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<DISPLAY-NAME xmlns:dctm="http://www.documentum.com" xmlns:fmt="http://java.sun.com/jstl/fmt" xmlns:jsp="jsp">Southern Medical Journal</DISPLAY-NAME>
<ARTICLE-TITLE xmlns:dctm="http://www.documentum.com" xmlns:fmt="http://java.sun.com/jstl/fmt" xmlns:jsp="jsp" xmlns:xlink="http://www.w3.org/1999/xlink">Androgen Abuse and Increased Cardiac Risk</ARTICLE-TITLE>
<!--***Template for articlediscussion***-->Abstract and Introduction
Abstract
The objectives of this article were to review the anabolic androgen steroids, specifically the direct and indirect effects on the cardiovascular system of the individuals who use them, and to summarize the evidence regarding the effects of androgens on the cardiovascular system. A search of the English-language scientific literature from 1976 to March 2012 was performed primarily by searching the MEDLINE and Embase databases and Google. Anabolic androgenic steroids are associated with direct effects such as cardiac muscle hypertrophy and myocardial fibrosis and indirect effects, including dyslipidemia, hypertension, arrhythmia, and myocardial infarction. It is likely that chronic exposure to these agents can result in significant alterations in the cardiovascular system, and their safety has not been fully established.
Introduction
The abuse of performance-enhancing drugs among competitive and noncompetitive athletes, including high school and college students, is a major public health issue and of significant concern. Anabolic androgen steroids (AAS) are the most commonly used ergogenic drugs.
AAS are synthetic derivatives of testosterone. The term androgenic indicates masculinization.The term anabolic indicates tissue building and is the component of a steroid that is responsible for thickened vocal cords, enlargement of the larynx, increase in libido, linear growth acceleration before epiphyseal plate closure, and increased muscle bulk and strength through dose-dependent hypertrophy, while decreasing body fat.The physiological effects on muscles and other tissues are summarized in Table 1.
Testosterone, nandrolone, stanozolol, and methandienone are the most frequently abused androgens. Physiological replacement of androgens has been used therapeutically to restore levels in hypogonadal men to increase fat-free mass, muscle size, and bone density.A number of clinical trials also have shown benefits of physiological dose replacement of AAS in wasting syndrome secondary to HIV infection,depression,and age-related sarcopenia. The major goals of androgen therapy are to replace testosterone at levels as close to regular physiological levels as is possible and to avoid the adverse effects.
Athletes usually consume supraphysiologic doses of AAS. Steroids are generally taken in 4- to 12-week cycles. Athletes often "stack" multiple steroids simultaneously and "pyramid" the dosing schedule, beginning with low dosage and increasing amounts during the middle and end of a cycle. Between dosing cycles, it is typical for users to have a period of abstinence, known as a "drug holiday," which usually occurs during the competition phases.This method provides 50 to 100 times the physiologically needed dose of steroids, resulting in levels that are far higher than physiological levels.The increased prevalence of AAS abuse in massive doses among athletes has led to numerous reports linking the adverse effects on multiple body systems, as well as premature mortality. In one study, competitive athletes using AAS had 4.6 times the mortality rate of the population not using AAS.
Abuse of AAS is now common in nonathletes. It is estimated that more than 1 million Americans abuse AAS, including many high school and college athletes.Other studies suggest that approximately 5% of boys and 2% of girls in high school admit to using AAS.
Get the summary from the
Agency for Healthcare Research and Quality
Another area for concern is the abuse of a precursor to AAS known as prohormones, such as androstenediol. Many prohormone synthetic chemicals have been banned, but numerous clones have been made with a minor change in the formulation. These prohormones increase hormone levels within the body leading to many of the same benefits and side effects as the AAS. This article reviews the adverse effects of AAS on the cardiovascular system.
A search of the English-language scientific literature from 1976 through March 2012 was performed primarily by searching the MEDLINE, Embase, and Google databases. The key words used in the search included androgens, anabolic, androgenic, steroids, exercise, athlete, cardiovascular, effects. The bibliographies of articles from the above search also were searched for relevant articles; links on Web sites containing published articles were searched for pertinent information.
AAS have been associated with direct and indirect cardiovascular effects, as described in the following sections.
Direct Cardiovascular Effects
Myocardial Histologic Changes
A 2005 study reported two cases of sudden cardiac death in young male athletes related to AAS abuse. Both cases involved healthy individuals without any history of coronary artery disease (CAD) and no evidence of significant abnormality in arterial microscopic examination. Autopsy of both hearts showed focal myocardial fibrosis suggestive of prior myocardial injury. In a study of a sudden unexpected death in a female fitness athlete using steroids and ephedrine, the only pathological finding was a few small foci of granulation tissue, which was interpreted as evidence of earlier myocardial necrosis.Sudden cardiac arrhythmia resulting from inflammatory process and myocardial fibrosis was suggested to be the cause of death in these cases. Other researchers have reported sudden cardiac deaths related to steroids that also showed myocardial fibrosis in the absence of CAD.
Cardiac Hypertrophy
Get the summary
Left ventricular hypertrophy (LVH) has been reported in androgen abusers.Several groups have shown that athletes using AAS have reduced end diastolic dimension, a thicker posterior wall and interventricular septum, and a larger left ventricular mass than athletes not using AAS.Cardiac muscle cells have receptors for androgens, and both testosterone and dihydrotestosterone produce a hypertrophic response by acting directly on cardiac muscle cells, increasing amino acid incorporation into protein.The problem is that LVH may persist after discontinuation of AAS.
Reduced Cardiac Function
An echocardiographic study of 47 strength-training individuals (46 male subjects), 28 of whom were regular AAS users, revealed a lower systolic function in AAS users versus nonusers, ejection fractions 58% versus 63%, respectively.In addition, there was evidence of reduced diastolic function by tissue Doppler measurement in the AAS users (ie, their hearts were weaker and stiffer). Another study of 12 long-term AAS users noted that compared with controls, they were noted to have significant systolic cardiac dysfunction as measured by lower left ventricular ejection fraction (50.1% vs 59.1%; P = 0.003), leading the authors to suggest that further work is needed to determine the extent of this problem.An Italian Doppler imaging study also showed reduced systolic function but in a regional distribution.\
Indirect Cardiovascular Effects
Abnormal Plasma Lipoprotein
Many studies have shown that AAS can cause dyslipidemia by increasing low-density lipoprotein as high as 596 mg/dL and decreasing high-density lipoprotein as low as 5 mg/dL.18,26–28 Alterations in high- and low-density lipoprotein levels occur in a dose-dependent manner within 9 weeks of self-administration of steroids.These changes could accelerate coronary artery atherosclerosis over the long term, resulting in an increased risk of coronary heart disease three to six times that of normal. The effects of androgens on lipid profile have been shown to be reversible after the discontinuation of administration.
Alterations in Blood Pressure
Although not shown in all studies, an association between elevated blood pressure and AAS abuse has been reported.Enhanced reactivity of the vasculature to norepinephrine, increased plasma renin activity, stimulation of aldosterone production by testosterone, and sodium retention by the kidneys are suggested mechanisms for high blood pressure following AAS use in athletes. Blood pressure response to androgen use typically shows a dose-response relation.The effects of AAS abuse on blood pressure may persist for long periods; some studies have shown persistent elevations for 5 to 12 months after discontinuing steroids. Clearly, additional studies are necessary to reveal a link between AAS and blood pressure.
Cardiac Arrhythmia
Sudden cardiac arrhythmia resulting from inflammatory process and myocardial fibrosis has been suggested to be the cause of death in athletes using AAS.AAS cause the deepest and most prolonged depression of stimulation threshold in the heart muscles.Long-term use may be responsible for an alteration in the electrophysiology of the myocardium that may predispose to reentry mechanism. It also has been shown that QTc interval and dispersion are increased in individuals who abuse androgens, suggesting the presence of ventricular repolarization abnormalities that could increase the risk of cardiac arrhythmias and sudden cardiac death.Atrial fibrillation secondary to high-dose steroids was reported in two cases of athletes who were using AAS and had no other known cause of atrial fibrillation.
Myocardial Infarction
Sudden cardiac deaths secondary to myocardial infarction and related to AAS use in previously healthy athletes have been reported; however, it must be pointed out that these effects are reported in individual case reports and no large, randomized study has been conducted to verify these results.
Exposure to AAS alters endothelial cell growth with a strong antiproliferative effect, induces apoptosis, and modifies intracellular levels of calcium. These observed endothelial alterations may be considered events that predispose to serious damage at the cell vasculature level.Androgens impair arterial vasomotor response and consequently increase collagen and other fibrous proteins in arterial vascular tissue and they impair flow-mediated, endothelium-dependent vasodilation.This effect may improve after the discontinuation of agents.Moreover, experimental studies have shown that androgens potentiate platelet aggregation in vitro and in vivo.Androgens may exert their effect on platelets through an effect on the prostaglandin system and lead to increasing platelet production of thromboxane A2 (a potent platelet aggregator), decreasing the production of prostacycline (prostaglandin I2, an inhibitor of platelet aggregation) and increasing fibrinogen levels.They also increase human platelet thromboxane A2 receptor density and their aggregation responses.
Get the summary from the
Agency for Healthcare Research and Quality
The above-mentioned physiological changes may predispose individuals to be at higher risk for myocardial infarction. Stergiopoulos et al reported a case of an acute ST segment elevation myocardial infarction immediately following supraphysiologic doses of intramuscular testosterone in a patient with no known risk factors for CAD with associated dramatic polycythemia. They proposed an association and a potential interplay of traditional cardiovascular risk factors, high-dose testosterone use, and possibly elevated plasma viscosity as possible contributors to this cardiovascular event.
It also has been shown that aortic distensibility decreases in athletes who use AAS. This went against previously reported increases in aortic distensibility in athletes in comparison with age-matched sedentary volunteers. Aortic stiffness by increasing ventricular load predisposes to the development of LVH, progressing to left ventricular dysfunction and cardiac failure, and creating an unfavorable oxygen supply/demand ratio. It also causes a reduction in aortic pressure during diastole, which decreases the coronary perfusion pressure and contributes to myocardial ischemia even in the absence of coronary artery atherosclerotic narrowing.These direct and indirect effects of AAS are summarized in Table 3.
Cardiovascular Effects of Androgen Deficiency
Get the summary
Interestingly, if androgen levels are too low, cardiac risk may increase. Androgen-deprivation therapy (ADT) is a widely used treatment for prostate cancer, and several studies have reported an association between ADT and an increased risk of myocardial infarction and cardiovascular mortality. Antiandrogens (eg, flutamide, bicalutamide) block the binding of androgen to its receptor, and they are often coupled with gonadotropin-releasing hormone (GnRH) agonists (eg, leuprolide, goserelin, triptorelin). In one population-based Medicare study, the use of a GnRH agonist in men with prostate cancer for at least 1 to 4 months was associated with an increased risk of incident coronary heart disease (adjusted hazard ratio
1.16, 95% confidence interval [CI] 1.10–1.21), myocardial infarction (adjusted HR 1.11, 95% CI 1.01–1.21), and sudden cardiac death or life-threatening ventricular arrhythmia (adjusted HR 1.16, 95% CI 1.05–1.27).Another population-based study noted that the use of ADT was associated with a 20% higher risk of cardiovascular morbidity (HR 1.20, 95% CI 1.15–1.26) during 5 years of follow-up.
In addition, androgen deficiency has been associated with cardiovascular risk factors by causing increased serum total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides.There is also an association between low androgen levels and an adverse metabolic profile (insulin resistance, metabolic syndrome, and diabetes).
Conclusions
Get the findings from the Agency for Healthcare Research and Quality
Coaches and athletic departments should take the initiative in addressing and educating student athletes about the detrimental effects and risks of abusing AAS. They also should stress the moral cheating aspects of such artificial enhancement. Although the negative effects of long-term use of AAS have not been conclusively proven, caution should be applied because both the direct and indirect effects could lead to accelerated CAD and sudden cardiac death. It appears that too many (androgen abuse) or too few androgens (androgen deficiency) may result in excess cardiovascular morbidity and mortality. More evaluation of individuals exposed to high-dose AAS is needed, including thorough evaluation of cardiac function, in addition to cardiac risk factors that may have been accelerated by the indirect effects of AAS. The practical implications are that long-term and high-dose use of AAS is associated with complications involving the cardiovascular system; AAS have direct and indirect effects on the cardiovascular system that can lead to increased morbidity and mortality of individuals who abuse them; and until more safety and efficacy research on the study of these agents is done, we recommend that individuals refrain from using high-dose AAS to improve performance.
<ARTICLE-TITLE xmlns:dctm="http://www.documentum.com" xmlns:fmt="http://java.sun.com/jstl/fmt" xmlns:jsp="jsp" xmlns:xlink="http://www.w3.org/1999/xlink">Androgen Abuse and Increased Cardiac Risk</ARTICLE-TITLE>
<!--***Template for articlediscussion***-->Abstract and Introduction
Abstract
The objectives of this article were to review the anabolic androgen steroids, specifically the direct and indirect effects on the cardiovascular system of the individuals who use them, and to summarize the evidence regarding the effects of androgens on the cardiovascular system. A search of the English-language scientific literature from 1976 to March 2012 was performed primarily by searching the MEDLINE and Embase databases and Google. Anabolic androgenic steroids are associated with direct effects such as cardiac muscle hypertrophy and myocardial fibrosis and indirect effects, including dyslipidemia, hypertension, arrhythmia, and myocardial infarction. It is likely that chronic exposure to these agents can result in significant alterations in the cardiovascular system, and their safety has not been fully established.
Introduction
The abuse of performance-enhancing drugs among competitive and noncompetitive athletes, including high school and college students, is a major public health issue and of significant concern. Anabolic androgen steroids (AAS) are the most commonly used ergogenic drugs.
AAS are synthetic derivatives of testosterone. The term androgenic indicates masculinization.The term anabolic indicates tissue building and is the component of a steroid that is responsible for thickened vocal cords, enlargement of the larynx, increase in libido, linear growth acceleration before epiphyseal plate closure, and increased muscle bulk and strength through dose-dependent hypertrophy, while decreasing body fat.The physiological effects on muscles and other tissues are summarized in Table 1.
Testosterone, nandrolone, stanozolol, and methandienone are the most frequently abused androgens. Physiological replacement of androgens has been used therapeutically to restore levels in hypogonadal men to increase fat-free mass, muscle size, and bone density.A number of clinical trials also have shown benefits of physiological dose replacement of AAS in wasting syndrome secondary to HIV infection,depression,and age-related sarcopenia. The major goals of androgen therapy are to replace testosterone at levels as close to regular physiological levels as is possible and to avoid the adverse effects.
Athletes usually consume supraphysiologic doses of AAS. Steroids are generally taken in 4- to 12-week cycles. Athletes often "stack" multiple steroids simultaneously and "pyramid" the dosing schedule, beginning with low dosage and increasing amounts during the middle and end of a cycle. Between dosing cycles, it is typical for users to have a period of abstinence, known as a "drug holiday," which usually occurs during the competition phases.This method provides 50 to 100 times the physiologically needed dose of steroids, resulting in levels that are far higher than physiological levels.The increased prevalence of AAS abuse in massive doses among athletes has led to numerous reports linking the adverse effects on multiple body systems, as well as premature mortality. In one study, competitive athletes using AAS had 4.6 times the mortality rate of the population not using AAS.
Abuse of AAS is now common in nonathletes. It is estimated that more than 1 million Americans abuse AAS, including many high school and college athletes.Other studies suggest that approximately 5% of boys and 2% of girls in high school admit to using AAS.
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Research summary examines approaches for screening, diagnosing, and treatment based on a review of 234 clinical studies.
Get the summary from the
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Another area for concern is the abuse of a precursor to AAS known as prohormones, such as androstenediol. Many prohormone synthetic chemicals have been banned, but numerous clones have been made with a minor change in the formulation. These prohormones increase hormone levels within the body leading to many of the same benefits and side effects as the AAS. This article reviews the adverse effects of AAS on the cardiovascular system.
A search of the English-language scientific literature from 1976 through March 2012 was performed primarily by searching the MEDLINE, Embase, and Google databases. The key words used in the search included androgens, anabolic, androgenic, steroids, exercise, athlete, cardiovascular, effects. The bibliographies of articles from the above search also were searched for relevant articles; links on Web sites containing published articles were searched for pertinent information.
AAS have been associated with direct and indirect cardiovascular effects, as described in the following sections.
Direct Cardiovascular Effects
Myocardial Histologic Changes
A 2005 study reported two cases of sudden cardiac death in young male athletes related to AAS abuse. Both cases involved healthy individuals without any history of coronary artery disease (CAD) and no evidence of significant abnormality in arterial microscopic examination. Autopsy of both hearts showed focal myocardial fibrosis suggestive of prior myocardial injury. In a study of a sudden unexpected death in a female fitness athlete using steroids and ephedrine, the only pathological finding was a few small foci of granulation tissue, which was interpreted as evidence of earlier myocardial necrosis.Sudden cardiac arrhythmia resulting from inflammatory process and myocardial fibrosis was suggested to be the cause of death in these cases. Other researchers have reported sudden cardiac deaths related to steroids that also showed myocardial fibrosis in the absence of CAD.
Cardiac Hypertrophy
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Left ventricular hypertrophy (LVH) has been reported in androgen abusers.Several groups have shown that athletes using AAS have reduced end diastolic dimension, a thicker posterior wall and interventricular septum, and a larger left ventricular mass than athletes not using AAS.Cardiac muscle cells have receptors for androgens, and both testosterone and dihydrotestosterone produce a hypertrophic response by acting directly on cardiac muscle cells, increasing amino acid incorporation into protein.The problem is that LVH may persist after discontinuation of AAS.
Reduced Cardiac Function
An echocardiographic study of 47 strength-training individuals (46 male subjects), 28 of whom were regular AAS users, revealed a lower systolic function in AAS users versus nonusers, ejection fractions 58% versus 63%, respectively.In addition, there was evidence of reduced diastolic function by tissue Doppler measurement in the AAS users (ie, their hearts were weaker and stiffer). Another study of 12 long-term AAS users noted that compared with controls, they were noted to have significant systolic cardiac dysfunction as measured by lower left ventricular ejection fraction (50.1% vs 59.1%; P = 0.003), leading the authors to suggest that further work is needed to determine the extent of this problem.An Italian Doppler imaging study also showed reduced systolic function but in a regional distribution.\
Indirect Cardiovascular Effects
Abnormal Plasma Lipoprotein
Many studies have shown that AAS can cause dyslipidemia by increasing low-density lipoprotein as high as 596 mg/dL and decreasing high-density lipoprotein as low as 5 mg/dL.18,26–28 Alterations in high- and low-density lipoprotein levels occur in a dose-dependent manner within 9 weeks of self-administration of steroids.These changes could accelerate coronary artery atherosclerosis over the long term, resulting in an increased risk of coronary heart disease three to six times that of normal. The effects of androgens on lipid profile have been shown to be reversible after the discontinuation of administration.
Alterations in Blood Pressure
Although not shown in all studies, an association between elevated blood pressure and AAS abuse has been reported.Enhanced reactivity of the vasculature to norepinephrine, increased plasma renin activity, stimulation of aldosterone production by testosterone, and sodium retention by the kidneys are suggested mechanisms for high blood pressure following AAS use in athletes. Blood pressure response to androgen use typically shows a dose-response relation.The effects of AAS abuse on blood pressure may persist for long periods; some studies have shown persistent elevations for 5 to 12 months after discontinuing steroids. Clearly, additional studies are necessary to reveal a link between AAS and blood pressure.
Cardiac Arrhythmia
Sudden cardiac arrhythmia resulting from inflammatory process and myocardial fibrosis has been suggested to be the cause of death in athletes using AAS.AAS cause the deepest and most prolonged depression of stimulation threshold in the heart muscles.Long-term use may be responsible for an alteration in the electrophysiology of the myocardium that may predispose to reentry mechanism. It also has been shown that QTc interval and dispersion are increased in individuals who abuse androgens, suggesting the presence of ventricular repolarization abnormalities that could increase the risk of cardiac arrhythmias and sudden cardiac death.Atrial fibrillation secondary to high-dose steroids was reported in two cases of athletes who were using AAS and had no other known cause of atrial fibrillation.
Myocardial Infarction
Sudden cardiac deaths secondary to myocardial infarction and related to AAS use in previously healthy athletes have been reported; however, it must be pointed out that these effects are reported in individual case reports and no large, randomized study has been conducted to verify these results.
Exposure to AAS alters endothelial cell growth with a strong antiproliferative effect, induces apoptosis, and modifies intracellular levels of calcium. These observed endothelial alterations may be considered events that predispose to serious damage at the cell vasculature level.Androgens impair arterial vasomotor response and consequently increase collagen and other fibrous proteins in arterial vascular tissue and they impair flow-mediated, endothelium-dependent vasodilation.This effect may improve after the discontinuation of agents.Moreover, experimental studies have shown that androgens potentiate platelet aggregation in vitro and in vivo.Androgens may exert their effect on platelets through an effect on the prostaglandin system and lead to increasing platelet production of thromboxane A2 (a potent platelet aggregator), decreasing the production of prostacycline (prostaglandin I2, an inhibitor of platelet aggregation) and increasing fibrinogen levels.They also increase human platelet thromboxane A2 receptor density and their aggregation responses.
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The above-mentioned physiological changes may predispose individuals to be at higher risk for myocardial infarction. Stergiopoulos et al reported a case of an acute ST segment elevation myocardial infarction immediately following supraphysiologic doses of intramuscular testosterone in a patient with no known risk factors for CAD with associated dramatic polycythemia. They proposed an association and a potential interplay of traditional cardiovascular risk factors, high-dose testosterone use, and possibly elevated plasma viscosity as possible contributors to this cardiovascular event.
It also has been shown that aortic distensibility decreases in athletes who use AAS. This went against previously reported increases in aortic distensibility in athletes in comparison with age-matched sedentary volunteers. Aortic stiffness by increasing ventricular load predisposes to the development of LVH, progressing to left ventricular dysfunction and cardiac failure, and creating an unfavorable oxygen supply/demand ratio. It also causes a reduction in aortic pressure during diastole, which decreases the coronary perfusion pressure and contributes to myocardial ischemia even in the absence of coronary artery atherosclerotic narrowing.These direct and indirect effects of AAS are summarized in Table 3.
Cardiovascular Effects of Androgen Deficiency
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Interestingly, if androgen levels are too low, cardiac risk may increase. Androgen-deprivation therapy (ADT) is a widely used treatment for prostate cancer, and several studies have reported an association between ADT and an increased risk of myocardial infarction and cardiovascular mortality. Antiandrogens (eg, flutamide, bicalutamide) block the binding of androgen to its receptor, and they are often coupled with gonadotropin-releasing hormone (GnRH) agonists (eg, leuprolide, goserelin, triptorelin). In one population-based Medicare study, the use of a GnRH agonist in men with prostate cancer for at least 1 to 4 months was associated with an increased risk of incident coronary heart disease (adjusted hazard ratio
1.16, 95% confidence interval [CI] 1.10–1.21), myocardial infarction (adjusted HR 1.11, 95% CI 1.01–1.21), and sudden cardiac death or life-threatening ventricular arrhythmia (adjusted HR 1.16, 95% CI 1.05–1.27).Another population-based study noted that the use of ADT was associated with a 20% higher risk of cardiovascular morbidity (HR 1.20, 95% CI 1.15–1.26) during 5 years of follow-up.
In addition, androgen deficiency has been associated with cardiovascular risk factors by causing increased serum total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides.There is also an association between low androgen levels and an adverse metabolic profile (insulin resistance, metabolic syndrome, and diabetes).
Conclusions
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Coaches and athletic departments should take the initiative in addressing and educating student athletes about the detrimental effects and risks of abusing AAS. They also should stress the moral cheating aspects of such artificial enhancement. Although the negative effects of long-term use of AAS have not been conclusively proven, caution should be applied because both the direct and indirect effects could lead to accelerated CAD and sudden cardiac death. It appears that too many (androgen abuse) or too few androgens (androgen deficiency) may result in excess cardiovascular morbidity and mortality. More evaluation of individuals exposed to high-dose AAS is needed, including thorough evaluation of cardiac function, in addition to cardiac risk factors that may have been accelerated by the indirect effects of AAS. The practical implications are that long-term and high-dose use of AAS is associated with complications involving the cardiovascular system; AAS have direct and indirect effects on the cardiovascular system that can lead to increased morbidity and mortality of individuals who abuse them; and until more safety and efficacy research on the study of these agents is done, we recommend that individuals refrain from using high-dose AAS to improve performance.
