ArticleBMC cardiovascular disorders2025
Impact of low-density lipoprotein cholesterol-lowering therapy on intermediate stenosis in non-culprit vessels of acute coronary syndrome.
Article in BMC cardiovascular disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Non-invasive identification of high-risk plaques in non-culprit lesions of acute coronary syndrome.Heart and vessels · 2026Article
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Authors and funding
12 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundAssociations 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).
methodsWe 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 (maxLCBI
resultsThe 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
conclusionAggressive LDL-C-lowering therapy for non-culprit intermediate stenosis in ACS appears to promote plaque stabilization and improve coronary flow.
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