Webb Carolyn M, Elkington Andrew G, Kraidly Mustafa M, Keenan Niall, Pennell Dudley J, Collins Peter
Cardiac Medicine, Royal Brompton Campus, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Am J Cardiol. 2008 Mar 1;101(5):618-24. doi: 10.1016/j.amjcard.2007.09.114. Epub 2007 Dec 21.
Intracoronary testosterone infusions induce coronary vasodilatation and increase coronary blood flow. Longer term testosterone supplementation favorably affected signs of myocardial ischemia in men with low plasma testosterone and coronary heart disease. However, the effects on myocardial perfusion are unknown. Effects of longer term testosterone treatment on myocardial perfusion and vascular function were investigated in men with CHD and low plasma testosterone. Twenty-two men (mean age 57 +/- 9 [SD] years) were randomly assigned to oral testosterone undecanoate (TU; 80 mg twice daily) or placebo in a crossover study design. After each 8-week period, subjects underwent at rest and adenosine-stress first-pass myocardial perfusion cardiovascular magnetic resonance, pulse-wave analysis, and endothelial function measurements using radial artery tonometry, blood sampling, anthropomorphic measurements, and quality-of-life assessment. Although no difference was found in global myocardial perfusion after TU compared with placebo, myocardium supplied by unobstructed coronary arteries showed increased perfusion (1.83 +/- 0.9 vs 1.52 +/- 0.65; p = 0.037). TU decreased basal radial and aortic augmentation indexes (p = 0.03 and p = 0.02, respectively), indicating decreased arterial stiffness, but there was no effect on endothelial function. TU significantly decreased high-density lipoprotein cholesterol and increased hip circumference, but had no effect on hemostatic factors, quality of life, and angina symptoms. In conclusion, oral TU had selective and modest enhancing effects on perfusion in myocardium supplied by unobstructed coronary arteries, in line with previous intracoronary findings. The TU-related decrease in basal arterial stiffness may partly explain previously shown effects of exogenous testosterone on signs of exercise-induced myocardial ischemia.
冠状动脉内注入睾酮可诱导冠状动脉扩张并增加冠状动脉血流量。长期补充睾酮对血浆睾酮水平低且患有冠心病的男性的心肌缺血症状有积极影响。然而,其对心肌灌注的影响尚不清楚。我们研究了长期睾酮治疗对冠心病且血浆睾酮水平低的男性心肌灌注和血管功能的影响。在一项交叉研究设计中,22名男性(平均年龄57±9[标准差]岁)被随机分配至口服十一酸睾酮(TU;80毫克,每日两次)组或安慰剂组。在每个8周周期后,受试者接受静息和腺苷负荷下的首次通过心肌灌注心血管磁共振成像、脉搏波分析以及使用桡动脉张力测量法、血液采样、人体测量和生活质量评估来测量内皮功能。虽然与安慰剂相比,TU治疗后整体心肌灌注无差异,但由无阻塞冠状动脉供血的心肌灌注增加(1.83±0.9对1.52±0.65;p = 0.037)。TU降低了基础桡动脉和主动脉增强指数(分别为p = 0.03和p = 0.02),表明动脉僵硬度降低,但对内皮功能无影响。TU显著降低高密度脂蛋白胆固醇并增加臀围,但对止血因子、生活质量和心绞痛症状无影响。总之,口服TU对无阻塞冠状动脉供血的心肌灌注有选择性且适度的增强作用,与先前冠状动脉内研究结果一致。TU相关的基础动脉僵硬度降低可能部分解释了先前显示的外源性睾酮对运动诱导心肌缺血症状的影响。