Subscribe to RSS
DOI: 10.1055/s-0037-1615178
Plasma Lp(a) Levels Are Increased in Patients with Chronic Thromboembolic Pulmonary Hypertension
Publication History
Received
11 December 1997
Accepted after revision
21 April 1998
Publication Date:
08 December 2017 (online)
Summary
Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease resulting from the thromboembolic obstruction of the segmental and/or large size pulmonary arteries, subsequently leading to pulmonary arterial hypertension. Incomplete resolution of acute pulmonary emboli and thrombus organization are believed to be important for the development of the disease. Primary pulmonary hypertension (PPH) is a further disease that at present is poorly understood but shows a clinical picture similar to CTEPH. Since lipoprotein(a) [Lp(a)], a genetically determined risk factor for atherosclerosis and thrombosis, has been found increased in plasma of patients with deep vein thrombosis and pulmonary embolism, we measured plasma Lp(a) levels in 40 patients with CTEPH and 50 patients with PPH and compared them to 50 matched controls. The median for Lp(a) plasma levels was significantly higher in CTEPH patients (26.6 mg/dl) than in PPH patients (9.6 mg/dl) and controls (7.2 mg/dl). Increased plasma Lp(a) could, therefore, play a significant role in the mechanisms of ongoing thrombosis and thrombus organization in CTEPH, while its possible role in PPH can be limited to a small number of patients.
-
References
- 1 Moser K. Venous thromboembolism: State of the art.. Am Rev Respir Dis 1990; 141: 235-49.
- 2 Fedullo PF, Moser KM. Advances in acute pulmonary embolism and chronic pulmonary hypertension.. Adv Intern Med 1997; 42: 67-104.
- 3 Anderson E, Simon G, Reid L. Primary and thromboembolic pulmonary hypertension: A quantitative pathologic study.. J Pathol 1973; 110: 237-93.
- 4 Moser K, Daily P, Peterson K, Dembitsky W, Vapnek J, Shure D. Thrombendarterectomy for chronic major vessel thromboembolic pulmonary hypertension in 42 patients: Immediate and long term results.. Ann Intern Med 1980; 107: 560-5.
- 5 Rubin JL. Pathology and Pathophysiology of primary pulmonary hypertension.. Am J Card 1995; 75: 51-4.
- 6 Karadi I, Kostner GM, Gries A, Nimpf J, Romics L, Malle E. Lipoprotein(a) and plasminogen are immunochemically related.. Biochim Biophys Acta 1988; 960: 91-7.
- 7 Loscalzo J, Weinfold M, Fless GM, Scanu AM. Lipoprotein (a), fibrin binding and plasminogen activation.. Arteriosclerosis 1990; 10: 240-45.
- 8 Aznar J, Estelles A, Breto M, Espana F. Euglobulin clot lysis induced by tissue type plasminogen activator in subjects with increased levels and different isoforms of lipoprotein (a).. Thromb Res 1993; 72: 459-65.
- 9 Csaszar A, Karadi I, Juhasz E, Romics L. High lipoprotein(a) levels with predominance of high molecular weight apo(a) isoforms in patients with pulmonary embolism.. Eur Journ of Clin Invest 1995; 25: 368-70.
- 10 Kruithof E, Gudinchet A, Bachmann F. PAI-1 and PAI-2 in various disease states.. Thromb Haemost 1988; 59: 7-12.
- 11 Olman MA, Marsh JJ, Lang IM, Moser KM, Binder BR, Schleef RR. Endogenous fibrinolytic system in chronic large-vessel thromboembolic pulmonary hypertension.. Circulation 1992; 86: 1241-8.
- 12 Hajar KA, Gavish D, Breslow JL, Nachmann RL. Lipoprotein (a) modulation of endothelial cell surface fibrinolysis and its potential role in atherosclerosis.. Nature 1989; 339: 303-5.
- 13 Haider AW, Andreotti F, Thompson GR, Kluft C, Maseri A, Davies GJ. Serum Lp(a) level is related to thrombin generation and spontaneous intermittent coronary occlusion in patients with acute myocardial infarction.. Circulation 1996; 94: 2072-6.
- 14 Moser KM, Fedullo PF, Finkbeiner WE, Golden J. Do patients with primary pulmonary hypertension develop extensive central thrombi?. Circulation 1995; 91 (03) 741-5.