Impact of Anabolic Steroids on Cardiovascular Health

Introduction
The misuse of Androgenic Anabolic Steroids (AAS) is associated with various cardiovascular complications in athletes. This includes the emergence of left ventricular hypertrophy, cardiomyopathy, arrhythmias, myocardial infarction, heart failure, hypertension, arterial thrombosis, and pulmonary embolism.

Cardiovascular Consequences of AAS Misuse

AAS misuse disrupts serum levels of various lipoproteins and cholesterol, significantly lowering high-density lipoprotein (HDL) and increasing low-density lipoprotein (LDL) and Lipoprotein A (Lp-A). This imbalance heightens atherogenesis risk, leading to coronary heart disease. A notable elevation in LDL coincides with HDL reduction. Enhanced LDL/Total Cholesterol ratios distort the atheromatic index and amplify the risk of acute myocardial infarction (AMI). LDL levels may rise due to hepatic triglyceride lipase activation and catabolism of very low-density lipoprotein. This process can also deplete HDL levels. Lipoprotein abnormalities can potentially increase coronary artery disease risk by three to six times. Hyperhomocysteinemia, a result of AAS abuse, can damage endothelial cells, disrupt normal endothelial function, and promote atherosclerosis. The impact on serum lipids and homocysteine varies based on AAS type, administration method, drug combination, dosage, and duration of abuse. Post-AAS cessation recovery of serum lipids is more dependent on abuse duration rather than dosage. However, vascular endothelium damage remains irreversible.

AAS are also linked to arrhythmias like atrial and ventricular fibrillation, and tachycardia. This is partly due to electrolyte imbalance, notably hypercalcemia, as AAS in high doses increase electrolyte and mineral absorption. The risk of fatal arrhythmias and sudden death is heightened with AAS use.

Echocardiographic studies reveal that high doses of AAS induce morphological and functional heart changes, leading to myocardial hypertrophy, potential enlargement of heart chamber diameters, and likely compromised left ventricular contractile function. These changes can result in left ventricular hypertrophy, cardiomegaly, and elevated risks of chronic heart failure, hypertension, and arrhythmias. These adverse effects become evident with prolonged AAS misuse. Studies also show that former AAS-using strength athletes may exhibit a slight concentric left ventricular hypertrophy and reduced diastolic function compared to non-using athletes.

Androgens in AAS may elevate blood pressure by stimulating aldosterone production in the kidneys. The extent of this increase correlates with the duration of abuse. Certain AAS, like Flyoxymesterone and trenbolone, known for suppressing cortisol, also influence blood pressure without causing water retention.

AAS affect blood composition, leading to erythrocytosis and potentially polycythemia, a risk factor for cardiovascular disease due to increased blood viscosity. AAS also affect platelet aggregation and coagulation cascade, contributing to a hypercoagulable state. These effects, combined with dehydration and physical stress, increase the risk of cardiovascular events.

Contrarily, AAS can prolong bleeding time, disrupt hemostasis, and heighten fibrinolysis, paradoxically coexisting with clot formation tendencies due to elevated hematocrit and fibrinogen levels.

Cardiovascular Risk Prevention Strategies

  • A 30-minute low-intensity aerobic activity at 60% maximum heart rate helps improve myocardial shape and size, resembling an endurance athlete's heart. It also helps manage body mass index, a crucial factor for those overweight, even with low fat percentage, as their heart requires more oxygen.
  • Sustained aerobic exercise can increase HDL, improving the atheromatic index and reducing cardiovascular disease risk.
  • Low-intensity aerobic activities can establish collateral circulation around the myocardium, enhancing oxygen supply and potentially aiding survival during myocardial infarction.

Cardiac adaptation varies with training type and sport, with significant changes like heart rate reduction and left ventricle mass increase observed in endurance athletes. Conversely, weightlifting combined with Performance Enhancing Drugs leads to distinct hemodynamic heart changes.

Steroid users who smoke , avoid aerobic activity, and consume unhealthy fats risk developing poor physical condition, inadequate collateral circulation, high blood pressure, and coronary heart disease.

To prevent cardiovascular disease, AAS abusers should engage in moderate aerobic activities, avoid unhealthy fats, and consume a diet rich in lean proteins, vegetables, fruits, and fiber. Regular monitoring of blood pressure, heart rate, and annual medical examinations are crucial. Regular assessments of hematocrit, hemoglobin, platelets, lipids, and glucose levels are essential for managing risks of metabolic syndrome, dyslipidemia, polycythemia, and type 2 diabetes. Optimal control of LDL-C levels and blood pressure is vital for all AAS abusers.