Large abdominal aortic aneurysms (AAAs) are associated with coagulation abnormalities, which are significantly reduced by low molecular weight heparin (LMWH). Considering anti-inflammatory properties of heparin we verified, whether LMWH influences MMP-2/-9 in AAA patients. The study involved 26 AAA individuals, 10 patients with coagulation abnormalities received LMWH and 16 were a control group. The plasma activity of MMP-2/-9 was measured using zymography. We found that, in addition to the reduction of coagulation abnormalities, LMWH treatment was associated with the decreased MMP-9 but not MMP-2 activity. Therefore, LMWH use could be considered as a valuable pretreatment before an elective aneurysm repair.

SummaryHuman factor VIII was purified from cryoprecipitate and incubated for up to 24 hours with four neutral proteases of human blood leukocytes, namely, with elastase-like protease (ELP), chymotrypsin-like protease (CLP), collagenase and gelatinase. Electrophoretic patterns showed a reproducible sequence of degradation of factor VIII and of its 230,000 molecular weight subunit by ELP and CLP. Intermediate products were similar but those resulting from exhaustive proteolysis by ELP and CLP differed distinctly from each other. Procoagulant activity of factor VIII was rapidly and completely destroyed by ELP and CLP before visible electrophoretic changes would be detected. No increase in this activity was observed prior to its destruction. Von Willebrand factor (ristocetin cofactor) activity was considerably more resistant to ELP and CLP and declined in rough relation to degradation of highly aggregated forms of factor VIII. ELP and CLP produced a pronounced progressive increase in the Laurell reaction antigen. Normal human plasma showed a high potency to inhibit ELP and CLP. Large doses of these enzymes (300 ug per ml) produced in the plasma medium only a moderate fall in factor VIII procoagulant activity. Collagenase and gelatinase did neither degrade factor VIII nor change its biological properties.

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Fibrin clot retraction (FCR) and collagen gel retraction (CGR) were studied in patients with inherited platelet defects, i.e. in Glanzmann’s thrombasthenia, Hermansky-Pudlak syndrome, May-Hegglin anomaly, giant platelet syndrome, as well as in patients with von Willebrand disease and factor XIII deficiency. FCR was abnormal only in thrombasthenia, while CGR was found to be reduced in 2 patients with Hermansky-Pudlak syndrome and in 4 out of 5 cases with von Willebrand disease. Both FCR and CGR were normal in May-Hegglin anomaly, giant platelet syndrome and severe factor XIII deficiency. In none of the examined bleeding disorders was a concomitant FCR and CGR reduction detected. Natural polyamines and anti-fibronectin antibodies did not affect platelet potency in FCR or CGR. Peroxidation of platelet membrane components by sodium periodate abolished the platelet-induced FCR and CGR. This effect was reversed by subsequent reduction by sodium borohydride.