SERUM MARKERS OF APOPTOSIS AND CONVENTIONAL RISK FACTORS IN PATIENTS WITH MYOCARDIAL INFARCTION AND HEALTHY RESIDENTS OF ARKHANGELSK REGION: TRENDS, CAUSES, AND CONSEQUENCES
https://doi.org/10.15829/1728-8800-2013-3-18-23
Abstract
Aim. To improve the risk stratification in young patients with myocardial infarction (MI), using the data on the Fas-mediated apoptosis activity in early and late post-infarction periods.
Material and methods. The study included 28 young MI patients (mean age 42,5±5,6 years), 56 elderly MI patients (mean age 63,0±7,8 years), and 66 healthy volunteers. The following parameters were assessed 2 weeks and 7 months (5,7–10,9 months) after MI: conventional risk factors of coronary heart disease (CHD), lipid profile, electrocardiography, echocardiography, and coronary angiography parameters, the levels of apoptosis biomarkers (sFas, sFasL), Cys C, and BNP-32 (immunoenzymatic method).
Results. The mean concentration of sFasL varied by gender, reaching 65,09±36,95 pg/ml in women vs. 77,27±27,48 pg/ml in men (р=0,008). The levels of sFasL were higher in young MI patients (80,18±40,54 pg/ ml), compared to healthy volunteers (58,38±25,79 pg/ml; р=0,012), while there was no marked variation in the levels of sFas. Smoking was associated with higher sFas levels. The concentration of sFasL was associated with the levels of blood lipids, fibrinogen, and body mass index. Patients with arterial hypertension had a higher concentration of sFasL (81,80±37,98 pg/ml) than their non-hypertensive peers (55,30±11,96 pg/ml; р=0,029). The sFas/sFasL ratio was linked to the number of metabolic syndrome (MS) components. Among young MI patients, the levels of sFasL, measured 2 weeks after MI, could be used for the prediction of a new coronary event in the next 6–8 months (sensitivity 75% and specificity 90%).
Conclusion. The concentration of sFasL was higher in young MI patients than in healthy individuals. The levels of sFasL were inversely associated with the number of MS components and also demonstrated predictive value for the assessment of the 6–8-month risk of recurrent angina in young MI patients.About the Authors
A. S. YakovlevaRussian Federation
tel.: 8 (8182) 63 29
O. A. Mirolyubova
Russian Federation
T. V. Supryadkina
Russian Federation
References
1. Napoli C. Oxidation of LDL, atherogenesis, and apoptosis. Ann NY Acad Sci 2003; 1010: 698–709.
2. Martinet W, Kockx MM. Apoptosis in atherosclerosis: implications for plaque destabilization. Acad Geneeskd Belg 2004; 66 (1): 61–79.
3. Ishiyama S, Hiroe M, Nishikawa T, et al. The Fas/Fas Ligand system is involved in the pathogenesis of autoimmune myocarditis in rats. J Immunol 2011; 161: 4695–701.
4. Gupta S. Molecular mechanisms of apoptosis in the cells of the immune system in human aging. Immunol Rev 2005; 205: 114–29.
5. Yamaguchi S, Yamaoka M, Okuyama M, et al. Elevated circulating levels and cardiac secretion of soluble Fas-ligand in patients with congestive heart failure. J Cardiol 1999; 83: 1500–3.
6. Boos CJ, Balakrishnan B, Blann AD, et al. Endothelial damage/dysfunction and apoptosis in acute coronary syndromes: implications for prognosis. J Thromb Haemost 2008; 6 (11): 1841–50.
7. Suda T, Takahashi T, Golstein P, et al. Molecular cloning and expression of the Fas-ligand, a novel member of the tumor necrosis factor family. Cell 1993; 75 (6):1169–78.
8. Zhao W S, Xu L, Wang LF, et al. A 60-s postconditioning protocol by percutaneous coronary intervention inhibits myocardial apoptosis in patients with acute myocardial infarction. Apoptosis 2009; 14 (10): 1204–11.
9. Bjorkerud S, Bjorkerud B. Apoptosis is abundant in human atherosclerotic lesions, especially in inflammatory cells (macrophages and T-cells), and may contribute to the accumulation of gruel and plague instability. Am J Pathol 1996; 149: 367–80.
10. M llauer L, Gruber P, Sebinger D, et al. Mutations in apoptosis genes: a pathogenetic factor for human disease. Mutat Res 2001; 488 (3): 211–31.
11. Deftereos S, Giannopoulos G, Kossyvakis C, et al. Effect of radiographic contrast media on markers of complement activation and apoptosis in patients with chronic coronary artery disease undergoing coronary angiography. J Invasive Cardiol 2009; 21 (9): 473–7.
12. Blanco-Colio LM, Martin-Ventura JL, Sol JM, et al. Decreased circulating Fas-ligand in patients with familial combined hyperlipidemia or carotid atherosclerosis. JACC 2011; 43: 1188–94.
13. Shimizu M, Fukuo K, Nagata S, et al. Increased plasma levels of the soluble form of Fas-ligand in patients with acute myocardial infarction and unstable angina pectoris. JACC 2002; 39: 585–90.
14. Feinberg MS, Schwartz R, Behar S. Impact of metabolic syndrome in patients with acute coronary syndrome. Adv Cardiol 2008; 45: 114–26.
Review
For citations:
Yakovleva A.S., Mirolyubova O.A., Supryadkina T.V. SERUM MARKERS OF APOPTOSIS AND CONVENTIONAL RISK FACTORS IN PATIENTS WITH MYOCARDIAL INFARCTION AND HEALTHY RESIDENTS OF ARKHANGELSK REGION: TRENDS, CAUSES, AND CONSEQUENCES. Cardiovascular Therapy and Prevention. 2013;12(3):18-23. (In Russ.) https://doi.org/10.15829/1728-8800-2013-3-18-23