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Thrombosed, ruptured atheromatous plaques in saphenous vein coronary artery bypass grafts: ten years' experience

A E Walts1, M C Fishbein, J M Matloff

  • 1Division of Anatomic Pathology, Cedars-Sinai Medical Center, Los Angeles, CA 90048.

American Heart Journal
|October 1, 1987
PubMed

Insights

Saphenous vein grafts used in coronary artery bypass grafting (CABG) frequently occlude due to thrombosis on ruptured plaques. This common mechanism necessitates repeat procedures and can lead to adverse outcomes.

Area of Science:

  • Cardiovascular Surgery
  • Vascular Biology
  • Pathology

Background:

  • Coronary artery bypass grafting (CABG) using saphenous vein grafts has seen increased utilization globally.
  • Late graft occlusion remains a significant concern, with an annual rate of approximately 4% and a rising incidence of reoperations.
  • Reoperations for occluded grafts increased from 0.8% in 1976 to 12.4% by 1985 at the institution.

Purpose of the Study:

  • To investigate the pathological mechanisms underlying late saphenous vein graft occlusion after CABG.
  • To identify the prevalence and characteristics of the lesion causing graft failure.
  • To determine the clinical significance and potential therapeutic targets for graft occlusion.

Main Methods:

  • Analysis of 119 excised, occluded saphenous vein grafts from patients undergoing reoperation.
  • Examination of 10 autopsy cases with occluded saphenous vein grafts.
  • Histopathological assessment to identify the nature of the occlusive lesion.

Main Results:

  • Thrombosis superimposed on ruptured atheromatous plaques was identified in 44% (52 of 119) of excised grafts.
  • Similar lesions were observed in grafts from autopsy cases.
  • The occlusive lesion occurred between 3 and 14 years post-CABG, with a peak incidence 5 to 10 years after implantation.
  • Graft occlusion mechanism was independent of patient age, sex, or bypassed coronary artery.

Conclusions:

  • Thrombosed, ruptured atheromatous plaque is a prevalent and clinically significant cause of late saphenous vein graft occlusion.
  • This mechanism is associated with recurrent symptoms, repeat revascularization, and potential mortality.
  • The identified lesion may be a target for interventions such as thrombolytic therapy or angioplasty.

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