Cardiovascular effects are one of the most serious and least recognized risks of anabolic steroids. They develop without obvious symptoms and appear years later. Metenolone acetate is often considered "soft" for the heart, because it does not aromatize and does not retain water. The editors analyze how this fits with what is known about lipids, blood pressure and blood clotting.

Why androgens affect the heart

Androgen receptors are not only in muscles and genitals, but also in cardiomyocytes, cells of the vascular wall, liver and bone marrow. Therefore, any agonist of the androgen receptor, introduced in a supraphysiological amount, in one way or another changes the work of the cardiovascular system.

A scientific review by the American Heart Association (Baggish et al., 2017) identifies several main mechanisms: adverse changes in lipoproteins, increased blood pressure, direct effects on the myocardium with the development of hypertrophy and fibrosis, increased haematocrit, and susceptibility to thrombosis.

None of these mechanisms are related to aromatization. Therefore, the lack of oestrogenic effects in metenolone does not give it "immunity" from cardiovascular risks. On the contrary, part of the protective effect on lipids in men is provided by oestradiol, which metenolone does not produce.

It is also important that most of the data comes from people who have used combinations of several steroids, often for years. It is impossible to single out the contribution of metenolone, but the class regularity can be traced stably.

Lipid profile: the main weak link of oral forms

The most reproducible effect of anabolic steroids on lipids is the reduction of high-density lipoprotein (HDL) cholesterol. This effect is associated with the stimulation of hepatic lipase, an enzyme that destroys HDL. At the same time, the level of low-density lipoprotein (LDL) often increases.

For oral androgens, this effect is particularly pronounced. The reason is pharmacokinetic: after absorption, the entire dose enters the portal vein and acts on the liver in a high concentration even before entering the general bloodstream. Metenolone acetate, although not 17α-alkylated, also enters the liver in this way.

The work of Friedl et al. (1990), whose conclusion is stated simply in the title of the article, showed that HDL did not decrease when an aromatizable androgen was administered. This is indirect evidence that oestradiol partially protects the lipid profile, while non-aromatized androgens, to which metenolone belongs, are deprived of such protection.

Lipid changes are generally reversible after cessation of use, but long-term atherogenic dyslipidemia promotes the development of atherosclerosis. A review by Achar et al. (2010) systematizes data on changes in lipids, pressure, and heart structure in response to anabolic steroids.

IndexTypical direction of changes against the background of androgensWhy it matters
HDLDecrease, especially with oral formsReduction of "reverse transport" of cholesterol
LDLOften increasesThe main atherogenic factor
TriglyceridesVariable changesDepends on nutrition and body weight
Lipoprotein(a)May decreaseThe clinical significance against the background of other changes is unclear
Metenolone acetate and cardiovascular health
Photo: Louis Reed / Unsplash

Blood pressure and myocardium

An increase in blood pressure with the background of anabolic steroids has been described in many studies, although the effect varies. Mechanisms include effects on the renin-angiotensin system, vascular tone, and sodium retention. Metenolone does not cause oestrogenic fluid retention, but the androgenic component of the effect on pressure is preserved.

Studies using echocardiography and cardiac MRI have shown that long-term users of anabolic steroids have higher left ventricular myocardial mass and worse systolic and diastolic function compared with those who exercise without steroids. Baggish et al also describe a higher incidence of coronary atherosclerosis in this group.

These changes develop slowly and may not produce symptoms for a long time. The first signs — shortness of breath during exercise, reduced tolerance to physical work, rhythm disturbances — are often attributed to fatigue or overtraining.

There are no data specifically for metenolone in this context. However, the mechanism of myocardial hypertrophy is mediated by the androgen receptor, so it is logical to assume that the risk depends on the total "androgen load" and not on the specific name of the drug.

Androgen receptor↓ HDL, ↑ LDL↑ pressureMyocardial hypertrophy↑ haematocrit Atherosclerosis, arrhythmias, thrombosis
Fig. 1. The main pathways of cardiovascular risk of anabolic steroids — schematically, as reviewed by Baggish et al. (2017).

Haematocrit and blood viscosity

Androgens stimulate the formation of erythrocytes. This effect is so stable that in the 1960s and 1970s, anabolic steroids, including metenolone, were used to treat some forms of anemia. In a healthy person, the same mechanism leads to an increase in haematocrit above the norm.

Haematocrit is the fraction of blood volume occupied by erythrocytes. Its increase increases the viscosity of the blood, the load on the heart and the risk of thrombotic complications. For testosterone therapy, clinical guidelines of the Endocrine Society (Bhasin et al., 2018) provide for haematocrit monitoring and treatment correction if it is significantly increased.

The risk is increased by dehydration, which often accompanies pre-competition weight cutting before competition, as well as by smoking and sleep apnoea. In combination with increased pressure and atherogenic lipids, this creates an unfavourable background for cardiovascular events.

We do not state the exact value of the increase in haematocrit against the background of metenolone acetate: there are no reliable data, and the effect depends on the dose, duration and individual characteristics.

What can be evaluated in analyses

Cardiovascular risks are the area where laboratory and instrumental control provides the most information. Below are the indicators that a doctor usually evaluates in people who use or have used androgens.

  • Lipidogram: total cholesterol, HDL, LDL, triglycerides.
  • General blood analysis: haemoglobin, haematocrit, erythrocytes.
  • Blood pressure: regular home measurements, daily monitoring if necessary.
  • ECG and echocardiography: assessment of heart structure and function.

Anawalt (2019) in a clinical review on the management of patients using anabolic steroids emphasizes the importance of a non-judgmental approach: the patient should tell the doctor about the use of the drugs in order to receive an adequate evaluation.

It is important to understand the limitations: normal tests at a certain time do not guarantee the absence of hidden changes, for example, initial myocardial hypertrophy. Therefore, a one-time inspection does not replace a comprehensive assessment.

We tell you more about the list of analyzes in a separate editorial material.

Important. The article is purely informative and is not a recommendation for use. Metenolone acetate is a prescription anabolic steroid; cardiovascular risk assessment should be carried out by a doctor.

Editorial conclusions

The lack of aromatization does not make metenolone acetate safe for the heart. The most likely adverse effect of oral administration is a decrease in HDL and a worsening of the lipid profile.

Other class risks — increased pressure, myocardial hypertrophy, increased haematocrit — are associated with the androgen receptor and increase with dose and duration of use.

Cardiovascular changes are often asymptomatic, so the only way to detect them is regular examination under the supervision of a doctor.

We also advise you to read the editorial materials about what tests to monitor when using metenolone acetate, about a complete overview of its side effects and about the oral bioavailability of the drug.

List of used literature

  1. Baggish AL, Weiner RB, Kanayama G, et al. Cardiovascular toxicity of illicit anabolic-androgenic steroid use. Circulation. 2017;135(21):1991–2002.
  2. Achar S, Rostamian A, Narayan SM. Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. Am J Cardiol. 2010;106(6):893–901.
  3. Friedl KE, Hannan CJ Jr, Jones RE, Plymate SR. High-density lipoprotein cholesterol is not decreased if an aromatizable androgen is administered. Metabolism. 1990;39(1):69–74.
  4. Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
  5. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715–1744.
  6. Anawalt BD. Diagnosis and management of anabolic androgenic steroid use. J Clin Endocrinol Metab. 2019;104(7):2490–2500.