Atherosclerosis · 2025
Apolipoprotein CIII in statin-treated type 2 diabetic patients: Its implications for plaque progression and instability: The pre-specified analysis from the OPTIMAL randomized controlled trial.
СтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Kitahara Satoshi, Kataoka Yu, Nicholls Stephen J, Funabashi Sayaka, Nakatsuka Kiyomasa, Nishimura Kunihiro, Makino Hisashi, Matsubara Masaki, Matsuo Miki, Omura-Ohata Yoko, Koezuka Ryo, Tochiya Mayu, Tamanaha Tamiko, Tomita Tsutomu, Honda-Kohmo Kyoko, Noguchi Michio, Murai Kota, Iwai Takamasa, Sawada Kenichiro, Matama Hideo, Honda Satoshi, Fujino Masashi, Yoneda Shuichi, Takagi Kensuke, Otsuka Fumiyuki, Asaumi Yasuhide, Hosoda Kiminori, Yasuda Satoshi, Noguchi Teruo
Аннотация
AIMS: Apolipoprotein CIII (ApoCIII) has a variety of proatherogenic properties. Given that hyperglycemia induces ApoCIII transcription, this apolipoprotein may promote coronary atherosclerosis in type 2 diabetic patients. We aimed to elucidate whether ApoCIII affects plaque progression and instability in statin-treated type 2 diabetic patients.
METHODS AND RESULTS: The OPTIMAL study was a prospective randomized controlled trial that employed serial NIRS/IVUS imaging to evaluate the efficacy of glycemic control on coronary atherosclerosis in 94 statin-treated type 2 diabetic patients (UMIN000036721). Of these, 78 patients with both ApoCIII levels and NIRS/IVUS images at baseline and week 48 were analyzed. Any increase in ApoCIII levels at week 48 was observed in 47.4 % of study participants. On-treatment LDL-C levels did not differ among participants with and without any increase in ApoCIII levels (1.76 ± 0.55 vs. 1.74 ± 0.55 mmol/L, p = 0.91). Serial changes in IVUS-derived atheroma volume were similar between two groups (-0.7 ± 2.2 vs. -2.4 ± 1.6 mm3, p = 0.51). However, greater progression in NIRS-derived maxLCBI4mm was observed in those with any increase in ApoCIII levels (91.2 ± 24.8 vs. -44.2 ± 23.5, p < 0.001). Even after adjusting for clinical characteristics, maxLCBI4mm in participants with any increase in ApoCIII levels still progressed (87.0 ± 24.9 vs. -44.2 ± 23.5, p < 0.001). Moreover, maxLCBI4mm less likely regressed in patients with any increase in ApoCIII levels (16.2 vs. 80.5 %, p < 0.001). Even in those achieving on-treatment LDL-C<1.4 mmol/L, maxLCBI4mm progressed in association with any increase in ApoCIII levels.
CONCLUSION: Circulating ApoCIII promoted the accumulation of lipidic plaque components in statin-treated type 2 diabetic patient, suggesting ApoCIII as a residual risk that requires therapeutic intervention.
METHODS AND RESULTS: The OPTIMAL study was a prospective randomized controlled trial that employed serial NIRS/IVUS imaging to evaluate the efficacy of glycemic control on coronary atherosclerosis in 94 statin-treated type 2 diabetic patients (UMIN000036721). Of these, 78 patients with both ApoCIII levels and NIRS/IVUS images at baseline and week 48 were analyzed. Any increase in ApoCIII levels at week 48 was observed in 47.4 % of study participants. On-treatment LDL-C levels did not differ among participants with and without any increase in ApoCIII levels (1.76 ± 0.55 vs. 1.74 ± 0.55 mmol/L, p = 0.91). Serial changes in IVUS-derived atheroma volume were similar between two groups (-0.7 ± 2.2 vs. -2.4 ± 1.6 mm3, p = 0.51). However, greater progression in NIRS-derived maxLCBI4mm was observed in those with any increase in ApoCIII levels (91.2 ± 24.8 vs. -44.2 ± 23.5, p < 0.001). Even after adjusting for clinical characteristics, maxLCBI4mm in participants with any increase in ApoCIII levels still progressed (87.0 ± 24.9 vs. -44.2 ± 23.5, p < 0.001). Moreover, maxLCBI4mm less likely regressed in patients with any increase in ApoCIII levels (16.2 vs. 80.5 %, p < 0.001). Even in those achieving on-treatment LDL-C<1.4 mmol/L, maxLCBI4mm progressed in association with any increase in ApoCIII levels.
CONCLUSION: Circulating ApoCIII promoted the accumulation of lipidic plaque components in statin-treated type 2 diabetic patient, suggesting ApoCIII as a residual risk that requires therapeutic intervention.