AAS and Cardiovascular/Pulmonary Function

I'm 35. And no, the doctor didn't do an EKG analysis. And she has no idea that I'm thinking of running any cycles. Maybe I have too little TT? I can definitely ask that that be tested right? Sorry, I actually haven't had a doctor for years until recently. I didn't even have insurance until 3 years ago, and then the deductible was 6500 so I never went to the doctor. And yes, I know that I have to be healthier, but substances like caffeine are hard to kick
 
Improvement of Arterial Endothelial Function Following Initiation of Testosterone Replacement Therapy
http://www.aua2016.org/abstracts/abstractprint.cfm?id=PD50-08


Introduction and Objectives - Isolated recent studies have suggested an increased risk of heart attack as early as 3 months following testosterone replacement therapy (TRT) initiation. Such a rapid risk increase would likely require rapid deterioration of arterial endothelial function since atherosclerosis would be unlikely to develop so quickly de novo. Our goal was to assess arterial endothelial function in hypogonadal men prior to and at least 3 months after initiation of TRT

Methods - Adult men were consented for the study if they had symptoms of hypogonadism, a total testosterone < 350 ng/dl, and planned to begin TRT. Endothelial function was non-invasively assessed using the Endo-PAT2000 machine, an FDA approved test of cardiac risk.

We measured the Augmentation Index(AI) (normal < 3%), a measure of arterial stiffness and Reactive Hyperemia Index(RHI), a measure of endothelial vasodilation (normal > 1.69). Prior studies suggest that a 10% level of day to day test variability is expected.

Topical gels or Testopel were used for TRT and target testosterone confirmed post therapy. Endothelial function was reassessed at the next clinic visit, between 3 and 6 months after treatment started if the patients were compliant with therapy. Changes in continuous variables were assessed with the paired t test and significance set at p<0.05

Results - 23 patients were consented with a mean age of 52.7 (range 34-68) and starting testosterone 196.9 ng/dl (range 35-339). There was a history of diabetes in 4, hypertension in 10 and coronary artery disease in 5 men.

Mean RHI was 1.67+/-0.37 (70% were abnormal) and mean AI was 2.57%+/-14.0 (39% were abnormal). No patient subsequently developed a clinical cardiac event. At follow up 20 patients were compliant with therapy and retested. Mean total testosterone increased from 203 to 511 (p<0.0001). Mean RHI improved from 1.70 to 2.14 (p=0.01). Mean AI improved from 2.9% to -1.75% (p=0.01). In 4 men RHI was unchanged and any lower values were within the 10% error of the test (1.3-6.3%). No man had worsening of AI.

Conclusions - Men with symptomatic hypogonadism often have abnormal arterial endothelial function. Following TRT, this endothelial function either remains unchanged or improves. This improvement would be expected to reduce the risk of subsequent cardiac events.
 
Acute Myocardial Infarction in A Young Bodybuilder Taking Anabolic Androgenic Steroids: A Case Report and Critical Review of the Literature
[For Full-Text Email mike.scally@asih.net (Include Title)]


We describe a case report of a 30-year-old bodybuilder suffering acute myocardial infarction (AMI). He had been taking stanozolol and testosterone for two months. The coronary angiogram showed high thrombotic burden in the left anterior descending artery without underlying atherosclerosis.

Few case reports of AMI in athletes taking anabolic androgenic steroids (AASs) have been reported so far. AAS-related AMI is possibly underreported in the medical literature due to the desire of the affected individuals to hide AAS use. Physicians should always consider the possibility of AAS abuse in the context of a young athlete suffering AMI. AASs can predispose to AMI through the acceleration of coronary atherosclerosis.

Additionally, thrombosis without underlying atherosclerosis or vasospasm is highly possible to cause AMI in AAS users. Complications after AMI may be more frequent in AAS users.

Christou GA, Christou KA, Nikas DN, Goudevenos JA. Acute myocardial infarction in a young bodybuilder taking anabolic androgenic steroids: A case report and critical review of the literature. Eur J Prev Cardiol. http://cpr.sagepub.com/content/early/2016/05/14/2047487316651341.abstract
 
Chronic Anabolic Androgenic Steroid Usage Associated With Acute Coronary Syndrome

INTRODUCTION: It has been argued in current studies that anabolic androgenic steroids (AAS) are misused by a great number of bodybuilders and athletes. However, there is diverse and often conflicting scientific data on the cardiac and metabolic complications caused by the misuse of AAS. There may be various reasons for myocardial infarction (MI) with normal coronary arteries. However, for the majority of patients, the exact cause is still unknown.

CASE REPORT: A 32 year-old male who was complaining about severe chest pain was admitted to our emergency department. He had been taking methenolone acetate 200 mg weekly for a period of three years for body building. His cardiac markers were significantly elevated and electrocardiogram (ECG) showed peaked T waves in all derivations, which did not show ST elevation or depression. Both right and left coronary artery systems were found to be completely normal as a result of the angiogram.

CONCLUSION: The purpose of this study is to show that AAS induced MI can be encountered with normal coronary arteries during acute coronary syndrome.

Sonmez E, Turkdogan KA, Yilmaz C, Kucukbuzcu S, Ozkan A, Sogutt O. Chronic anabolic androgenic steroid usage associated with acute coronary syndrome in bodybuilder. Turk J Emerg Med 2016;16(1):35-7. Chronic anabolic androgenic steroid usage associated with acute coronary syndrome in bodybuilder
 
Nikolic TR, Zivkovic VI, Srejovic IM, et al. Acute effects of nandrolone decanoate on cardiodynamic parameters in isolated rat heart. Can J Physiol Pharmacol. An Error Occurred Setting Your User Cookie

Despite worldwide use of anabolic steroids in last decades, there is still contradictory information about their acute influence on myocardium. The aim of this study was to examine the acute effects of nandrolone decanoate (ND) on cardiodynamics and coronary flow in isolated rat heart. The hearts of male Wistar albino rats (n = 48, 12 per group, age 8 weeks, body mass 180-200 g) were excised and perfused according to the Langendorff technique at gradually increased coronary perfusion pressures (40-120 cmH2O). After the control sets of experiments, the hearts in different groups were perfused with different doses of ND (1, 10, or 100 mumol/L separately). Using a sensor placed in the left ventricle, we registered maximum and minimum rate of pressure development in the left ventricle (dP/dtmax and dP/dtmin), systolic and diastolic left ventricular pressure (SLVP and DLVP), and heart rate (HR). Coronary flow (CF) was measured flowmetrically. The results clearly show the depression in cardiac function caused by higher doses of ND. The highest concentration of ND (100 mumol/L) induced the most deleterious impact on the myocardial function and perfusion of the heart (coronary circulation), which could be of clinical significance.
 
This is a subgroup analysis of patients with a pre-existing cardiovascular disease (CVD, defined as diagnosed coronary artery disease, myocardial infarction and/or stroke). 12.4% of all patients in the registries fulfilled this criterion. During treatment with testosterone with three-monthly depot injections for a duration of up to 8 years, not a single cardiovascular event or death occurred.

All these high-risk patients with a life-threatening disease were monitored and treated for their CVD elsewhere (cardiologists, internists, general practitioners). What the urologists (the investigators of this study) did was treat patients’ hypogonadism with testosterone. Surprisingly, the baseline situation of these patients suggested that they were far from being well managed: they were obese (mean BMI: 37 kg/m2), hypertensive (mean systolic blood pressure: 164 mmHg), dyslipidaemic (mean total cholesterol: 302 mg/dl = 7.8 mmol/L) and had poor glycaemic control (mean fasting glucose: 108 mg/dl = 6 mmol/L, mean HbA1c: 7.6%). 60% of these patients had diabetes.

With testosterone treatment in addition to the standard therapy patients were receiving, every one of the known cardiometabolic risk factors improved in a clinically meaningful, progressive and sustained fashion. The mean weight loss was 20% achieving a mean BMI of 29 kg/m2 and a mean HbA1c of 5.7%, just to name a few of the effects.

Haider A, Yassin A, Haider KS, Doros G, Saad F, Rosano GM. Men with testosterone deficiency and a history of cardiovascular diseases benefit from long-term testosterone therapy: observational, real-life data from a registry study. Vascular Health and Risk Management. 2016;12 251—61. Men with testosterone deficiency and a history of cardiovascular disea | VHRM

Background/objectives: Long-term testosterone therapy (TTh) in men with hypogonadism has been shown to improve all components of the metabolic syndrome. In this study, we investigated the effects of long-term TTh up to 8 years in hypogonadal men with a history of cardiovascular disease (CVD).

Patients and methods: In two urological clinics observational registries, we identified 77 hypogonadal men receiving TTh who also had a history of CVD. The effects of TTh on anthropometric and metabolic parameters were investigated for a maximum duration of 8 years. Any occurrence of major adverse cardiovascular events was reported. All men received long-acting injections of testosterone undecanoate at 3-monthly intervals.

Results: In 77 hypogonadal men with a history of CVD who received TTh, we observed a significant weight loss and a decrease in waist circumference and body mass index. Mean weight decreased from 114±13 kg to 91±9 kg, change from baseline: −24±1 kg and –20.2%±0.5%. Waist circumference decreased from 112±8 cm to 99±6 cm, change from baseline: −13±0.3 cm. Body mass index decreased from 37±4 to 29±3, change from baseline: −8±0.2 kg/m2. Cardiometabolic parameters such as lipid pattern, glycemic control, blood pressure, heart rate, and pulse pressure all improved significantly and sustainably. No patient suffered a major adverse cardiovascular event during the full observation time.

Conclusion: In men with hypogonadism, TTh appears to be effective in achieving sustained improvements in all cardiometabolic risk factors and may be effective as an add-on measure in the secondary prevention of cardiovascular events in hypogonadal men with a history of CVD.
 
Hvid-Jensen HS, Rasmussen F, Bendstrup E. Pulmonary hemorrhage following anabolic agent abuse: Two cases. Respir Med Case Rep 2016;18:45-7. https://www.sciencedirect.com/science/article/pii/S2213007116300260

Numerous adverse effects follow anabolic agent abuse. Pulmonary hemorrhage is not considered one of them.

We present two cases of young male bodybuilders who developed diffuse alveolar bleeding as a result of anabolic steroid abuse. Diffuse alveolar hemorrhage associated with anabolic agent abuse has not been described previously in the literature.

Both patients developed acute dyspnea and hemoptysis with consistent radiological findings. In both cases symptoms promptly resolved with cessation of exposure and no medical intervention was required and no signs of persistent lung damage were seen.

It is crucial to be aware of pulmonary hemorrhage as an acute complication of anabolic agent abuse. It should be considered an important differential diagnosis in the athletic patient presenting with respiratory symptoms.

 
Damn... What would be healthier for the heart:
- Low T + sedentary life style + some alcohol
- High T + active weight lifting + active cardiovascular exercise (daily) + no alcohol (on VERY rate occasion)
???

High T levels were also associated with drug and alcohol abuse. Maybe those are the factors that contribute...

I am on Clomid + Anastrozole. I am not sure if that means I am on "AAS". Could it be that synthetic T (steroids) is not fully compatible with human body? Clomid raises natural T and I really hope it doesn't increase my chances of getting a heart attack...
 
Hvid-Jensen HS, Rasmussen F, Bendstrup E. Pulmonary hemorrhage following anabolic agent abuse: Two cases. Respir Med Case Rep 2016;18:45-7. https://www.sciencedirect.com/science/article/pii/S2213007116300260

Numerous adverse effects follow anabolic agent abuse. Pulmonary hemorrhage is not considered one of them.

We present two cases of young male bodybuilders who developed diffuse alveolar bleeding as a result of anabolic steroid abuse. Diffuse alveolar hemorrhage associated with anabolic agent abuse has not been described previously in the literature.

Both patients developed acute dyspnea and hemoptysis with consistent radiological findings. In both cases symptoms promptly resolved with cessation of exposure and no medical intervention was required and no signs of persistent lung damage were seen.

It is crucial to be aware of pulmonary hemorrhage as an acute complication of anabolic agent abuse. It should be considered an important differential diagnosis in the athletic patient presenting with respiratory symptoms.
Great articles Dr. If I could add when I was 26 I was diagnosed with dialated cardiomyopathy with an ejection fraction of 20%. I was passing out at gym due to high doses of ephedrine and a local cardiologist performed a cardiac cath to find the results. I was hospitalized for 2 weeks at Yale New Haven and seen by a electro physiologist. He found I also have inappropriate sinus tachycardia. I take coreg for heart protection and xarelto to protect against strokes. After a year I did my first cycle and ejection fraction went from 40% to 50%. It has stayed there since and I am 39 now and doing my 5th cycle. I have only used sustanon. Nothing else. I am not saying testosterone has helped me, and my Dr. Does not like it, but as of now it hasn't hurt me. Wish there were more studies about AAS and the heart. Any feedback from you would be great.
 
I feel like there is a lack of "layman's information" in this thread and many of these studies leave me with a lot of questions.

It would be nice to see some information that relates to AAS use and also describes other variables, such as diet of patients, family illness/disease history, and any other relevant information.

Is the general theme of these articles that AAS use causes heart problems, even at TRT dosages?
 
I feel like there is a lack of "layman's information" in this thread and many of these studies leave me with a lot of questions.

It would be nice to see some information that relates to AAS use and also describes other variables, such as diet of patients, family illness/disease history, and any other relevant information.

Is the general theme of these articles that AAS use causes heart problems, even at TRT dosages?
Great point! I definitely go above TRT doses, but your right about genetics, diet, family history.
 
Ge Y, Liu S, Singh S. A Strong Man with a Weak Heart: The Ill-Effects of Performance Enhancing Drug Use. Am J Med. http://www.amjmed.com/article/S0002-9343(16)30693-3/abstract

An undisclosed habit accounted for severe left ventricular dysfunction and hepatic lesions in a young bodybuilder. A 25-year-old bodybuilder with a history of liver cysts presented with a five day history of epigastric discomfort, nausea, vomiting, diaphoresis, and intermittent shortness of breath.

The patient was not on prescription medications and denied use of tobacco, alcohol, supplements, or illicit drugs. Family history was unremarkable. He appeared anxious, uncomfortable, and diaphoretic.


 

Attachments

Ge Y, Liu S, Singh S. A Strong Man with a Weak Heart: The Ill-Effects of Performance Enhancing Drug Use. Am J Med. http://www.amjmed.com/article/S0002-9343(16)30693-3/abstract

An undisclosed habit accounted for severe left ventricular dysfunction and hepatic lesions in a young bodybuilder. A 25-year-old bodybuilder with a history of liver cysts presented with a five day history of epigastric discomfort, nausea, vomiting, diaphoresis, and intermittent shortness of breath.

The patient was not on prescription medications and denied use of tobacco, alcohol, supplements, or illicit drugs. Family history was unremarkable. He appeared anxious, uncomfortable, and diaphoretic.
Excellent article Dr. If I could ask something. What do you make of my cardiovascular situation.
 
Is there anything that would remedy symptoms of high cholesterol levels outside of stopping the use of AS?
Cholesterol medication. LOL. But seriously, if you know you already have high cholesterol I would keep your doctor in the loop about AAS use.
 
Cholesterol medication. LOL. But seriously, if you know you already have high cholesterol I would keep your doctor in the loop about AAS use.
no prior issue with cholesterol. slightly high bp. just borderline. diet and exercise are non issues. considered taking winny for longer but I'm noticing symptoms of vascular issues. associating them to the as and Winstol.was hoping to counter it somehow. maybe fuckloads of cardio?

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no prior issue with cholesterol. slightly high bp. just borderline. diet and exercise are non issues. considered taking winny for longer but I'm noticing symptoms of vascular issues. associating them to the as and Winstol.was hoping to counter it somehow. maybe fuckloads of cardio?

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Don't take Winny for longer then advised. Could really fuk up your hematocrit and cause a clot. You don't need fuk loads of cardio, but I do it 4x a week for 25-30 minutes. Cardio will help BP and could help cholesterol. Watch your red meat consumption and your saturated fats. Its your triglycerides you have to watch. Keep an eye on your BP bro. Mine got up to 132/82 on my last cycle. Slightly elevated but in the norm for a 39 year old. Get blood work done during and after cycles and always monitor your BP. Do those things and you should be good.
 
Don't take Winny for longer then advised. Could really fuk up your hematocrit and cause a clot. You don't need fuk loads of cardio, but I do it 4x a week for 25-30 minutes. Cardio will help BP and could help cholesterol. Watch your red meat consumption and your saturated fats. Its your triglycerides you have to watch. Keep an eye on your BP bro. Mine got up to 132/82 on my last cycle. Slightly elevated but in the norm for a 39 year old. Get blood work done during and after cycles and always monitor your BP. Do those things and you should be good.
thx. I'm gonna get blood work this week


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