Anabolic steroids exert a range of effects on the cardiovascular system. These effects include the development of atherosclerosis, systemic hypertension, impairment of diastolic and systolic ventricular function, and disruptions in lipid metabolism, all of which have been documented in cases of anabolic steroid abuse. Additionally, heightened platelet activity is observed in individuals using these substances, which may contribute to the occurrence of Myocardial Infarctions (MI) and potentially even strokes [3] .

Numerous instances exist of young athletes who have abused androgenic anabolic steroids, experiencing cardiovascular issues such as MI or thrombosis in various vessels, including the renal artery [4].

Another consequence of prolonged androgenic anabolic steroid abuse is left ventricular (LV) dysfunction, which can increase the risk of sudden death in affected individuals [5]. Pathological investigations in these cases have revealed thickening of small arteriole walls and intimal hyperplasia, factors that could be responsible for ischemic damage to the heart muscles and subsequent impairment of ventricular function [6].

Furthermore, the use of anabolic steroids can induce acute hyperhomocysteinemia, leading to associated thrombotic events [7].A increased level of homocysteine could be seen with lower HDL concentration, higher plasma LDL, and triglycerides.

Elevated homocysteine levels are often accompanied by lower high-density lipoprotein (HDL) concentrations, higher levels of Low-Density Lipoprotein (LDL), and triglycerides. Homocysteine is a sulfhydryl amino acid not typically found in natural human diets, and it can be toxic to endothelial cells, promoting the proliferation of smooth muscle in vessel walls and affecting the coagulation process [8, 9]. High levels of homocysteine have been associated with multivessel coronary artery disease and acute MI [10] . Anabolic steroids may interfere with the absorption of vitamins B6 and B12, potentially resulting in elevated homocysteine levels [11] . This effect might explain the elevated homocysteine levels in our patient, possibly contributing to stenosis and thrombosis.

The varied spectrum of steroid profiles and the unclear risk associated with each specific agent, along with variations in dosing, make it challenging to assess the risk for this particular patient population. Additionally, the off-label use of both animal and human compounds, coupled with the lack of regulation regarding concentration doses during production, further complicates the interpretation of the clinical risks [12].

While the administration of folate supplements may be debated, a more favorable approach involves normalizing plasma homocysteine levels through a healthy diet rich in vegetables and fresh fruits, along with moderate exercise [8]. High-dose vitamin B6 and folic acid administration after an acute MI does not reduce the risk of death of the recurrence of cardiovascular disease [13]. In fact, it may potentially harm myocardial repair and increase morbidity and mortality among patients with cardiovascular disease.