Cardiovascular Health and Impacts of Anabolic Steroid Use

The increasing instances of sudden, unforeseen deaths among specific groups of athletes have intensified discussions about cardiovascular health in the sports world. Heart disease is the foremost cause of sudden fatalities in both the general populace and among athletes. Athletes, known for their intense physical training, are generally presumed to be in prime heart health. However, this notion is often challenged by the use of substances aimed at enhancing performance, which can adversely affect their health outcomes. Athletes choose such substances based on their particular sport, including anabolic androgenic steroids, peptide hormones, stimulants, erythropoietin, and various other compounds. A notable number of sudden deaths in the past years have been among athletes in disciplines where high usage of anabolic steroids is prevalent. Additionally, the misuse of these substances, involving extremely high dosages, has been observed. This article aims to explore the impact of anabolic steroids on athletes' cardiac health and other relevant factors.

Sudden Heart Failure and Its Differential Diagnoses

The primary reason for sudden heart failure in the general populace is a deadly arrhythmia caused by coronary artery disease (CAD). Older athletes with CAD risk factors also have a heightened risk of ischemic heart events leading to fatal arrhythmias. Young athletes, although less commonly, are at risk if they have congenital heart conditions. Unlike older athletes where CAD is more common, younger ones are more likely to experience coronary vasospasm and vasculitis. It's essential to note that ventricular fibrillation or pulseless electrical activity is often the ultimate cause of cardiac fatalities. While CAD is a frequent pathological cause of fatal arrhythmias, a wide spectrum of causes should be considered.

Immediate Causes

  • Acute myocardial infarction
  • Low/high potassium levels
  • Hypothermia
  • Acidosis
  • Low blood sugar
  • Lack of oxygen
  • Low blood volume
  • Excessive intake of certain drugs
  • Rapid, irregular heartbeats
  • Compression of the heart
  • Physical injury
  • Rupture of the aorta

Developed Heart Conditions

  • Coronary artery disease/atherosclerosis
  • Enlargement of the left heart chamber
  • Mitral valve issues
  • Enlarged heart (cardiomyopathy)
  • Inflammation of the heart muscle

Inborn Heart Conditions

  • Thickened heart muscle (HOCM)
  • Coronary artery abnormalities
  • Abnormal left ventricular muscle
  • Enlarged heart (cardiomyopathy)
  • Right ventricular dysplasia
  • Congenital narrowing of the aortic valve

Congenital Electrical Issues in the Heart

  • Prolonged QT syndrome
  • Short QT syndrome
  • Catecholaminergic polymorphic ventricular tachycardia
  • Wolff-Parkinson-White syndrome
  • Brugada syndrome
  • Unexplained ventricular tachycardia
  • Mixed sodium channel disorder
  • Atrioventricular blockages

These varied acute incidents, structural defects, and electrical malfunctions can lead to unstable and life-threatening arrhythmias. It's crucial to understand these causes when considering cardiac arrest induced by performance-enhancing drugs. The highlighted clinical conditions show potential causes of sudden heart failure in athletes. While some acute causes like trauma or aortic rupture are incidental, others are often self-induced. For instance, low potassium levels might result from the misuse of diuretics, while low blood sugar can be a consequence of improper insulin use. Similarly, overdosing on stimulants can cause irregular heartbe ats.

This article will delve deeper into other acquired conditions. It's vital to recognize that all listed conditions can increase the risk of heart events throughout an athlete’s career, independently of any performance-enhancing drug use. Thus, the misuse of these drugs further escalates the risk in the presence of pre-existing, and possibly undiagnosed, cardiac diseases.

Influence of Performance Enhancing Substances on Cardiac Arrest

Various long-term cardiac risks are associated with the use of performance-enhancing drugs. These risks can be categorized into direct and indirect structural changes, arrhythmia risks, and the development of atherosclerotic disease. Anabolic androgenic steroids are particularly linked to these changes, though other factors often go unrecognized, such as the use of peptide hormones, stimulants, and diuretics. Notably, while hormones like human growth hormone significantly impact cardiac structure, the role of stimulants and diuretics in triggering cardiac events should not be underestimated.

Direct Heart Structure Alterations

Extensive research has linked anabolic steroid use to changes in the left side of the heart. These hormones, when they bind to heart muscle receptors, stimulate continuous growth. Different substances result in varying levels of growth, with some, like Trenbolone, causing substantial long-term enlargement. While vigorous exercise also contributes to this growth, the process is distinct from the enlargement caused by steroids. Co-use of certain peptide hormones often accompanies and exacerbates this growth. Regrettably, most evidence points to the irreversibility of these changes following prolonged abuse.

A pathological state of heart enlargement often leads to a mismatch in oxygen and nutrient delivery relative to demand. This can result in cell death and shifts in cell calcium levels, culminating in heart failure due to increased metabolic demands and other microscopic alterations.

Indirect Structural Modifications

High blood pressure is a common precursor to heart enlargement and subsequent failure. Anabolic steroids, depending on their type, can cause blood pressure elevation, with orally ingested ones that promote water retention being particularly impactful. Long-term use of stimulants that directly increase blood pressure, as well as fat-loss substances like thyroid drugs, contribute significantly to chronic heart enlargement, often irreversible in many steroid users.

Arrhythmia Risks

While fatal arrhythmias are the ultimate outcome leading to cardiac arrest, evidence directly linking anabolic steroids to arrhythmia risks is limited. Some studies have indicated prolonged electrophysiologic variables, but the direct correlation to increased arrhythmia risk remains unclear. However, testosterone replacement therapy at normalizing doses has been linked to a lower incidence of atrial fibrillation. Athletes are more prone to arrhythmias due to stimulant use and diuretics, which can lead to electrolyte imbalances and exacerbate arrhythmic conditions, especially under severe structural heart impairments.

Development of Atherosclerosis

Atherosclerotic coronary artery disease is a leading factor in sudden cardiac death. This condition evolves over years due to unmanaged lipid levels and other risk factors. Steroids are known to significantly lower beneficial cholesterol (HDL) while moderately increasing harmful cholesterol (LDL), thus affecting overall cholesterol balance. This leads to plaque build-up in arteries, increasing the risk of ischemic heart events. Other lifestyle habits, like smoking, significantly contribute to this process. Furthermore, the use of drugs that lower estrogen levels in conjunction with steroids can exacerbate lipid profile disturbances, often severely.

Additional factors tied to steroids, like increased red blood cell counts and kidney conditions, can further elevate the risk of cardiac events. For instance, the growing incidence of specific kidney diseases in steroid users can have dire implications for heart health.

Preventative Strategies and Management

Prevention remains the best approach against cardiac diseases, as they can sometimes present suddenly and fatally. Considering the various pathways through which steroids induce cardiac issues, management needs to be holistic, addressing overlapping pathological processes. Thorough medical histories and physical exams focusing on cardiovascular assessment are crucial, alongside tests for symptoms like fainting, chest pain, or exercise intolerance.

For cardiac health monitoring, regular checks of lipid levels, complete blood counts, chemistry panels, and kidney function are advisable, with bi-annual testing being a potential norm. Distorted lipid profiles are common in steroid users, necessitating early intervention, possibly including statin therapy.

While there may be hesitation in prescribing statins to younger patients, their continued steroid use elevates their atherosclerosis risk. Statins not only improve lipid profiles but also have beneficial effects on the arteries themselves. However, they can deplete coenzyme Q10, making supplementation a viable option. Omega-3s and high-dose garlic have also shown some efficacy in improving lipid profiles and reducing blood viscosity. The use of other supplements, like niacin, remains a topic of debate.

Managing Steroid-Induced High Blood Pressure

Addressing steroid-induced high blood pressure involves stopping the offending drugs, with specific attention to those causing excessive water retention or having strong hypertensive properties. Beyond drug cessation, initiating medications to manage blood pressure is often necessary, following standard guidelines but with careful consideration of the individual's medical history. ACE inhibitors or ARB medications are beneficial not only for blood pressure control but also for preventing or reducing heart enlargement. Beta blockers might be another option, especially for those with existing heart enlargement, as they improve heart blood flow and reduce arrhythmia risks. Lifestyle modifications, including diet and exercise, are also vital components of the management plan.

Diagnosing and Managing Heart Enlargement

Diagnosing and managing heart enlargement poses challenges, given its prevalence due to intense physical training in athletes. The primary screening tool is an electrocardiogram (ECG), but its broad use is debated due to the risk of false positives. The Seattle criteria provide a methodology for minimizing false positives in athletes. For diagnosing heart enlargement, criteria like the Cornell or Sokolow-Lyon voltage criteria or the Romhilt-Estes point system are used. Echocardiograms are the most reliable method for diagnosis but should be reserved for those with significant risk factors or symptoms. Once diagnosed, discontinuing the causative agents and managing blood pressure are critical, with medications like ACE inhibitors or beta blockers being potential treatments.

Conclusion

In summary, the challenge of preventing and treating heart-related conditions in athletes, especially considering the use of performance-enhancing drugs, is multifaceted. Identifying and treating congenital issues, preventing drug-induced cardiac diseases, and fostering a strong physician-patient relationship are key to achieving optimal health outcomes for athletes.