Main Article Content
Background. The purpose of this work was to study endogenous coagulation/fibrinolysis markers in patients with coronary heart disease (CHD) and concomitant type 2 diabetes mellitus (DM) and to compare these indices with respect to microvascular complications. Materials and methods. We have examined fifty four patients with CHD and concomitant type 2 DM (divided into 2 groups, with and without complications), who were hospitalized in the cardiology and endocrinology unit of the Kyiv Clinical Railway Hospital. Results. Prolonged prothrombin time in the coagulation system was detected in two groups (CHD + type 2 DM and CHD + type 2 DM + diabetic complications): by 7.64 % — in patients without microvascular complications and by 7.49 % — with complications, as well as and a significant increase in fibrinogen (by 36 and 42 %, respectively), but no significant changes were observed between the groups. The study of the anticoagulant blood system indexes revealed that the activity of antithrombin III and protein C in patients with CHD and concomitant type 2 DM with diabetic complications was lower (by 26 and 19.4 %, respectively) compared to the control group. A significant inhibition of the fibrinolytic activity of the blood plasma was detected. Conclusions. The obtained data indicate an inhibition of fibrinolytic and anticoagulant plasma activity, which was most pronounced in patients with CHD and concomitant type 2 DM with microvascular complications. The correlation between fibrinolysis and vascular diseases may depend on the condition of the vascular bed, which significantly increases with the development of macro and microvascular lesions in patients with CHD and concomitant type 2 DM.
This work is licensed under a Creative Commons Attribution 4.0 International License.
Our edition uses the copyright terms of Creative Commons for open access journals.
Authors, who are published in this journal, agree with the following terms:
- The authors retain rights for authorship of their article and grant to the edition the right of first publication of the article on a Creative Commons Attribution 4.0 International License, which allows others to freely distribute the published article, with the obligatory reference to the authors of original works and original publication in this journal.
- Directing the article for the publication to the editorial board (publisher), the author agrees with transmitting of rights for the protection and using the article, including parts of the article, which are protected by the copyrights, such as the author’s photo, pictures, charts, tables, etc., including the reproduction in the media and the Internet; for distributing; for the translation of the manuscript in all languages; for export and import of the publications copies of the writers’ article to spread, bringing to the general information.
- The rights mentioned above authors transfer to the edition (publisher) for the unlimited period of validity and on the territory of all countries of the world.
- The authors guarantee that they have exclusive rights for using of the article, which they have sent to the edition (publisher). The edition (the publisher) is not responsible for the violation of given guarantees by the authors to the third parties.
- The authors have the right to conclude separate supplement agreements that relate to non-exclusive distribution of their article in the form in which it had been published in the journal (for example, to upload the work to the online storage of the journal or publish it as part of a monograph), provided that the reference to the first publication of the work in this journal is included.
- The policy of the journal permits and encourages the publication of the article in the Internet (in institutional repository or on a personal website) by the authors, because it contributes to productive scientific discussion and a positive effect on efficiency and dynamics of the citation of the article.
Erem C, Hacihasanoğlu A, Celik S, et al. Coagulation and fibrinolysis parameters in type 2 diabetic patients with and without diabetic vascular complications. Med Princ Pract. 2005 Jan-Feb;14(1):22-30. doi:10.1159/000081919.
Fox CS, Golden SH, Anderson C, et al. Update on Prevention of Cardiovascular Disease in Adults With Type 2 Diabetes Mellitus in Light of Recent Evidence: A Scientific Statement From the American Heart Association and the American Diabetes Association. Diabetes Care. 2015 Sep;38(9):1777-803. doi: 10.2337/dci15-0012.
Kampoli AM, Tousoulis D, Briasoulis A, Latsios G, Papageorgiou N, Stefanadis C. Potential pathogenic inflammatory mechanisms of endothelial dysfunction induced by type 2 diabetes mellitus. Curr Pharm Des. 2011;17(37):4147-4158.
Derosa G, D’Angelo A, Salvadeo SA, et al. Modification of vascular and inflammation biomarkers after OGTT in overweight healthy and diabetic subjects. Microvasc Res. 2010 Mar;79(2):144-9. doi: 10.1016/j.mvr.2010.01.002.
Derosa G, D’Angelo A, Salvadeo SA, et al. Oral glucose tolerance test effects on endothelial inflammation markers in healthy subjects and diabetic patients. Horm Metab Res. 2010 Jan;42(1):8-13. doi: 10.1055/s-0029-1237728.
Kearney K, Tomlinson D, Smith K, Ajjan R. Hypofibrinolysis in diabetes: a therapeutic target for the reduction of cardiovascular risk. Cardiovasc Diabetol. 2017;16(1):34. doi:10.1186/s12933-017-0515-9.
Hameed I, Masoodi SR, Mir SA, Nabi M, Ghazanfar K, Ganai BA. Type 2 diabetes mellitus: from a metabolic disorder to an inflammatory condition. World J Diabetes. 2015 May 15;6(4):598-612. doi: 10.4239/wjd.v6.i4.598.
Asakawa H, Tokunaga K, Kawakami F. Elevation of fibrinogen and thrombin-antithrombin III complex levels of type 2 diabetes mellitus patients with retinopathy and nephropathy. J Diabetes Complications. 2018;14(3):121-126.
Donath MY, Dalmas É, Sauter NS, Böni-Schnetzler M. Inflammation in obesity and diabetes: islet dysfunction and therapeutic opportunity. Cell Metab. 2013 Jun 4;17(6):860-72. doi: 10.1016/j.cmet.2013.05.001.
McBane RD, Hardison RM, Sobel BE; BARI 2D Study Group. Comparison of plasminogen activator inhibitor-1, tissue type plasminogen activator antigen, fibrinogen, and D-dimer levels in various age decades in patients with type 2 diabetes mellitus and stable coronary artery disease (from the BARI 2D trial). Am J Cardiol. 2010 Jan 1;105(1):17-24. doi: 10.1016/j.amjcard.2009.08.643.