Journal of clinical lipidology · 2025
Different response of plaque regression following achievement of LDL-C <1.8 mmol/L in obese and nonobese patients with diabetes and coronary artery disease: OPTIMAL sub-analysis.
СтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Salib Anthony, Kataoka Yu, Nicholls Stephen J, Kitahara Satoshi, Funabashi Sayaka, Makino Hisashi, Matsubara Masaki, Matsuo Miki, Omura-Ohata Yoko, Koezuka Ryo, Tochiya Mayu, Tamanaha Tamiko, Tomita Tsutomu, Honda-Kohmo Kyoko, Noguchi Michio, Mitsui Kentaro, Murai Kota, Iwai Takamasa, Sawada Kenichiro, Matama Hideo, Honda Satoshi, Fujino Masashi, Yoneda Shuichi, Nakao Kazuhiro, Takagi Kensuke, Otsuka Fumiyuki, Asaumi Yasuhide, Hosoda Kiminori, Yasuda Satoshi, Noguchi Teruo
Аннотация
BACKGROUND: Obesity is a major risk factor for atherosclerotic cardiovascular disease (ASCVD). While lowering low-density lipoprotein cholesterol (LDL-C) reduces ASCVD, it remains unclear whether patients with obesity exhibit distinct plaque responses to LDL-C control.
OBJECTIVE: The current study sought to compare disease progression under achieving LDL-C <1.8 mmol/L in patients with type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD) with and without obesity.
METHODS: This prespecified sub-analysis of the OPTIMAL randomized trial (jRCT1052180152; UMIN000036721) evaluated 78 statin-treated patients with T2DM and CAD who underwent serial intravascular ultrasound imaging. Change in percent atheroma volume (PAV) was compared in those with obesity (body mass index [BMI] ≥ 25 kg/m2, n = 31) and without (BMI <25 kg/m2, n = 47) stratified by achievement of LDL-C<1.8 mmol/l at 48 weeks.
RESULTS: LDL-C<1.8 mmol/L was attained in 41.9% with obesity and 57.4% without (P = .18). In participants without obesity, achieving LDL-C<1.8 mmol/L was not associated with significant change in PAV (-0.5 ± 0.4 vs -0.3 ± 0.4%, P = .74) or regression frequency (59.3 vs 62.0%, P = .85). In contrast, patients with obesity achieving LDL-C<1.8 mmol/L more often received high-intensity statins and demonstrated significant PAV regression (-0.9 ± 0.3 vs 0.4 ± 0.2%, P = .006) and greater regression frequency (79.6 vs 25.2%, P = .01).
CONCLUSION: A greater regression of coronary atheroma following LDL-C<1.8 mmol/L was observed in obese patients. Future dedicated study is warranted to further elucidate atheroma regression in response to LDL-C control in obese and nonobese patients.
OBJECTIVE: The current study sought to compare disease progression under achieving LDL-C <1.8 mmol/L in patients with type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD) with and without obesity.
METHODS: This prespecified sub-analysis of the OPTIMAL randomized trial (jRCT1052180152; UMIN000036721) evaluated 78 statin-treated patients with T2DM and CAD who underwent serial intravascular ultrasound imaging. Change in percent atheroma volume (PAV) was compared in those with obesity (body mass index [BMI] ≥ 25 kg/m2, n = 31) and without (BMI <25 kg/m2, n = 47) stratified by achievement of LDL-C<1.8 mmol/l at 48 weeks.
RESULTS: LDL-C<1.8 mmol/L was attained in 41.9% with obesity and 57.4% without (P = .18). In participants without obesity, achieving LDL-C<1.8 mmol/L was not associated with significant change in PAV (-0.5 ± 0.4 vs -0.3 ± 0.4%, P = .74) or regression frequency (59.3 vs 62.0%, P = .85). In contrast, patients with obesity achieving LDL-C<1.8 mmol/L more often received high-intensity statins and demonstrated significant PAV regression (-0.9 ± 0.3 vs 0.4 ± 0.2%, P = .006) and greater regression frequency (79.6 vs 25.2%, P = .01).
CONCLUSION: A greater regression of coronary atheroma following LDL-C<1.8 mmol/L was observed in obese patients. Future dedicated study is warranted to further elucidate atheroma regression in response to LDL-C control in obese and nonobese patients.