AAS and Cardiovascular/Pulmonary Function

[Michael Scally MD]

Androgenic-Anabolic Steroids Inhibited Post-Exercise Hypotension

Highlights
· Post-exercise hypotension did not occur in anabolic steroid users.
· The rehabilitation of hypertension is blunted by anabolic steroids.
· Damage caused by anabolic steroids should be reported in educational programs.

BACKGROUND: There is evidence of hypertensive effects caused by anabolic androgenic steroids (AAS). A single exercise session promotes the acute reduction of blood pressure, but the effects of AAS on this phenomenon are unknown.

OBJECTIVES: To investigate the post-exercise blood pressure response in androgenic-anabolic steroid users.

METHODS: Thirteen AAS users (23.9+/-4.3 years old) and sixteen controls (22.1+/-4.5 years old) performed a session of aerobic exercise. Heart rate and blood pressure were assessed before exercise and during a 60min post-exercise resting period. Repeated ANOVA measures were used to determine differences between the groups.

RESULTS: While the control group had a significant reduction in post-exercise systolic blood pressure of up to 13.9+/-11.6mmHg at 40min, this phenomenon was limited among AAS users who reached a maximum of 6.2+/-11.5mmHg at 60min.

The between groups comparison revealed significant higher post-exercise hypotension (PEH) for the control group at 30min (-12.9+/-14.1mmHg versus -2.9+/-7.6mmHg), 40min (-13.9+/-11.6mmHg versus -2.5+/-8.3mmHg), 50min (-13.9+/-13.9mmHg versus -5.0+/-7.9mmHg) and 60min (-12.5+/-12.8mmHg versus -6.2+/-11.5mmHg).

There was no significant diastolic PEH in any of the groups.

CONCLUSIONS: This study demonstrated impaired systolic post-exercise hypotension as a new adverse effect of AAS usage.

Junior J, Silva AS, Cardoso GA, Silvino VO, Martins MCC, Santos MAP. Androgenic-anabolic steroids inhibited post-exercise hypotension: a case control study. Braz J Phys Ther. Androgenic-anabolic steroids inhibited post-exercise hypotension: a case control study

 

[hurricane]

Androgenic-Anabolic Steroids Inhibited Post-Exercise Hypotension

Highlights
· Post-exercise hypotension did not occur in anabolic steroid users.
· The rehabilitation of hypertension is blunted by anabolic steroids.
· Damage caused by anabolic steroids should be reported in educational programs.

BACKGROUND: There is evidence of hypertensive effects caused by anabolic androgenic steroids (AAS). A single exercise session promotes the acute reduction of blood pressure, but the effects of AAS on this phenomenon are unknown.

OBJECTIVES: To investigate the post-exercise blood pressure response in androgenic-anabolic steroid users.

METHODS: Thirteen AAS users (23.9+/-4.3 years old) and sixteen controls (22.1+/-4.5 years old) performed a session of aerobic exercise. Heart rate and blood pressure were assessed before exercise and during a 60min post-exercise resting period. Repeated ANOVA measures were used to determine differences between the groups.

RESULTS: While the control group had a significant reduction in post-exercise systolic blood pressure of up to 13.9+/-11.6mmHg at 40min, this phenomenon was limited among AAS users who reached a maximum of 6.2+/-11.5mmHg at 60min.

The between groups comparison revealed significant higher post-exercise hypotension (PEH) for the control group at 30min (-12.9+/-14.1mmHg versus -2.9+/-7.6mmHg), 40min (-13.9+/-11.6mmHg versus -2.5+/-8.3mmHg), 50min (-13.9+/-13.9mmHg versus -5.0+/-7.9mmHg) and 60min (-12.5+/-12.8mmHg versus -6.2+/-11.5mmHg).

There was no significant diastolic PEH in any of the groups.

CONCLUSIONS: This study demonstrated impaired systolic post-exercise hypotension as a new adverse effect of AAS usage.

Junior J, Silva AS, Cardoso GA, Silvino VO, Martins MCC, Santos MAP. Androgenic-anabolic steroids inhibited post-exercise hypotension: a case control study. Braz J Phys Ther. Androgenic-anabolic steroids inhibited post-exercise hypotension: a case control study

Very interesting study. Never would of thought your BP would drop that much post exercise. I wonder if that's why I used to pass out after working out. Plus my ejection fraction was found to be very low once they sent me for a cardiac cath. Something to be aware of. Even though I'm done with AAS.

 

[Michael Scally MD]

Elkhoury FF, Rambhatla A, Mills JN, Rajfer J. Cardiovascular Health, Erectile Dysfunction, and Testosterone Replacement: Controversies and Correlations. Urology. http://www.goldjournal.net/article/S0090-4295(17)30777-X/abstract

Erectile dysfunction (ED) and cardiovascular disease (CVD) share a similar underlying pathophysiology, and low serum testosterone, known as hypogonadism, is a significant player in both conditions. Hypogonadism is a known risk factor for cardiovascular events and worsened mortality, thus influencing physicians to recommend testosterone replacement in such patients. However, at least four recent reports suggest that testosterone replacement may worsen cardiovascular risk, heightening hesitancy in the medical community to treat hypogonadal men with testosterone. This review highlights the triad of CVD, ED, and testosterone therapy and provides the physician with some guiding principles to navigate these recent concerns.

 

[hurricane]

@Michael Scally MD. Hey Doc just wanted to let you know I'm back in the hospital. The last 2 days I've been in and out of atrial flutter. Dr. Marieb decided we need to go back in and do a "touch up" ablation. Scheduled for tomorrow morning. I've been reading a lot of your work. Your a smart mother fukr!! Very informative studies and interviews. I'll update you once I'm out of surgery.

 

[hurricane]

Surgery was a success. Resting with the family.

 

[hurricane]

@Michael Scally MD . Hey Doc I was just put on Isosorbide along with my coreg, ivabradine, and Xarelto. I know the basics of what it is, just wondering your thoughts on it. I am worried about headaches with it. Thanks.

 

[Michael Scally MD]

Increased Blood Pressure and Aortic Stiffness Among Abusers of Anabolic Androgenic Steroid

BACKGROUND: Abuse of anabolic androgenic steroids (AAS) is prevalent among recreational athletes and adverse effects on blood pressure (BP) and arterial stiffness could be substantial. Testosterone decreases natriuretic peptides which are key components in BP-regulation and may impair BP-homeostasis in AAS abusers.

OBJECTIVE: To investigate BP and aortic stiffness in relation to natriuretic peptides among current AAS abusers, former AAS abusers and controls.

METHODS: In this cross-sectional study, 37 current AAS abusers, 33 former AAS abusers and 30 controls were included. All participants were men involved in recreational strength training. We used 24-h BP monitoring, assessed proximal aorta distensibility index (ADI) by MRI and obtained overnight fasting blood samples to measure: midregional proatrial natriuretic peptide (MR-proANP), aldosterone, noradrenaline and copeptin.

RESULTS: Current AAS abusers exhibited higher mean (95% confidence interval) 24-h systolic BP than controls [132 (129; 135) versus 124 (120; 128) mmHg, P = 0.005] and systolic hypertension was more frequent among current AAS abusers than controls (51 versus 17%, P = 0.009).

ADI was lower among both current and former AAS abusers suggesting higher aortic stiffness; %-difference (95% confidence interval) from controls: -21% (-35; -5) and -21% (-36; -4), P < 0.05.

Plasma MR-proANP was decreased, whereas aldosterone and noradrenaline were increased among current AAS abusers compared with former AAS abusers and controls.

Decreased MR-proANP was independently associated with increased systolic BP and reduced ADI in multivariate linear regressions.

CONCLUSION: Current AAS abusers displayed increased 24-h systolic BP and decreased plasma MR-proANP. Both current and former AAS abusers exhibited higher aortic stiffness.

Rasmussen JJ, Schou M, Madsen PL, et al. Increased blood pressure and aortic stiffness among abusers of anabolic androgenic steroids: potential effect of suppressed natriuretic peptides in plasma? J Hypertens. https://insights.ovid.com/crossref?an=00004872-900000000-97622

 

[Michael Scally MD]

Bayat G, Javan M, Khalili A, Safari F, Shokri S, Hajizadeh S. Chronic endurance exercise antagonizes the cardiac UCP2 and UCP3 protein up-regulation induced by nandrolone decanoate. J Basic Clin Physiol Pharmacol. Chronic endurance exercise antagonizes the cardiac UCP2 and UCP3 protein up-regulation induced by nandrolone decanoate : Journal of Basic and Clinical Physiology and Pharmacology

BACKGROUND: Several lines of evidence revealed that chronic treatment of anabolic androgenic steroids (AASs) is accompanied with some cardiovascular side effects and in addition they also negatively mask the beneficial effects of exercise training on cardiac performance.

METHODS: The present study examined whether the nandrolone decanoate (ND)-induced cardiac effects were mediated by changing the cardiac uncoupling protein 2 (UCP2) and 3 (UCP3) expression. Five groups of male wistar-albino rats including sedentary control (SC), sedentary vehicle (SV), sedentary nandrolone decanoate (SND), exercise control (EC), and exercise nandrolone decanoate (END) were used. ND was injected (10 mg/kg/week, intramuscular) to the animals in the SND and END groups and endurance exercise training was performed on a treadmill five times per week.

RESULTS: The protein expressions of cardiac UCP2 and UCP3 have significantly increased in both the SND and EC groups compared to the SC ones. In contrast to UCP3, no significant differences were found between UCP2 protein expressions of the END and SC groups. Compared with the SND group, the exercise training significantly decreased the UCP2 and UCP3 protein expressions in the END group.

CONCLUSIONS: The study has indicated that endurance exercise in combination with ND can result in that the exercise effectively antagonizes the effects of ND treatment on UCP2 and UCP3 up-regulation.

 

[Dr JIM]

Over the past few years the literature has become replete with evidence AAS pose a real and legitimate Cardio-Vascular risk, and Ive every reason to believe this risk will only be amplified now that GH has become a major part of "the stack".

I can only hope those whom have cycled PEDs for years on end will pursue and inquire about "risk stratification" with their physician, less they become another "undocumented" AAS related cause of sudden cardiac death!

JIM

 

[Michael Scally MD]

[OA] "Testosterone replacement therapy and cardiovascular events."

A low testosterone level and hypogonadism are associated with cardiovascular disease. Aging, chronic health problems, and obesity are all associated with a low testosterone level as well as the presence and severity of cardiovascular disease. Testosterone is increasingly prescribed for patients with clinical hypogonadism and a low testosterone level.

The information we have is still contradictory regarding testosterone replacement therapy (TRT) and its association with adverse cardiovascular events. Older patients and patients who are susceptible to cardiovascular diseases could be at risk with a testosterone prescription. This is a review of the literature to discuss the cardiovascular safety of TRT.

Catakoglu, A. B. and M. Kendirci "Testosterone replacement therapy and cardiovascular events." Turk Kardiyol Dern Ars 2017;45(7):664-672. Testosterone replacement therapy and cardiovascular events [Turk Kardiyol Dern Ars]=

 

[Dr JIM]

[OA] "Testosterone replacement therapy and cardiovascular events."

A low testosterone level and hypogonadism are associated with cardiovascular disease. Aging, chronic health problems, and obesity are all associated with a low testosterone level as well as the presence and severity of cardiovascular disease. Testosterone is increasingly prescribed for patients with clinical hypogonadism and a low testosterone level.

The information we have is still contradictory regarding testosterone replacement therapy (TRT) and its association with adverse cardiovascular events. Older patients and patients who are susceptible to cardiovascular diseases could be at risk with a testosterone prescription. This is a review of the literature to discuss the cardiovascular safety of TRT.

Catakoglu, A. B. and M. Kendirci "Testosterone replacement therapy and cardiovascular events." Turk Kardiyol Dern Ars 2017;45(7):664-672. Testosterone replacement therapy and cardiovascular events [Turk Kardiyol Dern Ars]=

Perhaps I'm wrong but since many of the cases before the courts include a number of patients with considerable CV risk factors, providing TRT is used to maintain and mimic PHYSIOLOGIC TT within age established ranges, I've reason to suspect the "risk" is likely to approximate that of "maleness".

And I can say from personal experience MANY "older patients" are in search of TRT that enables them to approximate youthful values and for those individuals the risk likely increases in a manner proportional to the level achieved, especially when other C-V risk factors are present.

Stated another way not all "TRT" is created equal, and thats something the courts and contemporary research has overlooked IMO.

JIM

 

[Michael Scally MD]

Barbosa Neto, O., G. R. da Mota, et al. "Long-term anabolic steroids in male bodybuilders induce cardiovascular structural and autonomic abnormalities." Clin Auton Res. Long-term anabolic steroids in male bodybuilders induce cardiovascular structural and autonomic abnormalities

OBJECTIVE: The aims of this study were to examine the hypothesis that users of anabolic androgenic steroids (AAS) would have cardiac autonomic disorders and that there is a correlation between sympathetic modulation, high blood pressure (BP) and alterations to cardiac dimensions.

METHODS: Forty-five male subjects were enrolled in the study. They were categorized into three groups comprising bodybuilders actively using AAS (AAS users; n = 15), bodybuilders who had never used AAS (nonusers; n = 15) and age-paired healthy sedentary controls (n = 15). Hemodynamic parameters, linear and nonlinear analyses of heart rate variability and electrocardiography and echocardiography analyses were performed at rest.

RESULTS: Bodybuilders in the AAS group had a higher mean BP than those in the ASS nonuser group (p < 0.05) and the sedentary controls (p < 0.001). Cardiac sympathetic modulation was higher in AAS users than in AAS nonusers (p < 0.05) and the sedentary controls (p < 0.001), and parasympathetic modulation was lower in AAS users than in nonusers and the sedentary controls (p < 0.05). Shannon entropy was lower in AAS users than in the sedentary (p < 0.05) controls, and the corrected QT interval and QT dispersion were higher in AAS users than in the sedentary controls (p < 0.05). The interventricular septal thickness, left ventricle posterior wall thickness and relative diastolic wall thickness were higher in AAS users than in AAS nonusers and the sedentary controls (p < 0.001). AAS users showed a positive correlation between increased sympathetic modulation and high BP (r = 0.48, p < 0.005), as well as sympathetic modulation and cardiac hypertrophy (r = 0.66, p < 0.001).

CONCLUSION: There was a marked cardiac autonomic alteration in AAS users, with a shift toward sympathetic modulation predominance and vagal attenuation. The high BP observed in our group of bodybuilders using AAS was associated with increased sympathetic modulation, and this increased sympathetic modulation was associated with structural alterations in the heart. This association may constitute an important mechanism linking AAS abuse to increased cardiovascular risk.

 

[Michael Scally MD]

Polito MV, Dellegrottaglie S, Matturro R, Bonadies D, R DER, Galasso G. Androgenic-anabolic steroids: the new insidious killer leading to heart failure. Minerva Cardioangiol 2017;65(6):663-6. https://www.minervamedica.it/en/journals/minerva-cardioangiologica/article.php?cod=R05Y2017N06A0663

We report a case of a 41-years-old man, amateur athlete, admitted to our hospital with clinical findings of heart failure. Echocardiography documented a dilated cardiomyopathy with severely reduced (25%) left ventricular (LV) ejection fraction, right ventricular dysfunction and diffuse parietal hypertrophy. Coronary arteries were normal and cardiac magnetic resonance revealed myocardial edema and late gadolinium enhancement. A more careful history documented a long term anabolic steroids abuse. Therefore, a cardiomiopathy caused by toxic damage was considered the most likely diagnosis. At 1 year-follow up, after absolute anabolic steroids withdrawing, the patient was asymptomatic showing a good recovery of LV contractility and volumes.

 

[Dr JIM]

Barbosa Neto, O., G. R. da Mota, et al. "Long-term anabolic steroids in male bodybuilders induce cardiovascular structural and autonomic abnormalities." Clin Auton Res. Long-term anabolic steroids in male bodybuilders induce cardiovascular structural and autonomic abnormalities

OBJECTIVE: The aims of this study were to examine the hypothesis that users of anabolic androgenic steroids (AAS) would have cardiac autonomic disorders and that there is a correlation between sympathetic modulation, high blood pressure (BP) and alterations to cardiac dimensions.

METHODS: Forty-five male subjects were enrolled in the study. They were categorized into three groups comprising bodybuilders actively using AAS (AAS users; n = 15), bodybuilders who had never used AAS (nonusers; n = 15) and age-paired healthy sedentary controls (n = 15). Hemodynamic parameters, linear and nonlinear analyses of heart rate variability and electrocardiography and echocardiography analyses were performed at rest.

RESULTS: Bodybuilders in the AAS group had a higher mean BP than those in the ASS nonuser group (p < 0.05) and the sedentary controls (p < 0.001). Cardiac sympathetic modulation was higher in AAS users than in AAS nonusers (p < 0.05) and the sedentary controls (p < 0.001), and parasympathetic modulation was lower in AAS users than in nonusers and the sedentary controls (p < 0.05). Shannon entropy was lower in AAS users than in the sedentary (p < 0.05) controls, and the corrected QT interval and QT dispersion were higher in AAS users than in the sedentary controls (p < 0.05). The interventricular septal thickness, left ventricle posterior wall thickness and relative diastolic wall thickness were higher in AAS users than in AAS nonusers and the sedentary controls (p < 0.001). AAS users showed a positive correlation between increased sympathetic modulation and high BP (r = 0.48, p < 0.005), as well as sympathetic modulation and cardiac hypertrophy (r = 0.66, p < 0.001).

CONCLUSION: There was a marked cardiac autonomic alteration in AAS users, with a shift toward sympathetic modulation predominance and vagal attenuation. The high BP observed in our group of bodybuilders using AAS was associated with increased sympathetic modulation, and this increased sympathetic modulation was associated with structural alterations in the heart. This association may constitute an important mechanism linking AAS abuse to increased cardiovascular risk.

This citation is one of several that eludes to the risk posed to long term AAS runners AND "stimulant" like drugs.

Users need to understand several "bad things" occur when heart muscle undergoes "hypertrophic changes" (AKA LVH) the most important of which is altered electrical impulse conduction.

The net effect being the use of "bypass tracts" which enhances the occurrence of ectopy, and the development of potentially FATAL ventricular arrhythmia's.

I good example appears to be Rich Piana, in which he suddenly collapsed while sitting after using Cocaine ----- as his history was classic description of VENTRICULAR ARRHYTHMIA

And who knows the number of AAS related "sudden cardiac deaths" were a direct or indirect result of stimulant drugs challenging an already stressed heart -

The point AAS and stimulant drugs are a recipe for disaster, especially in long term cyclists IMO.

And I've been SHOCKED at the risks MANY "Pros" are willing to accept in an effort to maintain or exceed their "gains" in spite of clear cut AGE RELATED physiologic and metabolic limitations.

JIM

 

[Dr JIM]

Sounds all to familair of late

 

[Michael Scally MD]

The Role of Androgen Receptors in Atherosclerosis

Highlights
· The influence of androgens on cardiovascular disease is not clear.
· This has implications for androgen replacement and androgen deprivation therapies.
· Use of (cell-specific) knockout models is helping clarify the influence of androgen-androgen receptor signalling in cardiovascular disease.
· Androgens may be atheroprotective but the importance of dose, duration of exposure and source of androgen is poorly understood.
· Defining the influence of androgen-androgen receptor signalling on cardiovascular disease will be important for the development of new approaches to androgen replacement and androgen deprivation therapy.

Male disadvantage in cardiovascular health is well recognised. However, the influence of androgens on atherosclerosis, one of the major causes of many life-threatening cardiovascular events, is not well understood.

With the dramatic increase in clinical prescription of testosterone in the past decade, concerns about the cardiovascular side-effects of androgen supplementation or androgen deprivation therapy are increasing. Potential atheroprotective effects of testosterone could be secondary to (aromatase-mediated) conversion into oestradiol or, alternatively, to direct activation of androgen receptors (AR).

Recent development of animal models with cell-specific AR knockout has indicated a complex role for androgen action in atherosclerosis. Most studies suggest androgens are atheroprotective but the precise role of AR remains unclear. Increased use of AR knockout models should clarify the role of AR in atherogenesis and, thus, lead to exploitation of this pathway as a therapeutic target.

Takov, K., J. Wu, et al. "The role of androgen receptors in atherosclerosis." Mol Cell Endocrinol. Redirecting

 

[Michael Scally MD]

Holmes MV, Smith GD. Dyslipidaemia: Revealing the effect of CETP inhibition in cardiovascular disease. Nat Rev Cardiol;advance online publication. http://www.nature.com/nrcardio/journal/vaop/ncurrent/full/nrcardio.2017.156.html

Initial randomized trials of cholesteryl ester transfer protein (CETP) inhibitors were terminated early owing to adverse effects or futility. The REVEAL trial now shows the benefit of CETP inhibition in coronary heart disease. Despite raising HDL-cholesterol levels, the cardiovascular effect of CETP inhibitors is probably due to lowering of non-HDL-cholesterol levels.

 

[Michael Scally MD]

Pickering TG, Hall JE, Appel LJ, et al. Recommendations for Blood Pressure Measurement in Humans and Experimental Animals. Hypertension 2005;45(1):142-61. http://hyper.ahajournals.org/content/45/1/142

Accurate measurement of blood pressure is essential to classify individuals, to ascertain blood pressure-related risk, and to guide management. The auscultatory technique with a trained observer and mercury sphygmomanometer continues to be the method of choice for measurement in the office, using the first and fifth phases of the Korotkoff sounds, including in pregnant women. The use of mercury is declining, and alternatives are needed.

Aneroid devices are suitable, but they require frequent calibration. Hybrid devices that use electronic transducers instead of mercury have promise. The oscillometric method can be used for office measurement, but only devices independently validated according to standard protocols should be used, and individual calibration is recommended. They have the advantage of being able to take multiple measurements.

Proper training of observers, positioning of the patient, and selection of cuff size are all essential. It is increasingly recognized that office measurements correlate poorly with blood pressure measured in other settings, and that they can be supplemented by self-measured readings taken with validated devices at home.

There is increasing evidence that home readings predict cardiovascular events and are particularly useful for monitoring the effects of treatment. Twenty-four-hour ambulatory monitoring gives a better prediction of risk than office measurements and is useful for diagnosing white-coat hypertension. There is increasing evidence that a failure of blood pressure to fall during the night may be associated with increased risk. In obese patients and children, the use of an appropriate cuff size is of paramount importance.

 

[Dr JIM]

Users need to understand several "bad things" occur when heart muscle undergoes "hypertrophic changes" (AKA LVH) the most important of which is altered electrical impulse conduction.

The net effect being the use of "bypass tracts" which enhances the occurrence of ectopy, and the development of potentially FATAL ventricular arrhythmia's.

JIM

FYI

 

[hurricane]

This citation is one of several that eludes to the risk posed to long term AAS runners AND "stimulant" like drugs.

Users need to understand several "bad things" occur when heart muscle undergoes "hypertrophic changes" (AKA LVH) the most important of which is altered electrical impulse conduction.

The net effect being the use of "bypass tracts" which enhances the occurrence of ectopy, and the development of potentially FATAL ventricular arrhythmia's.

I good example appears to be Rich Piana, in which he suddenly collapsed while sitting after using Cocaine ----- as his history was classic description of VENTRICULAR ARRHYTHMIA

And who knows the number of AAS related "sudden cardiac deaths" were a direct or indirect result of stimulant drugs challenging an already stressed heart -

The point AAS and stimulant drugs are a recipe for disaster, especially in long term cyclists IMO.

And I've been SHOCKED at the risks MANY "Pros" are willing to accept in an effort to maintain or exceed their "gains" in spite of clear cut AGE RELATED physiologic and metabolic limitations.

JIM

Stimulants and AAS are definitely a bad combo. Learned the hard way.