beta-endorphin and Angina--Unstable

There is strong comorbidity between atherosclerosis (ATS) and depression which is attributed to increased atherogenicity, insulin resistance (IR), and immune and oxidative stress.. To examine the role of the above pathways and mu-opioid receptor (MOR), β-endorphin levels, zinc, copper, vitamin D3, calcium, and magnesium in depression due to ATS/unstable angina (UA).. Biomarkers were assayed in 58 controls and 120 ATS patients divided into those with moderate and severe depression according to the Beck Depression Inventory-II (BDI-II) scores >19 and >29, respectively.. Neural network and logistic regression models showed that severe depression due to ATS/UA was best predicted by interleukin-6 (IL-6), UA, MOR, zinc, β-endorphin, calcium and magnesium, and that moderate depression was associated with IL-6, zinc, MOR, β-endorphin, UA, atherogenicity, IR, and calcium. Neural networks yielded a significant discrimination of severe and moderate depression with an area under the receiver operating curves of 0.831 and 0.931, respectively. Using Partial Least Squares path analysis, we found that 66.2% of the variance in a latent vector extracted from ATS/UA clinical features, and the BDI-II scores, atherogenicity, and IR could be explained by the regression on IL-6, IL-10, zinc, copper, calcium, MOR, and age. The BDI-II scores increased from controls to ATS to UA class III to UA class IV.. Immune activation, the endogenous opioid system, antioxidants, trace elements, and macrominerals modulate a common core shared by increased depressive symptoms, ATS, UA, atherogenicity, and IR.

Topics: Analgesics, Opioid; Angina, Unstable; Atherosclerosis; beta-Endorphin; Calcium; Comorbidity; Copper; Depression; Humans; Interleukin-6; Magnesium; Oxidative Stress; Phenotype; Zinc

In animal models of circulatory shock and heart failure concentrations of the endogenous opioid peptide beta endorphin are raised and opioid receptor blockade improves haemodynamic variables and survival. This study was performed to identify whether acute myocardial ischaemia provokes the release of beta endorphin in humans.. Observational study in a university cardiology centre. Serial measurements of beta endorphin made by specific radioimmunoassay were correlated with other clinical and neuroendocrine variables that were measured prospectively. Fifty five patients with acute myocardial ischaemia and 26 patients undergoing elective coronary angioplasty of the left anterior descending coronary artery were studied.. beta endorphin concentrations were raised above the upper limit of normal in 31/42 (74%) patients with confirmed myocardial infarction, 3/13 (23%) patients with unstable angina, and 10/24 (42%) patients after coronary angioplasty. There was no evidence of myocardial release of beta endorphin. There were significant positive correlations between beta endorphin and the concentrations of adrenocorticotrophic hormone, cortisol, and arginine vasopressin. In patients with acute myocardial ischaemia there was a significant positive correlation between the peak concentrations of creatine kinase and beta endorphin but no correlation with visual analogue scores of the intensity of chest pain. The highest beta endorphin concentrations were seen in patients whose clinical course was complicated by the development of heart failure.. beta endorphin release is a component of the neuroendocrine activation associated with myocardial ischaemia/infarction.

Topics: Acute Disease; Adrenocorticotropic Hormone; Adult; Aged; Angina, Unstable; Angioplasty, Balloon, Coronary; Arginine Vasopressin; beta-Endorphin; Coronary Disease; Creatine Kinase; Female; Humans; Hydrocortisone; Male; Middle Aged; Myocardial Infarction; Prospective Studies; Radioimmunoassay