Authors
- Ersel Onrat — Faculty of Medicine, Afyonkarahisar, Turkey
- Sezgin Barlak — Faculty of Medicine, Afyonkarahisar, Turkey
- Serap Tutgun Onrat — Faculty of Medicine, Afyonkarahisar, Turkey
- İsmet Dogan — Faculty of Medicine, Afyonkarahisar, Turkey
- Hayri Demirbas — Faculty of Medicine, Afyonkarahisar, Turkey
- Serkan Gokaslan — Faculty of Medicine, Afyonkarahisar, Turkey
- Cigdem Gokaslan — Faculty of Medicine, Afyonkarahisar, Turkey
- Alaettin Avsar — Faculty of Medicine, Afyonkarahisar, Turkey
Abstract
**Introduction**: Carotid artery disease (CAD) is the narrowing of carotid arteries due to atherosclerosis. It can cause stroke. Some hereditary determinants can affect atherosclerosis formation. (1) In present study, we investigated the hereditary thrombophilia on the formation of CAD. **Patients and Methods**: We evaluated the effects of Factor V LEIDEN, Factor V H1299R, Prothrombin G20210A, Factor XIII V34L, B-Fibrinogen -455 G>A, PAI-1 4G/5G, HPA1, MTHFR C677T, MTHFR A1298C, ACE I/D, APO B R3500Q, and APO E polymorphisms on CAD formation by using a ViennaLab CVD Strip Assay. Group A includes 41 patients (70.2 ± 8.6 years, 30 men) with CAD and Group B includes 39 healthy controls (67.3 ± 9.2 years, 28 men). Twenty patients had transient ischemic attack or stroke, 21 had carotid artery stenosis, more than 50% in Group A. Hyperlipidemia is more frequent in Group A compared Group B (71%, 49%; pA, MTHFR C677T and MTHFR A1298C were more frequent in Group A compared with Group B significantly [(2.6%, 7.3% pA, MTHFR C677T and MTHFR A1298C heterozygous mutation seems to be determinant (p<0.05). We have some difficulty on the explication that why heterozygous form is significant even though homozygous form is not significant. This is a pilot study. We will go on working on the project to evaluate the hereditary thrombophilia.
Keywords
carotid artery disease, hereditary thrombophilia
DOI
https://doi.org/10.15836/ccar2017.385Literature
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