The discussion around cardiac health in sports is intensifying due to a rising incidence of unexpected sudden deaths in certain athlete populations.
Heart disease is a leading cause of sudden death in both the general population and athletes.
Given that athletes consistently engage in strenuous physical activity, it is generally assumed their cardiac health is in optimal condition.
While this may be true, the use of performance-enhancing drugs (PEDs) can skew health outcomes.
The types of PEDs vary significantly by sport and include anabolic-androgenic steroids (AAS), peptide hormones, stimulants, erythropoietin (EPO), and other drugs.
A significant number of unexpected deaths over the past decade have occurred in sports where AAS use is prominent.
Notably, these sports are characterized by the high-dose abuse of multiple agents.
This article aims to evaluate AAS use in athletes within the context of cardiac health and confounding variables.
Sudden Cardiac Death and Differential Diagnosis
In the general population, the primary cause of sudden cardiac death is a fatal arrhythmia resulting from coronary artery disease (CAD).
Similarly, older athletes with risk factors for CAD are at an increased risk of suffering from ischemic heart disease, which can trigger a fatal arrhythmia.
Younger athletes are also exposed to the risk of fatal arrhythmias if they have congenital risk factors.
Unlike older athletes where acquired CAD is prominent, younger athletes rarely experience the same condition, with the exception of coronary artery spasm and vasculitis.
The most common terminal cause of a fatal cardiac event is ventricular fibrillation or pulseless electrical activity.
While CAD is the main pathological driver of fatal arrhythmias, a wide range of causes must be considered.
Acute Causes
-Acute Myocardial Infarction
-Hypokalemia/Hyperkalemia
-Hypothermia
-Acidosis
-Hypoglycemia
-Hypoxia
-Hypovolemia
-Drug Overdose
-Unstable Tachycardia
-Cardiac Tamponade
-Trauma
-Aortic Rupture
Acquired Structural Heart Diseases
-Coronary Artery Disease/Atherosclerosis
-Left Ventricular Hypertrophy (LVH)
-Mitral Valve Prolapse (MVP)
-Dilated Cardiomyopathy
-Myocarditis
Congenital Structural Heart Diseases
-Hypertrophic Obstructive Cardiomyopathy (HOCM)
-Coronary Artery Anomalies
-Left Ventricular Non-compaction
-Dilated Cardiomyopathy
-Arrhythmogenic Right Ventricular Dysplasia
-Congenital Aortic Stenosis
Congenital Electrophysiological Disorders
-Long QT Syndrome
-Short QT Syndrome
-Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)
-Wolff-Parkinson-White Syndrome
-Brugada Syndrome
-Idiopathic Ventricular Tachycardia
-Mixed Sodium Channelopathy
-Atrioventricular Block
Various acute events, structural issues, and electrophysiological defects can trigger unstable and potentially fatal arrhythmias.
Understanding the multiple etiologies of sudden cardiac death is crucial for clinically contextualizing cardiac arrest due to PEDs.
The listed clinical conditions highlight the potential causes of sudden cardiac death in athletes.
While certain acute causes (e.g., trauma, aortic rupture) may be incidental, other causes are self-induced.
Electrolyte changes (e.g., hypokalemia) can result from diuretic abuse, while hypoglycemia can be caused by improper insulin use.
Stimulant overdose can induce unstable tachycardia.
While this article will detail acquired conditions, all other listed conditions can increase the risk of cardiac disease over a long athletic career.
This can occur independent of PED use, and the risk may be greater when abusing PEDs in the presence of a pre-existing (or undiagnosed) cardiac condition.
Performance-Enhancing Drugs and Cardiac Arrest
For PED users, there are several long-term mechanisms that can elevate the risk of sudden cardiac death.
These cardiac mechanisms can be classified as direct structural changes, indirect structural changes, arrhythmogenicity, and atherosclerotic disease.
The use of AAS is primarily associated with these potential changes, but there are often underestimated confounding variables.
These include peptide hormones, stimulants, and diuretics.
While peptide hormones (e.g., human growth hormone) can play a significant role in cardiac structural changes, it is important to note that the use of stimulants and diuretics can be confounding variables that contribute to cardiac pathology, as mentioned earlier.
The use of AAS has been extensively linked in the literature to left ventricular hypertrophy.
These hormones bind to myocardial androgen receptors in the heart, inducing sustained growth.
Certain agents, such as testosterone, induce less significant growth.
Other agents, like trenbolone, cause severe LVH in the long term.
While a significant portion of left ventricular growth can also be attributed to intensive exercise, the mechanism differs from AAS-induced left ventricular growth.
The concurrent use of certain peptide hormones, which is relatively common, is another major contributor to left ventricular growth.
Unfortunately, most evidence suggests these changes are irreversible with long-term abuse.
A state of pathological left ventricular hypertrophy typically means that the hypertrophied myocardial cells are not accompanied by a proportional increase in capillaries.
The result is a mismatch between oxygen and nutrient supply relative to demand.
Furthermore, myocardial cell death can occur, along with changes in intracellular calcium.
The clinical consequence of increased oxygen and metabolic demand, combined with other micro-level changes, can lead to a reduced compensatory capacity and heart failure.
Indirect Structural Changes
Elevated blood pressure is the most common cause of LVH in the general population and is a major preceding clinical factor leading to heart failure.
Anabolic steroids exhibit hypertensive effects that vary depending on the specific agent.
Oral steroids that cause extensive water retention are typically more hypertensive than agents that cause minimal water retention.
Certain steroids have vasoconstrictive effects and can suppress natriuretic peptides, which can induce hypertension.
These effects are amplified by the long-term use of stimulants/pre-workout supplements, which directly raise blood pressure.
Similarly, thyroid medications and clenbuterol, used for fat loss, also significantly contribute to a state of sustained hypertension.
In summary, these hypertensive effects contribute to the chronic and often irreversible LVH seen in many AAS users.
Arrhythmias
While a fatal arrhythmia is the final step before cardiac arrest, there is no clear evidence that AAS are directly arrhythmogenic.
Studies suggest that electrophysiological variables such as QTc, JTc, and Tp-e/QTc may be prolonged, but it is difficult to definitively link this to an increased risk of ventricular tachycardia.
However, it is noteworthy that testosterone replacement therapy is associated with a reduced incidence of atrial fibrillation.
The primary arrhythmogenic triggers in athletes are stimulants and diuretics.
For athletes with structural heart damage, arrhythmias can occur when cardiac demand increases or conditions are suboptimal.
Stimulants increase heart rate and contractility, raising myocardial oxygen demand, which can trigger ectopic and irregular beats.
Diuretics cause electrolyte shifts, and hypokalemia, hypomagnesemia, and hypocalcemia increase the risk of arrhythmias.
Atherosclerosis
The leading cause of sudden cardiac death is atherosclerotic coronary artery disease.
This disease develops from a chronically unmanaged lipid profile and risk factors.
AAS are associated with lowered HDL, elevated LDL, and overall changes in cholesterol.
AAS break down lipoproteins and alter apolipoprotein synthesis, increasing the risk of arterial plaque formation and ischemic heart disease.
Lifestyle factors, such as smoking, also cannot be ignored.
Furthermore, aromatase inhibitors, often used alongside AAS, can reduce estradiol, which can worsen the lipid profile.
AAS cause erythrocytosis, which increases blood viscosity, and also increases platelet aggregation, raising the risk of ischemic heart disease.
In particular, focal segmental glomerulosclerosis and kidney problems caused by trenbolone also impact the heart.
Solutions and Preventive Measures
The best treatment for heart disease is prevention.
Since AAS-related cardiac pathologies overlap, comprehensive management is essential.
A medical history and cardiovascular assessment are necessary, and a history of syncope, chest pain, or shortness of breath should be investigated.
Lipid profiles, CBC, chemistry panels, and kidney function should be monitored, with testing recommended every two years.
If low HDL or elevated LDL is present, statin therapy should be considered.
Statins improve the lipid profile worsened by reduced estradiol, but Coenzyme Q10 supplementation may be necessary.
PCSK9 inhibitors may not offer significant benefits to AAS users, whose lipid issues primarily affect HDL.
Omega-3s and high-dose garlic are effective for improving lipids.
For treating AAS-induced hypertension, discontinuing the offending agent is the priority.
Through consultation, the use of oral steroids or hypertensive injectable agents should be ceased.
Stimulants containing caffeine should be discontinued, and caffeine intake should be minimized.
If medication is required, ACE inhibitors or ARBs can be useful, with beta-blockers and calcium channel blockers being options depending on ethnicity.
Beta-blockers can improve coronary perfusion and lower arrhythmia risk in patients with left ventricular hypertrophy.
Garlic has benefits for both lipid improvement and blood pressure reduction.
An echocardiogram is used to diagnose left ventricular hypertrophy, and a wall thickness of 15mm or more is diagnosed as pathological LVH.
Physiological LVH is assessed at 11-13mm, and the “gray area” requires further evaluation.
If pathological LVH is diagnosed, treatment with ACE/ARB medications and beta-blockers should be considered.
