Lipoprotein(a) concentration is not associated with venous thromboembolismin a case control study

Background and Objective. Lipoprotein(a) is an LDL-like particle displaying strong athero-thrombotic properties. Although Lp(a) plays a pivotal role i n the genesis and progression of thrombosis in the arterial district, its r ole in promoting thrombosis in the venous district is still unclear. Design and Methods. To give further insight into the thrombotic potential o f Lp(a), 100 potentially eligible consecutive outpatients who had suffered from previous episodes of venous thrombosis (deep vein thrombosis with or w ithout pulmonary embolism) were enrolled into the study. Thirty-six of thes e patients who did not fulfil the entry criteria were then excluded from th e study. The concentration of Lp(a) was thus measured in 64 patients, and c ompared to that of 64 control subjects, matched for sex (p=0.46), age (p=0. 25) and pharmacological treatment; no subject belonging to the control grou p had a familial or personal history of venous thromboembolism. Exclusion c riteria for both groups included: diabetes mellitus, liver or kidney diseas es and malignancy, as established by both laboratory analysis and physical examination. To rule out false elevations of Lp(a) due to the presence of a concurrent acute phase response, C reactive protein (CRP) was measured in both groups using a commercial immunonephelometric assay. Results. No statistically significant differences were observed in the medi an Lp(a) concentration between patients and controls (median: 69 vs 83 mg/L , respectively; p=0.34). Neither were any significant differences found bet ween patients who had suffered from deep venous thrombosis with (n=18) or w ithout (n=46) pulmonary embolism (median: 73 vs 69 mg/L, respectively; p=0. 83). The concentration of CRP did not differ significantly between cases an d controls (median: 1.8 vs 2.3 g/L, respectively; p=0.37). Interpretation and Conclusions. Although there are several plausible biolog ical mechanisms to explain the strong thrombogenicity of Lp(a) in vitro, we failed to demonstrate a convincing association between Lp(a) and thrombosi s in the venous district. Besides the proven prothrombotic role of Lp(a) in some selected clinical settings, it is thus conceivable that the contribut ion of Lp(a) to genesis and progression of the venous thrombosis might be m arginal or efficiently counterbalanced In vivo. The clinical usefulness of including the measurement of Lp(a) among the screening tests for thrombophi lic patients, therefore, remains questionable. (C)1999, Ferrata Storti Foun dation.