International Journal of Pharma and Bio Sciences RELATIONSHIP OF TESTOSTERONE LEVELS IN MALES WITH CORONARY HEART DISEASE
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1 International Journal of Pharma and Bio Sciences RESEARCH ARTICLE BIO CHEMISTRY RELATIONSHIP OF TESTOSTERONE LEVELS IN MALES WITH CORONARY HEART DISEASE MAMTA SETH *1, ASHUMA SACHDEVA 2, PRASANTA SAHAROY 2, SHASHI SETH 2 AND HIMANSHU MADAAN 2 1. College of Pharmacy, Pt. B.D. Sharma University of Health Sciences, Rohtak Haryana (India) 2. Department of Biochemistry, Pt. B.D. Sharma University of Health Sciences, Rohtak Haryana (India) MAMTA SETH College of Pharmacy, Pt. B.D. Sharma University of Health Sciences, Rohtak Haryana (India) *Corresponding author ABSTRACT Males are more than twice at the risk of dying from coronary disease than women. The finding that estrogen has a protective role in females led to the speculation that testosterone is deleterious to the male cardiovascular system and contributes to the vascular risk, but subsequent research showed little evidence that endogenous testosterone is an adverse risk factor, but the role of testosterone status and replacement therapy on male health is controversial. We studied the levels of testosterone in 60 males with recent coronary heart disease confirmed by the levels of troponin I ultra and compared them with the age matched controls from normal population. These parameters were assayed using chemiluminescent technology. We found that in males with CHD the testosterone levels were significantly reduced. This article discusses the cardioprotective role of testosterone in males. B - 566
2 KEYWORDS Troponin I ultra, Coronary artery disease, Testosterone INTRODUCTION Coronary artery disease (CAD) is a leading cause of mortality and morbidity in the western world. It is a chronic progressive condition, and treatment is required indefinitely. Men have more than twice the risk of dying from coronary disease than women, an effect that persists after controlling for cardiovascular risk factors 1. The finding that estrogen has a protective role in females led to the speculation that testosterone may be deleterious to the male cardiovascular system, but subsequent research showed little evidence that endogenous testosterone is an adverse risk factor, but the role of testosterone status and replacement therapy on male health is controversial 2. Testosterone replacement reduces waist circumference, cholesterol, circulating pro-inflammatory cytokines and improves insulin sensitivity and glycemic control 3. Studies in male animals have shown that castration or induced hypogonadism increases atherosclerosis and testosterone replacement abrogates this 4,5. In addition, testosterone has beneficial effects in men with cardiac disease. Little attention has been paid to the role of testosterone in the pathogenesis of CAD. Males do not have a menopause equivalent, but sex hormones levels do fall with advancing age 6. Testosterone has well-established functions in the adult male. It induces secondary sexual characteristics, and is important for preserving sexual function, muscle strength, bone mineral density and mood in male 7. The hormone has a circadian and circannual rhythm, with peak blood levels in the morning and in the spring season, respectively. Testosterone is a potent coronary vasodilator, an effect mediated by a calcium channel antagonist action, and consequently has benefits on the angina threshold, particularly in men with low baseline testosterone 8,9. Testosterone therapy reduces total cholesterol, fat mass, waist circumference and pro-inflammatory cytokines associated with atherosclerosis, diabetes and the metabolic syndrome Testosterone also improves functional capacity and insulin resistance in men with heart failure 13, 14. The more elderly population, in which the prevalence of CAD is highest, has relatively low testosterone levels. Furthermore, males with CAD have lower testosterone levels when compared with age matched men with normal coronary angiograms 3. There is evidence that testosterone therapy delays the onset of cardiac ischemia, probably as a consequence of a coronary vasodilator mechanism, and improving the symptom of angina 15. Testosterone deficiency may cause undesirable effects such as loss of bone and lean body mass, increased adiposity, low energy and impaired physical and sexual function. Until recently, these effects were viewed as the natural physiology of ageing; however, recent studies have found low testosterone to be associated with increased mortality after controlling for baseline morbidity and age The effect of testosterone on mortality is independent after adjustment for baseline covariates. The majority of the hormone (68%) is present bound tightly to the sex-hormone- binding globulin, with about 30% being loosely bound to albumin and only 2 3% in the free form. The biologically active moiety is the albumin bound and free testosterone; this is called the bio-available portion 18. MATERIAL AND METHODS This study was conducted in the Deptt. Of Biochemistry, Pt. B D Sharma PGIMS, Rohtak, Haryana, on 60 patients of recent MI (within 6-12 hrs). The study group comprised of 60 male patients in the age group 30- B - 567
3 85years, with high levels of troponin I ultra confirming MI (Reference Range 0-1.5ng/ml). Their sample was evaluated for Testosterone, Lipid profile and Aspartate amino transferase (AST) and Alanine amino transferase (ALT). The levels of testosterone and troponin I ultra were estimated by chemiluminiscence based immunoassay method on Advia Centaur CP Chemiluminiscence system supplied by Siemens (Germany) using kits supplied by the same company. The Lipid profile and AST/ALT levels were estimated on Konelab Hitachi Autoanalyser using kits supplied by Roche Diagnostics. The results were analyzed statistically and compared with 60 age matched controls. OBSERVATIONS AND RESULTS On evaluation of the results it was found that the mean testosterone levels (Reference range ng/dl) were significantly lower than the controls (p<0.05). The levels of Troponin I ultra were raised significantly (p<0.005). The values of Lipid profile parameters i.e. T. Cholesterol, Triglycerides, HDL, LDL and VLDL were compared with the controls and the levels of AST and ALT were as expected. TABLE Parameters Cases Mean + SD Controls Mean + SD Troponin I * Testosterone ± ** TG ± TC ± HDL ± LDL ± VLDL ± AST ± ALT ± *p < 0.05; **p<0.005 DISCUSSION This study demonstrates a strong inverse relationship between the baseline level of total testosterone and MI. Myocardial infarction is caused by thrombosis of the coronary artery in 90% of cases. Thrombosis occurs when a coronary plaque erodes or ruptures, and the endothelium is breached. Thrombosis is a complicated process with its own intrinsic promoters and antagonists which together determine the prevailing coagulation status 14. Hypogonadism, the state of testosterone deficiency, has a prevalence of 7% in the general population, rising to 20% in very elderly males 6. In a small observational study comparing men presenting for scheduled angiography, the levels of bioavailable testosterone were significantly lower in males with CAD compared to men with normal coronaries. The EPIC-Norfolk study 17 excluded men with cardiovascular disease and cancer at baseline and yet found that all-cause mortality and cardiovascular mortality was increased for every 6 nmol/l reduction in serum testosterone. Low testosterone status is therefore associated with mortality, yet larger studies on the prevalence of hypogonadism in males with CAD have yet to be published. However data have been presented to suggest that the prevalence of biochemical hypogonadism in these patients, as defined by a total testosterone of < 7.5 nmol/l or a bio-available testosterone of < 2.5 nmol/l, may be as high as 23.4% 20. Lower circulating B - 568
4 testosterone concentrations are associated with metabolic syndrome, type 2 diabetes, changes in carotid intimamedia thickness, and aortic and lower limb arterial disease in men. Altered patterns of lipid profile and apoproteins are associated with CAD. In particular, high total cholesterol, high LDL fraction, hypertriglyceridaemia and elevated lipoproteina are pro-atherogenic, whereas HDL has a protective role. The majority of crosssectional studies have found a positive correlation of endogenous testosterone with HDL and a negative correlation with total cholesterol, LDL,and triglycerides. Thus, normal men with low testosterone appear to have adverse lipid profiles, and hypogonadal men have a potentially atherogenic dyslipidaemia prior to treatment 10. A few cross-section studies have found no correlation between endogenous androgens and lipid profile Testosterone has also been shown to influence the coagulation status of an individual. Androgens and in particular testosterone have an inverse relationship with fibrinogen which is the final component of the coagulation cascade and the building block of a stable clot. It is also an acute-phase protein and is raised in any disease characterized by inflammation and it has been confirmed in a meta-analysis that fibrinogen is an independent risk factor for CAD. Low endogenous testosterone is associated with elevated fibrinogen levels and also testosterone administration causes a significant fall in fibrinogen. Although the exact mechanism behind this reduction is not known but it has been postulated that because androgens are metabolized extensively in the liver, therefore androgen therapy may alter coagulation protein production,for example a high factor VII has been associated with low serum testosterone. An alternative explanation is that testosterone by its intrinsic immunemodulating properties, damps down the inflammation in atherosclerotic plaques causing the reduction of acute-phase proteins in general, including fibrinogen 14. Fundamentally, all men suffering with AMI are temporarily hypogonadal,and this phenomenon leads to a prothrombotic state that may prevent thrombolysis or cause reinfarction. Replacement therapy of testosterone to prevent MI in elderly is still under experimental stages and the long term results of the studies are awaited. CONCLUSION Patients with overt hypogonadism clearly require treatment. However, given that a substantial proportion of men with CAD appear to have relative testosterone deficiency, would correcting this afford any benefit to them? Certain studies have suggested objective improvements in symptoms, but would male HRT have beneficial effects on established risk factors, and would this be translated into a clinically relevant reduction in cardiovascular endpoints? Moreover would the known side effects of testosterone therapy make it any worthwhile starting this treatment regimen at all? These questions need to be addressed before embarking upon such line of treatment and hence the need for larger, long term studies. REFERENCES 1. Njolstad I, Arnesen E, Lund-Larsen PG. Smoking, serum lipids, blood pressure, and sex differences in myocardial infarction. A 12-year follow-up of the Finnmark Study. Circulation 1996; 93: Haddad R.M., Kennedy C.L., Caples S.M et al, Testosterone and cardiovascular risk in men: a systematic B - 569
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