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Levels of lipoprotein (a) in pulmonary arterial hypertension

Published online by Cambridge University Press:  01 July 2011

Raul D. Santos ,
Antonio Foronda ,
José A. F. Ramires  and
Raul C. Maranhão
Raul D. Santos
Affiliation:
Heart Institute (InCor) of the Medical School Hospital, Brazil
Antonio Foronda
Affiliation:
Heart Institute (InCor) of the Medical School Hospital, Brazil
José A. F. Ramires
Affiliation:
Heart Institute (InCor) of the Medical School Hospital, Brazil
Raul C. Maranhão*
Affiliation:
Heart Institute (InCor) of the Medical School Hospital, Brazil Faculty of Pharmaceutical Sciences University of Sao Paulo- Sao Paul, Brazil
*
Correspondence to: Raul C. Maranhão, Av. Dr. En.as C. Aguiar 44, 05403–000 Sao Paulo-SP, Brazil. Tel/Fax: 55 11 30630779; E-mail: [email protected]
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Abstract

We compared the levels of lipoprotein (a) in 48 Caucasian patients with pulmonary arterial hypertension, comprising 32 females and 16 males, aged 28.0 ± 12.0 years, with a range from 4 through 52 years, with 48 normal Caucasian subjects matched for age and sex. Pulmonary hypertension was secondary in 41 patients with Eisenmenger's syndrome, these comprising 27 females and 14 males aged 27.0 ± 12.0 years, with a range from 4 through 51 years, and primary in the other 7 patients, 5 females and 2 males, whose age was 30.0 ± 14.0 years, with a range from 9 through 52 years. Lipoprotein (a) was measured using an immunoprecipitation and turbidimetric assay after a 12 hour fast. Levels of the protein, expressed as the median (% 25; % 75), were higher in those with Eisenmenger's syndrome than in normal controls (p = 0.003). In addition, there was a greater prevalence of levels of lipoprotein greater than 30.0 mg/dl in those with secondary pulmonary arterial hypertension patients than in our normal population (p = 0.03). We have found no differences, however, in the levels of lipoprotein(a) in those who had primary pulmonary arterial hypertension when compared with their matched controls, albeit that the number of patients studied was small. We conclude that increased levels of lipoprotein (a) may be secondary to pulmonary arterial hypertension as a marker of tissue damage or may be genetically determined. In either way, the increase in lipoprotein (a) could be an additional factor predisposing to the vascular alterations known to occur in this disease.

Keywords

Lipoprotein (a)pulmonary hypertensioncongenital cardiac malformations
Type
Original Articles
Information
Cardiology in the Young , Volume 11 , Issue 1 , January 2001 , pp. 25 - 29
Copyright
Copyright © Cambridge University Press 2001

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References

1.Utterrman, G. Lipoprotein(a). In: The metabolic and molecular bases of inherited disease. Scriver, CL, Beaudet, AL, Williams, SS, Valle, D eds. New YorkMc Graw-Hill, 1995:1887–1912.Google Scholar
2.Grainger, DJ, Kirschenlohr, HL, Metcalfe, JC, Weissberg, PL, Wade, DP, Lawn, RM. Proliferation of human muscle cells promoted by lipoprotein(a). Science 1993;260:1655–1658.CrossRefGoogle ScholarPubMed
3.Gaw, A, Hobbs, HH. Molecular genetics of lipoprotein(a):New pieces to the puzzle. Curr Op Lipidol 1994;5:149–155.CrossRefGoogle Scholar
4.Kostner, GM, Avogaro, P, Cazzolato, G, Morth, E, Bittolo-Bon, G, Quina, GB. Lipoprotein(a) Lp(a) and the risk for myocardial infarction. Atherosclerosis 1981;38:51–61.CrossRefGoogle Scholar
5.Scott, J. Thrombogenesis linked to atherogenesis at last? Nature 1989;34l:22–23.CrossRefGoogle Scholar
6.Maeda, S, Abe, A, Seishima, M, Makino, K, Noma, A, Kawade, M. Transient changes of serum lipoprotein(a) as an acute phase protein. Atherosclerosis 1989;78:145–150.CrossRefGoogle ScholarPubMed
7.Oshima, S, Uchida, K, Yasu, T, Uno, K, Nonogi, H, Haze, K. Transient increase of plasma lipoprotein(a) in patients with unstable angina pectoris. Arterioscler and Thromb 1991;11:1772–1777.CrossRefGoogle ScholarPubMed
8.Rich, S, Brundage, BH. Pulmonary hypertension: a cellular basis for understanding the pathophysiology and treatment. J Amer Coll Cardiol 1989;14:545–550.CrossRefGoogle Scholar
9.Chaouat, A, Weitzenblum, E, Higenbottam, TThe role of thrombosis in severe pulmonary hypertension. Eur Respir J 1996;9:356–363.CrossRefGoogle ScholarPubMed
10.Voelkel, NF, Tuder, RM. Cellular and molecular mechanisms in the pathogenesis of severe pulmonary hypertension. Eur Respir J 1995;8:2129–2138CrossRefGoogle ScholarPubMed
11.Greenberg, HE, Scharf, FM. Pulmonary hypertension: pathophysiology and clinical disorders. In: Baum, GL, Wolinsky, E; eds. Textbook of Pulmonary Diseases. Boston: Little, Brown and Co; 1994:1285–1304.Google Scholar
12.Rich, S, Braunwald, E, Grossman, W Pulmonary Hypertension. In Heart Disease. Braunwald, E ed. Philadelphia, WB. Saunders Co; 1997;780–806.Google Scholar
13.Rich, S, Dantzker, DR, Ayres, SM, Bergofsky, EH, Brundage, BH, Detre, KM, Fishman, AP, Goldring, RM, Groves, BM, Koerner, SK. Primary Pulmonary Hypertension. A National prospective study Ann Intern Med 1987;107:216–223.CrossRefGoogle ScholarPubMed
14.Friedewald, WT, Levy, RI, Fredrickson, DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without the use of preparative ultracentrifuge. Clin Chem 1972;18: 499–502.CrossRefGoogle ScholarPubMed
15.Tuder, RM, groves, B, Badesch, DB, Voelkel, NF. Exuberant endothelial cell growth and elements of inflammation are present in plexiform lesions of pulmonary hypertension, Amer J Pathol 1994;144:275–85.Google Scholar
16.Borba, EF, Santos, RD, Bonfa, E, Vinagre, CG, Pileggi, FJ, Cossermelli, W, Maranhao, RC. Lipoprotein(a) levels in systemic lupus erithematosus. J Rheumatol 1994;21:220–3.Google Scholar
17.Takami, S, Kubo, M, Yamashita, S, Kameda-Takemura, K, Kawasaki, T, Kanbayashi, J, Nakamura, Y, Yokoi, Y, Ohnishi, K, Matsuzawa, YHigh levels of serum lipoprotein(a) in patients with ischemic heart disease with normal coronary angiogram and thromboangiitis obliterans. Atherosclerosis 1995;112:253–60.CrossRefGoogle ScholarPubMed
18.Wade, DP, Clarke, JG, Lindahl, GE, Liu, AC, Zysow, BR, Meer, K, Schwartz, K, Lawn, RM. 5' Control regions of the apolipoprotein(a) gene and members of the related plasminogen gene family. Proc Nad Acad Sci USA 1993;90:1369–73.CrossRefGoogle ScholarPubMed
19.Grainger, DJ, Kemp, PR, Metcalfe, JC, Liu, AC, Lawn, RM, Williams, NR, Grace, AA, Schofield, PM, Chauhan, A. The serum concentration of active transforming growth factor-β is severely depressed in advanced atherosclerosis. Nat Med 1995;l:74–79.CrossRefGoogle Scholar
20.Kinlay, S, Dobson, AJ, Heller, RF, McElduff, P, Alexander, H, Dickeson, J. Risk of primary and recurrent acute myocardial infarction from lipoprotein(a) in men and women. J Amer Coll Cardiol 1996;28:870–5.CrossRefGoogle ScholarPubMed
21.Galie, N, Grigioni, F, Uguccioni, L, Cervi, V, Di Luzio, S, Serafini, F, Catanzariti, P, Callegari, G, Fracchia, C, Branzi, A, Magnani, B. Increased levels of α-TNF in patients with primary pulmonary hypertension. Eur Heart J 1997;18 supl:528.Google Scholar
22.Braunwald, E, Colucci, WS, Grossman, W Clinical Aspects of heart failure: high —output, heart failure, pulmonary edema. In Heart Disease. Braunwald, E ed. Philadelphia, WB. Saunders Co; 1997;445–470.Google Scholar