki
AU - Tamaki, Nagara
N1 - Funding Information:
Dr. Yoshinaga has received research grants through the Imura Clinical Research Award (Adult Vascular Disease Research Foundation, Kyoto, Japan). This work was in part supported by FUJIFILM RI Pharma Co., Ltd. (Tokyo, Japan).
Publisher Copyright:
© 2016, Masuda et al.
PY - 2016
Y1 - 2016
N2 - Background: 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. 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). 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 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). 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 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). Conclusions: Segments with accelerated MIBI clearance showed reduced oxidative metabolism in ACS. Loss of MIBI retention may be associated with mitochondrial dysfunction.
AB - Background: 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. 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). 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 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). 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 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). 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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U2 - 10.1186/s13550-016-0196-5
DO - 10.1186/s13550-016-0196-5
M3 - Article
AN - SCOPUS:84971303968
VL - 6
JO - EJNMMI Research
JF - EJNMMI Research
SN - 2191-219X
IS - 1
M1 - 41
ER -