The abuse of androgenic anabolic steroids (AAS) can cause a variety of cardiovascular side effects in athletes, including left ventricular hypertrophy, cardiomyopathy, arrhythmias, myocardial infarction, heart failure, hypertension, arterial thrombosis, and pulmonary embolism [1-4].
Effects of Anabolic Steroid (AAS) Abuse
AASs disrupt serum levels of high-density lipoprotein (HDL), low-density lipoprotein (LDL), lipoprotein A (Lp-A), total cholesterol (TC), triglycerides, and homocysteine.
Significant decreases in HDL and elevations in LDL and Lp-A increase the risk of atherogenesis (plaque formation), leading to atherosclerosis and coronary heart disease.
Elevated LDL is similar to a decrease in HDL levels.
A decrease in HDL leads to an increase in LDL/TC, resulting in an atheroma index distortion (> 5) and an increased risk of acute myocardial infarction (AMI).
Studies have shown that serum LDL levels can increase through induction of the hepatic triglyceride lipase enzyme and catabolism of very low density lipoproteins.
Induction of hepatic triglyceride lipase can also catabolize HDL, reducing its serum levels.
By some estimates, these lipoprotein abnormalities increase the risk of coronary artery disease by a factor of 3 to 6. [4].
Hyperhomocysteinemia causes endothelial damage and endothelial dysfunction and increases platelet aggregation at sites of microvascular injury, leading to atherosclerosis.
Adverse effects on serum lipids and homocysteine depend on the type of AAS used, route of administration, drug combination, dose, and time of abuse.
However, studies have shown that the recovery of serum lipids after AAS use is highly dependent on the duration of AAS abuse rather than the dose.
It is important to note that although homocysteine levels decrease upon discontinuation of AAS, the damage to the vascular endothelium is irreversible. [1-4,8]
Steroids are also associated with arrhythmias (atrial fibrillation, ventricular fibrillation, tachycardia).
One of the reasons for this is electrolyte imbalance and hypercalcemia, as it is well known that they increase the absorption of electrolytes and minerals (sodium, calcium, phosphorus, magnesium), especially at doses that exceed physiologic doses.[1-3][4
In addition, the use of anabolic steroids (AAS) appears to increase the risk of sudden death from life-threatening arrhythmias. [1]
Echocardiographic studies have shown that supraphysiologic doses of AAS result in morphologic and functional changes in the heart.
These changes include a tendency to cause myocardial hypertrophy, a possible increase in ventricular diameter, and clinically impaired left ventricular contractile function.
These changes lead to left ventricular hypertrophy (LVH), cardiomegaly, and increase the risk of chronic heart failure, hypertension, and arrhythmias.
It is important to note that long-term AAS abuse can adversely affect cardiac structure and function. [1].
Additionally, studies have shown that compared to non-steroidal strength athletes, strength athletes who use AAS have mild concentric left ventricular hypertrophy and show signs of decreased diastolic function several years after stopping AAS abuse.
Anabolic steroid (AAS) abuse, especially androgens, can increase blood pressure (BP) because they stimulate the production of the hormone aldosterone in the kidneys. [1,4,7]
The amount of increase is related to the duration of abuse.
Some AAS are also aromatizing, meaning they are converted to estrogen by the aromatase enzyme.
Estrogenic activity is associated with water retention and edema.
Therefore, bodybuilders who abuse aromatizing steroids in the off-season are more likely to develop high blood pressure.
However, few non-aromatizing AAS can increase blood pressure.
Plyoxymesterone and trenbolone are two of them.
Both inhibit the catabolic glucocorticosteroid cortisol (this is the reason for their high anabolic effect).
But they also suppress the mineralocorticosteroid aldosterone.
This is why they have zero water retention.
Nevertheless, other mechanisms related to the inhibition of the enzyme 11-hydroxylase will eventually lead to an increase in blood pressure.
The kidneys have this particular enzyme to protect them from cortisol-induced increases in blood pressure.
This enzyme converts cortisol into inactive cortisone (the synthetic form), due to the fact that the receptors for aldosterone sometimes bind to cortisol and that's where the problem starts.
When inhibition of 11-hydroxylase occurs, the overproduction of 11-beta-deoxycorticosterone by the adrenal cortex may be responsible for the increase in blood pressure. [7]
Anabolic steroids (AAS) affect hematopoiesis, causing erythrocytosis and eventually polycythemia.
Polycythemia vera can be a risk factor for cardiovascular disease because of the rapid increase in blood viscosity.
AAS also affect platelet aggregation due to increased production of thromboxane A2 and decreased production of prostacyclin.
In addition, changes in the coagulation cascade can occur, including an increase in thrombin activity, which also contributes to a hypercoagulable state.
These adverse effects are exacerbated by dehydration and catecholaminergic stress, which often occurs in association with strenuous physical activity.
Hypercoagulable state increases the risk of cardiovascular disease (myocardial infarction, thrombotic stroke, cerebrovascular hemorrhage).
AAS prolong bleeding time and impede hemostasis, while INR, APTT increase and intensify fibrinolysis. This mechanism contradicts their platelet aggregation effect.
In conclusion, AAS (anabolic steroids) break down the coagulation process, but on the other hand, they induce thrombus formation through elevated hematocrit and elevated fibrinogen.
Preventing cardiovascular disease risk
Because anabolic steroid (AAS) users have higher rates of cardiovascular disease morbidity and mortality compared to non-users, cardiovascular physical activity is important for the following reasons
1) Bodybuilders and weightlifters should perform 30 seconds of slow-paced aerobic exercise at 60% of their maximal oxygen uptake.
This kind of exercise will eventually improve the shape and size of your myocardium, and as long as you stop taking AAS, or at least take them moderately and wisely, your LVF will decrease and your ventricles will change into the model of an endurance athlete's heart.
BMI is also a factor to consider, as an overweight person, even with a low body fat percentage, has a higher oxygen demand on the myocardium.
Therefore, the heart has to perform harder, and this puts it at risk of ischemic episodes.
2) Long-term aerobic exercise increases HDL, which can improve the atherogenic index (HDL/LDL) and reduce the risk of atherothrombotic cardiovascular disease (CVD).
3) Low-speed aerobic activity establishes the so-called "collateral circulation".
This fact translates practically into a vast network of blood vessels that surround the myocardium and supply oxygen to the heart muscle.
It is through this kind of blood vessels that someone can survive a heart attack ischemic episode (AMI). [8,9]
Many studies have shown that cardiac regulation depends on the type of training (dynamic or static) and the type of sport.
It has been shown that at least 3 hours of exercise per week is required to observe adaptive changes such as decreased heart rate and increased left ventricular (LV) mass.
Marathon and triathlon athletes have a "drop heart" shape with enlarged ventricles and thin ventricular walls.
This helps to provide a functionally greater ejection fraction (EF) and stroke volume (the ability of the heart muscle to pump blood and the amount of blood in each pulse) hemodynamically.
On the other hand, exercise that combines weight resistance training with chemical enhancement through performance-enhancing drugs (PEDs) results in specific hemodynamic changes in the heart.
Specifically, heart rate increases, stroke volume, and ejection fraction (EF) decreases.
The left ventricle adapts to these hemodynamic changes, with a smaller ventricular cavity and thickening of the ventricular wall.[8,9][10
Steroid users who smoke cigarettes, avoid cardiovascular aerobic physical activity, and consume saturated trans fats are more likely to develop coronary heart disease due to inadequate collateral circulation, poor physical condition with hypertension, and atherosclerosis.
Their maximal oxygen uptake and aerobic respiratory capacity are significantly reduced.
Because atherosclerotic CVD is usually the result of a combination of risk factors, all current guidelines on CVD prevention in clinical practice recommend assessing total CVD risk.
The higher the risk, the more intensive measures should be taken.
Therefore, AAS abusers are in a high-risk group and should follow certain rules for longevity and medical prevention. [9]
1.Engage in moderate aerobic physical activity at a rate of 60% of your maximal oxygen uptake (MHR) for 30 minutes daily.
2.Avoid excess saturated and trans fats/refined carbohydrates and sugars
3.Eat a diet rich in white lean meat, fish, egg whites, vegetables, fruits, nuts, oats, and fiber to prevent oxidation of LDL and elevation of triglycerides and total cholesterol, lower insulin resistance, and contribute to blood sugar-lowering effects.
4.Anticoagulants (EPA, DHA, salicylic acid) are preferably used with breakfast, not after exercise, as AAS abuse leads to elevated hemoglobin (Htc) and increased blood viscosity.
5.Regular use of niacin (B3), coenzyme Q10 and magnesium, which have the ability to improve HDL/LDL ratio and increase aerobic energy production in the myocardium using phytosterol % red yeast, and L-carnitine, which has mild antiarrhythmic and energy-enhancing properties.
6.Monitor blood pressure and heart rate weekly and have a stress test, electrocardiogram, and Holter 24-hour test once a year.
Elevated blood pressure is one of the strongest and most modifiable risk factors for CVD.
The beneficial effects of blood pressure-lowering therapy in reducing stroke, myocardial infarction, heart failure, and death have been demonstrated in numerous meta-analyses.
7.Routine assessment of hematocrit, hemoglobin, platelets, HDL, LDL, total cholesterol, triglycerides, and fasting blood glucose. These assessments ensure that there is no evidence of metabolic syndrome, hyperlipidemia, hypertriglyceridemia, and type 2 diabetes.
Optimal control of LDL-C levels and blood pressure is critical for all AAS abusers.
References.
[1].Androgenic anabolic steroid abuse and the cardiovascular system. Vanberg P , Atar D , et al. Handb express Pharmacol. 2010; (195):411-57.
[2].Cardiovascular disease and androgens: A review. Manu Kaushik , Siva P. Sontineni , et al. International Journal of Cardiology 2010;142: 8-14
[3].Cardiovascular toxicity of illicit anabolic-androgenic steroid use. Aaron L. Baggish, Rory B. Weiner, et al. 2017; 135:1991-2002.
[4].Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions and rhythm. Suraj Achar , Armand Rostamian , et al. J Cardiol. 2010 Sep 15; 106(6):893-901.
[5].Performance-enhancing drug abuse and cardiovascular risk in athletes: implications for clinicians. Peter J Angell , Neil Chester et al. Br J Sports Med 2012; 46: i78-i84
[6].Anabolic steroids and cardiovascular risk. Peter Angell, Chester N, et al. Sports Med 2012; 42(2):119-134
[7].Cardiovascular expression of anabolic steroids in relation to demographic variables in bodybuilding athletes. Farzad Gheslaghi , Mohammad-Reza Piri-Ardakani , et al. J Res Med Sci . Feb 2015; 20(2): 165-168.
[8].Echocardiographic prospective evaluation of androgen-anabolic steroid effects on cardiac structure and function in strength athletes. H Kuipers, et al. Int J Sports Med 2003; 24: 344-351
[9].Cardiovascular disease prevention: recent achievements and remaining challenges. Guy Barker. Electronic journal of cardiology practice.
Available at: https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/prevention-of-cardiovascular-disease-recent-achievements-and-remaining-challeng
