Scholarlink

Background <p>Associations between optimal low-density lipoprotein cholesterol (LDL-C) level and changes in coronary flow and plaque characteristics are unclear. Therefore, we examined the effect of LDL-C lowering changes lipid-rich coronary plaques and flow using near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) and quantitative flow ratio (QFR) in non-culprit vessels of patients with acute coronary syndrome (ACS).</p> Methods <p>We prospectively examined 72 patients with ACS who underwent NIRS-IVUS for intermediate stenosis in non-culprit vessels at baseline and at follow-up. According to patients’ LDL-C levels at follow-up, they were classified into two groups. Patients with LDL-C levels &lt; 55&#xa0;mg/dL were categorized into the very low LDL-C group (VL group), while those with LDL-C levels ≥ 55&#xa0;mg/dL were categorized into the low LDL-C group (L group). Changes in the lesion lipid core burden index (LCBI) and maximum 4-mm lipid core burden index (maxLCBI<sub>4mm</sub>) were assessed using NIRS-IVUS. Coronary flow was assessed using the QFR. The differences (Δ) between each value at follow-up and at baseline were determined.</p> Results <p>The median LDL-C level at follow-up was 48 (42–53) mg/dL in the VL group and 64 (60–68) mg/dL in the L group. There was a strong correlation between reduction of maxLCBI<sub>4mm</sub> and improvement of QFR (R<sup>2</sup> = 0.58). The VL group showed a significant decrease in maxLCBI<sub>4mm</sub> along with improvement in QFR value compared with the L group (<i>P</i> = 0.003; <i>P</i> = 0.008, respectively). The proportion of plaques with a maxLCBI<sub>4mm</sub> ≥ 400 (18.1% vs. 53.6%, <i>P</i> = 0.002) and the lesion LCBI (35.5(8.25–74) vs. 88.5(42.8–132), <i>P</i> = 0.03) at follow-up was lower in the VL group than in the L group. Plaques with a maxLCBI<sub>4mm</sub> ≥ 400 at baseline changed more frequently to a maxLCBI<sub>4mm</sub> &lt; 400 at follow-up in the VL group than in the L group (36% vs. 4%, <i>P</i> = 0.001).</p> Conclusion <p>Aggressive LDL-C-lowering therapy for non-culprit intermediate stenosis in ACS appears to promote plaque stabilization and improve coronary flow.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Impact of low-density lipoprotein cholesterol-lowering therapy on intermediate stenosis in non-culprit vessels of acute coronary syndrome

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月28日

查看全文
  • Kazuyoshi Kakehi,
  • Masafumi Ueno,
  • Masaru Kayama,
  • Nobuhiro Yamada,
  • Kyohei Onishi,
  • Keishiro Sugimoto,
  • Yohei Funauchi,
  • Takayuki Kawamura,
  • Kosuke Fujita,
  • Hiroki Matsuzoe,
  • Koichiro Matsumura,
  • Gaku Nakazawa

摘要

Background

Associations between optimal low-density lipoprotein cholesterol (LDL-C) level and changes in coronary flow and plaque characteristics are unclear. Therefore, we examined the effect of LDL-C lowering changes lipid-rich coronary plaques and flow using near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) and quantitative flow ratio (QFR) in non-culprit vessels of patients with acute coronary syndrome (ACS).

Methods

We prospectively examined 72 patients with ACS who underwent NIRS-IVUS for intermediate stenosis in non-culprit vessels at baseline and at follow-up. According to patients’ LDL-C levels at follow-up, they were classified into two groups. Patients with LDL-C levels < 55 mg/dL were categorized into the very low LDL-C group (VL group), while those with LDL-C levels ≥ 55 mg/dL were categorized into the low LDL-C group (L group). Changes in the lesion lipid core burden index (LCBI) and maximum 4-mm lipid core burden index (maxLCBI4mm) were assessed using NIRS-IVUS. Coronary flow was assessed using the QFR. The differences (Δ) between each value at follow-up and at baseline were determined.

Results

The median LDL-C level at follow-up was 48 (42–53) mg/dL in the VL group and 64 (60–68) mg/dL in the L group. There was a strong correlation between reduction of maxLCBI4mm and improvement of QFR (R2 = 0.58). The VL group showed a significant decrease in maxLCBI4mm along with improvement in QFR value compared with the L group (P = 0.003; P = 0.008, respectively). The proportion of plaques with a maxLCBI4mm ≥ 400 (18.1% vs. 53.6%, P = 0.002) and the lesion LCBI (35.5(8.25–74) vs. 88.5(42.8–132), P = 0.03) at follow-up was lower in the VL group than in the L group. Plaques with a maxLCBI4mm ≥ 400 at baseline changed more frequently to a maxLCBI4mm < 400 at follow-up in the VL group than in the L group (36% vs. 4%, P = 0.001).

Conclusion

Aggressive LDL-C-lowering therapy for non-culprit intermediate stenosis in ACS appears to promote plaque stabilization and improve coronary flow.