Diagnostic value of hormonal, lipid and ultrasonographic myocardial parameters in metabolic syndrome complicated by chronic coronary artery disease and type 2 diabetes mellitus

Main Article Content

R.Ya. Dutka
N.V. Chmyr
Z.R. Leontieva
Y.M. Fedechko

Abstract

Background. Concomitant diseases due to a combination of metabolic and hormonal changes lead to the development of cardiovascular complications as a direct cause of death and reduced duration or quality of population’s life. The role of hormones in this combined pathology, especially their nosotropic and clinical relationship and correlation with the morphofunctional parameters of the myocardium, has not been studied thoroughly. It is difficult to analyse a lot of laboratory indexes in many comparison groups. The purpose is to set diagnostic markers in metabolic syndrome (MS) and also their relationship compared to combined pathology such as chronic coronary artery disease (CAD) and type 2 diabetes mellitus (DM). Materials and methods. Three hundred and nineteen patients were examined and divided into 6 groups: 82 people with metabolic syndrome were in the first group; 39 with compensated type 2 DM which developed as a result of МS — in the second group; 35 with DM and decompensated type 2 DM — in the third group; 44 individuals with МS complicated by CAD — in the fourth group; 44 with CAD and compensated type 2 DM which developed against the background of МS — in the fifth group; 75 with CAD and decompensated type 2 DM — in the sixth group. The control group consisted of 40 healthy individuals (17 men and 23 females). Then, the levels of prolactin, cortisol, free thyroxinе, thyroid-sti­mulating hormone, blood lipids were measured and cardiac ultrasonography was performed. An integral index for evaluating the significance of study results was used. It was calculated by the ratio of comparison group median to the control group median. The level ≥ 1.2 was set as a significance result. The sum of indexes (∑і) was calculated to describe changes in group indexes. Results. It is found that diagnosis of CAD objectively was not confirmed in female patients younger than 40 years with МS without type 2 DM with increased prolactin, cortisol, and thyroid-stimulating hormone. Thus, there already were initial changes of lipid exchange due to an increase in triglycerides and very low-density lipoprotein choleste­rol levels. Occurrence of CAD on the MS background (only in the absence of type 2 DM) is characterized by almost normal levels of prolactin and cortisol with significantly increased content of thyroid-stimulating hormone in all patients, regardless of gender. Me­tabolic disorders of blood lipids (increased triglycerides, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, total cholesterol, decreased high-density lipoprotein cholesterol), changes in the structural and functional state of the myocar­dium (increased left atrial anteroposterior dia­meter, left ventricular end-diastolic dimension, interventricular septal thickness and left ventricular posterior wall thickness) were observed in patients with CAD on the background of MS. Analysis of the correlation of ∑і of blood lipids, hormones with ultrasonography parameters found that in the 4th group of patients with CAD, the high value of blood lipid ∑і corresponds to the lowest ∑і of hormone indices. The 6th group of individuals with CAD combined with the decompensated type 2 DM is characterized by highest ∑і of both lipid exchange and hormones. The changes in the structural and functional state of myocardium are nonspeci­fic, more expressed with the combined pathology. In MS combined with CAD and compensated type 2 DM, the levels of hormones and lipids did not differ from those in MS with CAD without type 2 DM. There were increased levels of cortisol and prolactin with normal level of ТSH in MS complicated by decompensated type 2 DM and CAD. Analysis of blood lipids demonstrated increased levels of thyroid-stimulating hormone, triglycerides, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol and decreased content of high-density lipoprotein cholesterol with significant ultrasonography changes as an increase in the left atrial anteroposterior diameter, left ventri­cular end-diastolic dimension, interventricular septal thickness, left ventricular posterior wall thickness and decreased ejection fraction. Conclusions. Diagnostic markers (hormone levels, blood lipid parameters and ultrasonographic changes in the myocardium) were determined in metabo­lic syndrome, and also their relationship was studied compared to combined pathology of CAD and type 2 DM.

Article Details

How to Cite
Dutka, R., N. Chmyr, Z. Leontieva, and Y. Fedechko. “Diagnostic Value of Hormonal, Lipid and Ultrasonographic Myocardial Parameters in Metabolic Syndrome Complicated by Chronic Coronary Artery Disease and Type 2 Diabetes Mellitus”. INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine), vol. 17, no. 2, May 2021, pp. 127-35, doi:10.22141/2224-0721.17.2.2021.230567.
Section
Original Researches

References

van Herpt TT, Dehghan A, van Hoek M, et al. The clinical value of metabolic syndrome and risks of cardiometabolic events and mortality in the elderly: the Rotterdam study. Cardiovasc Diabetol. 2016 Apr 27;15:69. doi:10.1186/s12933-016-0387-4.

Montazerifar F, Bolouri A, Mahmoudi Mozaffar M, Karajibani M. The Prevalence of Metabolic Syndrome in Coronary Artery Disease Patients. Cardiol Res. 2016 Dec;7(6):202-208. doi:10.14740/cr507w.

van Vliet-Ostaptchouk JV, Nuotio ML, Slagter SN, et al. The prevalence of metabolic syndrome and metabolically healthy obesity in Europe: a collaborative analysis of ten large cohort studies. BMC Endocr Disord. 2014 Feb 1;14:9. doi:10.1186/1472-6823-14-9.

Kleinherenbrink W, Osei E, den Hertog HM, Zandbergen AAM. Prediabetes and macrovascular disease: Review of the association, influence on outcome and effect of treatment. Eur J Intern Med. 2018 Sep;55:6-11. doi:10.1016/j.ejim.2018.07.001.

Kautzky-Willer A, Harreiter J, Pacini G. Sex and Gender Differences in Risk, Pathophysiology and Complications of Type 2 Diabetes Mellitus. Endocr Rev. 2016 Jun;37(3):278-316. doi:10.1210/er.2015-1137.

Popovic D, Damjanovic S, Djordjevic T, et al. Stress hormones at rest and following exercise testing predict coronary artery disease severity and outcome. Stress. 2017 Sep;20(5):523-531. doi:10.1080/10253890.2017.1368488.

Joseph JJ, Golden SH. Cortisol dysregulation: the bidirectional link between stress, depression, and type 2 diabetes mellitus. Ann N Y Acad Sci. 2017 Mar;1391(1):20-34. doi:10.1111/nyas.13217.

Velarde GP, Sherazi S, Kraemer DF, et al. Clinical and Biochemical Markers of Cardiovascular Structure and Function in Women With the Metabolic Syndrome. Am J Cardiol. 2015 Dec 1;116(11):1705-10. doi:10.1016/j.amjcard.2015.09.010.

International Diabetes Federation Epidemiology Task Force Consensus Group. The IDF consensus worldwide definition of the metabolic syndrome. International Diabetes Federation. Brussels. 2005. Available from: https://www.idf.org/e-library/consensus-statements/60-idfconsensus-worldwide-definitionof-the-metabolic-syndrome.html#:~:text=IDF%20Consensus%20Worldwide%20Definition%20of%20the%20Metabolic%20Syndrome&text=The%20metabolic%20syndrome%20is%20a,cholesterol%20and%20high%20blood%20pressure .

Bhatheja S, Panchal HB, Ventura H, Paul TK. Obesity Cardiomyopathy: Pathophysiologic Factors and Nosologic Reevaluation. Am J Med Sci. 2016 Aug;352(2):219-22. doi:10.1016/j.amjms.2016.05.014.

Incollingo Rodriguez AC, Epel ES, White ML, Standen EC, Seckl JR, Tomiyama AJ. Hypothalamic-pituitary-adrenal axis dysregulation and cortisol activity in obesity: A systematic review. Psychoneuroendocrinology. 2015 Dec;62:301-18. doi:10.1016/j.psyneuen.2015.08.014.

Raaz D, Wallaschofski H, Stumpf C, et al. Increased prolactin in acute coronary syndromes as putative Co-activator of ADP-stimulated P-selectin expression. Horm Metab Res. 2006 Nov;38(11):767-72. doi:10.1055/s-2006-955090.

Al-Kuraishy HM, Al-Gareeb AI, Awad MS, Alrifai SB. Assessment of serum prolactin levels in acute myocardial infarction: The role of pharmacotherapy. Indian J Endocrinol Metab. 2016 Jan-Feb;20(1):72-9. doi:10.4103/2230-8210.172240.

Balbach L, Wallaschofski H, Völzke H, Nauck M, Dörr M, Haring R. Serum prolactin concentrations as risk factor of metabolic syndrome or type 2 diabetes? BMC Endocr Disord. 2013 Mar 21;13:12. doi:10.1186/1472-6823-13-12.

Therkelsen KE, Abraham TM, Pedley A, et al. Association Between Prolactin and Incidence of Cardiovascular Risk Factors in the Framingham Heart Study. J Am Heart Assoc. 2016 Feb 23;5(2):e002640. doi:10.1161/JAHA.115.002640.

Yang L, Lv X, Yue F, Wei D, Liu W, Zhang T. Subclinical hypothyroidism and the risk of metabolic syndrome: A meta-analysis of observational studies. Endocr Res. 2016 May;41(2):158-65. doi:10.3109/07435800.2015.1108332.