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Efficacy of aggressive lipid controlling therapy for preventing saphenous vein graft disease

Mitsumasa Hata1, Tadateru Takayama, Akira Sezai

  • 1Department of Cardiovascular Surgery, Nihon University School of Medicine, Tokyo, Japan. mihata@med.nihon-u.ac.jp

The Annals of Thoracic Surgery
|October 27, 2009
PubMed

Insights

Aggressive lipid controlling therapy (ALCT) significantly prevents saphenous vein graft disease after coronary bypass surgery. ALCT maintains low-density lipoprotein cholesterol below 80 mg/dL, avoiding plaque and thrombus formation in grafts.

Area of Science:

  • Cardiovascular Medicine
  • Interventional Cardiology
  • Vascular Biology

Background:

  • Coronary artery bypass grafting (CABG) using saphenous vein grafts (SVGs) is a common revascularization procedure.
  • Saphenous vein graft disease (SVGD) remains a significant cause of graft failure and adverse cardiovascular events.
  • Intracoronary imaging techniques are crucial for assessing SVG morphology and disease progression.

Purpose of the Study:

  • To evaluate the efficacy of aggressive lipid-controlling therapy (ALCT) in preventing post-CABG SVG disease.
  • To assess the impact of ALCT on lipid profiles and inflammatory markers in CABG patients.
  • To investigate the presence of atherosclerotic plaques and thrombi in SVGs under different lipid management strategies.

Main Methods:

  • A prospective study involving 21 patients post-CABG, divided into two groups based on lipid control.
  • Group I (n=10) received rosuvastatin for ALCT (LDL-C < 80 mg/dL, LDL/HDL < 1.5).
  • Group II (n=11) had uncontrolled hyperlipidemia (LDL-C > 100 mg/dL, LDL/HDL > 2.5) despite pravastatin.
  • Intracoronary angioscopy and intravascular ultrasound (IVUS) were used to assess 27 SVGs 12-16 months post-CABG.

Main Results:

  • Group I demonstrated significantly lower LDL-C (64.1 vs 130.2 mg/dL), LDL/HDL ratio (1.36 vs 2.64), and hs-CRP levels compared to Group II.
  • IVUS revealed eccentric plaques in 78.6% of SVGs in Group II.
  • Angioscopy showed yellow plaques in 100% and thrombi in 78.6% of SVGs in Group II, whereas Group I SVGs were free of these findings.

Conclusions:

  • Aggressive lipid-controlling therapy is highly effective in preventing the development of atherosclerotic plaques and thrombi in SVGs post-CABG.
  • Maintaining low LDL-C and LDL/HDL ratios is crucial for long-term SVG patency.
  • Prophylactic management of lipid profiles is a promising strategy to avoid early and late SVG disease.
Abstract

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