MACROAGGREGATION OF PLATELETS IN PLASMA, AS DISTINCT FROM MICROAGGREGATION IN WHOLE-BLOOD (AND PLASMA), AS DETERMINED USING OPTICAL AGGREGOMETRY AND PLATELET COUNTING RESPECTIVELY, IS SPECIFICALLY IMPAIRED FOLLOWING CARDIOPULMONARY BYPASS IN MAN

We determined changes in platelet aggregability following cardiopulmon ary bypass, using optical aggregometry to assess macroaggregation in p latelet-rich plasma (PRP), and platelet counting to assess microaggreg ation both in whole blood and PRP. Hirudin was used as the anticoagula nt to maintain normocalcaemia. Microaggregation (%, median and interqu artile range) in blood stirred with collagen (0.6 mu g/ml) was only ma rginally impaired following bypass (91 [88, 93] at 10 min postbypass v 95 (99, 96] prebypass; n = 22), whereas macroaggregation (amplitude o f response; cm) in PRP stirred with collagen (1.0 mu g/ml) was markedl y impaired (9.5 [8.0, 10.8], n = 41 v 13.4 [12.7, 14.3], n = 10; p <0. 0001). However, in PRP, despite impairment of macroaggregation (9.1 [8 .5, 10.1], n = 12), microaggregation was near-maximal (93 [91, 94]), a s in whole blood stirred with collagen. In contrast, in aspirin-treate d patients (n = 14), both collagen-induced microaggregation in whole b lood (49 [47, 52]) and macroaggregation in PRP (5.1 [3.8, 6.6]) were m ore markedly impaired, compared with control (both p <0.001). Similarl y, in PRP, macroaggregation with ristocetin (1.5 mg/ml) was also impai red following bypass (9.4 [7.2, 10.7], n = 38 v 12.4 [10.0, 13.4]; p < 0.0002, n = 20), but as found with collagen, despite impairment of mac roaggregation (7.2 [3.5, 10.9], n = 12), microaggregation was again ne ar-maximal(96 [93, 97]). The response to ristocetin was more markedly impared after bypass in succinylated gelatin (Gelo-fusine) treated pat ients (5.6 [2.8, 8.6], n = 17; p <0.005 v control), whereas the respon se to collagen was little different (9.3 v 9.5). In contrast to findin gs with collagen in aspirin-treated patients, the response to ristocet in was little different to that in controls (8.0 v 8.3). Impairment of macroaggregation with collagen or ristocetin did not correlate with t he duration of bypass or the platelet count, indicating that haemodilu tion is not a contributory factor. In conclusion: (1) Macroaggregation in PRP, as determined using optical aggregometry, is specifically imp aired following bypass, and this probably reflects impairment of the b uild-up of small aggregates into larger aggregates. (2) Impairment of aggregate growth and consolidation could contribute to the haemostatic defect following cardiac surgery.