Thrombogenicity of the human arterial wall after interventional thermal injury

Thermal injury has been shown to reduce platelet adhesion (PA) in vitro but not in vivo. The controversy may be based on the mode of thermal injury, the anticoagulation regimen, or species differences. Human and rabbit arteries were dilated by a radio-frequency (RF)-heated balloon (RF dilation) or by immersion in heated buffer. The artery segments were perfused in an annular perfusion chamber with blood anticoagulant by citrate or heparin (37 degrees C, 5 min, shear rate: 1,300 s-1). To determine PA to deep wall layers, 6-micron cross-sections of heated arteries were perfused in a rectangular perfusion chamber (37 degrees C, 5 min, 1,300 s-1). After RF dilation of human arteries at 55 and 90 degrees C, subendothelical PA (citrated blood) decreased from 28.9% at 37 degrees C to 6.8%, and increased to 39.6%, respectively (in both cases p<0.05). Heparin anticoagulation resulted in subendothelial fibrin deposition that was equal after 37 and 90 degrees C, and decreased after 55 degrees C. Heating of cross-sections of atherosclerotic coronary arteries to 55 and 90 degrees C, showed increased and decreased PA, respectively, to the intima and media. No effect was observed on the highly reactive adventitia and atherosclerotic plaque. We conclude that thermal balloon angioplasty at 90 degrees C reduces PA to the arterial subendothelium, but not to the adventitia or the atherosclerotic plaque. As thermal balloon angioplasty in patients will always produce a region with increased PA at 55 degrees C and as heparin anticoagulation permits fibrin deposition that is not affected by heat, it is unlikely that thermal balloon angioplasty alone will reduce thrombotic complications.