Your age is what?
MESO-Rx
Anabolic Steroids
AAS and Cardiovascular/Pulmonary Function
- Thread starter Michael Scally MD
- Start date
Of course there’s a risk but that doesn’t stop users from using AAS.
I’d suggest you investivaget your need for TRT at age “35”, right.
Or better yet ask your doc “considering the risk do I really NEED TRT”!
I’d suggest you investivaget your need for TRT at age “35”, right.
Or better yet ask your doc “considering the risk do I really NEED TRT”!
I’m 56 and wondering the same thing...
My understanding is, That even though there has been some conflicting evidence, the balance of evidence suggests that TRT in men who truly need it, with low testosterone levels, actually improves cardiac health / lowers cardiac risk
It could be debated whether 200 mg per week is excessive I’m sure
usually keeps me around 1000,
I was just over in the drugsgear thread, And happened to notice your username, posting about how you run 250 mg / week on a cruise, which puts you at 1200 test. Using UGL test. Now you’re here saying you’re on Dr. TRT at 200 a week. lol
Yes that's correct, I had a good job with insurance and got laid off, "hard times"thus losing my insurance. Had to go the underground route for a while, until I got some more insurance. My script was for test c 200, I been doing just under 1 ml of the 250 when i got my last bloods and it put me at 1186 to be exact, which is a little higher than usual. I also do a cycle of some sort 1 or 2x a year, so I keep other things on hand, but I always just run test at my trt dose, it's been good for me at that dose and never wanted to screw with it.
I was just concerned if my trt was to high, and what the risk where?
I was just concerned if my trt was to high, and what the risk where?
Ah ok didn’t know if you were trolling or something lol That makes sense though
A drug derived from fish oil cut the rate of cardiovascular problems, including heart attacks and strokes, by 25%, a result that will likely transform the fortunes of its maker, Amarin Pharmaceuticals, and upend decades of thinking about cardiovascular disease.
Amarin's drug, Vascepa, is already approved by the Food and Drug Administration to cut triglycerides in patients in whom levels have risen above 500 milligrams per deciliter, triple normal. But there had been skepticism regarding whether it would provide a benefit in heart disease, because other fish oil pills had used much lower doses and because it has proved difficult for any drug significantly to reduce the risk of heart attacks and strokes when given on top of cholesterol-lowering medicines, which are already very effective.
But the results from the 8,179-patient study, reported in a press release with few details, seem to leave little doubt that the effect of the drug was substantial in people who had high triglycerides (median triglyceride levels in the study were 219 mg/dL, 50% more than normal) and had either had previous cardiovascular problems, such as a heart attack or stroke, or had diabetes and another risk factor for heart disease.
Patients who received four grams of Vascepa had a 25% lower risk of a cardiovascular problem, defined as a heart attack, a stroke, a heart procedure to open a clogged artery, or chest pain requiring a hospitalization, compared to those who received a placebo. (Half the patients received Vascepa, and half a placebo made of mineral oil.) The result was highly statistically significant, with a p value of less than 0.001. (A result is considered significant if this statistic is less than 0.05).
"What??!!! Fantastic! Wow!" said Sekar Kathiresan, a cardiologist who is director of the Cardiovascular Disease Initiative at the Broad Institute and the Center for Genomic Medicine at Massachusetts General Hospital. "That's awesome! Such great news for patients!"
REDUCE-IT™ CARDIOVASCULAR OUTCOMES STUDY OF VASCEPA® (ICOSAPENT ETHYL) CAPSULES MET PRIMARY ENDPOINT
REDUCE-IT™ Cardiovascular Outcomes Study of Vascepa® (icosapent ethyl) Capsules Met Primary Endpoint | Amarin Corporation plc
REDUCE-IT Is First Outcomes Study to Assess Treatment of Patients with LDL-C Controlled by Statin Therapy, Persistent Elevated Triglycerides and Other Cardiovascular Risk Factors
Results Specific to Pure EPA Vascepa at 4 Grams Daily
BEDMINSTER, N.J. and DUBLIN, Ireland, Sept. 24, 2018 (GLOBE NEWSWIRE) -- Amarin Corporation plc (NASDAQ:AMRN), announced today topline results from the Vascepa® cardiovascular (CV) outcomes trial, REDUCE-IT™, a global study of 8,179 statin-treated adults with elevated CV risk. REDUCE-IT met its primary endpoint demonstrating an approximately 25% relative risk reduction, to a high degree of statistical significance (p<0.001), in major adverse CV events (MACE) in the intent-to-treat patient population with use of Vascepa 4 grams/day as compared to placebo.
Patients enrolled in REDUCE-IT had LDL-C between 41-100 mg/dL (median baseline LDL-C 75 mg/dL) controlled by statin therapy and various cardiovascular risk factors including persistent elevated triglycerides (TGs) between 150-499 mg/dL (median baseline 216 mg/dL) and either established cardiovascular disease (secondary prevention cohort) or diabetes mellitus and at least one other CV risk factor (primary prevention cohort).
Key topline results include:
Efficacy: Approximately 25% relative risk reduction, demonstrated to a high degree of statistical significance (p<0.001), in the primary endpoint composite of the first occurrence of MACE, including cardiovascular death, nonfatal myocardial infarction (MI), nonfatal stroke, coronary revascularization, or unstable angina requiring hospitalization. This result was supported by robust demonstrations of efficacy across multiple secondary endpoints.
Safety: Vascepa was well tolerated with a safety profile consistent with clinical experience associated with omega-3 fatty acids and current FDA-approved labeling. The proportions of patients experiencing adverse events and serious adverse events in REDUCE-IT were similar between the active and placebo treatment groups. Median follow-up time in REDUCE-IT was 4.9 years.
REDUCE-IT™ Cardiovascular Outcomes Study of Vascepa® (icosapent ethyl) Capsules Met Primary Endpoint | Amarin Corporation plc
REDUCE-IT Is First Outcomes Study to Assess Treatment of Patients with LDL-C Controlled by Statin Therapy, Persistent Elevated Triglycerides and Other Cardiovascular Risk Factors
Results Specific to Pure EPA Vascepa at 4 Grams Daily
BEDMINSTER, N.J. and DUBLIN, Ireland, Sept. 24, 2018 (GLOBE NEWSWIRE) -- Amarin Corporation plc (NASDAQ:AMRN), announced today topline results from the Vascepa® cardiovascular (CV) outcomes trial, REDUCE-IT™, a global study of 8,179 statin-treated adults with elevated CV risk. REDUCE-IT met its primary endpoint demonstrating an approximately 25% relative risk reduction, to a high degree of statistical significance (p<0.001), in major adverse CV events (MACE) in the intent-to-treat patient population with use of Vascepa 4 grams/day as compared to placebo.
Patients enrolled in REDUCE-IT had LDL-C between 41-100 mg/dL (median baseline LDL-C 75 mg/dL) controlled by statin therapy and various cardiovascular risk factors including persistent elevated triglycerides (TGs) between 150-499 mg/dL (median baseline 216 mg/dL) and either established cardiovascular disease (secondary prevention cohort) or diabetes mellitus and at least one other CV risk factor (primary prevention cohort).
Key topline results include:
Efficacy: Approximately 25% relative risk reduction, demonstrated to a high degree of statistical significance (p<0.001), in the primary endpoint composite of the first occurrence of MACE, including cardiovascular death, nonfatal myocardial infarction (MI), nonfatal stroke, coronary revascularization, or unstable angina requiring hospitalization. This result was supported by robust demonstrations of efficacy across multiple secondary endpoints.
Safety: Vascepa was well tolerated with a safety profile consistent with clinical experience associated with omega-3 fatty acids and current FDA-approved labeling. The proportions of patients experiencing adverse events and serious adverse events in REDUCE-IT were similar between the active and placebo treatment groups. Median follow-up time in REDUCE-IT was 4.9 years.
Anabolic Steroids Induced Cardiomyopathy
Background - Anabolic steroids are a very rare and reversible cause of dilated cardiomyopathy. Early diagnosis and treatment of steroid induced cardiomyopathy can prevent potentially fatal effects.
Case - 28-year-old male with no past medical history presented with one week of history of coughing up blood and shortness of breath. Physical exam demonstrated tachycardia, JVD, 4+ swelling in bilateral extremities and up to umbilicus. Labs were significant for elevated liver enzymes and creatinine. An electrocardiogram showed sinus tachycardia.
Transthoracic and subsequently Transesophageal echocardiogram showed ejection fraction of 20%, severe mitral stenosis, severe aortic regurgitation, and left atrial mass. On further history, patient admitted to using anabolic steroids called trenbolone one week on and one week off cycle for the past 2 years.
Decision-making - Due to high suspicion of anabolic steroid induced cardiomyopathy rather than myxoma, prompt treatment with diuresis was initiated. Decision was made to immediately consult cardiothoracic surgeon. Patient had resection of left atrial mass which was biopsied revealing a thrombus. Patient had a mechanical aortic valve replacement and prosthetic mitral valve replacement. After surgery, Patient's kidney function and liver function were also improved.
Conclusion - Awareness of the complication of anabolic steroid use can lead to prompt treatment and prevent further deterioration of congestive heart failure.
Patel M, Shere A, Ghali J. ANABOLIC STEROIDS INDUCED CARDIOMYOPATHY. Journal of the American College of Cardiology 2018;71:A2416. https://www.sciencedirect.com/science/article/pii/S0735109718329577
Background - Anabolic steroids are a very rare and reversible cause of dilated cardiomyopathy. Early diagnosis and treatment of steroid induced cardiomyopathy can prevent potentially fatal effects.
Case - 28-year-old male with no past medical history presented with one week of history of coughing up blood and shortness of breath. Physical exam demonstrated tachycardia, JVD, 4+ swelling in bilateral extremities and up to umbilicus. Labs were significant for elevated liver enzymes and creatinine. An electrocardiogram showed sinus tachycardia.
Transthoracic and subsequently Transesophageal echocardiogram showed ejection fraction of 20%, severe mitral stenosis, severe aortic regurgitation, and left atrial mass. On further history, patient admitted to using anabolic steroids called trenbolone one week on and one week off cycle for the past 2 years.
Decision-making - Due to high suspicion of anabolic steroid induced cardiomyopathy rather than myxoma, prompt treatment with diuresis was initiated. Decision was made to immediately consult cardiothoracic surgeon. Patient had resection of left atrial mass which was biopsied revealing a thrombus. Patient had a mechanical aortic valve replacement and prosthetic mitral valve replacement. After surgery, Patient's kidney function and liver function were also improved.
Conclusion - Awareness of the complication of anabolic steroid use can lead to prompt treatment and prevent further deterioration of congestive heart failure.
Patel M, Shere A, Ghali J. ANABOLIC STEROIDS INDUCED CARDIOMYOPATHY. Journal of the American College of Cardiology 2018;71:A2416. https://www.sciencedirect.com/science/article/pii/S0735109718329577
Ha E T, Weinrauch M L, Brensilver J (September 17, 2018) Non-ischemic Cardiomyopathy Secondary to Left Ventricular Hypertrophy due to Long-term Anabolic-androgenic Steroid Use in a Former Olympic Athlete. Cureus. Non-ischemic Cardiomyopathy Secondary to Left Ventricular Hypertrophy due to Long-term Anabolic-androgenic Steroid Use in a Former Olympic Athlete
Currently, the cardiovascular risk associated with the use of anabolic steroids is not well documented. Recent studies have shown that its use may potentiate the development of cardiac dysfunction in the short term.
This case report describes an encounter that supports a causal link between anabolic-androgenic steroid use (AAS) and cardiomyopathy later in life. We herein present a case study of a 73-year-old prior Olympic athlete who had misused AAS for 20 years and subsequently was found to have developed a systolic and diastolic cardiomyopathy, presumably due to long-standing left ventricular hypertrophy.
A 73-year-old man presented to our medical center with symptoms of lightheadedness and palpitations. He was found to be in ventricular tachycardia and was converted to sinus rhythm with medical pharmacotherapy. Further workup with two-dimensional trans-thoracic echocardiogram and cardiac catheterization showed severe left ventricular (LV) hypertrophy in the absence of hypertension and a combined systolic and diastolic heart failure with reduced ejection fraction in the absence of significant coronary artery disease or dilated cardiac chambers.
The patient denies any family or personal history of cardiac issues until the time of presentation. By exclusion, he was diagnosed with a non-ischemic cardiomyopathy secondary to his prior regimented use of anabolic steroids. Although causality can only be inferred, this case presents a potentially delayed long-term cardiac consequences of extreme AAS use over many years.
Notably, our patient had remained asymptomatic, until the development of arrhythmias, eventuating in ventricular tachycardia and contributing to heart failure with reduced ejection fraction. Physicians should caution users about the risk of possible long-term cardiac complications linked with AAS use.
Currently, the cardiovascular risk associated with the use of anabolic steroids is not well documented. Recent studies have shown that its use may potentiate the development of cardiac dysfunction in the short term.
This case report describes an encounter that supports a causal link between anabolic-androgenic steroid use (AAS) and cardiomyopathy later in life. We herein present a case study of a 73-year-old prior Olympic athlete who had misused AAS for 20 years and subsequently was found to have developed a systolic and diastolic cardiomyopathy, presumably due to long-standing left ventricular hypertrophy.
A 73-year-old man presented to our medical center with symptoms of lightheadedness and palpitations. He was found to be in ventricular tachycardia and was converted to sinus rhythm with medical pharmacotherapy. Further workup with two-dimensional trans-thoracic echocardiogram and cardiac catheterization showed severe left ventricular (LV) hypertrophy in the absence of hypertension and a combined systolic and diastolic heart failure with reduced ejection fraction in the absence of significant coronary artery disease or dilated cardiac chambers.
The patient denies any family or personal history of cardiac issues until the time of presentation. By exclusion, he was diagnosed with a non-ischemic cardiomyopathy secondary to his prior regimented use of anabolic steroids. Although causality can only be inferred, this case presents a potentially delayed long-term cardiac consequences of extreme AAS use over many years.
Notably, our patient had remained asymptomatic, until the development of arrhythmias, eventuating in ventricular tachycardia and contributing to heart failure with reduced ejection fraction. Physicians should caution users about the risk of possible long-term cardiac complications linked with AAS use.
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 is poorly understood.
· Understanding the link between androgens and atherosclerosis is key to improving androgen replacement/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, Wu J, Denvir MA, Smith LB, Hadoke PWF. The role of androgen receptors in atherosclerosis. Molecular and Cellular Endocrinology 2018;465:82-91. https://www.sciencedirect.com/science/article/pii/S0303720717305269
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 is poorly understood.
· Understanding the link between androgens and atherosclerosis is key to improving androgen replacement/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, Wu J, Denvir MA, Smith LB, Hadoke PWF. The role of androgen receptors in atherosclerosis. Molecular and Cellular Endocrinology 2018;465:82-91. https://www.sciencedirect.com/science/article/pii/S0303720717305269
[OA] Differentiating Athlete's Heart From Cardiomyopathies - The Left Side
In athletes who undertake a high volume of high intensity exercise, the resultant changes in cardiac structure and function which develop as a result of physiological adaptation to exercise (so called "Athlete's Heart") may overlap with some features of pathological conditions.
This chapter will focus on the left side of the heart, where left ventricular cavity enlargement, increase in left ventricular wall thickness and increased left ventricular trabeculation associated with athletic remodelling may sometimes be difficult to differentiate from conditions such as dilated cardiomyopathy, hypertrophic cardiomyopathy or isolated left ventricular non-compaction.
The distinction between physiological versus pathological changes in athletes is imperative as an incorrect diagnosis can have important consequences, such as exclusion from competitive sport, or false reassurance and missed opportunity for effective therapeutic intervention.
Brosnan MJ, Rakhit D. Differentiating Athlete's Heart From Cardiomyopathies - The Left Side. Heart, lung & circulation 2018;27:1052-62. https://www.heartlungcirc.org/article/S1443-9506(18)30468-2/fulltext
In athletes who undertake a high volume of high intensity exercise, the resultant changes in cardiac structure and function which develop as a result of physiological adaptation to exercise (so called "Athlete's Heart") may overlap with some features of pathological conditions.
This chapter will focus on the left side of the heart, where left ventricular cavity enlargement, increase in left ventricular wall thickness and increased left ventricular trabeculation associated with athletic remodelling may sometimes be difficult to differentiate from conditions such as dilated cardiomyopathy, hypertrophic cardiomyopathy or isolated left ventricular non-compaction.
The distinction between physiological versus pathological changes in athletes is imperative as an incorrect diagnosis can have important consequences, such as exclusion from competitive sport, or false reassurance and missed opportunity for effective therapeutic intervention.
Brosnan MJ, Rakhit D. Differentiating Athlete's Heart From Cardiomyopathies - The Left Side. Heart, lung & circulation 2018;27:1052-62. https://www.heartlungcirc.org/article/S1443-9506(18)30468-2/fulltext
Brosnan MJ. Athlete's ECG - Simple Tips for Navigation. Heart, lung & circulation 2018;27:1042-51. https://www.heartlungcirc.org/article/S1443-9506(18)30587-0/fulltext
Regular exercise training results in structural and electrical cardiac adaptations which are reflected in the resting 12-lead electrocardiograph (ECG), thus an athlete's ECG can be quite different to that of a sedentary person of the same age, gender and ethnicity.
This has been recognised as an issue in the setting of pre-participation ECG screening of athletes in whom false positive findings are commonplace when using normative ECG values derived from sedentary populations.
As such, athlete ECG interpretation guidelines have been devised and modified several times over the past decade, with the ultimate goal of reducing the number of athletes undergoing unnecessary secondary investigations to exclude cardiac pathology whilst maintaining the sensitivity of the ECG in detecting cardiac diseases associated with sudden cardiac death (SCD).
By no means exhaustive, the following series of athlete ECG examples is aimed at providing the reader with a basic understanding of what ECG changes are considered normal for an athlete, and what changes should prompt further investigation to exclude cardiac pathology, even in the absence of symptoms.
Regular exercise training results in structural and electrical cardiac adaptations which are reflected in the resting 12-lead electrocardiograph (ECG), thus an athlete's ECG can be quite different to that of a sedentary person of the same age, gender and ethnicity.
This has been recognised as an issue in the setting of pre-participation ECG screening of athletes in whom false positive findings are commonplace when using normative ECG values derived from sedentary populations.
As such, athlete ECG interpretation guidelines have been devised and modified several times over the past decade, with the ultimate goal of reducing the number of athletes undergoing unnecessary secondary investigations to exclude cardiac pathology whilst maintaining the sensitivity of the ECG in detecting cardiac diseases associated with sudden cardiac death (SCD).
By no means exhaustive, the following series of athlete ECG examples is aimed at providing the reader with a basic understanding of what ECG changes are considered normal for an athlete, and what changes should prompt further investigation to exclude cardiac pathology, even in the absence of symptoms.
Sandesara PB, Virani SS, Fazio S, Shapiro MD. The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk. Endocrine reviews 2018:er.2018-00184-er.2018-. Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk | Endocrine Reviews | Oxford Academic
Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide. Low-density lipoprotein cholesterol (LDL-C) is a well-established mediator of atherosclerosis and a key target for intervention for the primary and secondary prevention of ASCVD. However, despite significant reduction in LDL-C, patients continue to have recurrent ASCVD events. Hypertriglyceridemia maybe an important contributor of this residual risk. Observational and genetic epidemiological data strongly support a causal role of triglycerides and the cholesterol content within triglyceride-rich lipoproteins (TGRL) and/or remnant cholesterol (RC) in the development of ASCVD. TGRL are comprised of hepatically derived very low-density lipoprotein (VLDL) and intestinally derived chylomicrons. RC is the cholesterol content of all TGRL and plasma triglycerides serve as a surrogate measure of TGRL and RC. Although lifestyle modification remains the cornerstone for management of hypertriglyceridemia, many novel drugs are in development and have shown impressive TG lowering efficacy. Several ongoing randomized controlled trials are under way to examine the impact of these novel agents on ASCVD outcomes. In this comprehensive review, we provide an overview of the biology, epidemiology and genetics of triglycerides and ASCVD and discuss current and novel triglyceride lowering therapies under development.
Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide. Low-density lipoprotein cholesterol (LDL-C) is a well-established mediator of atherosclerosis and a key target for intervention for the primary and secondary prevention of ASCVD. However, despite significant reduction in LDL-C, patients continue to have recurrent ASCVD events. Hypertriglyceridemia maybe an important contributor of this residual risk. Observational and genetic epidemiological data strongly support a causal role of triglycerides and the cholesterol content within triglyceride-rich lipoproteins (TGRL) and/or remnant cholesterol (RC) in the development of ASCVD. TGRL are comprised of hepatically derived very low-density lipoprotein (VLDL) and intestinally derived chylomicrons. RC is the cholesterol content of all TGRL and plasma triglycerides serve as a surrogate measure of TGRL and RC. Although lifestyle modification remains the cornerstone for management of hypertriglyceridemia, many novel drugs are in development and have shown impressive TG lowering efficacy. Several ongoing randomized controlled trials are under way to examine the impact of these novel agents on ASCVD outcomes. In this comprehensive review, we provide an overview of the biology, epidemiology and genetics of triglycerides and ASCVD and discuss current and novel triglyceride lowering therapies under development.
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