Aaron L Baggish1, Rory B Weiner2, Gen Kanayama2, James I Hudson2, Michael T Lu2, Udo Hoffmann2, Harrison G Pope1. 1. From Cardiovascular Performance Program, Division of Cardiology, Massachusetts General Hospital, Boston (A.L.B., R.B.W.); Department of Medicine, Harvard Medical School, Boston, MA (A.L.B., R.B.W.); Biological Psychiatry Laboratory and Psychiatric Epidemiology Research Program, McLean Hospital, Belmont, MA (G.K., J.I.H., H.G.P.); Department of Psychiatry, Harvard Medical School, Boston, MA (G.K., J.I.H., H.G.P.); Cardiac MR PET CT Program, Massachusetts General Hospital and Department of Radiology, Harvard Medical School, Boston (M.T.L., U.H.). abaggish@partners.org hpope@mclean.harvard.edu. 2. From Cardiovascular Performance Program, Division of Cardiology, Massachusetts General Hospital, Boston (A.L.B., R.B.W.); Department of Medicine, Harvard Medical School, Boston, MA (A.L.B., R.B.W.); Biological Psychiatry Laboratory and Psychiatric Epidemiology Research Program, McLean Hospital, Belmont, MA (G.K., J.I.H., H.G.P.); Department of Psychiatry, Harvard Medical School, Boston, MA (G.K., J.I.H., H.G.P.); Cardiac MR PET CT Program, Massachusetts General Hospital and Department of Radiology, Harvard Medical School, Boston (M.T.L., U.H.).
Abstract
BACKGROUND: Millions of individuals have used illicit anabolic-androgenic steroids (AAS), but the long-term cardiovascular associations of these drugs remain incompletely understood. METHODS: Using a cross-sectional cohort design, we recruited 140 experienced male weightlifters 34 to 54 years of age, comprising 86 men reporting ≥2 years of cumulative lifetime AAS use and 54 nonusing men. Using transthoracic echocardiography and coronary computed tomography angiography, we assessed 3 primary outcome measures: left ventricular (LV) systolic function (left ventricular ejection fraction), LV diastolic function (early relaxation velocity), and coronary atherosclerosis (coronary artery plaque volume). RESULTS: Compared with nonusers, AAS users demonstrated relatively reduced LV systolic function (mean±SD left ventricular ejection fraction = 52±11% versus 63±8%; P<0.001) and diastolic function (early relaxation velocity = 9.3±2.4 cm/second versus 11.1±2.0 cm/second; P<0.001). Users currently taking AAS at the time of evaluation (N=58) showed significantly reduced LV systolic (left ventricular ejection fraction = 49±10% versus 58±10%; P<0.001) and diastolic function (early relaxation velocity = 8.9±2.4 cm/second versus 10.1±2.4 cm/second; P=0.035) compared with users currently off-drug (N=28). In addition, AAS users demonstrated higher coronary artery plaque volume than nonusers (median [interquartile range] 3 [0, 174] mL3 versus 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 [0.16-1.03 SD units]; P=0.008). CONCLUSIONS: 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 underrecognized public-health problem.
BACKGROUND: Millions of individuals have used illicit anabolic-androgenic steroids (AAS), but the long-term cardiovascular associations of these drugs remain incompletely understood. METHODS: Using a cross-sectional cohort design, we recruited 140 experienced male weightlifters 34 to 54 years of age, comprising 86 men reporting ≥2 years of cumulative lifetime AAS use and 54 nonusing men. Using transthoracic echocardiography and coronary computed tomography angiography, we assessed 3 primary outcome measures: left ventricular (LV) systolic function (left ventricular ejection fraction), LV diastolic function (early relaxation velocity), and coronary atherosclerosis (coronary artery plaque volume). RESULTS: Compared with nonusers, AAS users demonstrated relatively reduced LV systolic function (mean±SD left ventricular ejection fraction = 52±11% versus 63±8%; P<0.001) and diastolic function (early relaxation velocity = 9.3±2.4 cm/second versus 11.1±2.0 cm/second; P<0.001). Users currently taking AAS at the time of evaluation (N=58) showed significantly reduced LV systolic (left ventricular ejection fraction = 49±10% versus 58±10%; P<0.001) and diastolic function (early relaxation velocity = 8.9±2.4 cm/second versus 10.1±2.4 cm/second; P=0.035) compared with users currently off-drug (N=28). In addition, AAS users demonstrated higher coronary artery plaque volume than nonusers (median [interquartile range] 3 [0, 174] mL3 versus 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 [0.16-1.03 SD units]; P=0.008). CONCLUSIONS: 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 underrecognized public-health problem.
Authors: Andreas Breenfeldt Andersen; Glenn A Jacobson; Jacob Bejder; Dino Premilovac; Stephen M Richards; Jon J Rasmussen; Søren Jessen; Morten Hostrup Journal: Sports Med Date: 2021-04-02 Impact factor: 11.136
Authors: James I Hudson; Gen Kanayama; Harrison G Pope; Samantha Muse; Marc J Kaufman; Aaron Baggish; Sushrut S Waikar Journal: Am J Kidney Dis Date: 2020-04-30 Impact factor: 8.860