Cardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid Use.
Cardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid Use.
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DOI：
10.1161/circulationaha.116.026945
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发表时间：
2017-05-23
期刊：
影响因子：
37.8
通讯作者：
Pope HG Jr
中科院分区：
文献类型：
--
作者：
Baggish AL;Weiner RB;Kanayama G;Hudson JI;Lu MT;Hoffmann U;Pope HG Jr
数以百万计的人使用非法合成代谢雄激素类固醇（AAS），但这些药物的长期心血管协会仍然不完全清楚。采用横断面队列设计，我们招募了140名年龄在34-54岁的有经验的男性举重运动员，其中86名男性报告至少2年的累积终身AAS使用和54名非使用男性。使用经胸超声心动图和冠状动脉计算机断层扫描血管造影术，我们评估了3个主要结局指标：左心室（LV）收缩功能（左心室射血分数[LVEF]）、LV舒张功能（早期舒张速度[E ′]）和冠状动脉粥样硬化（冠状动脉斑块体积）。与非使用者相比，AAS使用者表现出相对降低的LV收缩功能（平均值±SD LVEF = 52±11% vs. 63±8%; P<0.001）和舒张功能（E ′ = 9.3±2.4 cm/s vs. 11.1±2.0 cm/s; P<0.001）。与目前停药的使用者（N = 28）相比，在评价时目前正在服用AAS的使用者（N = 58）显示LV收缩功能（LVEF = 49±10% vs. 58±10%; P<0.001）和舒张功能（E ′ = 8.9±2.4 cm/s vs. 10.1±2.4 cm/s; P=0.035）显著降低。此外，AAS使用者的冠状动脉斑块体积高于非使用者（中位数[四分位距] 3 [0，174] mL 3 vs. 0 [0，69] mL 3，P = 0.012）。终生AAS剂量与冠状动脉粥样硬化负荷密切相关（AAS用途：使用累积时间每增加10年，斑块体积等级增加[95%置信区间]：0.60 SD单位[0.16 - 1.03 SD单位]; P = 0.008）。长期使用AAS似乎与心肌功能障碍和加速冠状动脉粥样硬化有关。这些形式的AAS相关的不良心血管表型可能代表了以前认识不足的公共卫生问题。
Millions of individuals have used illicit anabolic-androgenic steroids (AAS), but the long-term cardiovascular associations of these drugs remains incompletely understood. Employing a cross-sectional cohort design, we recruited 140 experienced male weightlifters aged 34–54 years, comprising 86 men reporting at least 2 years of cumulative lifetime AAS use and 54 non-using men. Using transthoracic echocardiography and coronary computed tomography angiography, we assessed 3 primary outcome measures: left ventricular (LV) systolic function (left ventricular ejection fraction [LVEF]), LV diastolic function (early relaxation velocity [E´]), and coronary atherosclerosis (coronary artery plaque volume). Compared to non-users, AAS users demonstrated relatively reduced LV systolic function (mean±SD LVEF = 52±11% vs. 63±8%; P<0.001) and diastolic function (E´ = 9.3±2.4 cm/s vs. 11.1±2.0 cm/s; P<0.001). Users currently taking AAS at the time of evaluation (N = 58) showed significantly reduced LV systolic (LVEF = 49±10% vs. 58±10%; P<0.001) and diastolic function (E´ = 8.9±2.4 cm/s vs. 10.1±2.4 cm/s; P=0.035) compared to users currently off-drug (N = 28). Additionally, AAS users demonstrated higher coronary artery plaque volume then nonusers (median [interquartile range] 3 [0, 174] mL3 vs. 0 [0, 69] mL3, P = 0.012). Lifetime AAS dose was strongly associated with coronary atherosclerotic burden (increase [95% confidence interval] in rank of plaque volume for each 10-year increase in cumulative duration of AAS use: 0.60 SD units [0.16 to 1.03 SD units]; P = 0.008). Long-term AAS use appears to be associated with myocardial dysfunction and accelerated coronary atherosclerosis. These forms of AAS-associated adverse cardiovascular phenotypes may represent a previously under-recognized public-health problem.