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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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