Serum free testosterone level in coronary artery disease in candidates for coronary artery bypass graft surgery: A cross-sectional study


Background: Due to the controversy over the effect of serum testosterone levels on coronary artery diseases, this survey explores the serum levels of free testosterone, luteinizing hormone, and follicle-stimulating hormone in candidates for coronary artery bypass graft compared with an age-matched control group and evaluates the associated factors in these participants.

Objective: To determine the testosterone level in elective coronary artery bypass grafting participants.

Materials and Methods: In this cross-sectional study, all male patients aged > 40 yr as candidates for elective coronary artery bypass grafting, who were referred to the Afshar Hospital, Yazd, Iran, from March 2018 to March 2019, were included. In total, 100 men were enrolled (50 cases and 50 controls). Their serum levels of free and total testosterone, luteinizing hormone, and follicle-stimulating hormone were measured and the results were compared.

Results: The findings indicated a significant difference between the two groups in total and free testosterone (both p < 0.001); they were lower in the case group. There was also a significant difference in the total testosterone of the participants with diabetes mellitus compared with no-diabetic individuals (p = 0.007). Free testosterone of diabetic subjects taking insulin was lower compared with those taking no insulin (p = 0.04). There was also an association between the body mass index and free testosterone, left ventricular ejection fraction and total testosterone, and a significant and negative relation between the duration of hospital admissions and free testosterone (p < 0.05).

Conclusion: This study illustrates that participants with coronary artery disease bear a significantly low testosterone level in comparison with the healthy control group.

Key words: Coronary artery disease, Testosterone, Coronary artery bypass graft surgery.

[1] McAloon CJ, Boylan LM, Hamborg T, Stallard N, Osman F, Lim PB, et al. The changing face of cardiovascular disease 2000-2012: An analysis of the world health organisation global health estimates data. Int J Cardiol 2016; 224: 256–264.

[2] NCD Countdown. 2030: Worldwide trends in noncommunicable disease mortality and progress towards Sustainable Development Goal target 3.4. Lancet 2018; 392: 1072–1088.

[3] Townsend N, Wilson L, Bhatnagar P, Wickramasinghe K, Rayner M, Nichols M. Cardiovascular disease in Europe: Epidemiological update 2016. Eur Heart J 2016; 37: 3232–3245.

[4] Roth GA, Forouzanfar MH, Moran AE, Barber R, Nguyen G, Feigin VL, et al. Demographic and epidemiologic drivers of global cardiovascular mortality. New Eng J Med 2015; 372: 1333–1341.

[5] Piepoli MF, Hoes AW, Agewall S, Albus C, Brotons C, Catapano AL, et al. 2016 European guidelines on cardiovascular disease prevention in clinical practice: The sixth joint task force of the european society of cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of 10 societies and by invited experts) developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR). Atherosclerosis 2016; 252: 207–274.

[6] Wong ND. Epidemiological studies of CHD and the evolution of preventive cardiology. Nat Rev Cardiol 2014; 11: 276–289.

[7] Kiani F, Hesabi N, Arbabisarjou A. Assessment of risk factors in participants with myocardial infarction. Glob J Health Sci 2016; 8: 255–262.

[8] Pedersen LR, Frestad D, Michelsen MM, Mygind ND, Rasmusen H, Suhrs HE, et al. Risk factors for myocardial infarction in women and men: A review of the current literature. Curr Pharmaceut Design 2016; 22: 3835–3852.

[9] Fairweather D. Sex differences in inflammation during atherosclerosis. Clin Med Insights Cardiol 2014; 8: S17068: 49–59.

[10] Perez-Lopez FR, Larrad-Mur L, Kallen A, Chedraui P, Taylor HS. Gender differences in cardiovascular disease: Hormonal and biochemical influences. Reprod Sci 2010; 17: 511–531.

[11] Schwarz ER, Phan A, Willix Jr RD. Andropause and the development of cardiovascular disease presentation—more than an epi-phenomenon. J Geriatr Cardiol 2011; 8: 35–43.

[12] Xu L, Freeman G, Cowling BJ, Schooling CM. Testosterone therapy and cardiovascular events among men: A systematic review and meta-analysis of placebo-controlled randomized trials. BMC Med 2013; 11: 108–120.

[13] Ahmadi A, Soori H, Sajjadi H, Nasri H, Mehrabi Y, Etemad K. Current status of the clinical epidemiology of myocardial infarction in men and women: A national cross-sectional study in iran. Int J Prevent Med 2015; 6: 14–18.

[14] Hu X, Rui L, Zhu T, Xia H, Yang X, Wang X, et al. Low testosterone level in middle-aged male participants with coronary artery disease. Eur J Int Med 2011; 22: 133–136.

[15] Allameh F, Pourmand GH, Bozorgi A, Nekuie S, Namdari F. The association between androgenic hormone levels and the risk of developing coronary artery disease (CAD). Iran J Public Health 2016; 45: 14–19.

[16] Malkin CJ, Pugh PJ, Morris PD, Asif S, Jones TH, Channer KS. Low serum testosterone and increased mortality in men with coronary heart disease. Heart 2010; 96: 1821–1825.

[17] Dellal FD, Mutlu Niyazoğlu T, Niyazoğlu M, Çeviker T, Görar S, Taşan E. Evaluation of androgen levels in participants with acute coronary syndrome. Med Sci 2012; 1: 323–330.

[18] Davoodi G, Amirezadegan A, Borumand MA, Dehkori MR, Kazemisaeid A, Yaminisharif A. The relationship between level of androgenic hormones and coronary artery disease in men. Cardiovasc J Afr 2007; 18: 362–366.

[19] Kloner RA, Carson C, Dobs A, Kopecky S, Mohler ER. Testosterone and cardiovascular disease. J Am College Cardiol 2016; 67: 545–557.

[20] Ruige JB, Mahmoud AM, De Bacquer D, Kaufman JM. Endogenous testosterone and cardiovascular disease in healthy men: A meta-analysis. Heart 2011; 97: 870–875.

[21] Morris PD, Channer KS. Testosterone and cardiovascular disease in men. Asian J Androl 2012; 14: 428–435.

[22] Trost LW, Mulhall JP. Challenges in testosterone measurement, data interpretation, and methodological appraisal of interventional trials. J Sex Med 2016; 13: 1029–1046.

[23] Mattack N, Devi R, Kutum T, Patgiri D. The evaluation of serum levels of testosterone in type 2 diabetic men and its relation with lipid profile. J Clin Diagn Res 2015; 9: BC04–BC07.

[24] Moulana M, Lima R, Reckelhoff JF. Metabolic syndrome, androgens, and hypertension. Curr Hypertens Reports 2011; 13: 158–162.

[25] Dhindsa S, Miller MG, McWhirter CL, Mager DE, Ghanim H, Chaudhuri A, et al. Testosterone concentrations in diabetic and nondiabetic obese men. Diabetes Care 2010; 33: 1186–1192.

[26] Rao PM, Kelly DM, Jones TH. Testosterone and insulin resistance in the metabolic syndrome and T2DM in men. Nat Rev Endocrinol 2013; 9: 479–493.

[27] Kelly DM, Jones TH. Testosterone: A metabolic hormone in health and disease. J Endocrinol 2013; 217: R25–R45.

[28] Kelly DM, Jones TH. Testosterone: A vascular hormone in health and disease. J Endocrinol 2013; 217: R47–R71.

[29] Shamim MO, Ali Khan FM, Arshad R. Association between serum total testosterone and body mass index in middle aged healthy men. Pak J Med Sci 2015; 31: 355–359.

[30] Gupta V, Bhasin S, Guo W, Singh R, Miki R, Chauhan P, et al. Effects of dihydrotestosterone on differentiation and proliferation of human mesenchymal stem cells and preadipocytes. Mol Cell Endocrinol 2008; 296: 32–40.