Loss of blood platelet adhesion after heating native and cultured human subendothelium to 100  Celcius

Borst, Cornelius; Bos, A N; Zwaginga, Jaap‐Jan; Rienks, Rienk; Groot, P. G. De; Sixma, JJ

doi:10.1093/cvr/24.8.665

Cited by 27 publications

(13 citation statements)

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“…No enhanced PA was found in the rabbit artery after heating it to 55°C. In this and previous in vitro studies [10,11] using human subendothelium, we found enhanced PA after heating to 55°C and this phenomenon therefore seems to be species-specific. In human specimens, we established that thermally denaturated von Willebrand factor in the subendothelium is responsible not only for a decrease in adhesion after exposure to temperatures high er than 71 °C, but also for an increase in adhesion after exposure to temperatures around 55 °C, provided the von Willebrand factor concentration is low [11], We tentative ly attribute the absence of an increase in adhesion to rab bit artery subendothelium to a high von Willebrand factor content in the subendothelium.…”

Section: Species Differencessupporting

confidence: 85%

“…In several other catheter-based tech niques of arterial revascularization, such as the low-pres sure radio frequency (RF) thermal balloon [4,7,8] or the excimer laser [9], thermal energy is also delivered to the arterial wall. Initial in vitro perfusion studies of thermally damaged vessel wall constituents suggested that heating the arterial wall to temperatures over 70 °C reduces its thrombogcnicity [10][11][12], In vivo animal studies with high-temperature thermal balloon angioplasty, however, show thrombogenicity to be increased [7] or at best equal to conventional balloon angioplasty [13]. Accordingly, clinical results have been disappointing because of an increased restenosis rate, tentatively attributed to exces sive thermal damage of the arterial wall [14].…”

Section: Introductionmentioning

confidence: 99%

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Thrombogenicity of the Human Arterial Wall after Interventional Thermal Injury

Post

Graaf-Bos²,

Zanten³

et al. 1996

J Vasc Res

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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°C, 5 min, shear rate: 1,300 s^–1). To determine PA to deep wall layers, 6-µm cross-sections of heated arteries were perfused in a rectangular perfusion chamber (37 °C, 5 min, 1,300 s^–1)- After RF dilation of human arteries at 55 and 90 °C, subendothelical PA (citrated blood) decreased from 28.9% at 37°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°C, and decreased after 55°C. Heating of cross-sections of atherosclerotic coronary arteries to 55 and 90°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°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°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.

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Section: Species Differencessupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Thrombogenicity of the Human Arterial Wall after Interventional Thermal Injury

Post

Graaf-Bos²,

Zanten³

et al. 1996

J Vasc Res

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“…In previous experiments in our laboratory [14], in creased platelet adhesion was observed after exposure to 55 °C. whereas platelet adhesion was much decreased after heating to 90 °C.…”

Section: Platelet Adhesionmentioning

confidence: 61%

“…In a recent in vitro study with human subendothelium in our laboratory, however, the much reduced thrombogenicity after exposure to temperatures above 70 °C was accompanied by a small increase in thrombogenicity after exposure to a temperature of 55 °C [14], The latter increase might interfere with the possible beneficial ef fects of the higher temperatures.…”

Section: Introductionmentioning

confidence: 73%

“…Thermal fusion of dissections and a decrease in elastic recoil were demonstrated with laser balloon angio plasty (LBA) at temperatures between 80 and 120 °C [9][10][11], In several other experimental studies, reduced thrombogcnicity of the arterial wall after exposure to tempera tures over 70 °C was found [12][13][14], The prevalent thought when LBA was introduced was, that a reduction in the number of platelets adhering to the arterial wall might be accompanied by a decrease in the release of growth factors and enzymes, which have been implicated in the pathogenesis of restenosis. Also, thermal destruc tion of viable tissue would reduce the number of smooth muscle cells capable of a proliferative response to injury, thereby decreasing the likelihood of restenosis [9],…”

Section: Introductionmentioning

confidence: 99%

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Thrombogenicity and Intimal Hyperplasia after Conventional and Thermal Balloon Dilation in Normal Rabbit Iliac Arteries

Erven

Velema²,

Bos³

et al. 1992

J Vasc Res

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Acute occlusion and restenosis are the major complications of percutaneous transluminal coronary balloon angioplasty. Application of heat during balloon dilation was postulated to reduce these complications. We evaluated thrombogenicity and intimal hyperplasia of normal rabbit iliac arteries after conventional (37 °C) and thermal balloon dilation. Thermal dilation was performed with a radio-frequency-heated balloon, provided with three thermocouples attached to the inside of the balloon skin. In a previous in vitro study, thrombogenicity of human subendothelium was increased at 55°C and greatly decreased at temperatures over 70°C. Thermal balloon dilation was therefore performed at 55 and 90°C in vivo. Rabbits survived 2 h for evaluation of platelet adhesion or either 3 or 8 weeks for intimal hyperplasia. Angiograms revealed no occlusions or thrombi after any procedure. Platelet adhesion was quantified on 20 scanning electron microscopic pictures per balloon dilation site and was expressed as the percentage of the luminal surface covered by platelets. Platelet adhesion was similar in all groups, although large thrombi were present in the 90°C group. Intimal hyperplasia was measured morphometrically at regular intervals over the balloon site. After 3 weeks, the average intimal hyperplasia was significantly reduced in the 90°C balloon dilation group, which was mainly due to the absence of intimal hyperplasia in the mid-part of these segments. After 8 weeks, intimal hyperplasia was equal in all groups. Thus, in the applied model, platelet coverage was equal after conventional balloon angioplasty and after 55 and 90°C balloon angioplasty. Our data suggest that intimal hyperplasia is delayed but not diminished after balloon dilation at 90°C.

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