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Plasminogen activator inhibitor-1, free fatty acids, and insulin resistance in patients with myocardial infarction

Authors Gruzdeva O, Uchasova E, Dyleva Y, Belik E, Shurygina E, Barbarash O

Received 11 April 2013

Accepted for publication 31 May 2013

Published 13 August 2013 Volume 2013:6 Pages 293—301


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 5

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Olga Gruzdeva, Evgenya Uchasova, Yulia Dyleva, Ekaterina Belik, Ekaterina Shurygina, Olga Barbarash

Research Institute for Complex Issues of Cardiovascular Diseases under the Siberian Branch of the Russian Academy of Medical Sciences, Kemerovo, Russian Federation

Background: Insulin resistance is known to be a common feature of type 2 diabetes mellitus and is regarded as an important mechanism in the pathogenesis of this disease. The key pathogenetic mechanisms of insulin resistance progression are free fatty acids metabolism impairment and enhanced activity of plasminogen activator inhibitor 1. Both free fatty acids and plasminogen activator inhibitor 1 are recognized as risk factors for coronary heart disease.
Methods: The patients were divided into two groups: group 1 included 65 non-diabetic myocardial infarction patients and group 2 enrolled 60 diabetic myocardial infarction patients. The control group consisted of 30 sex- and age-matched volunteers. The concentration of serum free fatty acids, glucose, C-peptide, and insulin were measured on the 1st and 12th days of the study. All the patients had their postprandial glycemia, insulin, and C-peptide concentrations measured 2 hours after a standard carbohydrate breakfast containing 360 kcal (protein 20 g, carbohydrate 57 g, and fat 9 g).
Results: Free fatty acids levels in group 1 and in group 2 exceeded the control group values by 7-fold and 11-fold, respectively. Plasminogen activator inhibitor 1 concentration was 2.5-fold higher in group 1 and 4.6-fold higher in group 2 compared to the control group on the 1st day from the myocardial infarction onset. In addition, plasminogen activator inhibitor 1 concentration was significantly reduced in both groups on the 12th day from the myocardial infarction onset; however, it did not achieve the control group values.
Conclusion: Increased postprandial glucose level, insulinemia, and elevated levels of free fatty acids and plasminogen activator inhibitor are associated with myocardial infarction-associated progression of insulin resistance. However, insulin resistance metabolic markers are of great predictive capacity in the assessment of risk of acute coronary events.

Keywords: free fatty acids, type 2 diabetes mellitus, myocardial infarction, insulin resistance, plasminogen activator inhibitor 1

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