Skip to main content

14-09-2009 | Cardiology | Article

SVG occlusion independent of HIT antibodies


Free abstract

MedWire News: US research indicates that the antibodies that cause heparin-induced thrombocytopenia (HIT) do not increase the risk for early saphenous vein graft (SVG) occlusion in patients undergoing coronary artery bypass graft surgery (CABG).

Antibodies to complexes of heparin and platelet factor 4 (PF4) can induce HIT in patients given unfractionated heparin (UFH), and may be prothrombogenic even in patients who do not develop HIT, observe Jeffrey Rade and co-workers, from John Hopkins School of Medicine in Baltimore, Maryland.

To investigate whether anti-PF4/heparin antibodies predict the risk for SVG occlusion or other poor outcomes in CABG patients, the team measured antibody levels in 386 patients before and again 4 days, 6 weeks, and 6 months after CABG.

As reported in the Journal of Thrombosis and Haemostasis, 3% of patients were seropositive for anti-PF4/heparin antibodies before surgery, rising to 18.4% and 52.0% of patients at 4 and 6 weeks’ postoperatively, respectively. After 6 months, 16.4% of patients were seropositive.

Serotonin release assays conducted 6 weeks after surgery indicated that 9% of patients carried antibodies that were capable of stimulating heparin-dependent platelet activation.

Computed tomography coronary angiography was performed on 297 of the patients 6 months after surgery to determine SVG patency and showed 21% were totally occluded, and 3% had high-grade stenosis.

However, there was no significant difference in the percentage of occluded SVG in seropositive and seronegative patients (19% vs 20%), or the rate of adverse events (21% vs 24%).

“Induction of anti-PF4/heparin antibodies consequent to UFH exposure is not an independent risk factor for either early SVG thrombosis or adverse clinical outcome within the first 6 months after CABG surgery,” Rade et al comment.

Nevertheless, they conclude: “Early SVG thrombosis in the modern era remains substantial, highlighting the need for new research into the mechanisms of SVG failure and therapies to prevent it.”

MedWire ( is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

By Lynda Williams

Related topics