Association of genetic polymorphisms with endothelial dysfunction in chronic heart failure

M. Kose, T.S. Akpinar, O.K. Bakkaloglu, A. Tufan, A. Sumnu, S. Emet, M. Kocaaga, O. Erk, M.S. Kayacan, K. Güler, A.S. Demirel

Department of Internal Medicine, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey. doktortimur@gmail.com

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• Cardiology

OBJECTIVES: Endothelial dysfunction can be shown very early in the cardiovascular disease. In the present study the association between congestive heart failure (CHF), endothelial function and 3 gene polymorphisms was investigated.

PATIENTS AND METHODS: In 104 healthy controls and 104 CHF patients, endothelial constitutive nitric oxide synthase (ecNOS), angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) gene polymorphisms were assessed. The cause of CHF was ischemic in 68 patients and dilated cardiomyopathy (DCMP) in 36 patients. High resolution brachial artery ultrasound was used in 37 CHF patients and 37 healthy controls to assess the endothelial function. Endothelium-dependent vasodilation (EDD) and endothelium-independent vasodilation (EID) were determined.

RESULTS: There no was difference between controls and CHF patients for the ACE, ecNOS, and AT1R genotype frequencies. Compared to controls CHF patients had significantly impaired EDD (9.0+5% vs 16±7%, p < 0.001) and EID (13±6% vs 19+8%, p = 0.001). EDD (7±4% vs 12+6%, p = 0.005), but not EID, was significantly impaired in ischemic CHF as compared to DCMP patients. In the CHF group ecNOS a allele and AT1R C allele influence the EDD.

CONCLUSIONS: Endothelial dysfunction was present in CHF group and the presence of ecNOS a allele and AT1R C allele further impaired EDD.

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