Lipoprotein (a) in patients with spontaneous venous thromboembolism

• Published in: Thrombosis research 2007-01, Vol.120 (1), p.15-20
• Main Authors: Vormittag, Rainer, Vukovich, Thomas, Stain, Milena, Lehr, Stephan, Minar, Erich, Pabinger, Ingrid
• Format: Article
• Language: English
• Subjects: Adult; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Blood. Blood coagulation. Reticuloendothelial system; Cardiology. Vascular system; Case-Control Studies; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous; Female; Hematology, Oncology and Palliative Medicine; Humans; Lipoprotein (a); Lipoprotein(a) - blood; Male; Medical sciences; Middle Aged; Pharmacology. Drug treatments; Prevalence; Pulmonary embolism; Pulmonary Embolism - blood; Pulmonary Embolism - etiology; Risk Factors; Venous thromboembolism; Venous thrombosis; Venous Thrombosis - blood; Venous Thrombosis - etiology
• ISSN: 0049-3848; 1879-2472
• DOI: 10.1016/j.thromres.2006.03.002

Abstract Introduction Elevated lipoprotein (a) (Lp (a)) has been established as a risk factor of coronary heart disease and stroke. Findings concerning the risk of venous thromboembolism (VTE) in adults are contradictory. The aim of our study was to investigate, whether elevated Lp (a) levels are an independent risk factor of spontaneous symptomatic venous thromboembolism (VTE). Our study was further designed to detect differences in risk profiles between thrombosis patients with and without symptomatic PE. Materials and methods We investigated Lp (a) in 128 patients with spontaneous symptomatic deep vein thrombosis (DVT, group 1), 105 with spontaneous symptomatic pulmonary embolism with or without DVT (PE, group 2) and 122 healthy controls. Lp (a) was measured with an immunoturbidimetric assay (Tina-quant®, Roche, Grenzach-Wyhlen, Germany) on a Hitachi-Modular system. Results Lp (a) levels (mg/L) were not significantly different among groups, median levels (25th–75th percentiles) were 170 (51–386) in group 1, 140 (< 20–427) in group 2 and 126 (54–331) in controls, respectively. As continuous variable, odds ratios for VTE for a 100 mg/L increase of Lp (a) were 1.1 [95% confidence interval 0.98–1.2] for group 1 versus controls and 1.1 [0.95–1.2] for group 2 versus controls. The prevalence of Lp (a) above 300 mg/L was not significantly different among patients and controls (group 1: 30%, group 2: 32% and controls: 25%, p = 0.4, p = 0.2, respectively). Conclusions In conclusion we found no association between Lp (a) and VTE regardless whether DVT occurred together with PE or not.