Key result
High molecular weight heparin caused a significant fall in platelet count and enhanced platelet aggregation and thromboxane A2 release, which reversed after contrast medium injection.
Why the study?
Does high molecular weight heparin and contrast medium alter platelet function in patients undergoing coronary angiography?
Observational
Does high molecular weight heparin and contrast medium alter platelet function in patients undergoing coronary angiography?
High molecular weight heparin induces significant platelet activation during coronary angiography, which is partially reversed by contrast medium, suggesting a potential mechanism for procedure-related ischaemia.
Answers are grounded in this paper and cite their sources.
May link heparin to angiography-related ischemia via platelet effects; leaves open whether contrast reversal warrants practice change.
Platelet function was studied during coronary angiography of patients complaining of chest pain. The following changes occurred 5 min after injecting 100 IU.kg-1 body weight of a conventional high molecular weight heparin: (a) a significant fall in platelet count; (b) a significant enhancement of platelet aggregation in platelet rich plasma (turbidometric technique) and in whole blood (platelet aggregation technique); and (c) significantly enhanced release of platelet thromboxane A2, a vasoconstrictor. These changes tended to reverse towards baseline values 5 min after injecting a contrast medium (Conray 420), which was found to inhibit platelet aggregation. Thus heparinisation with a high molecular weight heparin seems to cause pronounced activation of platelets in patients undergoing coronary angiography, and this may contribute to the pathogenesis of cardiac ischaemia that may occur during this procedure. Since coronary artery bypass surgery in similar patients involves the use of heparin at much higher doses without the concomitant use of an antiaggregatory contrast medium, it is possible that platelet hyperaggregability may contribute to the well documented ischaemic brain injury associated with this form of surgery. Furthermore, the use of high molecular weight heparin after successful coronary angioplasty or thrombosis may influence the incidence of reocclusion. These findings therefore suggest that low molecular weight heparinoids should be evaluated in these situations since these anticoagulants are only weak activators of platelet aggregation.
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Greenbaum et al. (1987) conducted an observational in Chest pain requiring coronary angiography. High molecular weight heparin and contrast medium (Conray 420) vs. Baseline (pre-injection) was evaluated on Platelet function (platelet count, platelet aggregation, and thromboxane A2 release). High molecular weight heparin caused a significant fall in platelet count and enhanced platelet aggregation and thromboxane A2 release, which reversed after contrast medium injection.
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