Effect of heparin bonding on catheter-induced fibrin formation and platelet activation.

Abstract

Pathologic and experimental evidence indicates that platelet activation and fibrin formation contribute to the pathogenesis of angina pectoris, coronary vasospasm and myocardial infarction. Detection of localized intravascular platelet activation and fibrin formation in vivo by selective blood sampling requires catheters that do not induce coagulation ex vivo. We studied the effect of heparin bonding of catheter surfaces on activation of the coagulation system by cardiovascular catheters. Woven Dacron, polyvinylchloride, and polyurethane catheters were tested and compared with identical catheters with heparin-bonded surfaces in 47 patients undergoing percutaneous cardiac catheterization. Platelet activation was measured by radioimmunoassay of plasma platelet factor 4 (PF4), /3-thromboglobulin (BTG), and thromboxane B2 (TXB2) in blood samples withdrawn through catheters, and fibrin formation was assessed by determination of fibrinopeptide A (FPA) levels. In blood samples collected through conventional catheters, FPA, PF4, BTG, and TXB2 levels were markedly elevated; blood sampling through heparin-bonded catheters had no significant effect on FPA, PF4, BTG, or TXB2 levels. Scanning electron microscopy disclosed extensive platelet aggregates and fibrin strands adherent to the surface of conventional catheters but not to heparin-bonded catheter surfaces. This study demonstrates that (1) collection of blood samples through cardiovascular catheters causes artifactual elevation of FPA, PF4, BTG, and TXB2 levels, and (2) heparin-bonded catheter surfaces effectively prevent catheter-induced platelet a-granule release and fibrin formation on catheter surfaces. Heparin-bonded catheters will facilitate investigation of the role of intravascular coagulation in coronary artery disease by eliminating catheter-induced fibrin formation and platelet activation. Circulation 70, No. 5, 843-850, 1984. RECENT clinical and experimental evidence suggests that platelet activation and fibrin formation in vivo may be fundamentally important in clinical complications of atherosclerotic coronary artery disease, including unstable angina,1 myocardial infarction,24 and sudden death.5 Investigation of platelet release and fibrin formation in vivo has been facilitated by the recent development of radioimmunoassays for specific proteins and prostanoids released by activated platelets6'7 and peptides released during fibrin formation.8Platelet factor 4 (PF4) and ,3-thromboglobulin (BTG) are platelet-specific proteins secreted from platelet agranules during the platelet-release reaction.9 10

Platelet activation during coronary angioplasty in humans.

“…37 In the present study, no significant platelet activation by withdrawal of blood through a long catheter was seen in patients chronically treated with aspirin and pretreated with heparin. Our results might have been affected by changes in platelet activation that were related to the duration of the procedure, the sampling technique, or the duration between sampling and measurement.…”

Effects of balloon mitral valvuloplasty on systemic and regional left atrial levels of prothrombin fragment 1+2 in mitral stenosis

“…The conclusions of the present study regarding the immediate effects of balloon dilatation on systemic and left atrial levels of F1j2 are unlikely to have been influenced by factors known to affect other coagulation markers, such as the presence of intravascular catheters [28] or the use of heparin [29]. Thus a previous study has found that F1j2 levels are not influenced by the presence of intravascular catheters [30], and in the present study, despite the use of heparin, venous F1j2 levels did not change in the interval between baseline and post transseptal puncture sampling.…”

Increased left atrial thrombin generation in mitral stenosis is not reflected in arterial prothrombin fragment 1+2 levels

“…Thus, although coagulation markers such as fibrinopeptide A and thrombin-antithrombin complex are prone to undergo artefactual increases during blood sampling through catheters [14,15], thrombin generation in the present study was assessed by measurement of F1j2, a coagulation marker with a low propensity for sampling-related elevations [15,16]. These findings suggest that the association of increased left atrial with normal venous F1j2 levels in mitral stenosis is due principally to limited spillover of F1j2 from the left atrium into the systemic circulation.…”