Any advice on ways to mitigate the risks of heart issues from long term aas use? Is cardio a must or a must not? Supplements? Eating? Certain types of steroids to avoid? Great thread, thanks for the info!
MESO-Rx
Anabolic Steroids
AAS and Cardiovascular/Pulmonary Function
- Thread starter Michael Scally MD
- Start date
Fox R, Varadharajan K, Patel B, Beegun I. Blood, sweat and tears: androgenic-anabolic steroid misuse and recurrent primary post-tonsillectomy haemorrhage. BMJ Case Rep. 2014. http://casereports.bmj.com/content/2014/bcr-2014-207111.abstract
A 30-year-old male body builder and androgenic-anabolic steroid and insulin abuser was admitted for day case elective tonsillectomy (bipolar). He returned with primary post-tonsillectomy haemorrhage 18 h after the operation and required bipolar cautery to the multiple small bleeding points in the right and left tonsillar fossa. Thorough coagulation screen was normal. Recurrent primary haemorrhage occurred 3 h post-operatively requiring immediate surgical intervention, removal of the inferior poles, precautionary throat packs, intubation and observation on the intensive treatment unit (ITU). Re-examination in theatre revealed a bleeding left superior pole that was under-run to achieve haemostasis and the patient returned to ITU. Hypertensive episodes were noted in the emergency department and intraoperatively including one recording >200 mm Hg. Haemostasis was eventually achieved once the blood pressure was adequately controlled. A slow wean of steroids was also instigated and the patient was managed on a surgical ward for 2 weeks post-tonsillectomy.
A 30-year-old male body builder and androgenic-anabolic steroid and insulin abuser was admitted for day case elective tonsillectomy (bipolar). He returned with primary post-tonsillectomy haemorrhage 18 h after the operation and required bipolar cautery to the multiple small bleeding points in the right and left tonsillar fossa. Thorough coagulation screen was normal. Recurrent primary haemorrhage occurred 3 h post-operatively requiring immediate surgical intervention, removal of the inferior poles, precautionary throat packs, intubation and observation on the intensive treatment unit (ITU). Re-examination in theatre revealed a bleeding left superior pole that was under-run to achieve haemostasis and the patient returned to ITU. Hypertensive episodes were noted in the emergency department and intraoperatively including one recording >200 mm Hg. Haemostasis was eventually achieved once the blood pressure was adequately controlled. A slow wean of steroids was also instigated and the patient was managed on a surgical ward for 2 weeks post-tonsillectomy.
HDL Cholesterol Efflux Capacity and Incident Cardiovascular Events
A low level of high-density lipoprotein (HDL) cholesterol is a major independent risk factor for atherosclerotic cardiovascular disease. However, in randomized, controlled trials, high-dose niacin or inhibitors of cholesteryl ester transfer protein did not improve cardiovascular outcomes despite significantly increasing the HDL cholesterol level.
Furthermore, genetic variants associated with HDL cholesterol levels are often not associated with cardiovascular disease. These observations suggest that HDL cholesterol may not be causally associated with cardiovascular disease, and they highlight the potential limitations of using the HDL cholesterol level to assess risk or responses to therapies targeted at HDL cholesterol.
HDL has numerous antiatherosclerotic actions that are not readily reflected by HDL cholesterol levels. A key function of HDL is to promote reverse cholesterol transport from the periphery to the liver, and the critical initial step in reverse cholesterol transport is cholesterol efflux from macrophages to HDL. Macrophage-specific cholesterol efflux capacity has been directly and causally linked to the prevention of atherosclerosis in animal models.
The ability to assess the clinical relevance of reverse cholesterol transport in humans has been limited thus far. Recently, however, strategies to measure cholesterol efflux capacity have been used successfully in clinical studies, revealing inverse correlations between cholesterol efflux capacity and prevalent coronary artery disease, independently of the HDL cholesterol level.
It is not known whether cholesterol efflux capacity is associated with incident cardiovascular events (i.e., events occurring after time of sample collection) in unselected persons from the population. It is also not known whether sex, race, adiposity, relative insulin sensitivity or resistance, or inflammation influences cholesterol efflux capacity.
In a large, unselected, probability-based population cohort free from clinical cardiovascular disease at baseline, we investigated the epidemiology of cholesterol efflux capacity and evaluated the association of cholesterol efflux capacity with incident cardiovascular outcomes.
In this study, we found that a functional property of HDL, namely cholesterol efflux capacity, was inversely associated with incident atherosclerotic cardiovascular disease in a population-based cohort free from cardiovascular disease at baseline.
This association persisted after multivariate adjustment, suggesting that HDL function is associated with cardiovascular risk by means of processes distinct from those reflected by the HDL cholesterol level, HDL particle concentration, or traditional cardiovascular risk factors.
Rohatgi A, Khera A, Berry JD, et al. HDL Cholesterol Efflux Capacity and Incident Cardiovascular Events. New England Journal of Medicine. http://www.nejm.org/doi/full/10.1056/NEJMoa1409065
BACKGROUND - It is unclear whether high-density lipoprotein (HDL) cholesterol concentration plays a causal role in atherosclerosis. A more important factor may be HDL cholesterol efflux capacity, the ability of HDL to accept cholesterol from macrophages, which is a key step in reverse cholesterol transport. We investigated the epidemiology of cholesterol efflux capacity and its association with incident atherosclerotic cardiovascular disease outcomes in a large, multiethnic population cohort.
METHODS - We measured HDL cholesterol level, HDL particle concentration, and cholesterol efflux capacity at baseline in 2924 adults free from cardiovascular disease who were participants in the Dallas Heart Study, a probability-based population sample. The primary end point was atherosclerotic cardiovascular disease, defined as a first nonfatal myocardial infarction, nonfatal stroke, or coronary revascularization or death from cardiovascular causes. The median follow-up period was 9.4 years.
RESULTS - In contrast to HDL cholesterol level, which was associated with multiple traditional risk factors and metabolic variables, cholesterol efflux capacity had minimal association with these factors. Baseline HDL cholesterol level was not associated with cardiovascular events in an adjusted analysis (hazard ratio, 1.08; 95% confidence interval [CI], 0.59 to 1.99).
In a fully adjusted model that included traditional risk factors, HDL cholesterol level, and HDL particle concentration, there was a 67% reduction in cardiovascular risk in the highest quartile of cholesterol efflux capacity versus the lowest quartile (hazard ratio, 0.33; 95% CI, 0.19 to 0.55).
Adding cholesterol efflux capacity to traditional risk factors was associated with improvement in discrimination and reclassification indexes.
CONCLUSIONS - Cholesterol efflux capacity, a new biomarker that characterizes a key step in reverse cholesterol transport, was inversely associated with the incidence of cardiovascular events in a population-based cohort.
A low level of high-density lipoprotein (HDL) cholesterol is a major independent risk factor for atherosclerotic cardiovascular disease. However, in randomized, controlled trials, high-dose niacin or inhibitors of cholesteryl ester transfer protein did not improve cardiovascular outcomes despite significantly increasing the HDL cholesterol level.
Furthermore, genetic variants associated with HDL cholesterol levels are often not associated with cardiovascular disease. These observations suggest that HDL cholesterol may not be causally associated with cardiovascular disease, and they highlight the potential limitations of using the HDL cholesterol level to assess risk or responses to therapies targeted at HDL cholesterol.
HDL has numerous antiatherosclerotic actions that are not readily reflected by HDL cholesterol levels. A key function of HDL is to promote reverse cholesterol transport from the periphery to the liver, and the critical initial step in reverse cholesterol transport is cholesterol efflux from macrophages to HDL. Macrophage-specific cholesterol efflux capacity has been directly and causally linked to the prevention of atherosclerosis in animal models.
The ability to assess the clinical relevance of reverse cholesterol transport in humans has been limited thus far. Recently, however, strategies to measure cholesterol efflux capacity have been used successfully in clinical studies, revealing inverse correlations between cholesterol efflux capacity and prevalent coronary artery disease, independently of the HDL cholesterol level.
It is not known whether cholesterol efflux capacity is associated with incident cardiovascular events (i.e., events occurring after time of sample collection) in unselected persons from the population. It is also not known whether sex, race, adiposity, relative insulin sensitivity or resistance, or inflammation influences cholesterol efflux capacity.
In a large, unselected, probability-based population cohort free from clinical cardiovascular disease at baseline, we investigated the epidemiology of cholesterol efflux capacity and evaluated the association of cholesterol efflux capacity with incident cardiovascular outcomes.
In this study, we found that a functional property of HDL, namely cholesterol efflux capacity, was inversely associated with incident atherosclerotic cardiovascular disease in a population-based cohort free from cardiovascular disease at baseline.
This association persisted after multivariate adjustment, suggesting that HDL function is associated with cardiovascular risk by means of processes distinct from those reflected by the HDL cholesterol level, HDL particle concentration, or traditional cardiovascular risk factors.
Rohatgi A, Khera A, Berry JD, et al. HDL Cholesterol Efflux Capacity and Incident Cardiovascular Events. New England Journal of Medicine. http://www.nejm.org/doi/full/10.1056/NEJMoa1409065
BACKGROUND - It is unclear whether high-density lipoprotein (HDL) cholesterol concentration plays a causal role in atherosclerosis. A more important factor may be HDL cholesterol efflux capacity, the ability of HDL to accept cholesterol from macrophages, which is a key step in reverse cholesterol transport. We investigated the epidemiology of cholesterol efflux capacity and its association with incident atherosclerotic cardiovascular disease outcomes in a large, multiethnic population cohort.
METHODS - We measured HDL cholesterol level, HDL particle concentration, and cholesterol efflux capacity at baseline in 2924 adults free from cardiovascular disease who were participants in the Dallas Heart Study, a probability-based population sample. The primary end point was atherosclerotic cardiovascular disease, defined as a first nonfatal myocardial infarction, nonfatal stroke, or coronary revascularization or death from cardiovascular causes. The median follow-up period was 9.4 years.
RESULTS - In contrast to HDL cholesterol level, which was associated with multiple traditional risk factors and metabolic variables, cholesterol efflux capacity had minimal association with these factors. Baseline HDL cholesterol level was not associated with cardiovascular events in an adjusted analysis (hazard ratio, 1.08; 95% confidence interval [CI], 0.59 to 1.99).
In a fully adjusted model that included traditional risk factors, HDL cholesterol level, and HDL particle concentration, there was a 67% reduction in cardiovascular risk in the highest quartile of cholesterol efflux capacity versus the lowest quartile (hazard ratio, 0.33; 95% CI, 0.19 to 0.55).
Adding cholesterol efflux capacity to traditional risk factors was associated with improvement in discrimination and reclassification indexes.
CONCLUSIONS - Cholesterol efflux capacity, a new biomarker that characterizes a key step in reverse cholesterol transport, was inversely associated with the incidence of cardiovascular events in a population-based cohort.
Zhao J, Jiang C, Lam TH, et al. Genetically predicted testosterone and electrocardiographic QT interval duration in Chinese: a Mendelian randomization analysis in the Guangzhou Biobank Cohort Study. Int J Epidemiol. http://ije.oxfordjournals.org/content/early/2014/12/13/ije.dyu241.abstract
BACKGROUND: QT interval prolongation, a predictor of cardiac arrhythmias, and elevated heart rate are associated with higher risk of cardiovascular mortality. Observationally testosterone is associated with shorter corrected QT interval and slower heart rate; however, the evidence is open to residual confounding and reverse causality. We examined the association of testosterone with electrocardiogram (ECG) parameters using a separate-sample instrumental variable (SSIV) estimator.
METHODS: To minimize reverse causality, a genetic score predicting testosterone was developed in 289 young Chinese men from Hong Kong, based on a parsimonious set of single nuclear polymorphisms (rs10046, rs1008805 and rs1256031). Linear regression was used to examine the association of genetically predicted testosterone with QT interval, corrected QT interval [using the Framingham formula (QTf) and Bazett formula (QTb)] and heart rate in 4212 older (50+ years) Chinese men from the Guangzhou Biobank Cohort Study.
RESULTS: Predicted testosterone was not associated with QT interval [-0.08 ms per nmol/l testosterone, 95% confidence interval (CI) -0.81 to 0.65], QTf interval (0.40 ms per nmol/l testosterone, 95% CI -0.12 to 0.93) or heart rate (0.26 beats per minute per nmol/l testosterone, 95% CI -0.04 to 0.56), but was associated with longer QTb interval (0.66 ms per nmol/l testosterone, 95% CI 0.02 to 1.31).
CONCLUSIONS: Our findings do not corroborate observed protective associations of testosterone with QT interval or heart rate among men, but potentially suggest effects in the other direction. Replication in a larger sample is required.
BACKGROUND: QT interval prolongation, a predictor of cardiac arrhythmias, and elevated heart rate are associated with higher risk of cardiovascular mortality. Observationally testosterone is associated with shorter corrected QT interval and slower heart rate; however, the evidence is open to residual confounding and reverse causality. We examined the association of testosterone with electrocardiogram (ECG) parameters using a separate-sample instrumental variable (SSIV) estimator.
METHODS: To minimize reverse causality, a genetic score predicting testosterone was developed in 289 young Chinese men from Hong Kong, based on a parsimonious set of single nuclear polymorphisms (rs10046, rs1008805 and rs1256031). Linear regression was used to examine the association of genetically predicted testosterone with QT interval, corrected QT interval [using the Framingham formula (QTf) and Bazett formula (QTb)] and heart rate in 4212 older (50+ years) Chinese men from the Guangzhou Biobank Cohort Study.
RESULTS: Predicted testosterone was not associated with QT interval [-0.08 ms per nmol/l testosterone, 95% confidence interval (CI) -0.81 to 0.65], QTf interval (0.40 ms per nmol/l testosterone, 95% CI -0.12 to 0.93) or heart rate (0.26 beats per minute per nmol/l testosterone, 95% CI -0.04 to 0.56), but was associated with longer QTb interval (0.66 ms per nmol/l testosterone, 95% CI 0.02 to 1.31).
CONCLUSIONS: Our findings do not corroborate observed protective associations of testosterone with QT interval or heart rate among men, but potentially suggest effects in the other direction. Replication in a larger sample is required.
skywalker33
New Member
Thanks so much for all this info. I have been looking into all this myself recently and it's great to have this many studies in one place. I have some reading to do...
The Effect of Chronic Anabolic-Androgenic Steroid Use & 12-Lead Surface Electrocardiogram
Alizade E. The Effect of Chronic Anabolic-Androgenic Steroid Use on Tp-E Interval, Tp-E/Qt Ratio, and Tp-E/Qtc Ratio in Male Bodybuilders. Ann Noninvasive Electrocardiol. http://onlinelibrary.wiley.com/doi/10.1111/anec.12256/abstract
BACKGROUND: The chronic consumption of androgenic anabolic steroids has shown to cause atrial arrhythmias. Several studies have suggested that the interval from the peak to the end of the electrocardiographic T wave (Tp-e) may correspond to the transmural dispersion of repolarization and that increased Tp-e interval and Tp-e/QT ratio are associated with malignant ventricular arrhythmias.
The aim of this study was to evaluate repolarization dispersion measured from the 12-lead surface electrocardiogram (including Tp-e interval, Tp-e/QT ratio, and Tp-e/cQT ratio) in bodybuilders who are using anabolic androgenic steroids (AAS).
METHODS: We selected a population of 33 competitive bodybuilders, including 15 actively using AAS for >/= 2 years (users) and 18 who had never used AAS (nonusers), all men.
RESULTS: QT, cQT, QTd, cQTd, JT, and cJT were significantly increased in AAS users bodybulders compared to the nonusers (all P < 0.001). Tp-e interval, Tp-e/QT ratio, and Tp-e/cQT ratio were also significantly higher in AAS user group compared to the nonuser group (all P < 0.001). QRS duration was not different between the groups.
There were negative correlation between Em and Tp-e, Tp-e/QT ratio, Tp-e/cQT ration (r = -0.657, P < 0.01; r = -0.607, P = 0.02; r = -0.583, P = 0.02; respectively).There were also negative correlation between Sm and Tp-e, Tp-e/QT ratio, Tp-e/cQT ration (r = -0.681, P < 0.01; r = -0.549, P = 0.03; r = -0.544, P = 0.023; respectively).
CONCLUSION: In conclusion, we have presented a strong evidence suggesting that Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio were increased in AAS users, which suggest that there might be a link between AAS use and ventricular arrthymias and sudden death.
Alizade E. The Effect of Chronic Anabolic-Androgenic Steroid Use on Tp-E Interval, Tp-E/Qt Ratio, and Tp-E/Qtc Ratio in Male Bodybuilders. Ann Noninvasive Electrocardiol. http://onlinelibrary.wiley.com/doi/10.1111/anec.12256/abstract
BACKGROUND: The chronic consumption of androgenic anabolic steroids has shown to cause atrial arrhythmias. Several studies have suggested that the interval from the peak to the end of the electrocardiographic T wave (Tp-e) may correspond to the transmural dispersion of repolarization and that increased Tp-e interval and Tp-e/QT ratio are associated with malignant ventricular arrhythmias.
The aim of this study was to evaluate repolarization dispersion measured from the 12-lead surface electrocardiogram (including Tp-e interval, Tp-e/QT ratio, and Tp-e/cQT ratio) in bodybuilders who are using anabolic androgenic steroids (AAS).
METHODS: We selected a population of 33 competitive bodybuilders, including 15 actively using AAS for >/= 2 years (users) and 18 who had never used AAS (nonusers), all men.
RESULTS: QT, cQT, QTd, cQTd, JT, and cJT were significantly increased in AAS users bodybulders compared to the nonusers (all P < 0.001). Tp-e interval, Tp-e/QT ratio, and Tp-e/cQT ratio were also significantly higher in AAS user group compared to the nonuser group (all P < 0.001). QRS duration was not different between the groups.
There were negative correlation between Em and Tp-e, Tp-e/QT ratio, Tp-e/cQT ration (r = -0.657, P < 0.01; r = -0.607, P = 0.02; r = -0.583, P = 0.02; respectively).There were also negative correlation between Sm and Tp-e, Tp-e/QT ratio, Tp-e/cQT ration (r = -0.681, P < 0.01; r = -0.549, P = 0.03; r = -0.544, P = 0.023; respectively).
CONCLUSION: In conclusion, we have presented a strong evidence suggesting that Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio were increased in AAS users, which suggest that there might be a link between AAS use and ventricular arrthymias and sudden death.
Baumann S, Jabbour C, Huseynov A, Borggrefe M, Haghi D, et al. Myocardial Scar Detected by Cardiovascular Magnetic Resonance in a Competitive Bodybuilder With Longstanding Abuse of Anabolic Steroids. Asian J Sports Med. 2015;5(4):e24058. http://asjsm.com/?page=article&article_id=24058
INTRODUCTION: The self-administration intake of anabolic-androgenic steroids (AAS) is a widespread practice in competitive bodybuilders. Structural changes within the myocardium following AAS abuse including hypertrophy, restricted diastolic function as well as systolic dysfunction and impaired ventricular inflow have been reported.
CASE PRESENTATION: We present the case of a 39-year-old bodybuilder with a more than 20-year history of anabolic-androgenic steroids (AAS) abuse presenting with increasing exertional dyspnoea and fatigue.
Diagnostic work-up of the patient's current symptoms included a cine cardiovascular magnetic resonance (CMR). Using a T1-weighted inversion-recovery sequence 10 minutes after application of 0.1 mmol/kg gadolinium with diethylenetriaminepentaacetic acid (gadolinium DTPA), patchy midwall enhancement in the septal and posterolateral region of the left ventricle was demonstrated.
This enhancement pattern is different from the enhancement pattern found in patients with ischemic heart disease.
CONCLUSIONS: The present case illustrates for the first time, by CMR, myocardial scarring with severe left ventricular hypertrophy in a patient with normal coronary arteries after long lasting abuse of AAS. With that finding we could demonstrate a link between AAS abuse and the occurrence of myocardial scarring in humans. This finding may help raise awareness of the consequences of AAS use.
INTRODUCTION: The self-administration intake of anabolic-androgenic steroids (AAS) is a widespread practice in competitive bodybuilders. Structural changes within the myocardium following AAS abuse including hypertrophy, restricted diastolic function as well as systolic dysfunction and impaired ventricular inflow have been reported.
CASE PRESENTATION: We present the case of a 39-year-old bodybuilder with a more than 20-year history of anabolic-androgenic steroids (AAS) abuse presenting with increasing exertional dyspnoea and fatigue.
Diagnostic work-up of the patient's current symptoms included a cine cardiovascular magnetic resonance (CMR). Using a T1-weighted inversion-recovery sequence 10 minutes after application of 0.1 mmol/kg gadolinium with diethylenetriaminepentaacetic acid (gadolinium DTPA), patchy midwall enhancement in the septal and posterolateral region of the left ventricle was demonstrated.
This enhancement pattern is different from the enhancement pattern found in patients with ischemic heart disease.
CONCLUSIONS: The present case illustrates for the first time, by CMR, myocardial scarring with severe left ventricular hypertrophy in a patient with normal coronary arteries after long lasting abuse of AAS. With that finding we could demonstrate a link between AAS abuse and the occurrence of myocardial scarring in humans. This finding may help raise awareness of the consequences of AAS use.
When Testosterone Can Break Your Heart
https://endo.confex.com/endo/2015endo/webprogram/Paper19173.html
Testosterone replacement has been increasingly promoted over the past years and currently there is insufficient data regarding the potential associated cardiovascular morbidity. Potential mechanisms of cardiovascular toxicity are: atherogenic, thrombotic, vasospastic and direct myocardial injury.
We highlight the case of a young patient that presented with new onset congestive heart failure in the context of using supraphysiological doses of intramuscular testosterone.
A 52 year old previously healthy man presented to our hospital with worsening dyspnea on exertion for 2-3 weeks, 2 pillow orthopnea and paroxysmal nocturnal dyspnea accompanied by “band like” chest pain.
His past medical history was only positive for “low testosterone” and he denied smoking, habitual alcohol use or drug use. He is a firefighter and was previously very active with no limitations.
His home medications were: inhaled albuterol, montelukast and injectable intramuscular testosterone. On physical examination patient was noted to be very muscular, looking younger than his stated age. Exam was otherwise unremarkable except for bilateral rales in both lung bases.
Laboratory data revealed polycythemia with an elevated hematocrit level (62.9, n 37.0-50.0 %).
An echocardiogram showed a severely depressed left and right ventricular function and further cardiac workup revealed a non-ischemic etiology.
A total testosterone level was obtained because of the polycythemia and was noted to be markedly elevated (2240 ng/dL n 240-950 ng/dL).
On further interview patient disclosed that he was taking testosterone 200mg intramuscularly every 4 days and was not following up regularly with his physician to check testosterone levels. He was self-dosing the testosterone based on symptoms of low energy.
Patient was started on treatment with intravenous lasix and underwent phlebotomy with improvement in the symptoms and hematocrit level. Testosterone injections were discontinued.
The testosterone levels remained very elevated for more than 3 weeks after the last intramuscular testosterone injection, most likely because of the stacking effect of the frequent self-administered doses.
He was seen in follow up after a few months and at that time his systolic function had significantly improved.
This case illustrates the fact that supraphysiological levels of testosterone could be associated with new onset congestive heart failure in young fit men on testosterone replacement therapy.
A testosterone level should be obtained in these patients as part of the workup. Testing should be considered even in patients that do not disclose testosterone use.
https://endo.confex.com/endo/2015endo/webprogram/Paper19173.html
Testosterone replacement has been increasingly promoted over the past years and currently there is insufficient data regarding the potential associated cardiovascular morbidity. Potential mechanisms of cardiovascular toxicity are: atherogenic, thrombotic, vasospastic and direct myocardial injury.
We highlight the case of a young patient that presented with new onset congestive heart failure in the context of using supraphysiological doses of intramuscular testosterone.
A 52 year old previously healthy man presented to our hospital with worsening dyspnea on exertion for 2-3 weeks, 2 pillow orthopnea and paroxysmal nocturnal dyspnea accompanied by “band like” chest pain.
His past medical history was only positive for “low testosterone” and he denied smoking, habitual alcohol use or drug use. He is a firefighter and was previously very active with no limitations.
His home medications were: inhaled albuterol, montelukast and injectable intramuscular testosterone. On physical examination patient was noted to be very muscular, looking younger than his stated age. Exam was otherwise unremarkable except for bilateral rales in both lung bases.
Laboratory data revealed polycythemia with an elevated hematocrit level (62.9, n 37.0-50.0 %).
An echocardiogram showed a severely depressed left and right ventricular function and further cardiac workup revealed a non-ischemic etiology.
A total testosterone level was obtained because of the polycythemia and was noted to be markedly elevated (2240 ng/dL n 240-950 ng/dL).
On further interview patient disclosed that he was taking testosterone 200mg intramuscularly every 4 days and was not following up regularly with his physician to check testosterone levels. He was self-dosing the testosterone based on symptoms of low energy.
Patient was started on treatment with intravenous lasix and underwent phlebotomy with improvement in the symptoms and hematocrit level. Testosterone injections were discontinued.
The testosterone levels remained very elevated for more than 3 weeks after the last intramuscular testosterone injection, most likely because of the stacking effect of the frequent self-administered doses.
He was seen in follow up after a few months and at that time his systolic function had significantly improved.
This case illustrates the fact that supraphysiological levels of testosterone could be associated with new onset congestive heart failure in young fit men on testosterone replacement therapy.
A testosterone level should be obtained in these patients as part of the workup. Testing should be considered even in patients that do not disclose testosterone use.
Placci A, Sella G, Bellanti G, Margheri M. Anabolic androgenic steroid-induced Takotsubo cardiomyopathy. BMJ Case Rep. 2015. http://casereports.bmj.com/content/2015/bcr-2014-209089.short?rss=1
Anabolic steroid abuse, aimed at increasing muscle mass, has been growing in recent years. We describe a case of a 25-year-old bodybuilder who, after taking nandrolone and stanozolol, presented with Takotsubo syndrome. The angiography showed a normal coronary anatomy with the absence of stenosis. The left ventricular function was completely normalised after 1 week.
Virani SS, Khan AN, Mendoza CE, Ferreira AC, de Marchena E. Takotsubo Cardiomyopathy, or Broken-Heart Syndrome. Texas Heart Institute Journal. 2007;34(1):76-9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1847940/
Takotsubo cardiomyopathy mimics acute coronary syndrome and is accompanied by reversible left ventricular apical ballooning in the absence of angiographically significant coronary artery stenosis. In Japanese, “tako-tsubo” means “fishing pot for trapping octopus,” and the left ventricle of a patient diagnosed with this condition resembles that shape. Takotsubo cardiomyopathy, which is transient and typically precipitated by acute emotional stress, is also known as “stress cardiomyopathy” or “broken-heart syndrome.”
Herein, we describe the clinical angiographic characteristics of 4 patients who exhibited this syndrome, and we review the existing literature and propose reasons to conduct prospective studies.
Anabolic steroid abuse, aimed at increasing muscle mass, has been growing in recent years. We describe a case of a 25-year-old bodybuilder who, after taking nandrolone and stanozolol, presented with Takotsubo syndrome. The angiography showed a normal coronary anatomy with the absence of stenosis. The left ventricular function was completely normalised after 1 week.
Virani SS, Khan AN, Mendoza CE, Ferreira AC, de Marchena E. Takotsubo Cardiomyopathy, or Broken-Heart Syndrome. Texas Heart Institute Journal. 2007;34(1):76-9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1847940/
Takotsubo cardiomyopathy mimics acute coronary syndrome and is accompanied by reversible left ventricular apical ballooning in the absence of angiographically significant coronary artery stenosis. In Japanese, “tako-tsubo” means “fishing pot for trapping octopus,” and the left ventricle of a patient diagnosed with this condition resembles that shape. Takotsubo cardiomyopathy, which is transient and typically precipitated by acute emotional stress, is also known as “stress cardiomyopathy” or “broken-heart syndrome.”
Herein, we describe the clinical angiographic characteristics of 4 patients who exhibited this syndrome, and we review the existing literature and propose reasons to conduct prospective studies.
Last edited:
Thieme D, Buttner A. [German - Cardiovascular alterations associated with doping]. Herz. http://link.springer.com/article/10.1007/s00059-015-4218-2/fulltext.html
Doping -the abuse of anabolic-androgenic steroids in particular- is widespread in amateur and recreational sports and does not solely represent a problem of professional sports. Excessive overdose of anabolic steroids is well documented in bodybuilding or powerlifting leading to significant side effects.
Cardiovascular damages are most relevant next to adverse endocrine effects. Clinical cases as well as forensic investigations of fatalities or steroid consumption in connection with trafficking of doping agents provide only anecdotal evidence of correlations between side effects and substance abuse.
Analytical verification and self-declarations of steroid users have repeatedly confirmed the presumption of weekly dosages between 300 and 2000 mg, extra to the fact that co-administration of therapeutics to treat side-effects represent a routine procedure.
Beside the most frequent use of medications used to treat erectile dysfunction or estrogenic side-effects, a substantial number of antihypertensive drugs of various classes, i.e. beta-blockers, diuretics, angiotensin II receptor antagonists, calcium channel blockers, as well as ACE inhibitors were recently confiscated in relevant doping cases.
The presumptive correlation between misuse of anabolic steroids and self-treatment of cardiovascular side effects was explicitly confirmed by detailed user statements. Two representative fatalities of bodybuilders were introduced to outline characteristic, often lethal side effects of excessive steroid abuse.
Moreover, illustrative autopsy findings of steroid acne, thrombotic occlusion of Ramus interventricularis anterior and signs of cardiac infarctions are presented.
A potential steroid abuse should be carefully considered in cases of medical consultations of patients exhibiting apparent constitutional modifications and corresponding adverse effects. Moreover, common self-medications -as frequently applied by steroid consumers- should be taken into therapeutic considerations.
Doping -the abuse of anabolic-androgenic steroids in particular- is widespread in amateur and recreational sports and does not solely represent a problem of professional sports. Excessive overdose of anabolic steroids is well documented in bodybuilding or powerlifting leading to significant side effects.
Cardiovascular damages are most relevant next to adverse endocrine effects. Clinical cases as well as forensic investigations of fatalities or steroid consumption in connection with trafficking of doping agents provide only anecdotal evidence of correlations between side effects and substance abuse.
Analytical verification and self-declarations of steroid users have repeatedly confirmed the presumption of weekly dosages between 300 and 2000 mg, extra to the fact that co-administration of therapeutics to treat side-effects represent a routine procedure.
Beside the most frequent use of medications used to treat erectile dysfunction or estrogenic side-effects, a substantial number of antihypertensive drugs of various classes, i.e. beta-blockers, diuretics, angiotensin II receptor antagonists, calcium channel blockers, as well as ACE inhibitors were recently confiscated in relevant doping cases.
The presumptive correlation between misuse of anabolic steroids and self-treatment of cardiovascular side effects was explicitly confirmed by detailed user statements. Two representative fatalities of bodybuilders were introduced to outline characteristic, often lethal side effects of excessive steroid abuse.
Moreover, illustrative autopsy findings of steroid acne, thrombotic occlusion of Ramus interventricularis anterior and signs of cardiac infarctions are presented.
A potential steroid abuse should be carefully considered in cases of medical consultations of patients exhibiting apparent constitutional modifications and corresponding adverse effects. Moreover, common self-medications -as frequently applied by steroid consumers- should be taken into therapeutic considerations.
Luijkx T, Velthuis BK, Backx FJ, Buckens CF, Prakken NH, et al. Anabolic androgenic steroid use is associated with ventricular dysfunction on cardiac MRI in strength trained athletes. Int J Cardiol. 2013;167(3):664-8. http://www.internationaljournalofcardiology.com/article/S0167-5273(12)00277-X/fulltext
BACKGROUND: Uncertainty remains about possible cardiac adaptation to resistance training. Androgenic anabolic steroids (AAS) use plays a potential role and may have adverse cardiovascular effects.
OBJECTIVE: To elucidate the effect of resistance training and of AAS-use on cardiac dimensions and function.
PARTICIPANTS: Cardiac magnetic resonance (CMR) were performed in 156 male subjects aged 18-40 years: 52 non-athletes (maximum of 3 exercise hours/week), 52 strength-endurance (high dynamic-high static, HD-HS) athletes and 52 strength (low dynamic-high static, LD-HS) trained athletes (athletes >/= 6 exercise hours/week). 28 LD-HS athletes denied and 24 admitted to AAS use for an average duration of 5 years (range 3 months-20 years).
RESULTS: No significant differences were found between non-athletes and non-AAS-using LD-HS athletes. AAS-using LD-HS athletes had significantly larger LV and RV volumes and LV wall mass than non-AAS-using LD-HS athletes, but lower than HD-HS athletes. In comparison to all other groups AAS-using LD-HS athletes showed lower ejection fractions of both ventricles (LV/RV EF 51/48% versus 55-57/51-52%) and lower E/A ratios (LV/RV 1.5/1.2 versus 1.9-2.0/1.4-1.5) as an indirect measure of diastolic function. Linear regression models demonstrated a significant effect of AAS-use on LV EDV, LV EDM, systolic function and mitral valve E/A ratio (all ANOVA-tests p<0.05).
CONCLUSIONS: Strength athletes who use AAS show significantly different cardiac dimensions and biventricular systolic dysfunction and impaired ventricular inflow as compared to non-athletes and non-AAS-using strength athletes. Increased ventricular volume and mass did not exceed that of strength-endurance athletes. These findings may help raise awareness of the consequences of AAS use.
BACKGROUND: Uncertainty remains about possible cardiac adaptation to resistance training. Androgenic anabolic steroids (AAS) use plays a potential role and may have adverse cardiovascular effects.
OBJECTIVE: To elucidate the effect of resistance training and of AAS-use on cardiac dimensions and function.
PARTICIPANTS: Cardiac magnetic resonance (CMR) were performed in 156 male subjects aged 18-40 years: 52 non-athletes (maximum of 3 exercise hours/week), 52 strength-endurance (high dynamic-high static, HD-HS) athletes and 52 strength (low dynamic-high static, LD-HS) trained athletes (athletes >/= 6 exercise hours/week). 28 LD-HS athletes denied and 24 admitted to AAS use for an average duration of 5 years (range 3 months-20 years).
RESULTS: No significant differences were found between non-athletes and non-AAS-using LD-HS athletes. AAS-using LD-HS athletes had significantly larger LV and RV volumes and LV wall mass than non-AAS-using LD-HS athletes, but lower than HD-HS athletes. In comparison to all other groups AAS-using LD-HS athletes showed lower ejection fractions of both ventricles (LV/RV EF 51/48% versus 55-57/51-52%) and lower E/A ratios (LV/RV 1.5/1.2 versus 1.9-2.0/1.4-1.5) as an indirect measure of diastolic function. Linear regression models demonstrated a significant effect of AAS-use on LV EDV, LV EDM, systolic function and mitral valve E/A ratio (all ANOVA-tests p<0.05).
CONCLUSIONS: Strength athletes who use AAS show significantly different cardiac dimensions and biventricular systolic dysfunction and impaired ventricular inflow as compared to non-athletes and non-AAS-using strength athletes. Increased ventricular volume and mass did not exceed that of strength-endurance athletes. These findings may help raise awareness of the consequences of AAS use.
Ilic I, Djordjevic V, Stankovic I, Vlahovic-Stipac A, Putnikovic B, et al. The impact of anabolic androgenic steroids abuse and type of training on left ventricular remodeling and function in competitive athletes. Vojnosanit Pregl. 2014;71(4):383-9. http://www.doiserbia.nb.rs/Article.aspx?ID=0042-84501300046I
BACKGROUND/AIM: Long-term intensive training is associated with distinctive cardiac adaptations which are known as athlete's heart. The aim of this study was to determine whether the use of anabolic androgenic steroids (AAS) could affect echocardiographic parameters of left ventricular (LV) morphology and function in elite strength and endurance athletes.
METHODS: A total of 20 elite strength athletes (10 AAS users and 10 non-users) were compared to 12 steroid-free endurance athletes. All the subjects underwent comprehensive standard echocardiography and tissue Doppler imaging.
RESULTS: After being indexed for body surface area, both left atrium (LA) and LV end-diastolic diameter (LVEDD) were significantly higher in the endurance than strength athletes, regardless of AAS use (p < 0.05, for both). A significant correlation was found between LA diameter and LVEDD in the steroid-free endurance athletes, showing that 75% of LA size variability depends on variability of LVEDD (p < 0.001). No significant differences in ejection fraction and cardiac output were observed among the groups, although mildly reduced LV ejection fraction was seen only in the AAS users. The AAS-using strength athletes had higher A-peak velocity when compared to steroid-free athletes, regardless of training type (p < 0.05 for both). Both AAS-using and AAS-free strength athletes had lower e' peak velocity and higher E/e' ratio than endurance athletes (p < 0.05, for all).
CONCLUSIONS: There is no evidence that LV ejection fraction in elite athletes is altered by either type of training or AAS misuse. Long-term endurance training is associated with preferable effects on LV diastolic function compared to strength training, particularly when the latter is combined with AAS abuse.
BACKGROUND/AIM: Long-term intensive training is associated with distinctive cardiac adaptations which are known as athlete's heart. The aim of this study was to determine whether the use of anabolic androgenic steroids (AAS) could affect echocardiographic parameters of left ventricular (LV) morphology and function in elite strength and endurance athletes.
METHODS: A total of 20 elite strength athletes (10 AAS users and 10 non-users) were compared to 12 steroid-free endurance athletes. All the subjects underwent comprehensive standard echocardiography and tissue Doppler imaging.
RESULTS: After being indexed for body surface area, both left atrium (LA) and LV end-diastolic diameter (LVEDD) were significantly higher in the endurance than strength athletes, regardless of AAS use (p < 0.05, for both). A significant correlation was found between LA diameter and LVEDD in the steroid-free endurance athletes, showing that 75% of LA size variability depends on variability of LVEDD (p < 0.001). No significant differences in ejection fraction and cardiac output were observed among the groups, although mildly reduced LV ejection fraction was seen only in the AAS users. The AAS-using strength athletes had higher A-peak velocity when compared to steroid-free athletes, regardless of training type (p < 0.05 for both). Both AAS-using and AAS-free strength athletes had lower e' peak velocity and higher E/e' ratio than endurance athletes (p < 0.05, for all).
CONCLUSIONS: There is no evidence that LV ejection fraction in elite athletes is altered by either type of training or AAS misuse. Long-term endurance training is associated with preferable effects on LV diastolic function compared to strength training, particularly when the latter is combined with AAS abuse.
Parker MW, Thompson PD. Anabolic-Androgenic Steroids: Worse for the Heart Than We Knew? Circulation: Heart Failure. 2010;3(4):470-1. http://circheartfailure.ahajournals.org/content/3/4/470.full
Baggish AL, Weiner RB, Kanayama G, Hudson JI, Picard MH, et al. Long-term anabolic-androgenic steroid use is associated with left ventricular dysfunction. Circ Heart Fail. 2010;3(4):472-6. http://circheartfailure.ahajournals.org/content/3/4/472.long
BACKGROUND: Although illicit anabolic-androgenic steroid (AAS) use is widespread, the cardiac effects of long-term AAS use remain inadequately characterized. We compared cardiac parameters in weightlifters reporting long-term AAS use to those in otherwise similar weightlifters without prior AAS exposure.
METHODS AND RESULTS: We performed 2D tissue-Doppler and speckle-tracking echocardiography to assess left ventricular (LV) ejection fraction, LV systolic strain, and conventional indices of diastolic function in long-term AAS users (n=12) and otherwise similar AAS nonusers (n=7). AAS users (median [quartile 1, quartile 3] cumulative lifetime AAS exposure, 468 [169, 520] weeks) closely resembled nonusers in age, prior duration of weightlifting, and current intensity of weight training.
LV structural parameters were similar between the two groups; however, AAS users had significantly lower LV ejection fraction (50.6% [48.4, 53.6] versus 59.1% [58.0%, 61.7%]; P=0.003 by two-tailed Wilcoxon rank sum test), longitudinal strain (16.9% [14.0%, 19.0%] versus 21.0% [20.2%, 22.9%]; P=0.004), and radial strain (38.3% [28.5%, 43.7%] versus 50.1% [44.3%, 61.8%]; P=0.02). Ten of the 12 AAS users showed LV ejection fractions below the accepted limit of normal (>or=55%).
AAS users also demonstrated decreased diastolic function compared to nonusers as evidenced by a markedly lower early peak tissue velocity (7.4 [6.8, 7.9] cm/s versus 9.9 [8.3, 10.5] cm/s; P=0.005) and early-to-late diastolic filling ratio (0.93 [0.88, 1.39] versus 1.80 [1.48, 2.00]; P=0.003).
CONCLUSIONS: Cardiac dysfunction in long-term AAS users appears to be more severe than previously reported and may be sufficient to increase the risk of heart failure.
Baggish AL, Weiner RB, Kanayama G, Hudson JI, Picard MH, et al. Long-term anabolic-androgenic steroid use is associated with left ventricular dysfunction. Circ Heart Fail. 2010;3(4):472-6. http://circheartfailure.ahajournals.org/content/3/4/472.long
BACKGROUND: Although illicit anabolic-androgenic steroid (AAS) use is widespread, the cardiac effects of long-term AAS use remain inadequately characterized. We compared cardiac parameters in weightlifters reporting long-term AAS use to those in otherwise similar weightlifters without prior AAS exposure.
METHODS AND RESULTS: We performed 2D tissue-Doppler and speckle-tracking echocardiography to assess left ventricular (LV) ejection fraction, LV systolic strain, and conventional indices of diastolic function in long-term AAS users (n=12) and otherwise similar AAS nonusers (n=7). AAS users (median [quartile 1, quartile 3] cumulative lifetime AAS exposure, 468 [169, 520] weeks) closely resembled nonusers in age, prior duration of weightlifting, and current intensity of weight training.
LV structural parameters were similar between the two groups; however, AAS users had significantly lower LV ejection fraction (50.6% [48.4, 53.6] versus 59.1% [58.0%, 61.7%]; P=0.003 by two-tailed Wilcoxon rank sum test), longitudinal strain (16.9% [14.0%, 19.0%] versus 21.0% [20.2%, 22.9%]; P=0.004), and radial strain (38.3% [28.5%, 43.7%] versus 50.1% [44.3%, 61.8%]; P=0.02). Ten of the 12 AAS users showed LV ejection fractions below the accepted limit of normal (>or=55%).
AAS users also demonstrated decreased diastolic function compared to nonusers as evidenced by a markedly lower early peak tissue velocity (7.4 [6.8, 7.9] cm/s versus 9.9 [8.3, 10.5] cm/s; P=0.005) and early-to-late diastolic filling ratio (0.93 [0.88, 1.39] versus 1.80 [1.48, 2.00]; P=0.003).
CONCLUSIONS: Cardiac dysfunction in long-term AAS users appears to be more severe than previously reported and may be sufficient to increase the risk of heart failure.
Sondergaard EB, Thune JJ, Gustafsson F. Characteristics and outcome of patients with heart failure due to anabolic-androgenic steroids. Scand Cardiovasc J. 2014;48(6):339-42. http://informahealthcare.com/doi/abs/10.3109/14017431.2014.976837
OBJECTIVES: The objective of the study was to analyse the outcome of patients with advanced heart failure due to abuse of anabolic-androgenic steroids.
DESIGN: A retrospective chart review of patients admitted or referred for advanced heart failure, due to anabolic-androgenic steroid abuse, in the period 2009-2013 was performed.
RESULTS: In 6 of 9 patients (median age: 31, all males) referred in the study period, some potential for recovery of left ventricular (LV) function was seen (P < 0.002), with a maximal improvement in LV ejection fraction reached within 6 months of treatment with angiotensin-converting enzyme inhibitors and beta-blockers. The remaining 3 patients required implantation of a LV assist device (LVAD) and were listed for heart transplantation. No recovery of LV function in the patients treated with assist device was seen.
CONCLUSION: Anabolic-androgenic steroid-induced advanced heart failure is generally not a reversible condition. If diagnosed in the early stages some recovery of ventricular function is possible, but the long-term prognosis is uncertain. Likely, a substantial proportion of patients will eventually require LVADs or cardiac transplantation.
OBJECTIVES: The objective of the study was to analyse the outcome of patients with advanced heart failure due to abuse of anabolic-androgenic steroids.
DESIGN: A retrospective chart review of patients admitted or referred for advanced heart failure, due to anabolic-androgenic steroid abuse, in the period 2009-2013 was performed.
RESULTS: In 6 of 9 patients (median age: 31, all males) referred in the study period, some potential for recovery of left ventricular (LV) function was seen (P < 0.002), with a maximal improvement in LV ejection fraction reached within 6 months of treatment with angiotensin-converting enzyme inhibitors and beta-blockers. The remaining 3 patients required implantation of a LV assist device (LVAD) and were listed for heart transplantation. No recovery of LV function in the patients treated with assist device was seen.
CONCLUSION: Anabolic-androgenic steroid-induced advanced heart failure is generally not a reversible condition. If diagnosed in the early stages some recovery of ventricular function is possible, but the long-term prognosis is uncertain. Likely, a substantial proportion of patients will eventually require LVADs or cardiac transplantation.
Pongkan W, Chattipakorn SC, Chattipakorn N. Chronic Testosterone Replacement Exerts Cardioprotection against Cardiac Ischemia-Reperfusion Injury by Attenuating Mitochondrial Dysfunction in Testosterone-Deprived Rats. PLoS One. 2015;10(3):e0122503. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0122503
BACKGROUND: Although testosterone deficiency is associated with increased risks of heart disease, the benefits of testosterone therapy are controversial. Moreover, current understanding on the cardiac effect of testosterone during cardiac ischemia-reperfusion (I/R) periods is unclear. We tested the hypothesis that testosterone replacement attenuates the impairment of left ventricular (LV) function and heart rate variability (HRV), and reduces the infarct size and arrhythmias caused by I/R injury in orchiectomized (ORX) rats.
METHODOLOGY: ORX or sham-operated male Wistar rats (n = 24) were randomly divided and received either testosterone (2 mg/kg, subcutaneously administered) or the vehicle for 8 weeks. The ejection fraction (EF) and HRV were determined at baseline and the 4th and 8th week. I/R was performed by left anterior descending coronary artery ligation for 30 minutes, followed by a 120-minute reperfusion. LV pressure, arrhythmia scores, infarct size and cardiac mitochondrial function were determined.
RESULTS: Prior to I/R, EF and HRV were impaired in the ORX group, but were restored in the testosterone-treated group. During I/R, arrhythmia scores and the infarct size were greater, and cardiac mitochondrial function was impaired, whereas the time to 1st VT/VF onset and the LV end-systolic pressure were decreased in the ORX group when compared to the sham group. Testosterone replacement attenuated the impairment of these parameters in ORX rats during I/R injury, but did not show any benefit or adverse effect in non-ORX rats.
CONCLUSIONS: Testosterone replacement restores cardiac function and autonomic regulation, and exerts cardioprotective effects during the I/R period via mitochondrial protection in ORX rats.
BACKGROUND: Although testosterone deficiency is associated with increased risks of heart disease, the benefits of testosterone therapy are controversial. Moreover, current understanding on the cardiac effect of testosterone during cardiac ischemia-reperfusion (I/R) periods is unclear. We tested the hypothesis that testosterone replacement attenuates the impairment of left ventricular (LV) function and heart rate variability (HRV), and reduces the infarct size and arrhythmias caused by I/R injury in orchiectomized (ORX) rats.
METHODOLOGY: ORX or sham-operated male Wistar rats (n = 24) were randomly divided and received either testosterone (2 mg/kg, subcutaneously administered) or the vehicle for 8 weeks. The ejection fraction (EF) and HRV were determined at baseline and the 4th and 8th week. I/R was performed by left anterior descending coronary artery ligation for 30 minutes, followed by a 120-minute reperfusion. LV pressure, arrhythmia scores, infarct size and cardiac mitochondrial function were determined.
RESULTS: Prior to I/R, EF and HRV were impaired in the ORX group, but were restored in the testosterone-treated group. During I/R, arrhythmia scores and the infarct size were greater, and cardiac mitochondrial function was impaired, whereas the time to 1st VT/VF onset and the LV end-systolic pressure were decreased in the ORX group when compared to the sham group. Testosterone replacement attenuated the impairment of these parameters in ORX rats during I/R injury, but did not show any benefit or adverse effect in non-ORX rats.
CONCLUSIONS: Testosterone replacement restores cardiac function and autonomic regulation, and exerts cardioprotective effects during the I/R period via mitochondrial protection in ORX rats.
Binayi F, Joukar S, Najafipour H, Karimi A, Abdollahi F, et al. The Effects of Nandrolone Decanoate Along with Prolonged Low-Intensity Exercise on Susceptibility to Ventricular Arrhythmias. Cardiovasc Toxicol. http://link.springer.com/article/10.1007/s12012-015-9313-3
We examined the influence of chronic administration of nandrolone decanoate with low-intensity endurance swimming exercise on susceptibility to lethal ventricular arrhythmias in rat.
The animal groups included the control group, exercise group (EX), nandrolone group (Nan), vehicle group (Arach), trained vehicle group (Arach + Ex) and trained nandrolone group (Nan + Ex) that treated for 8 weeks.
Then, arrhythmia induction was performed by intravenous infusion of aconitine and electrocardiogram recorded. Then, malondialdehyde (MDA), hydroxyproline (HYP) and glutathione peroxidase of heart tissue were measured.
Chronic administration of nandrolone with low-intensity endurance swimming exercise had no significant effect on blood pressure, heart rate and basal ECG parameters except RR interval that showed increase (P < 0.05). Low-intensity exercise could prevent the incremental effect of nandrolone on MDA and HYP significantly. It also increased the heart hypertrophy index (P < 0.05) and reduced the abating effect of nandrolone on animal weighting.
Nandrolone along with exercise significantly increased the duration of VF (P < 0.05) and reduced the VF latency (P < 0.05). The findings suggest that chronic co-administration of nandrolone with low-intensity endurance swimming exercise to some extent facilitates the occurrence of ventricular fibrillation in rat.
Complementary studies are needed to elucidate the involved mechanisms of this abnormality.
We examined the influence of chronic administration of nandrolone decanoate with low-intensity endurance swimming exercise on susceptibility to lethal ventricular arrhythmias in rat.
The animal groups included the control group, exercise group (EX), nandrolone group (Nan), vehicle group (Arach), trained vehicle group (Arach + Ex) and trained nandrolone group (Nan + Ex) that treated for 8 weeks.
Then, arrhythmia induction was performed by intravenous infusion of aconitine and electrocardiogram recorded. Then, malondialdehyde (MDA), hydroxyproline (HYP) and glutathione peroxidase of heart tissue were measured.
Chronic administration of nandrolone with low-intensity endurance swimming exercise had no significant effect on blood pressure, heart rate and basal ECG parameters except RR interval that showed increase (P < 0.05). Low-intensity exercise could prevent the incremental effect of nandrolone on MDA and HYP significantly. It also increased the heart hypertrophy index (P < 0.05) and reduced the abating effect of nandrolone on animal weighting.
Nandrolone along with exercise significantly increased the duration of VF (P < 0.05) and reduced the VF latency (P < 0.05). The findings suggest that chronic co-administration of nandrolone with low-intensity endurance swimming exercise to some extent facilitates the occurrence of ventricular fibrillation in rat.
Complementary studies are needed to elucidate the involved mechanisms of this abnormality.
I love all the studies but I'd really like to hear from anyone with knowledge on the subject how you can mitigate the risks of heart disease while using steroids?
Alexandre J, Milliez P, Rouet R, Manrique A, Allouche S, et al. Aldosterone and testosterone: two steroid hormones structurally related but with opposite electrophysiological properties during myocardial ischemia-reperfusion. Fundam Clin Pharmacol. http://onlinelibrary.wiley.com/doi/10.1111/fcp.12122/abstract
Steroid hormones appear to be a key factor in the gender differences in the rates and severity of cardiovascular diseases. Aldosterone and testosterone have typical steroid ring structure but despite this, they demonstrate very different properties.
During acute myocardial ischemia-reperfusion, the deleterious impact of aldosterone is now well established. Conversely, the electrophysiological impact of testosterone in this context remained unknown.
We used female rabbit in vitro models and standard microelectrode technique including right ventricle mimicking the "border zone" existing between normal and ischemic/reperfused areas and isolated right ventricle experiments to assess the acute electrophysiological impact of both aldosterone and testosterone.
During ischemia-reperfusion, acute superfusion of 10 and 100 nmol/L testosterone decreased normoxic and reperfused action potential duration at 90% (APD90 ), systematically induced conduction blocks and decreased APD90 dispersion between ischemic and non-ischemic areas (from 98+/-4 ms to 57+/-7 ms and 66+/-3 ms, for respectively testosterone 10 and 100 nmol/L, P<0.05). Testosterone 10 and 100 nmol/L concomitantly decreased sustained premature ventricular contractions (PVCs) occurrence (from 55% to 0%, P<0.05).
Conversely, aldosterone 10 and 100 nmol/L increased normoxic and reperfused APD90 , APD90 dispersion and reperfusion-induced PVCs. Furthermore, testosterone demonstrated cycle length-dependent effects on APD90 for high heart rate, whereas aldosterone did not exhibit any significant effect compared with controls.
During acute myocardial ischemia-reperfusion, acute superfusion of physiological concentrations of testosterone seemed to be antiarrhythmic by removing a pro-arrhythmic substrate (APD90 dispersion), inducing conduction blocks and decreasing triggered activities (PVCs occurrence). Further experiments are warranted to confirm our results.
Steroid hormones appear to be a key factor in the gender differences in the rates and severity of cardiovascular diseases. Aldosterone and testosterone have typical steroid ring structure but despite this, they demonstrate very different properties.
During acute myocardial ischemia-reperfusion, the deleterious impact of aldosterone is now well established. Conversely, the electrophysiological impact of testosterone in this context remained unknown.
We used female rabbit in vitro models and standard microelectrode technique including right ventricle mimicking the "border zone" existing between normal and ischemic/reperfused areas and isolated right ventricle experiments to assess the acute electrophysiological impact of both aldosterone and testosterone.
During ischemia-reperfusion, acute superfusion of 10 and 100 nmol/L testosterone decreased normoxic and reperfused action potential duration at 90% (APD90 ), systematically induced conduction blocks and decreased APD90 dispersion between ischemic and non-ischemic areas (from 98+/-4 ms to 57+/-7 ms and 66+/-3 ms, for respectively testosterone 10 and 100 nmol/L, P<0.05). Testosterone 10 and 100 nmol/L concomitantly decreased sustained premature ventricular contractions (PVCs) occurrence (from 55% to 0%, P<0.05).
Conversely, aldosterone 10 and 100 nmol/L increased normoxic and reperfused APD90 , APD90 dispersion and reperfusion-induced PVCs. Furthermore, testosterone demonstrated cycle length-dependent effects on APD90 for high heart rate, whereas aldosterone did not exhibit any significant effect compared with controls.
During acute myocardial ischemia-reperfusion, acute superfusion of physiological concentrations of testosterone seemed to be antiarrhythmic by removing a pro-arrhythmic substrate (APD90 dispersion), inducing conduction blocks and decreasing triggered activities (PVCs occurrence). Further experiments are warranted to confirm our results.
Ayaz O, Howlett SE. Testosterone modulates cardiac contraction and calcium homeostasis: cellular and molecular mechanisms. Biol Sex Differ. 2015;6:9. http://www.bsd-journal.com/content/6/1/9
The incidence of cardiovascular disease rises dramatically with age in both men and women. Because a woman's risk of cardiovascular disease rises markedly after the onset of menopause, there has been growing interest in the effect of estrogen on the heart and its role in the pathophysiology of these diseases.
Much less attention has been paid to the impact of testosterone on the heart, even though the levels of testosterone also decline with age and low-testosterone levels are linked to the development of cardiovascular diseases.
The knowledge that receptors for all major sex steroid hormones, including testosterone, are present on individual cardiomyocytes suggests that these hormones may influence the heart at the cellular level. Indeed, it is well established that there are male-female differences in intracellular Ca(2+) release and contraction in isolated ventricular myocytes.
Growing evidence suggests that these differences arise from effects of sex steroid hormones on processes involved in intracellular Ca(2+) homeostasis.
This review considers how myocardial contractile function is modified by testosterone, with a focus on the impact of testosterone on processes that regulate Ca(2+) handling at the level of the ventricular myocyte.
The idea that testosterone regulates Ca(2+) handling in the heart is important, as Ca(2+) dysregulation plays a key role in the pathogenesis of a variety of different cardiovascular diseases.
A better understanding of sex hormone regulation of myocardial Ca(2+) homeostasis may reveal new targets for the treatment of cardiovascular diseases in all older adults.
The incidence of cardiovascular disease rises dramatically with age in both men and women. Because a woman's risk of cardiovascular disease rises markedly after the onset of menopause, there has been growing interest in the effect of estrogen on the heart and its role in the pathophysiology of these diseases.
Much less attention has been paid to the impact of testosterone on the heart, even though the levels of testosterone also decline with age and low-testosterone levels are linked to the development of cardiovascular diseases.
The knowledge that receptors for all major sex steroid hormones, including testosterone, are present on individual cardiomyocytes suggests that these hormones may influence the heart at the cellular level. Indeed, it is well established that there are male-female differences in intracellular Ca(2+) release and contraction in isolated ventricular myocytes.
Growing evidence suggests that these differences arise from effects of sex steroid hormones on processes involved in intracellular Ca(2+) homeostasis.
This review considers how myocardial contractile function is modified by testosterone, with a focus on the impact of testosterone on processes that regulate Ca(2+) handling at the level of the ventricular myocyte.
The idea that testosterone regulates Ca(2+) handling in the heart is important, as Ca(2+) dysregulation plays a key role in the pathogenesis of a variety of different cardiovascular diseases.
A better understanding of sex hormone regulation of myocardial Ca(2+) homeostasis may reveal new targets for the treatment of cardiovascular diseases in all older adults.
Nadimi A, Nasseri A, Nikookheslat S. Effects of resistance exercise and the use of anabolic androgenic steroids on hemodynamic characteristics and muscle damage markers in bodybuilders. J Sports Med Phys Fitness. http://www.minervamedica.it/en/jour...al-fitness/article.php?cod=R40Y9999N00A150097
AIM: Anabolic androgenic steroids (AAS), synthetic compounds of testosterone commonly used as sport performance enhancers, could cause cardiovascular dysfunction and cell damage. Even though the side effects of AAS intake have been widely studied, yet little is known about how resistance exercise can alter these side effects.
This study aimed to determine the effects of one session resistance exercise and the use of AAS on hemodynamic characteristics and muscle damage markers in professional bodybuilders.
METHODS: Sixteen bodybuilders were divided into two groups: bodybuilders using AAS for at least 5 years (users; n = 8) and AAS--free bodybuilders (non--users; n = 8). The exercise protocol was a circuit strength training session involved three sets of 8--9 repetitions at 80--85% of 1--RM. Heart rate (HR), blood pressure (BP) and concentrations of serum creatine kinase (CK) and lactate dehydrogenase (LDH) were measured at three different time points, immediately before and after the exercise session and 24--h following the exercise session.
RESULTS: The users group showed greater basal levels of hemodynamic characteristics (i.e. HR and BP) and cell damage markers (i.e. CK and LDH) compared to those in the non--users group (all P < 0.05). Furthermore, the exercise session significantly increased the levels of HR ( P = 0.02) and CK ( P = 0.01) in the users group compared to those in the non--users group immediately after the exercise. No significant differences were observed in BP and LDH responses to exercise between the users and the non--users groups ( P > 0.05).
CONCLUSIONS: These findings indicate that the use of AAS could be potentially harmful as it enhances the levels of the hemodynamic characteristics and the muscle enzymes. These harmful effects of AAS intake could be more evident in response to resistance exercise.
AIM: Anabolic androgenic steroids (AAS), synthetic compounds of testosterone commonly used as sport performance enhancers, could cause cardiovascular dysfunction and cell damage. Even though the side effects of AAS intake have been widely studied, yet little is known about how resistance exercise can alter these side effects.
This study aimed to determine the effects of one session resistance exercise and the use of AAS on hemodynamic characteristics and muscle damage markers in professional bodybuilders.
METHODS: Sixteen bodybuilders were divided into two groups: bodybuilders using AAS for at least 5 years (users; n = 8) and AAS--free bodybuilders (non--users; n = 8). The exercise protocol was a circuit strength training session involved three sets of 8--9 repetitions at 80--85% of 1--RM. Heart rate (HR), blood pressure (BP) and concentrations of serum creatine kinase (CK) and lactate dehydrogenase (LDH) were measured at three different time points, immediately before and after the exercise session and 24--h following the exercise session.
RESULTS: The users group showed greater basal levels of hemodynamic characteristics (i.e. HR and BP) and cell damage markers (i.e. CK and LDH) compared to those in the non--users group (all P < 0.05). Furthermore, the exercise session significantly increased the levels of HR ( P = 0.02) and CK ( P = 0.01) in the users group compared to those in the non--users group immediately after the exercise. No significant differences were observed in BP and LDH responses to exercise between the users and the non--users groups ( P > 0.05).
CONCLUSIONS: These findings indicate that the use of AAS could be potentially harmful as it enhances the levels of the hemodynamic characteristics and the muscle enzymes. These harmful effects of AAS intake could be more evident in response to resistance exercise.
Similar threads
Sponsors
Latest posts
-
MESO-Rx Sponsor PCT 24X7 "1 stop shop for all day healthcare"- Latest: PCT24X7 PHARMACY
-
