The study failed to show noninferiority of PRT-PLTs based on predefined CCI criteria. PLT and red blood cell utilization in the two groups was not significantly different suggesting that the slightly lower CCIs (PRT-PLTs) did not increase blood product utilization. Safety data showed similar findings in the two groups. Further studies are required to determine if the lower CCI observed with PRT-PLTs translates into an increased risk of bleeding.

SummaryThrombin-induced platelet aggregation has been generally believed to be irreversible. However, thrombin-induced aggregation of washed platelets is reversible if fibrin formation is prevented or the fibrin which binds the platelets together is removed from the platelet aggregates. After treatment with high concentrations of thrombin (0.5 units/ml) single platelets can be recovered that have lost practically all of their releasable serotonin and adenine nucleotides. These platelets are able to aggregate upon addition of low concentrations of ADP in the presence of fibrinogen. They aggregate in response to the ionophore A23, 187 in the absence of added fibrinogen, whereas sodium arachidonate-induced aggregation requires added fibrinogen. Thrombin-treated platelets change their shape in response to collagen in the absence of fibrinogen, and will aggregate upon the addition of collagen providing fibrinogen is present. This response to collagen can be blocked with aspirin but not with a mixture of creatine phosphate/creatine phosphokinase. Upon a second exposure to thrombin, thrombin-pretreated platelets do not change their shape and do not undergo aggregation. Thrombin-pretreated platelets will not retract a thrombin-induced fibrin clot unless ADP, sodium arachidonate, the ionophore A23, 187 or collagen are added together with thrombin.The ability of thrombin-treated platelets to adhere to the exposed subendothelial surface of the rabbit aorta is reduced, compared with untreated control platelets. The thrombin-treated platelets shorten the bleeding time of thrombocytopenic rabbits. However, they are not as effective in shortening the bleeding time as normal control platelets. When injected into rabbits with a normal platelet count, the thrombin-treated platelets that circulate after infusion survive for the same length of time as untreated control platelets. These findings indicate that thrombin-induced platelet aggregation with extensive release of granule constituents is not irreversible and that thrombin treatment does not cause irreversible damage of all platelets that would lead to their immediate elimination from the circulation. Furthermore, these platelets can still be haemostatically effective. It is conceivable that platelets that have lost their amine storage granule contents during a release reaction in vivo, such as may occur in certain cases of intravascular coagulation and repeated episodes of thrombosis, may be found in the circulation of man.

SummaryAn anticoagulant activity was isolated from the plasma of a patient with a strong lupus-like anticoagulant using gel filtration by high performance liquid chromatography. IgM were detected in this anticoagulant fraction which exhibited specificity towards 50% phosphatidylcholine - 50% phosphatidylserine vesicles and cardiolipin. These phospholipids were able to produce an apparent 3-fold enhancement of purified human protein C activation by human a-thrombin in the presence of purified human placenta thrombomodulin. In the absence of phospholipid, the anticoagulant fraction had no effect on thrombomodulin activity. The anticoagulant fraction could neutralize the enhancement of thrombomodulin activity by phospholipid in a dose-dependent manner. This study suggests that the neutralization of phospholipid might result in a reduced activation of protein C which could be responsible for the occurrence of thrombotic complications in a proportion of patients with lupus anticoagulants.

SummaryThe mechanisms involved in platelet deaggregation are unclear. Washed platelets from rabbits or humans aggregated by ADP can be deaggregated by EDTA or PGI2 if the release reaction has not occurred; during deaggregation 125I-fibrinogen dissociates from the platelets. Human platelets suspended in a medium without calcium undergo the release reaction during ADP-induced aggregation; EDTA, PGE, or PGI2 do not deaggregate these platelets although EDTA displaces much of the 125I-fibrinogen that associates with them during aggregation. Rabbit platelets aggregated by low concentrations of releaseinducing stimuli (sodium arachidonate, collagen or thrombin) can be deaggregated by EDTA, PGI2 or PGE1 and 125I-fibrinogen dissociates from them; with high concentrations of collagen or thrombin, deaggregation and dissociation of l25I-fibrinogen is slower. Human platelets that have undergone the release reaction in response to thrombin, collagen or a combination of sodium arachidonate and ADP are not readily deaggregated by EDTA or PGE1. Since aggregation and fibrinogen binding involving the glycoprotein IIb/IIIa complex are readily reversed by EDTA, and since Ca2+ is required for thrombospondin binding to activated platelets, there may be a third type of platelet-platelet adherence that is not disrupted by EDTA; this type of binding plays a greater role with human than with rabbit platelets.

Eighty patients undergoing pelvic or abdominal surgery for cancer were randomized in two groups for prevention of postoperative thromboembolism: 40 patients received a 15,000 IU day-1 Calciparine prophylaxis and 40 patients a 5000 anti-Xa U/d Fragmin prophylaxis for 10 days. In the Calciparine group, two patients (5%) developed postoperative pulmonary embolism but none developed it in the Fragmin group. Two patients in the Fragmin group (5%) developed isotopic DVT, which was not confirmed by phlebography. There was no deep vein thrombosis of the lower limbs in the two groups. Important postoperative bleeding (one patient in the Calciparine group and two patients in the Fragmin group) was similar in both groups. Moderate and minor bleeding were significantly lower in the Fragmin group. Haemoglobin and haematocrit changes, total blood loss and transfusion requirements were not different in both groups. It is concluded that, over a 10-day period, one daily 5000 U Fragmin prophylaxis was as effective and safe as three daily 5000 IU Calciparine injections.

SummaryBuckground: After successful coronary interventions, minor elevations of creatine kinase MB (CK-MB) identitied a population with a worse long-temi prognosis than that in patients without enzyme elevations. In that setting, cardiac troponin-I (cTn-I), a highly specific marker for myocardial injury, was considered for a small study; the results did not support the view that significant myocardial damage occurred during successful percutaneous transluminal coronary ang ioplasty (PTC A).Hypothesis: The present study was designed to assess the rate of elevated values ofcTn-I after successful PTCA and to determine its prognostic value.Merhods: CTn-I and CK-MB were measured in 44 patients before and daily for 3 days after PTCA. Two groups of patients were considered according to the presence or absence of elevated levels of cTn-I. The rate of free-event survival was estimated for the two groups using the Kaplan-Meier method and was compared with the log rank test.Rmdts: Globally, 36% of patients had an increase in cTn-I (normal values 0.35 ng/ml) and 9% had an increase in CK-MB. p = 0.002. The mean time to maximal enzyme level was 1.8 days for cTn-I and 2.2 days for CK-MB. Over a follow-up Conclusion: These results suggest that cTn-I is more sensitive than CK-MB in identifying minor myocardial damage after PTCA, but these elevated concentrations of cTn-I in the short-term aftermath of angioplasty do not seem to be a marker of worse long-term prognosis.

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