Cardiovascular action

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By Medifit Education


Medifit Education explains how Anabolic steroids shows action on cardio vascular system.

  • Enlarged heart – increased risk of heart attack
  • Water and salt retention = high blood pressure
  • Elevated cholesterol and triglycerides
  • Blood clotting disorders


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According to researchers, long-term use of anabolic steroids appears to weaken the heart, but it’s not clear if this weakening is reversible.

Abuse of anabolic androgenic steroids (AAS) has been linked to a variety of different cardiovascular side effects. In case reports, acute myocardial infarction is the most common event presented, but other adverse cardiovascular effects such as left ventricular hypertrophy, reduced left ventricular function, arterial thrombosis, pulmonary embolism and several cases of sudden cardiac death have also been reported. However, to date there are no prospective, randomized, interventional studies on the long-term cardiovascular effects of abuse of AAS.

Alterations in the structure of the heart, such as enlargement and thickening of the left ventricle, which impairs its contraction and relaxation. Possible effects of these alterations in the heart are hypertension, cardiac arrhythmias, congestive heart failure, heart attacks, and sudden cardiac death. These changes are also seen in non-drug-using athletes, but steroid use may accelerate this process.

AAS use can cause harmful changes in cholesterol levels: Some steroids cause an increase in LDL “bad” cholesterol and a decrease in HDL “good” cholesterol. In addition, steroids provoke a rapid increase in body weight and an accompanying rise in blood pressure, both of which leave users more vulnerable to a cardiovascular event.


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Left ventricular hypertrophy (LVH) independently predicts cardiovascular mortality and morbidity across diverse disease states.1 While cardiac diastolic or contractile failure might result directly from structural change within the ventricle (such as altered capillary density or matrix deposition), the association of LVH with cardiovascular disease is more likely dependent upon the increased activity of shared physiological pathways driving both processes. The nature of these underlying mechanisms remains poorly understood. In this regard, escalating attention has focused on the potential role of steroid hormones on LV growth responses.

Pathological cardiovascular manifestations are reported in four male patients, who had taken massive amounts of anabolic steroids while undergoing many years of strength training. One patient was referred because of ventricular fibrillation during exercise, one because of clinically manifest heart failure, and one because of arterial thrombus in his lower left leg. The fourth patient was persuaded to attend for a check-up because of a long history of massive use of anabolic steroids. All four patients had cardiac hypertrophy. Two of the patients had symptoms and signs of heart failure, and one of these two had a massive thrombosis in both right and left ventricles of his heart. After cessation of the use of anabolic steroids in the other patient with heart failure, left ventricular wall thickness reduced quickly from 12 to 10·5 mm, and fractional shortening increased from 14% to 27%. Endomyocardial biopsy revealed increased fibrosis in the myocardium in two of the three cases. HDL-cholesterol was 0·58 mmol . 1−1 and 0·35 mmol . 1−1 in the two patients still using multiple anabolic steroids at the time of investigation. The cardio vascular findings described in the present paper should warn all physicians and athletes about the possible serious acute and long-term side effects of the massive use of anabolic steroids.

In an effort to better understand the impact of long-term anabolic steroid use on the heart, cardiologist and researcher Aaron L. Baggish, MD, of Harvard Medical School and Massachusetts General Hospital performed heart function testing on weightlifters – steroid users and non-users. (The study appears in the 4/2010 issue of the American Heart Association journal, Circulation: Heart Failure.)



12 weightlifters that took steroids

7 weightlifters that did not take drugs


Average age: 40

Average length of steroid use: 9 years

Duration of weightlifting, total physical activity level and weight: Groups were similar

Muscle mass: Steroid users had more than the non-users


A healthy left ventricle – the heart’s main pumping chamber – pumps 55% to 70% of the blood that fills the heart. This measurement is known as ejection fraction. When Doppler echocardiography ultrasound was used to examine blood flow through the heart, most of the steroid users showed evidence of weakness during contraction in the left ventricle.

10 of the 12 steroid users had ejection fractions of less than 55%, which has been linked to an increased risk for heart failure and sudden cardiac arrest

1 of the 7 weightlifters with no history of steroid use had a low ejection fraction

The steroid users also showed evidence of impaired diastolic function, which is the ability of the left ventricle to relax and fill with blood following contraction

Left ventricle relaxation was reduced by almost 50% among steroid users compared to non-users


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LVH in athletes is generally considered to be benign physiological LVH as opposed to the dangerous pathological LVH. Physiological LVH would include both anaerobic as well as aerobic training; the adaptation appears to be harmless and regresses over time when training is discontinued.

However, it seems as if the eccentric LVH from aerobic training is more beneficial since it causes an increase in hole diameter, relaxation, and elasticity as opposed to the concentric LVH from anaerobic training (e.g. resistance training) which may actually decrease hole diameter while simultaneously increase size, stiffness, and contraction. Is this true?

Pathological LVH is usually due to long-term uncontrolled hypertension (HTN) although it is very rarely caused by a pre-existing genetic condition known as hypercaridopmyopathy (HCM). Pathological LVH is a risk factor for myocardial infarction (MI), stroke, sudden cardiac death, and congestive heart failure (CHF). So, anything that causes pathologoical LVH should clearly be avoided.

Do you know why AAS causes LVH and what type of LVH it causes? Is it due to androgen receptor (AR) activation in the heart? Is it more likely to be concentric since most bodybuilders and powerlifters, drug-free or natural, already have concentric LVH due to the nature of their training routines?


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Sodium and water retention resulting in edema can occur. Cautious administration and careful monitoring is recommended in patients with conditions aggravated by fluid retention.

Cardiovascular effects may be precipitated in patients adversely affected by fluid retention. Edema, with and without congestive heart failure, has occurred during anabolic steroid therapy.

Metabolic effects occurring during anabolic steroid therapy in immobilized patients or those with metastatic breast disease include osteolytic-induced hypercalcemia. Anabolic steroids effect electrolyte balance, nitrogen retention, and urinary calcium excretion. Edema, with and without congestive heart failure, has occurred during anabolic steroid therapy. The androgenic activity of anabolic steroids may decrease levels of thyroxin-binding globulin, resulting in decreased total T4 serum levels and increased resin uptake of T3 and T4. Free thyroid hormone levels remain unchanged, however, and there is no clinical evidence of thyroid dysfunction. Significant increases in low density lipoproteins (LDL) and decreases in high density lipoproteins (HDL) have occurred.

Anabolic steroids cause retention of nitrogen, sodium, potassium, chloride, water and phosphorus, and decrease urinary excretion of calcium. Patients should be instructed to report edema.


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The misuse of androgenic-anabolic steroids (AASs) in young, healthy strength athletes has been associated with the occurrence of premature cardiovascular events. These events may in part be mediated by the adverse effects on serum lipid variables that have been linked to AAS administration. Previous studies have indicated that the use of AAS results in decreases in high density lipoprotein cholesterol (HDL-C) and apolipoprotein A1 (Apo-A1; the major component of the HDL particle), and increases in low density lipoprotein cholesterol (LDL-C). A growing number of strength athletes misuse AASs to obtain a well shaped body or increase muscular strength. Most athletes take AASs for periods of 8–12 weeks several times a year. Self administration of AASs may result in much higher doses than recommended, with possibly more severe side effects and more profound effects on serum lipids and lipoproteins. In particular, the orally active 17-α-alkyl steroids have been shown to have severe effects on LDL-C and HDL-C.


Various studies have suggested that the concentration of lipoprotein (a) (Lp(a) is an independent risk indicator for the development of vascular disease. The fat composition of Lp(a) is comparable to that of LDL-C, but the most important difference is the presence of a specific apoprotein (a). This protein is attached to apolipoprotein B (Apo-B) by a disulphide bridge. A close correlation has been reported between the serum concentration of Lp(a) and the accumulation of this particle in the vascular wall. The serum concentration of Lp(a) seems to be genetically determined and, when raised, cannot be lowered by alterations in food intake or taking cholesterol lowering drugs. Previous reports have suggested that, in contrast with their detrimental effects on lipids, AASs may favourably lower Lp(a) concentrations.


The aim of the present studies was to investigate the effects of AASs on lipoproteins and lipids in healthy, young strength athletes. To obtain more insight into the relation between dose of AAS and the response on plasma lipid variables, we performed two prospective studies: one controlled, non-blinded investigation and a randomised, double blind, placebo controlled study. The first investigated the effects of self administration of high doses of AASs on these variables. In the second study, the effects of a commonly used single AAS, nandrolone decanoate, on lipoprotein risk factors and Lp(a) were examined. In both studies we also assessed the recovery of the lipoprotein and lipid variables after cessation of drug administration.

Conclusions: Self administration of several AASs simultaneously for eight or 14 weeks produces comparable profound unfavourable effects on lipids and lipoproteins, leading to an increased atherogenic lipid profile, despite a beneficial effect on Lp(a) concentration. The changes persist after AAS withdrawal, and normalisation depends on the duration of the drug abuse. Eight weeks of administration of nandrolone decanoate does not affect lipid and lipoprotein concentrations, although it may selectively reduce Lp(a) concentrations. The effect of this on atherogenesis remains to be established.


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According to a number of recent reports, persons using anabolic steroids may be subject to an increased risk of thromboembolism. We evaluated the effect of anabolic steroid use on the coagulation and fibrinolytic systems of 16 male bodybuilders to determine whether alterations occurred that would predispose them to a hypercoagulable state. No attempt was made to regulate or guide steroid use. Paired blood samples, both with and without steroid use, were obtained from six individuals, and the remaining subjects provided single samples obtained either during steroid use or nonuse. No differences were noted in most parameters, but we did find a significant increase in protein C antigen (p = 0.008) and free protein S antigen (p = 0.015), with a decreased euglobulin lysis time (p = 0.021) during steroid use. We also found a reduction in total cholesterol levels (p = 0.035) during steroid use. At least some of these findings suggest an activated fibrinolytic state, a known effect of anabolic steroids. The results do not support the presence of a hypercoagulable state. If anabolic steroids do produce a thrombotic tendency, they may do so through alterations in other hemostatic mechanisms or changes in lipid fractions, or more sensitive coagulation assays may be required for detection.

Steroids also increase the risk that blood clots will form in blood vessels, potentially disrupting blood flow and damaging the heart muscle so that it does not pump blood effectively.


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By Medifit Education

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