Anabolic androgenic steroid–induced acute myocardial infarction with multiorgan failure

Flo, Frederick J.; Kanu, Obiajulu; Teleb, Mohamed; Chen, Yuefeng; Siddiqui, Tariq

doi:10.1080/08998280.2018.1460130

Cited by 10 publications

(12 citation statements)

References 20 publications

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“…AAS may also stimulate erythropoiesis which results in polycythemia which in turn increases blood viscosity leading to thrombosis [6]. Direct toxicity of AAS can also result in fibrosis and intimal hyperplasia of the intramural coronary arteries [11].…”

Section: Discussionmentioning

confidence: 99%

“…Experimental studies showed that AAS can cause a decreased response to vasodilators due to inhibition of endothelial guanylate cyclase which leads to the reduction of nitric oxide-mediated relaxation [12]. Chronic AAS (Nandrolone) therapy was also found to cause decreased thoracic aorta relaxation due to decreased concentrations of arterial endothelial cyclic guanosine monophosphate [11].…”

Section: Discussionmentioning

confidence: 99%

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A Rare Case Report and Literature Review of Anabolic-Androgenic Steroids (AAS)-Induced Acute Myocardial Infarction

Zhang¹,

Shan²,

Raza³

et al. 2020

Cureus

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Anabolic-androgenic steroids (AAS) abuse is common in competitive athletes in order to enhance athletic performances. However, AAS abuse is often associated with deleterious side effects including but not limited to cardiovascular diseases, depression, hormonal abnormalities, and cancer. We present a case of a 31-year-old male with a history of Crohn's disease on infliximab and chronic AAS use who had persistent retrosternal chest pain found to have an acute myocardial infarction (MI) without obvious cardiovascular risk factors.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A Rare Case Report and Literature Review of Anabolic-Androgenic Steroids (AAS)-Induced Acute Myocardial Infarction

Zhang¹,

Shan²,

Raza³

et al. 2020

Cureus

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“…Some reports suggest that DHT induces cardiac hypertrophy in cultured rat cardiomyocytes (186,187) and in a rat model (188). On the other hand, treatment with finasteride, which inhibits the transformation of testosterone to DHT, reduces both cardiac hypertrophy and remodeling (187,189).…”

Section: Testosterone Metabolites In Agingmentioning

confidence: 99%

Androgen-Regulated Cardiac Metabolism in Aging Men

2020

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The prevalence of cardiovascular mortality is higher in men than in age-matched premenopausal women. Gender differences are linked to circulating sex-related steroid hormone levels and their cardio-specific actions, which are critical factors involved in the prevalence and features of age-associated cardiovascular disease. In women, estrogens have been described as cardioprotective agents, while in men, testosterone is the main sex steroid hormone. The effects of testosterone as a metabolic regulator and cardioprotective agent in aging men are poorly understood. With advancing age, testosterone levels gradually decrease in men, an effect associated with increasing fat mass, decrease in lean body mass, dyslipidemia, insulin resistance and adjustment in energy substrate metabolism. Aging is associated with a decline in metabolism, characterized by modifications in cardiac function, excitation-contraction coupling, and lower efficacy to generate energy. Testosterone deficiency-as found in elderly men-rapidly becomes an epidemic condition, associated with prominent cardiometabolic disorders. Therefore, it is highly probable that senior men showing low testosterone levels will display symptoms of androgen deficiency, presenting an unfavorable metabolic profile and increased cardiovascular risk. Moreover, recent reports establish that testosterone replacement improves cardiomyocyte bioenergetics, increases glucose metabolism and reduces insulin resistance in elderly men. Thus, testosterone-related metabolic signaling and gene expression may constitute relevant therapeutic target for preventing, or treating, age-and gender-related cardiometabolic diseases in men. Here, we will discuss the impact of current evidence showing how cardiac metabolism is regulated by androgen levels in aging men.

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“…The negative effects on the cardiovascular function have classically been divided into four categories: thrombotic, atherogenic, vasospastic, and cardiomyocyte direct toxicity [ 18 ]. AAS-induced cardiovascular events are mostly present in a young and healthy population, with no associated risk factors or proven atherosclerotic lesions [ 19 , 20 , 21 , 22 , 23 , 24 ]. This suggests that the pathophysiological mechanism might be atherothrombotic rather than atherogenic, or vasospastic.…”

Section: Introductionmentioning

confidence: 99%

“…This suggests that the pathophysiological mechanism might be atherothrombotic rather than atherogenic, or vasospastic. This conclusion seems more logical in the attempt to explain the basis for the severe adverse effects of androgens misuse [ 22 , 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Exogenous Androgens on Platelet Activity and Their Thrombogenic Potential in Supraphysiological Administration: A Literature Review

Roşca

Vlădăreanu

Mititelu

et al. 2021

JCM

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Anabolic androgenic steroids (AAS), simply called “androgens”, represent the most widespread drugs used to enhance performance and appearance in a sporting environment. High-dosage and/or long-term AAS administration has been associated frequently with significant alterations in the cardiovascular system, some of these with severe endpoints. The induction of a prothrombotic state is probably the most life-threatening consequence, suggested by numerous case reports in AAS-abusing athletes, and by a considerable number of human and animal studies assessing the influence of exogenous androgens on hemostasis. Despite over fifty years of research, data regarding the thrombogenic potential of exogenous androgens are still scarce. The main reason is the limited possibility of conducting human prospective studies. However, human observational studies conducted in athletes or patients, in vitro human studies, and animal experiments have pointed out that androgens in supraphysiological doses induce enhanced platelet activity and thrombopoiesis, leading to increased platelet aggregation. If this tendency overlaps previously existing coagulation and/or fibrinolysis dysfunctions, it may lead to a thrombotic diathesis, which could explain the multitude of thromboembolic events reported in the AAS-abusing population. The influence of androgen excess on the platelet activity and fluid–coagulant balance remains a subject of debate, urging for supplementary studies in order to clarify the effects on hemostasis, and to provide new compelling evidence for their claimed thrombogenic potential.

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Anabolic androgenic steroid–induced acute myocardial infarction with multiorgan failure

Cited by 10 publications

References 20 publications

A Rare Case Report and Literature Review of Anabolic-Androgenic Steroids (AAS)-Induced Acute Myocardial Infarction

A Rare Case Report and Literature Review of Anabolic-Androgenic Steroids (AAS)-Induced Acute Myocardial Infarction

Androgen-Regulated Cardiac Metabolism in Aging Men

Effects of Exogenous Androgens on Platelet Activity and Their Thrombogenic Potential in Supraphysiological Administration: A Literature Review

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