Association of serum testosterone with lipid abnormalities in patients with angiographically proven coronary artery disease

Context: Low testosterone levels are associated with an atherogenic lipid profile and may contribute to the pathogenesis of atherosclerosis. Aims: Our study aimed to investigate the relationship between serum total testosterone (TT) levels and lipid profile in angiographically confirmed coronary artery disease (CAD) in men. Settings and Design: This is a case-control hospital-based study at Teaching Hospital, Karapitiya, Galle, Sri Lanka. Materials and Methods: Two hundred and six men, 103 with angiographically proven CAD and 103 healthy men as a control group were studied. The serum levels of TT and lipids were assessed. Statistical Analysis: Data were analyzed using Minitab software (version 15 for Windows). Results: The mean concentrations of lipid parameters of patients and controls were as follows: Serum total cholesterol (TCh), 5.9 ± 2.8 vs. 5.2 ± 1.6 mmol/l (P = 0.022), low-density lipoprotein cholesterol (LDL-Ch), 3.9 ± 1.2 vs. 3.1 ± 0.5 mmol/l (P = 0.001), high-density lipoprotein cholesterol (HDL-Ch), 1.1 ± 0.5 vs. 1.4 ± 0.6 mmol/l (P = 0.001), and TGs, 2.0 ± 1.0 vs. 1.5 ± 0.8 mmol/l (P = 0.001); lipid levels were significantly different between the two groups. The mean levels of TT in the patients and controls were 11.4 ± 2.7 vs. 18.1 ± 7.2 nmol/l (P = 0.001), significantly different. Among CAD patients, a significant positive association was found between testosterone and HDL-Ch (r = 0.623, P = 0.001), whereas a negative association was found with LDL-Ch (r = -0.579, P = 0.001). Conclusions: Low levels of TT in men with CAD that appear together with an atherogenic lipid milieu may be involved in the pathogenesis of CAD. The observed association between testosterone and HDL-Ch suggests a protective effect of the hormone

Vascular dysfunction and atherosclerosis in chronic kidney disease; A distinct entity

Cardiovascular disease (CVD) is prevalent among patients with chronic kidney disease (CKD) and its occurrence and severity cannot be fully defined by the conventional cardiovascular risk factors namely age, hypertension, dyslipidaemia, diabetes mellitus and obesity. Contemporary studies have examined the role of non-conventional risk factors such as anemia, hyperhomocysteinemia, calcium and phosphate metabolism, vascular stiffness due to endothelial dysfunction ( ED), oxidative injury, and inflammation in the causation of CVD in CKD. Therapeutic interventions used in non-CKD patients are found to be less effective on patients with CKD. The purpose of this review was to gather available evidence on the CVD risk among CKD patients. Numerous mechanisms have been postulated to describe the increased atherogenicity in CKD patients. We discuss these mechanisms especially arterial stiffness, ED and inflammation in detail. In conclusion, CVD in CKD is still an unexplored area which needs further studies to uncover the possible mechanisms. Identifying newer therapies to improve health among this group of patients is of paramount importance