open access

Ahead of print
Research paper
Published online: 2020-11-13
Get Citation

Undercarboxylated matrix Gla protein in patients with ST-segment elevation myocardial infarction and chronic coronary syndromes

Ewa Konduracka, Marcin Pawłowski, Danuta Fedak, Grzegorz Gajos, Aleksander Siniarski, Paweł Rostoff, Marta Węgrzynowska, Jadwiga Nessler
DOI: 10.5603/FC.a2020.0047

open access

Ahead of print
Original Papers
Published online: 2020-11-13

Abstract

Intruduction. Matrix Gla proteins (MGPs) are usually considered as natural inhibitors of soft tissue calcification in chronic inflammatory disorders. However, MGP levels in acute inflammation related to myocardial ischemia have been poorly investigated. The aim of this study was to compare the serum concentrations of uncarboxylated MGPs (ucMGPs) between patients with ST-segment elevation myocardial infarction (STEMI) vs. with chronic coronary syndromes (CCS) and to investigate the association between ucMGP concentration and an increased risk of major adverse cardiovascular events (MACE) in STEMI patients. Material and methods. We enrolled 155 consecutive patients (mean ± standard deviation age, 64 ± 13 years), including 80 patients with a first STEMI and 75 ones with CCS as a controls. Blood samples were obtained within first 24 h from hospital admission to evaluate ucMGP levels. Combination of MACE [all-cause mortality, heart failure (HF) within the first 30 days after myocardial infarction] were evaluated. Results. ucMGP levels were higher in patients with STEMI than in controls (2929 ± 96.5 ng/mL vs. 67.3 + 32.3 ng/mL; p < 0.0001). A significant positive correlation between ucMGP and high-sensitivity C-reactive protein, troponin levels was found. Multivariate analysis showed that ucMGP was an independent associate of STEMI [odds ratio (OR) 1.39; confidence interval (CI): 0.78–2.14, p = 0.01]. Although ucMGP did not predict the combined MACE, however it was an independent associate of HF occurrence 30 days after STEMI (OR, 1.20; 95% CI: 1.07–1.30, p = 0.04). Conclusion. Elevated ucMGP levels in patients with STEMI indicate that some MGPs may be involved in disorders related not only to chronic but also acute inflammatory states.

Abstract

Intruduction. Matrix Gla proteins (MGPs) are usually considered as natural inhibitors of soft tissue calcification in chronic inflammatory disorders. However, MGP levels in acute inflammation related to myocardial ischemia have been poorly investigated. The aim of this study was to compare the serum concentrations of uncarboxylated MGPs (ucMGPs) between patients with ST-segment elevation myocardial infarction (STEMI) vs. with chronic coronary syndromes (CCS) and to investigate the association between ucMGP concentration and an increased risk of major adverse cardiovascular events (MACE) in STEMI patients. Material and methods. We enrolled 155 consecutive patients (mean ± standard deviation age, 64 ± 13 years), including 80 patients with a first STEMI and 75 ones with CCS as a controls. Blood samples were obtained within first 24 h from hospital admission to evaluate ucMGP levels. Combination of MACE [all-cause mortality, heart failure (HF) within the first 30 days after myocardial infarction] were evaluated. Results. ucMGP levels were higher in patients with STEMI than in controls (2929 ± 96.5 ng/mL vs. 67.3 + 32.3 ng/mL; p < 0.0001). A significant positive correlation between ucMGP and high-sensitivity C-reactive protein, troponin levels was found. Multivariate analysis showed that ucMGP was an independent associate of STEMI [odds ratio (OR) 1.39; confidence interval (CI): 0.78–2.14, p = 0.01]. Although ucMGP did not predict the combined MACE, however it was an independent associate of HF occurrence 30 days after STEMI (OR, 1.20; 95% CI: 1.07–1.30, p = 0.04). Conclusion. Elevated ucMGP levels in patients with STEMI indicate that some MGPs may be involved in disorders related not only to chronic but also acute inflammatory states.
Get Citation

Keywords

myocardial infarction, chronic coronary disease, undercarboxylated matrix Gla protein

About this article
Title

Undercarboxylated matrix Gla protein in patients with ST-segment elevation myocardial infarction and chronic coronary syndromes

Journal

Folia Cardiologica

Issue

Ahead of print

Article type

Research paper

Published online

2020-11-13

DOI

10.5603/FC.a2020.0047

Keywords

myocardial infarction
chronic coronary disease
undercarboxylated matrix Gla protein

Authors

Ewa Konduracka
Marcin Pawłowski
Danuta Fedak
Grzegorz Gajos
Aleksander Siniarski
Paweł Rostoff
Marta Węgrzynowska
Jadwiga Nessler

References (15)
  1. Roumeliotis S, Dounousi E, Eleftheriadis T, et al. Association of the inactive circulating matrix Gla protein with vitamin K intake, calcification, mortality, and cardiovascular disease: a review. Int J Mol Sci. 2019; 20(3): 628.
  2. Gheorghe SR, Crăciun AM. Matrix Gla protein in tumoral pathology. Clujul Med. 2016; 89(3): 319–321.
  3. Viegas CSB, Costa RM, Santos L, et al. Gla-rich protein function as an anti-inflammatory agent in monocytes/macrophages: implications for calcification-related chronic inflammatory diseases. PLoS One. 2017; 12(5): e0177829.
  4. Parker BD, Schurgers LJ, Brandenburg VM, et al. The associations of fibroblast growth factor 23 and uncarboxylated matrix Gla protein with mortality in coronary artery disease: the Heart and Soul Study. Ann Intern Med. 2010; 152(10): 640–648.
  5. Wei FF, Trenson S, Verhamme P, et al. Vitamin K-dependent matrix Gla protein as multifaceted protector of vascular and tissue integrity. Hypertension. 2019; 73(6): 1160–1169.
  6. Dalmeijer GW, van der Schouw YT, Magdeleyns EJ, et al. Circulating species of matrix Gla protein and the risk of vascular calcification in healthy women. Int J Cardiol. 2013; 168(6): e168–e170.
  7. Schlieper G, Westenfeld R, Krüger T, et al. Circulating nonphosphorylated carboxylated matrix gla protein predicts survival in ESRD. J Am Soc Nephrol. 2011; 22(2): 387–395.
  8. Morrow DA, Antman EM, Charlesworth A, et al. TIMI risk score for ST-elevation myocardial infarction: a convenient, bedside, clinical score for risk assessment at presentation: An intravenous nPA for treatment of infarcting myocardium early II trial substudy. Circulation. 2000; 102(17): 2031–2037.
  9. Karamat MA, Raja UY, Manley SE, et al. Prevalence of undiagnosed type 2 diabetes in patients admitted with acute coronary syndrome: the utility of easily reproducible screening methods. BMC Endocr Disord. 2017; 17(1): 3.
  10. Yao Y, Watson AD, Ji S, et al. Heat shock protein 70 enhances vascular bone morphogenetic protein-4 signaling by binding matrix Gla protein. Circ Res. 2009; 105(6): 575–584.
  11. Amanvermez R, Acar E, Günay M, et al. Hsp 70, hsCRP and oxidative stress in patients with acute coronary syndromes. Bosn J Basic Med Sci. 2012; 12(2): 102–107.
  12. Abedin M, Lim J, Tang TB, et al. N-3 fatty acids inhibit vascular calcification via the p38-mitogen-activated protein kinase and peroxisome proliferator-activated receptor-gamma pathways. Circ Res. 2006; 98(6): 727–729.
  13. Dahlberg S, Ede J, Schurgers L, et al. Desphospho-uncarboxylated matrix-Gla protein is increased postoperatively in cardiovascular risk patients. Nutrients. 2018; 10(1).
  14. Margonato A, Gorla R, Macchi A, et al. Role of plaque calcification regulators osteoprotegerin and matrix Gla-proteins in stable angina and acute myocardial infarction. J Cardiovasc Med (Hagerstown). 2015; 16(3): 156–162.
  15. Buyukterzi Z, Can U, Alpaydin S, et al. Enhanced serum levels of matrix Gla protein and bone morphogenetic protein in acute coronary syndrome patients. J Clin Lab Anal. 2018; 32(3).

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

 

Wydawcą serwisu jest  "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl