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Objectives <p>We aimed to evaluate associations between lipoprotein (a) [Lp(a)] levels and intravascular imaged coronary lesions morphology in coronary artery disease [CAD] patients. Additionally, we assessed the association of high-dose statins mediated Lp(a) changes with plaque morphology changes.</p> Methods <p>Post-hoc subanalysis of the YELLOW-II study. Lp(a) was measured in patients with stable CAD, who underwent percutaneous coronary intervention (PCI). Following PCI, optical coherence tomography (OCT), intravascular ultrasound and near-infrared spectroscopy were used to evaluate an obstructive non-culprit lesion. Subjects then received rosuvastatin 40&#xa0;mg for 8–12 weeks, after which the lesion was reimaged. Associations between Lp(a) quartiles and plaque characteristics before and after statins were assessed.</p> Results <p>Eighty-two patients were included (mean age 62 ± 11 years-old, 33% females, mean LDL-C 87 ± 40&#xa0;mg/dL). Median Lp(a) was 25 (IR 6.0-65.8) mg/dL (4.0, 12.5, 37.5, 97.0&#xa0;mg/dL in Q1, Q2, Q3, Q4, respectively). OCT minimal fibrous cap thickness (FCT) was lower in Q4 vs. Q1 (79.4 ± 29 vs. 111.1 ± 49&#xa0;μm, <i>p</i> = 0.045), indicative of high-risk unstable plaques. Following 8–12 weeks of statins, median Lp(a) increased to 34.0 (10.0–77.0) mg/dL (<i>p</i> &lt; 0.01), and minimal FCT increased in the overall cohort (99.2 ± 39.1 to 106.3 ± 36.9&#xa0;μm, <i>p</i> &lt; 0.001). However, there was no difference in FCT between Lp(a) quartiles at follow-up (<i>p</i> = 0.64). Furthermore, the increase in Lp(a) with statins did not impact FCT changes.</p> Conclusions <p>Higher levels of Lp(a) at baseline are associated with lower OCT fibrous caps in patients with stable CAD. After high-intensity statin therapy, Lp(a) significantly increased, however, changes in Lp(a) were not associated with changes in fibrous cap thickness.</p> Graphical Abstract <p>Lp(a) and Intracoronary Imaging after Statins in Patients with CAD.&#xa0;The central illustration presents lipoprotein (a) [Lp(a)] plasma levels and minimal fibrous cap thickness (FCT) at baseline and after 8-12 weeks of rosuvastatin, across baseline Lp(a) quartiles. Baseline Lp(a) means for each Lp(a)-quartile are presented in the left upper bar graph. After statins (right upper bar graph), mean Lp(a) increased across all Lp(a) quartiles, as shown by the blue arrows. Baseline FCT is shown across Lp(a) quartiles in the lower left bar graph. Notably, in the highest Lp(a) quartile [Lp(a)-Q4], baseline FCT is the thinnest. After rosuvastatin FCT increases in all Lp(a) quartiles but the lowest Lp(a) quartile [(Lp(a)-Q1)], as represented by the red arrows (lower right bar graph). Notably, the arrow is getting longer with the increase in quartiles, representative of greater absolute change in FCT with higher baseline Lp(a).</p> <p></p>

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Lipoprotein (a) and Coronary Atherosclerosis in Intracoronary Imaging - YELLOW II – Lp(a) Study

  • 期刊论文

  • 发表日期：

    2026年3月3日

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  • Chen Gurevitz,
  • Yuliya Vengrenyuk,
  • Shingo Minatoguchi,
  • Keisuke Yasumura,
  • Amit Hooda,
  • Prakash Krishnan,
  • Pedro Moreno,
  • Jagat Narula,
  • Samin Sharma,
  • Robert S. Rosenson,
  • Annapoorna S. Kini

摘要

Objectives

We aimed to evaluate associations between lipoprotein (a) [Lp(a)] levels and intravascular imaged coronary lesions morphology in coronary artery disease [CAD] patients. Additionally, we assessed the association of high-dose statins mediated Lp(a) changes with plaque morphology changes.

Methods

Post-hoc subanalysis of the YELLOW-II study. Lp(a) was measured in patients with stable CAD, who underwent percutaneous coronary intervention (PCI). Following PCI, optical coherence tomography (OCT), intravascular ultrasound and near-infrared spectroscopy were used to evaluate an obstructive non-culprit lesion. Subjects then received rosuvastatin 40 mg for 8–12 weeks, after which the lesion was reimaged. Associations between Lp(a) quartiles and plaque characteristics before and after statins were assessed.

Results

Eighty-two patients were included (mean age 62 ± 11 years-old, 33% females, mean LDL-C 87 ± 40 mg/dL). Median Lp(a) was 25 (IR 6.0-65.8) mg/dL (4.0, 12.5, 37.5, 97.0 mg/dL in Q1, Q2, Q3, Q4, respectively). OCT minimal fibrous cap thickness (FCT) was lower in Q4 vs. Q1 (79.4 ± 29 vs. 111.1 ± 49 μm, p = 0.045), indicative of high-risk unstable plaques. Following 8–12 weeks of statins, median Lp(a) increased to 34.0 (10.0–77.0) mg/dL (p < 0.01), and minimal FCT increased in the overall cohort (99.2 ± 39.1 to 106.3 ± 36.9 μm, p < 0.001). However, there was no difference in FCT between Lp(a) quartiles at follow-up (p = 0.64). Furthermore, the increase in Lp(a) with statins did not impact FCT changes.

Conclusions

Higher levels of Lp(a) at baseline are associated with lower OCT fibrous caps in patients with stable CAD. After high-intensity statin therapy, Lp(a) significantly increased, however, changes in Lp(a) were not associated with changes in fibrous cap thickness.

Graphical Abstract

Lp(a) and Intracoronary Imaging after Statins in Patients with CAD. The central illustration presents lipoprotein (a) [Lp(a)] plasma levels and minimal fibrous cap thickness (FCT) at baseline and after 8-12 weeks of rosuvastatin, across baseline Lp(a) quartiles. Baseline Lp(a) means for each Lp(a)-quartile are presented in the left upper bar graph. After statins (right upper bar graph), mean Lp(a) increased across all Lp(a) quartiles, as shown by the blue arrows. Baseline FCT is shown across Lp(a) quartiles in the lower left bar graph. Notably, in the highest Lp(a) quartile [Lp(a)-Q4], baseline FCT is the thinnest. After rosuvastatin FCT increases in all Lp(a) quartiles but the lowest Lp(a) quartile [(Lp(a)-Q1)], as represented by the red arrows (lower right bar graph). Notably, the arrow is getting longer with the increase in quartiles, representative of greater absolute change in FCT with higher baseline Lp(a).