The prognostic value of testosterone in chronic coronary artery disease

Background: Low serum testosterone (T) levels are associated with increased all-cause mortality in community-based studies while there are no data on the prognostic role of free T (FT), the most active fraction of total T, in patients with coronary artery disease (CAD). Objectives: We tested the hypothesis that endogenous FT predicts cardiovascular (CV) mortality in men with stable CAD.Methods: Serum FT, lipids, high-sensitivity C-reactive protein (hsCRP) and intereukin-6 levels were measured in 612 consecutive men with stable CAD. Primary endpoint was CV death, and secondary endpoint hospitalizations for acute coronary syndrome, ventricular arrhythmias, or ischemic stroke. Results: During a median follow-up of 5 years, 243 CV events (39.7%) occurred. Of these, 68 were CV deaths (11%), 140 acute coronary syndromes (22.9%), 7 strokes (1.1%), and 28 (4.6%) arrhythmic events. FT was inversely associated with CV death after adjustment for conventional risk factors for CAD (hazard ratio [HR]: 0.853; 95% confidence interval [CI]: 0.782 to 0.930; p7 pg/mL) after adjustment for traditional risk factors for CAD (HR: 2.815; 95% CI: 1.428 to 5.550; p=0.003). FT levels could not predict secondary endpoints (HR: 0.965; 95% CI: 0.920 to 1.013; p=0.151).Conclusions: In order to explore whether endogenous free testosterone (FT) predicts cardiovascular (CV) mortality in men with stable coronary artery disease (CAD) we recruited 612 coronary men. During a 5 years follow-up, 68 CV deaths occurred. FT was inversely associated with CV death after adjustment for classical risk factors (p7pg/mL) μετά από προσαρμογή ως προς τους παραδοσιακούς παράγοντες κινδύνου της ΣΝ (ΗR: 2,815, 95% CI: 1,428 έως 5,550, p=0,003). Τα επίπεδα ελεύθερης τεστοστερόνης ορού δεν προέβλεπαν τα δευτερογενή καταληκτικά σημεία (HR: 0,965, 95% CI: 0,920 έως 1,013, p=0,151).Συμπεράσματα: Τα χαμηλά επίπεδα της ελεύθερης τεστοστερόνης ορού συσχετίζονται με υψηλή πενταετή καρδιαγγειακή θνητότητα σε άνδρες με σταθερή ΣΝ, ανεξάρτητα από τους άλλους παραδοσιακούς παράγοντες καρδιαγγειακού κινδύνου

Amyloid-beta (1-40) and the risk of death from cardiovascular causes in patients with coronary heart disease

BACKGROUND: The amyloid beta peptide is the major protein constituent of neuritic plaques in Alzheimer disease and appears to play a central role in vascular inflammation pathophysiology. OBJECTIVES: This study sought to determine the clinical value of amyloid-beta 1-40 (Abeta40) measurement in predicting cardiovascular (CV) mortality in patients with coronary heart disease (CHD) and arterial stiffness progression in young healthy subjects. METHODS: Abeta40 was retrospectively measured in blood samples collected from 3 independent prospective cohorts and 2 case-control cohorts (total N = 1,464). Major adverse cardiac events (MACE) were assessed in the 2 prospective cohorts (n = 877) followed for a median of 4.4 years. To look at effects on subclinical disease, arterial stiffness was evaluated at baseline and after 5-year follow-up (n = 107) in young healthy subjects. The primary endpoint was the predictive value of Abeta40 for CV mortality and outcomes in patients with CHD. RESULTS: In Cox proportional hazards models adjusted for age, sex, estimated glomerular filtration rate, left ventricular ejection fraction, high-sensitivity C-reactive protein, and high-sensitivity troponin T, Abeta40 independently predicted CV death and MACE in patients with CHD (p < 0.05 for all). After multivariate adjustment, Abeta40 levels conferred a substantial enhancement of net reclassification index and integrated discrimination improvement of individuals at risk in the total combined CHD cohort over the best predictive model. Further cohort-based analysis revealed that Abeta40 levels were significantly and independently associated with arterial stiffness progression, incident subclinical atherosclerosis, and incident CHD. CONCLUSIONS: Measuring blood levels of Abeta40 identified patients at high risk for CV death

Amyloid-beta (1-40) and the risk of death from cardiovascular causes in patients with coronary heart disease

BACKGROUND: The amyloid beta peptide is the major protein constituent of neuritic plaques in Alzheimer disease and appears to play a central role in vascular inflammation pathophysiology. OBJECTIVES: This study sought to determine the clinical value of amyloid-beta 1-40 (Abeta40) measurement in predicting cardiovascular (CV) mortality in patients with coronary heart disease (CHD) and arterial stiffness progression in young healthy subjects. METHODS: Abeta40 was retrospectively measured in blood samples collected from 3 independent prospective cohorts and 2 case-control cohorts (total N = 1,464). Major adverse cardiac events (MACE) were assessed in the 2 prospective cohorts (n = 877) followed for a median of 4.4 years. To look at effects on subclinical disease, arterial stiffness was evaluated at baseline and after 5-year follow-up (n = 107) in young healthy subjects. The primary endpoint was the predictive value of Abeta40 for CV mortality and outcomes in patients with CHD. RESULTS: In Cox proportional hazards models adjusted for age, sex, estimated glomerular filtration rate, left ventricular ejection fraction, high-sensitivity C-reactive protein, and high-sensitivity troponin T, Abeta40 independently predicted CV death and MACE in patients with CHD (p < 0.05 for all). After multivariate adjustment, Abeta40 levels conferred a substantial enhancement of net reclassification index and integrated discrimination improvement of individuals at risk in the total combined CHD cohort over the best predictive model. Further cohort-based analysis revealed that Abeta40 levels were significantly and independently associated with arterial stiffness progression, incident subclinical atherosclerosis, and incident CHD. CONCLUSIONS: Measuring blood levels of Abeta40 identified patients at high risk for CV death