BACKGROUND: Experimental studies suggest that androgens induce coronary vasodilatation. We performed this pilot project to examine the clinical effects of long-term low-dose androgens in men with angina. METHODS AND RESULTS:Forty-six men with stable angina completed a 2-week, single-blind placebo run-in, followed by double-blind randomization to 5 mg testosterone daily by transdermal patch or matching placebo for 12 weeks, in addition to their current medication. Time to 1-mm ST-segment depression on treadmill exercise testing and hormone levels were measured and quality of life was assessed by SF-36 at baseline and after 4 and 12 weeks of treatment. Active treatment resulted in a 2-fold increase in androgen levels and an increase in time to 1-mm ST-segment depression from (mean+/-SEM) 309+/-27 seconds at baseline to 343+/-26 seconds after 4 weeks and to 361+/-22 seconds after 12 weeks. This change was statistically significant compared with that seen in the placebo group (from 266+/-25 seconds at baseline to 284+/-23 seconds after 4 weeks and to 292+/-24 seconds after 12 weeks; P:=0.02 between the 2 groups by ANCOVA). The magnitude of the response was greater in those with lower baseline levels of bioavailable testosterone (r=-0. 455, P:<0.05). There were no significant changes in prostate specific antigen, hemoglobin, lipids, or coagulation profiles during the study. There were significant improvements in pain perception (P:=0.026) and role limitation resulting from physical problems (P:=0.024) in the testosterone-treated group. CONCLUSIONS:Low-dose supplemental testosterone treatment in men with chronic stable angina reduces exercise-induced myocardial ischemia.
RCT Entities:
BACKGROUND: Experimental studies suggest that androgens induce coronary vasodilatation. We performed this pilot project to examine the clinical effects of long-term low-dose androgens in men with angina. METHODS AND RESULTS: Forty-six men with stable angina completed a 2-week, single-blind placebo run-in, followed by double-blind randomization to 5 mg testosterone daily by transdermal patch or matching placebo for 12 weeks, in addition to their current medication. Time to 1-mm ST-segment depression on treadmill exercise testing and hormone levels were measured and quality of life was assessed by SF-36 at baseline and after 4 and 12 weeks of treatment. Active treatment resulted in a 2-fold increase in androgen levels and an increase in time to 1-mm ST-segment depression from (mean+/-SEM) 309+/-27 seconds at baseline to 343+/-26 seconds after 4 weeks and to 361+/-22 seconds after 12 weeks. This change was statistically significant compared with that seen in the placebo group (from 266+/-25 seconds at baseline to 284+/-23 seconds after 4 weeks and to 292+/-24 seconds after 12 weeks; P:=0.02 between the 2 groups by ANCOVA). The magnitude of the response was greater in those with lower baseline levels of bioavailable testosterone (r=-0. 455, P:<0.05). There were no significant changes in prostate specific antigen, hemoglobin, lipids, or coagulation profiles during the study. There were significant improvements in pain perception (P:=0.026) and role limitation resulting from physical problems (P:=0.024) in the testosterone-treated group. CONCLUSIONS: Low-dose supplemental testosterone treatment in men with chronic stable angina reduces exercise-induced myocardial ischemia.