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Revista Portuguesa de Cardiologia 2001-Apr

[Can blood homocysteine explain the family history of vascular diseases?].

Vetëm përdoruesit e regjistruar mund të përkthejnë artikuj
Identifikohuni Regjistrohu
Lidhja ruhet në kujtesën e fragmenteve
R P Reis
E Gomes
R Duarte
M J Correia
A Cândido
H P Reis
J Azinheira
J E Pina
J M Correia
A S Luís

Fjalë kyçe

Abstrakt

OBJECTIVE

Family history of vascular disease is an important risk factor for vascular disease, independent of conventional risk factors. Homocysteinemia, a newly defined risk factor, is caused by genetics, such as cystathionine beta synthase deficiencies, and metabolic deficiencies. With the present work we intend to study the influence of family history of vascular disease in homocysteinemia.

METHODS

We studied 204 normal persons (153 males), average age 38.7 +/- 10.9 years, in terms of family history of vascular disease (death due to myocardial infarction or a stroke), conventional risk factors, routine laboratory tests, fasting homocysteinemia and after oral methionine loading (0.1 g/Kg body weight). We compared laboratory results, conventional risk factors and homocysteinemia levels in persons with and without a family history of vascular disease. We performed covariance analysis to evaluate, in a multivariate model, factors that were related to basal or after methionine loading homocysteinemia.

RESULTS

35% of persons presented a family history of vascular disease (FHVD). Persons with FHVD presented higher age (45.6 +/- 8.9 versus 35.0 +/- 10.1, p < 0.001), and higher prevalence of hypertension (p = 0.002), dyslipidemia (p = 0.001), obesity (p = 0.03), and physical inactivity (p = 0.03). They presented a tendency, without statistical significance, to have a higher prevalence of diabetes and of hyperhomocysteinemia, and to present higher levels of basal and afterload homocysteinemia. Performing covariance analysis, basal homocysteinemia did not present any relation to FHVD. After methionine load homocysteinemia was strongly influenced by basal homocysteinemia (p = 0.0000), and significantly related to FHVD (p = 0.039).

CONCLUSIONS

Homocysteinemia cannot explain most of the risk of family history of vascular disease, not explained by conventional risk factors. The only significant relationship between homocysteinemia and FHVD was observed with afterload homocysteinemia in the multivariate model. FHVD is clearly related to conventional risk factors.

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