Journal of the American Heart Association · 2026
Lipidic Plaque Features of Polyvascular Disease in Response to Low-Density Lipoprotein Cholesterol <55 mg/dL: Implication of Circulating Lipoprotein(a) Levels.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Katasako-Yabumoto Aya, Kataoka Yu, Nicholls Stephen J, Kiyoshige Eri, Nishimura Kunihiro, Puri Rishi, Murai Kota, Iwai Takamasa, Sawada Kenichiro, Matama Hideo, Honda Satoshi, Takagi Kensuke, Fujino Masashi, Yoneda Shuichi, Otsuka Fumiyuki, Nakao Kazuhiro, Nishihira Kensaku, Takamisawa Itaru, Asaumi Yasuhide, Tsujita Kenichi, Noguchi Teruo
Аннотация
BACKGROUND: Patients with polyvascular disease (PolyVD) or atherosclerosis in the coronaries and at least 1 additional arterial bed are at increased risk of subsequent clinical cardiovascular events. While lowering low-density lipoprotein cholesterol (LDL-C) is recommended in the secondary prevention settings, whether PolyVD favorably responds to LDL-C control remains unknown.
METHODS: The current study analyzed in 422 patients (422 target lesions) with coronary artery disease by using near-infrared spectroscopy imaging before percutaneous coronary intervention in the REASSURE-NIRS (Revelation of Pathophysiological Phenotypes of Vulnerable Lipid-Rich Plaque on Near-Infrared Spectroscopy; NCT04864171) multicenter registry. PolyVD was defined as concomitance of coronary artery disease and cerebrovascular disease or lower extremity arterial disease.
RESULTS: Maximum 4-mm lipid-core burden index, as a near-infrared spectroscopy-derived marker of plaque instability, and lipoprotein(a) [Lp(a)] were compared across LDL-C levels (<55, 55-69, and ≥70mg/dL) in patients with (n=189) and without PolyVD (n=233). The proportion of LDL-C <55 mg/dL was 15.3 and 9.4% in patients with and without PolyVD, respectively. In patients without PolyVD, LDL-C <55 mg/dL was associated with lower maximum 4-mm lipid-core burden index (P=0.045). Furthermore, a lower frequency of Lp(a) ≥50 mg/dL was observed in patients without PolyVD who achieved LDL-C <55 mg/dL (P=0.042). Only 4.5% of them presented with Lp(a) ≥50 mg/dL. However, achieved LDL-C <55 mg/dL was not associated with lower maximum 4-mm lipid-core burden index in patients with PolyVD (P=0.085). Moreover, Lp(a) remained comparable regardless of LDL-C levels (P=0.902). Of note, 20.7% of patients with PolyVD with LDL-C <55 mg/dL exhibited Lp(a) ≥50 mg/dL.
CONCLUSIONS: Coronary atheroma in patients with PolyVD was resistant to lowering LDL-C <55 mg/dL. Given that >20% of those with LDL-C <55 mg/dL exhibited Lp(a) ≥50 mg/dL, Lp(a) may be a potential therapeutic target to delipidate coronary atheroma.
METHODS: The current study analyzed in 422 patients (422 target lesions) with coronary artery disease by using near-infrared spectroscopy imaging before percutaneous coronary intervention in the REASSURE-NIRS (Revelation of Pathophysiological Phenotypes of Vulnerable Lipid-Rich Plaque on Near-Infrared Spectroscopy; NCT04864171) multicenter registry. PolyVD was defined as concomitance of coronary artery disease and cerebrovascular disease or lower extremity arterial disease.
RESULTS: Maximum 4-mm lipid-core burden index, as a near-infrared spectroscopy-derived marker of plaque instability, and lipoprotein(a) [Lp(a)] were compared across LDL-C levels (<55, 55-69, and ≥70mg/dL) in patients with (n=189) and without PolyVD (n=233). The proportion of LDL-C <55 mg/dL was 15.3 and 9.4% in patients with and without PolyVD, respectively. In patients without PolyVD, LDL-C <55 mg/dL was associated with lower maximum 4-mm lipid-core burden index (P=0.045). Furthermore, a lower frequency of Lp(a) ≥50 mg/dL was observed in patients without PolyVD who achieved LDL-C <55 mg/dL (P=0.042). Only 4.5% of them presented with Lp(a) ≥50 mg/dL. However, achieved LDL-C <55 mg/dL was not associated with lower maximum 4-mm lipid-core burden index in patients with PolyVD (P=0.085). Moreover, Lp(a) remained comparable regardless of LDL-C levels (P=0.902). Of note, 20.7% of patients with PolyVD with LDL-C <55 mg/dL exhibited Lp(a) ≥50 mg/dL.
CONCLUSIONS: Coronary atheroma in patients with PolyVD was resistant to lowering LDL-C <55 mg/dL. Given that >20% of those with LDL-C <55 mg/dL exhibited Lp(a) ≥50 mg/dL, Lp(a) may be a potential therapeutic target to delipidate coronary atheroma.