MESO-Rx
Anabolic Steroids
AAS and Cardiovascular/Pulmonary Function
- Thread starter Michael Scally MD
- Start date
hurricane
Well-known Member
I have to admit that as great as these studies are I'd still be scared to use trt with my heart.
Latest bloodwork came back this morning with Total test at 603. At 42 I'm cool with that.
If someone has CHF with low T do you think trt should be a "first line medication"?
I'm going to ask my doctors that question.
[Post below is from August 5]
Former IFBB and WBF Pro bodybuilder David Dearth dies
https://www.evolutionofbodybuilding.net/david-dearth-dies/
Sad news in the bodybuilding world with the death of David Dearth.
David was 56 years old.
The death of David is a shock to all his friends and fans as he was just on social media joking around a day ago.
According to his latest posts, David was in hospital having surgery to remove a number of abscess.
One of his close friends confirmed his death via a post on Facebook.
The cause of death was due to a heart attack while David was still in hospital.
Former IFBB and WBF Pro bodybuilder David Dearth dies
https://www.evolutionofbodybuilding.net/david-dearth-dies/
Sad news in the bodybuilding world with the death of David Dearth.
David was 56 years old.
The death of David is a shock to all his friends and fans as he was just on social media joking around a day ago.
According to his latest posts, David was in hospital having surgery to remove a number of abscess.
One of his close friends confirmed his death via a post on Facebook.
The cause of death was due to a heart attack while David was still in hospital.
Chamarthi G, Koratala A. Thoracoabdominal Aneurysm in a Professional Body Builder. Am J Med 2018;131:e201-e2. https://www.amjmed.com/article/S0002-9343(17)31289-5/abstract
A 33-year-old, otherwise healthy man presented with worsening epigastric and flank pain for 3 weeks. He denied having vomiting, diarrhea, fever, urinary symptoms or history of kidney stones. His vital signs were significant for a blood pressure of 140/72 mmHg and pulse rate of 94 bpm. Acute coronary syndrome was excluded by electrocardiography.
A computed tomography (CT) scan of the chest and abdomen with contrast demonstrated aneurysmal dilation of the entire length of descending thoracic and abdominal aorta with the proximal descending thoracic aorta measuring about 4.8 cm in diameter [Figure 1].
There was a focal saccular aneurysm in the infrarenal part with peri-aortic stranding suspicious for mycotic aneurysm, for which he was started on antibiotics. There were no stigmata of Marfan syndrome on physical examination and serologic testing for syphilis was negative.
His total cholesterol level was 144 mg/dL (ref: 140-199), LDL 85 mg/dL (optimal: <100) and HDL 41 mg/dL (optimal: >40). Vasculitic work up was negative.
He was a bodybuilder by profession and on further questioning, admitted to 10-year use of anabolic androgenic steroids including stanozolol, oxymetholone and testosterone, together with human growth hormone in cycles, which is the likely etiology of his aortic aneurysm. His plasma testosterone level was low at 144 ng/dL (ref: 230-800), consistent with long-term exogenous androgen use.
The infrarenal aneurysm was treated with resection and aortoiliac tube graft. Histologic examination showed dense adventitial fibrosis and lymphoplasmacytic infiltrate in the aortic wall.
A 33-year-old, otherwise healthy man presented with worsening epigastric and flank pain for 3 weeks. He denied having vomiting, diarrhea, fever, urinary symptoms or history of kidney stones. His vital signs were significant for a blood pressure of 140/72 mmHg and pulse rate of 94 bpm. Acute coronary syndrome was excluded by electrocardiography.
A computed tomography (CT) scan of the chest and abdomen with contrast demonstrated aneurysmal dilation of the entire length of descending thoracic and abdominal aorta with the proximal descending thoracic aorta measuring about 4.8 cm in diameter [Figure 1].
There was a focal saccular aneurysm in the infrarenal part with peri-aortic stranding suspicious for mycotic aneurysm, for which he was started on antibiotics. There were no stigmata of Marfan syndrome on physical examination and serologic testing for syphilis was negative.
His total cholesterol level was 144 mg/dL (ref: 140-199), LDL 85 mg/dL (optimal: <100) and HDL 41 mg/dL (optimal: >40). Vasculitic work up was negative.
He was a bodybuilder by profession and on further questioning, admitted to 10-year use of anabolic androgenic steroids including stanozolol, oxymetholone and testosterone, together with human growth hormone in cycles, which is the likely etiology of his aortic aneurysm. His plasma testosterone level was low at 144 ng/dL (ref: 230-800), consistent with long-term exogenous androgen use.
The infrarenal aneurysm was treated with resection and aortoiliac tube graft. Histologic examination showed dense adventitial fibrosis and lymphoplasmacytic infiltrate in the aortic wall.
Libby P, Buring JE, Badimon L, et al. Atherosclerosis. Nature Reviews Disease Primers 2019;5:56. https://doi.org/10.1038/s41572-019-0106-z
Atherosclerosis, the formation of fibrofatty lesions in the artery wall, causes much morbidity and mortality worldwide, including most myocardial infarctions and many strokes, as well as disabling peripheral artery disease.
Development of atherosclerotic lesions probably requires low-density lipoprotein, a particle that carries cholesterol through the blood. Other risk factors for atherosclerosis and its thrombotic complications include hypertension, cigarette smoking and diabetes mellitus. Increasing evidence also points to a role of the immune system, as emerging risk factors include inflammation and clonal haematopoiesis.
Studies of the cell and molecular biology of atherogenesis have provided considerable insight into the mechanisms that link all these risk factors to atheroma development and the clinical manifestations of this disease.
An array of diagnostic techniques, both invasive (such as selective coronary arteriography) and noninvasive (such as blood biomarkers, stress testing, CT and nuclear scanning), permit assessment of cardiovascular disease risk and targeting of therapies.
An expanding armamentarium of therapies that can modify risk factors and confer clinical benefit is available; however, we face considerable challenge in providing equitable access to these treatments and in maximizing adherence.
Yet, the clinical application of the fruits of research has advanced preventive strategies, enhanced clinical outcomes in affected individuals, and improved their quality of life.
Rapidly accelerating knowledge and continued research promise to provide further progress in combating this common chronic disease.
Atherosclerosis, the formation of fibrofatty lesions in the artery wall, causes much morbidity and mortality worldwide, including most myocardial infarctions and many strokes, as well as disabling peripheral artery disease.
Development of atherosclerotic lesions probably requires low-density lipoprotein, a particle that carries cholesterol through the blood. Other risk factors for atherosclerosis and its thrombotic complications include hypertension, cigarette smoking and diabetes mellitus. Increasing evidence also points to a role of the immune system, as emerging risk factors include inflammation and clonal haematopoiesis.
Studies of the cell and molecular biology of atherogenesis have provided considerable insight into the mechanisms that link all these risk factors to atheroma development and the clinical manifestations of this disease.
An array of diagnostic techniques, both invasive (such as selective coronary arteriography) and noninvasive (such as blood biomarkers, stress testing, CT and nuclear scanning), permit assessment of cardiovascular disease risk and targeting of therapies.
An expanding armamentarium of therapies that can modify risk factors and confer clinical benefit is available; however, we face considerable challenge in providing equitable access to these treatments and in maximizing adherence.
Yet, the clinical application of the fruits of research has advanced preventive strategies, enhanced clinical outcomes in affected individuals, and improved their quality of life.
Rapidly accelerating knowledge and continued research promise to provide further progress in combating this common chronic disease.
Effects of Icosapent Ethyl (Eicosapentaenoic Acid Ethyl Ester)
Icosapent ethyl is pure prescription eicosapentaenoic acid approved at 4 g/day as an adjunct to diet to reduce triglycerides (TG) in adults with TG ≥500 mg/dl. Elevated high-sensitivity C-reactive protein (hsCRP) is associated with increased cardiovascular risk.
The 12-week ANCHOR study randomized 702 statin-treated patients at increased cardiovascular risk with TG 200 to 499 mg/dl despite low-density lipoprotein cholesterol (LDL-C) control (40 to 99 mg/dl).
This post hoc analysis assessed 246 ANCHOR patients with baseline hsCRP ≥ 2.0 mg/L randomized to icosapent ethyl 4 g/day (n = 126; approved dose) or placebo (n = 120).
Without increasing LDL-C, icosapent ethyl significantly reduced
· median TG (−20%; p < 0.0001),
· non–high-density lipoprotein cholesterol (−12.3%; p < 0.0001),
· total cholesterol (−11.1%; p < 0.0001),
· high-density lipoprotein cholesterol (−5.2%; p = 0.0042),
· very LDL-C (−21.0%; p < 0.0001),
· very low-density lipoprotein TG (−22.9%; p < 0.0001),
· remnant lipoprotein cholesterol (−23.0%; p = 0.0125),
· apolipoprotein B (−7.4%; p = 0.0021),
· apolipoprotein C-III (−16%; p < 0.0001),
· oxidized LDL (−13.7%; p = 0.0020),
· lipoprotein-associated phospholipase A2 (−19.6%; p < 0.0001), and
· hsCRP (−17.9%; p = 0.0213) versus placebo,
while interleukin-6 and intercellular adhesion molecule-1 were not significantly changed.
Eicosapentaenoic acid increased with icosapent ethyl 4 g/day +637% in plasma and +632% in red blood cells versus placebo (both p < 0.0001). Icosapent ethyl exhibited a safety profile similar to placebo.
In conclusion, in statin-treated patients with hsCRP ≥ 2.0 mg/L and TG 200 to 499 mg/dl at baseline, icosapent ethyl 4 g/day significantly and safely reduced TG and other atherogenic and inflammatory parameters without increasing LDL-C versus placebo.
Miller M, Ballantyne CM, Bays HE, et al. Effects of Icosapent Ethyl (Eicosapentaenoic Acid Ethyl Ester) on Atherogenic Lipid/Lipoprotein, Apolipoprotein, and Inflammatory Parameters in Patients With Elevated High-Sensitivity C-Reactive Protein (from the ANCHOR Study). The American journal of cardiology 2019;124:696-701. https://www.sciencedirect.com/science/article/pii/S000291491930637X
Icosapent ethyl is pure prescription eicosapentaenoic acid approved at 4 g/day as an adjunct to diet to reduce triglycerides (TG) in adults with TG ≥500 mg/dl. Elevated high-sensitivity C-reactive protein (hsCRP) is associated with increased cardiovascular risk.
The 12-week ANCHOR study randomized 702 statin-treated patients at increased cardiovascular risk with TG 200 to 499 mg/dl despite low-density lipoprotein cholesterol (LDL-C) control (40 to 99 mg/dl).
This post hoc analysis assessed 246 ANCHOR patients with baseline hsCRP ≥ 2.0 mg/L randomized to icosapent ethyl 4 g/day (n = 126; approved dose) or placebo (n = 120).
Without increasing LDL-C, icosapent ethyl significantly reduced
· median TG (−20%; p < 0.0001),
· non–high-density lipoprotein cholesterol (−12.3%; p < 0.0001),
· total cholesterol (−11.1%; p < 0.0001),
· high-density lipoprotein cholesterol (−5.2%; p = 0.0042),
· very LDL-C (−21.0%; p < 0.0001),
· very low-density lipoprotein TG (−22.9%; p < 0.0001),
· remnant lipoprotein cholesterol (−23.0%; p = 0.0125),
· apolipoprotein B (−7.4%; p = 0.0021),
· apolipoprotein C-III (−16%; p < 0.0001),
· oxidized LDL (−13.7%; p = 0.0020),
· lipoprotein-associated phospholipase A2 (−19.6%; p < 0.0001), and
· hsCRP (−17.9%; p = 0.0213) versus placebo,
while interleukin-6 and intercellular adhesion molecule-1 were not significantly changed.
Eicosapentaenoic acid increased with icosapent ethyl 4 g/day +637% in plasma and +632% in red blood cells versus placebo (both p < 0.0001). Icosapent ethyl exhibited a safety profile similar to placebo.
In conclusion, in statin-treated patients with hsCRP ≥ 2.0 mg/L and TG 200 to 499 mg/dl at baseline, icosapent ethyl 4 g/day significantly and safely reduced TG and other atherogenic and inflammatory parameters without increasing LDL-C versus placebo.
Miller M, Ballantyne CM, Bays HE, et al. Effects of Icosapent Ethyl (Eicosapentaenoic Acid Ethyl Ester) on Atherogenic Lipid/Lipoprotein, Apolipoprotein, and Inflammatory Parameters in Patients With Elevated High-Sensitivity C-Reactive Protein (from the ANCHOR Study). The American journal of cardiology 2019;124:696-701. https://www.sciencedirect.com/science/article/pii/S000291491930637X
Higher Serum Sex Hormone-Binding Globulin (SHBG) Levels Are Associated with Incident Cardiovascular Disease (CVD)
Context - Sex hormone-binding globulin (SHBG) levels are associated with cardiovascular disease (CVD) risk factors. However, prospective data on the association between SHBG levels and CVD events are sparse, with conflicting results.
Objectives - To examine associations between serum SHBG, total testosterone (TT), and incident CVD and CVD-related mortality in middle-aged to elderly men.
Design and Methods - Data on 2563 community-dwelling men (35-80 years) were obtained from participants in the Men Androgen Inflammation Lifestyle Environment and Stress (MAILES) cohort.
The analytic sample included 1492 men without baseline (2002-2007) CVD and with fasted morning serum SHBG and TT available at both baseline and follow-up (2007-2010), and without medications affecting TT or SHBG.
Associations of baseline SHBG and TT, with incident CVD and CVD - mortality, were analysed using logistic regression for incident CVD and Cox’s proportional hazard regression for CVD mortality, adjusting for established CVD risk factors.
Results - In multivariable models, elevated baseline SHBG and lower baseline TT were independently associated with incident CVD (OR=1.54 [1.15, 2.06] per SD increase in SHBG, p=0.003) and (OR =0.71 [0.52, 0.97] per SD decrease in TT, p=0.03), respectively. A decrease in TT between time points was associated with incident CVD (OR=0.72 [0.56, 0.92], P=0.01). Neither SHBG nor TT were significantly associated with all-age CVD mortality (HR=0.69 [0.29, 1.63], p=0.40 & HR=0.60 [0.28, 1.26], p=0.18, respectively).
Conclusions - Among all men and men aged over 65, both elevated SHBG and lower TT were independently associated with both a greater risk of CVD and an increased CVD mortality risk.
Gyawali P, Martin SA, Heilbronn LK, et al. Higher serum sex hormone-binding globulin (SHBG) levels are associated with incident cardiovascular disease (CVD) in men [published online August 7, 2019]. J Clin Endocrinol Metab. Higher serum sex hormone-binding globulin (SHBG) levels are associated with incident cardiovascular disease (CVD) in men
Context - Sex hormone-binding globulin (SHBG) levels are associated with cardiovascular disease (CVD) risk factors. However, prospective data on the association between SHBG levels and CVD events are sparse, with conflicting results.
Objectives - To examine associations between serum SHBG, total testosterone (TT), and incident CVD and CVD-related mortality in middle-aged to elderly men.
Design and Methods - Data on 2563 community-dwelling men (35-80 years) were obtained from participants in the Men Androgen Inflammation Lifestyle Environment and Stress (MAILES) cohort.
The analytic sample included 1492 men without baseline (2002-2007) CVD and with fasted morning serum SHBG and TT available at both baseline and follow-up (2007-2010), and without medications affecting TT or SHBG.
Associations of baseline SHBG and TT, with incident CVD and CVD - mortality, were analysed using logistic regression for incident CVD and Cox’s proportional hazard regression for CVD mortality, adjusting for established CVD risk factors.
Results - In multivariable models, elevated baseline SHBG and lower baseline TT were independently associated with incident CVD (OR=1.54 [1.15, 2.06] per SD increase in SHBG, p=0.003) and (OR =0.71 [0.52, 0.97] per SD decrease in TT, p=0.03), respectively. A decrease in TT between time points was associated with incident CVD (OR=0.72 [0.56, 0.92], P=0.01). Neither SHBG nor TT were significantly associated with all-age CVD mortality (HR=0.69 [0.29, 1.63], p=0.40 & HR=0.60 [0.28, 1.26], p=0.18, respectively).
Conclusions - Among all men and men aged over 65, both elevated SHBG and lower TT were independently associated with both a greater risk of CVD and an increased CVD mortality risk.
Gyawali P, Martin SA, Heilbronn LK, et al. Higher serum sex hormone-binding globulin (SHBG) levels are associated with incident cardiovascular disease (CVD) in men [published online August 7, 2019]. J Clin Endocrinol Metab. Higher serum sex hormone-binding globulin (SHBG) levels are associated with incident cardiovascular disease (CVD) in men
[OA] Comparison of Testosterone Level in Patients with Myocardial Infarction with Control Group
Objective: To compare testosterone levels of patients with myocardial infarction with control group.
Methodology: In this case control study, the testosterone levels of male patients with myocardial infarction (cases) and men with coronary artery stenosis less than40% (control group measured by angiography) were compared with each other. This study was done at cardiovascular unit or CCU of Mehr and Aria hospital of Mashhad, Iran from 1st January to 31st December 2015.
Serum levels of testosterone of patients with myocardial infarction and control group were recorded and compared with the normal level of testosterone. SPSSv.18 and Statistics V.10 were used, the meaningful level of test was considered less than5%.
Results: This study consisted of 60 participants with 30 in each group. We examined serum samples for testosterone level, the mean serum level in controls and patient groups were 6.7ngr and 2.8ngr/lit respectively. Patient group level was higher than the control group and between the two study groups, there was significant statistical difference (p=0.0001).
In addition, significant differences in the level of testosterone were observed in both groups according to age stratification. The results showed that 70% of the patients had lower levels of testosterone, but in the control group all were normal.
Conclusion: Due to lower testosterone levels in patients with myocardial infarction compared with healthy subjects, it seems that reduced testosterone levels, may be considered as an independent risk factor.
Ariabod V, Qara M, Payan K. Comparison of testosterone level in patients with myocardial infarction with control group. Pak Heart J 2019;52 (02):132-6. COMPARISON OF TESTOSTERONE LEVEL IN PATIENTS WITH MYOCARDIAL INFARCTION WITH CONTROL GROUP | Ariabod | Pakistan Heart Journal
Objective: To compare testosterone levels of patients with myocardial infarction with control group.
Methodology: In this case control study, the testosterone levels of male patients with myocardial infarction (cases) and men with coronary artery stenosis less than40% (control group measured by angiography) were compared with each other. This study was done at cardiovascular unit or CCU of Mehr and Aria hospital of Mashhad, Iran from 1st January to 31st December 2015.
Serum levels of testosterone of patients with myocardial infarction and control group were recorded and compared with the normal level of testosterone. SPSSv.18 and Statistics V.10 were used, the meaningful level of test was considered less than5%.
Results: This study consisted of 60 participants with 30 in each group. We examined serum samples for testosterone level, the mean serum level in controls and patient groups were 6.7ngr and 2.8ngr/lit respectively. Patient group level was higher than the control group and between the two study groups, there was significant statistical difference (p=0.0001).
In addition, significant differences in the level of testosterone were observed in both groups according to age stratification. The results showed that 70% of the patients had lower levels of testosterone, but in the control group all were normal.
Conclusion: Due to lower testosterone levels in patients with myocardial infarction compared with healthy subjects, it seems that reduced testosterone levels, may be considered as an independent risk factor.
Ariabod V, Qara M, Payan K. Comparison of testosterone level in patients with myocardial infarction with control group. Pak Heart J 2019;52 (02):132-6. COMPARISON OF TESTOSTERONE LEVEL IN PATIENTS WITH MYOCARDIAL INFARCTION WITH CONTROL GROUP | Ariabod | Pakistan Heart Journal
[OA] Apolipoprotein B Underlies the Causal Relationship of Circulating Blood Lipids with Coronary Heart Disease
Background: Circulating blood lipids cause coronary heart disease (CHD). However, the precise way in which one or more lipoprotein lipid-related entities account for this relationship remains unclear. We sought to explore the causal relationships of blood lipid traits with risk of CHD using multivariable Mendelian randomization.
Methods: We conducted GWAS of circulating blood lipid traits in UK Biobank (up to n=440,546) for LDL cholesterol, triglycerides and apolipoprotein B to identify lipid-associated SNPs. Using data from CARDIoGRAMplusC4D for CHD (consisting of 60,801 cases and 123,504 controls), we performed univariable and multivariable Mendelian randomization (MR) analyses. Similar analyses were conducted for HDL cholesterol and apolipoprotein A-I.
Findings: GWAS identified multiple independent SNPs associated at P<5x10-8 for LDL cholesterol (220), apolipoprotein B (n=255), triglycerides (440), HDL cholesterol (534) and apolipoprotein AI (440). Between 56-93% of SNPs identified for each lipid trait had not been previously reported in large-scale GWAS.
Almost half (46%) of these SNPs were associated at P<5x10-8 with more than one lipid related trait. Assessed individually using MR, each of LDL cholesterol (OR 1.66 per 1 standard deviation higher trait; 95%CI: 1.49; 1.86; P=2.4x10-19), triglycerides (OR 1.34; 95%CI: 1.25, 1.44; P=9.1x10-16) and apolipoprotein B (OR 1.73; 95%CI: 1.56, 1.91; P=1.5x10-25) had effect estimates consistent with a higher risk of CHD.
In multivariable MR, only apolipoprotein B (OR 1.92; 95%CI: 1.31, 2.81; P=7.5x10-4) retained a robust effect with the estimate for LDL cholesterol (OR 0.85; 95%CI: 0.57; 1.27; P=0.44) reversing and that of triglycerides (OR 1.12; 95%CI: 1.02, 1.23; P=0.01) becoming markedly weaker. Individual MR analyses showed a 1-SD higher HDL-C (OR 0.80; 95%CI: 0.75, 0.86; P=1.7x10-10) and apolipoprotein A-I (OR 0.83; 95%CI: 0.77, 0.89; P=1.0x10-6) to lower the risk of CHD but these effect estimates weakened to include the null on accounting for apolipoprotein B.
Conclusions: Apolipoprotein B is of fundamental causal relevance in the aetiology of CHD, and underlies the relationship of LDL cholesterol and triglycerides with CHD.
Richardson TG, Sanderson E, Palmer TM, et al. Apolipoprotein B underlies the causal relationship of circulating blood lipids with coronary heart disease. medRxiv 2019:19004895. http://medrxiv.org/content/early/2019/08/29/19004895.abstract
Background: Circulating blood lipids cause coronary heart disease (CHD). However, the precise way in which one or more lipoprotein lipid-related entities account for this relationship remains unclear. We sought to explore the causal relationships of blood lipid traits with risk of CHD using multivariable Mendelian randomization.
Methods: We conducted GWAS of circulating blood lipid traits in UK Biobank (up to n=440,546) for LDL cholesterol, triglycerides and apolipoprotein B to identify lipid-associated SNPs. Using data from CARDIoGRAMplusC4D for CHD (consisting of 60,801 cases and 123,504 controls), we performed univariable and multivariable Mendelian randomization (MR) analyses. Similar analyses were conducted for HDL cholesterol and apolipoprotein A-I.
Findings: GWAS identified multiple independent SNPs associated at P<5x10-8 for LDL cholesterol (220), apolipoprotein B (n=255), triglycerides (440), HDL cholesterol (534) and apolipoprotein AI (440). Between 56-93% of SNPs identified for each lipid trait had not been previously reported in large-scale GWAS.
Almost half (46%) of these SNPs were associated at P<5x10-8 with more than one lipid related trait. Assessed individually using MR, each of LDL cholesterol (OR 1.66 per 1 standard deviation higher trait; 95%CI: 1.49; 1.86; P=2.4x10-19), triglycerides (OR 1.34; 95%CI: 1.25, 1.44; P=9.1x10-16) and apolipoprotein B (OR 1.73; 95%CI: 1.56, 1.91; P=1.5x10-25) had effect estimates consistent with a higher risk of CHD.
In multivariable MR, only apolipoprotein B (OR 1.92; 95%CI: 1.31, 2.81; P=7.5x10-4) retained a robust effect with the estimate for LDL cholesterol (OR 0.85; 95%CI: 0.57; 1.27; P=0.44) reversing and that of triglycerides (OR 1.12; 95%CI: 1.02, 1.23; P=0.01) becoming markedly weaker. Individual MR analyses showed a 1-SD higher HDL-C (OR 0.80; 95%CI: 0.75, 0.86; P=1.7x10-10) and apolipoprotein A-I (OR 0.83; 95%CI: 0.77, 0.89; P=1.0x10-6) to lower the risk of CHD but these effect estimates weakened to include the null on accounting for apolipoprotein B.
Conclusions: Apolipoprotein B is of fundamental causal relevance in the aetiology of CHD, and underlies the relationship of LDL cholesterol and triglycerides with CHD.
Richardson TG, Sanderson E, Palmer TM, et al. Apolipoprotein B underlies the causal relationship of circulating blood lipids with coronary heart disease. medRxiv 2019:19004895. http://medrxiv.org/content/early/2019/08/29/19004895.abstract
Clinical Characterization of Men with Long QT Syndrome and Torsades De Pointes Associated with Hypogonadism
Background - Long QT syndrome (LQTS) can cause the potentially fatal ventricular tachycardia torsades de pointes (TdP). QT interval corrected for heart rate (QTc) is shorter in men than in women, with testosterone contributing to shorten QTc. We recently described male hypogonadism as a reversible risk factor for acquired LQTS and TdP, but the clinical characteristics of such patients have not been characterized.
Aims - To describe the clinical characteristics of men with acquired LQTS or TdP associated with hypogonadism caused by endocrine conditions or androgen deprivation therapy (ADT), and to evaluate the relationship between testosterone concentrations and electrocardiographic changes.
Methods - We searched MEDLINE (to 04 January 2019) and the French pharmacovigilance database (to 09 August 2018) to identify male cases of acquired LQTS and TdP associated with endocrine hypogonadism or ADT; their narratives were gathered from reporting collaborators.
Results - We identified seven cases of TdP (one fatal) with endocrine hypogonadism, abnormally long QTc and morphologically abnormal T-wave notches.
After reversion of low testosterone concentrations in the surviving patients (N = 6), QTc shortened, T-wave morphology normalized and there was no TdP recurrence. Among these cases, none had mutation in the LQTS genes, three men required testosterone and three had reversible hypogonadism after resolution of a concurrent acute severe illness.
We found an additional 27 reports of men with LQTS (N = 6), TdP (N = 9; 2/9 fatal) or sudden death (N = 12; 10/12 fatal) suspected to be induced or favoured by ADT (24/27 for prostate cancer). Generally, after ADT withdrawal, QTc shortened and no TdP recurred.
Conclusion - We propose seeking for hypogonadism caused by endocrine conditions or ADT in men presenting with TdP. Caution is warranted when ADT is used in situations at risk of TdP. Testosterone may be useful to treat or prevent TdP.
Salem J-E, Bretagne M, Lebrun-Vignes B, et al. Clinical characterization of men with long QT syndrome and torsades de pointes associated with hypogonadism: A review and pharmacovigilance study. Archives of Cardiovascular Diseases 2019. https://www.sciencedirect.com/science/article/pii/S1875213619301408
Background - Long QT syndrome (LQTS) can cause the potentially fatal ventricular tachycardia torsades de pointes (TdP). QT interval corrected for heart rate (QTc) is shorter in men than in women, with testosterone contributing to shorten QTc. We recently described male hypogonadism as a reversible risk factor for acquired LQTS and TdP, but the clinical characteristics of such patients have not been characterized.
Aims - To describe the clinical characteristics of men with acquired LQTS or TdP associated with hypogonadism caused by endocrine conditions or androgen deprivation therapy (ADT), and to evaluate the relationship between testosterone concentrations and electrocardiographic changes.
Methods - We searched MEDLINE (to 04 January 2019) and the French pharmacovigilance database (to 09 August 2018) to identify male cases of acquired LQTS and TdP associated with endocrine hypogonadism or ADT; their narratives were gathered from reporting collaborators.
Results - We identified seven cases of TdP (one fatal) with endocrine hypogonadism, abnormally long QTc and morphologically abnormal T-wave notches.
After reversion of low testosterone concentrations in the surviving patients (N = 6), QTc shortened, T-wave morphology normalized and there was no TdP recurrence. Among these cases, none had mutation in the LQTS genes, three men required testosterone and three had reversible hypogonadism after resolution of a concurrent acute severe illness.
We found an additional 27 reports of men with LQTS (N = 6), TdP (N = 9; 2/9 fatal) or sudden death (N = 12; 10/12 fatal) suspected to be induced or favoured by ADT (24/27 for prostate cancer). Generally, after ADT withdrawal, QTc shortened and no TdP recurred.
Conclusion - We propose seeking for hypogonadism caused by endocrine conditions or ADT in men presenting with TdP. Caution is warranted when ADT is used in situations at risk of TdP. Testosterone may be useful to treat or prevent TdP.
Salem J-E, Bretagne M, Lebrun-Vignes B, et al. Clinical characterization of men with long QT syndrome and torsades de pointes associated with hypogonadism: A review and pharmacovigilance study. Archives of Cardiovascular Diseases 2019. https://www.sciencedirect.com/science/article/pii/S1875213619301408
[OA] Anabolic-Androgenic Steroids and Cardiovascular Risk
OBJECTIVE: Anabolic-androgenic steroids (AAS) represents a group of synthetic testosterone derivatives that play an important role in clinical treatment. These drugs are widely abused among the general public to increase lean weight and improve athletic performance.
It has been reported that AAS use can produce many adverse effects, especially the occurrence of cardiovascular risk. Although there are many related studies, there has been no consensus on AAS use and cardiovascular risk. The present study was to review the effect of AAS on the cardiovascular system.
DATA SOURCES: The data in this review were obtained from articles included in PubMed and the National Center for Biotechnology Information database.
STUDY SELECTION: Original articles, case reports, and systematic reviews about AAS were selected for the article.
RESULTS: The use/abuse of AAS is correlated with higher cardiovascular risks, and many AAS users/abusers had cardiovascular diseases. However, there are many confounding factors in the studies that explored the causality between AAS intake and disease development, and additional studies are required to determine AAS toxicity.
CONCLUSION: AAS produces toxic effects on the cardiovascular system, and it is necessary to ensure that more people know this about AAS, including medical personnel.
Liu JD, Wu YQ. Anabolic-androgenic steroids and cardiovascular risk. Chinese medical journal 2019. Anabolic-androgenic steroids and cardiovascular risk : Chinese Medical Journal
OBJECTIVE: Anabolic-androgenic steroids (AAS) represents a group of synthetic testosterone derivatives that play an important role in clinical treatment. These drugs are widely abused among the general public to increase lean weight and improve athletic performance.
It has been reported that AAS use can produce many adverse effects, especially the occurrence of cardiovascular risk. Although there are many related studies, there has been no consensus on AAS use and cardiovascular risk. The present study was to review the effect of AAS on the cardiovascular system.
DATA SOURCES: The data in this review were obtained from articles included in PubMed and the National Center for Biotechnology Information database.
STUDY SELECTION: Original articles, case reports, and systematic reviews about AAS were selected for the article.
RESULTS: The use/abuse of AAS is correlated with higher cardiovascular risks, and many AAS users/abusers had cardiovascular diseases. However, there are many confounding factors in the studies that explored the causality between AAS intake and disease development, and additional studies are required to determine AAS toxicity.
CONCLUSION: AAS produces toxic effects on the cardiovascular system, and it is necessary to ensure that more people know this about AAS, including medical personnel.
Liu JD, Wu YQ. Anabolic-androgenic steroids and cardiovascular risk. Chinese medical journal 2019. Anabolic-androgenic steroids and cardiovascular risk : Chinese Medical Journal
Safety First
New Member
Ive been reading through your posts plenty for the past 24 hours.
I've polished my knowledge quite a bit and reassured some of my earlier assumptions about AAS and its affects on the body.
Even a TRT dose of test seems to lead to
Some level of atherosclerosis. It seems there is no anabolic on the market that won't take a toll on your body in some way.
In your opinion, what are the most heart friendly anabolic compounds for human consumption?
The obvious answer seems to be there are none.
Thanks in Advance,
Saftey first
hurricane
Well-known Member
Dr. Scally is a wealth of knowledge for this community. Good on you for educating yourself.
Don't be offended if he doesn't answer your question directly. It's not his style for the most part.
Welcome to MESO.
Safety First
New Member
Thank you so much.
[OA] Sudden Cardiac Death in Anabolic Androgenic Steroids Abuse: Case Report and Literature Review
Anabolic androgenic steroids (AAS) have several adverse effects on the cardiovascular system that may lead to a sudden cardiac death (SCD). We herein report a case involving a 24-year-old male, AAS abuser with intramuscular delivery in the 6 months before, who suffered a cardiorespiratory arrest at home’s bathtub when returning from New Year’s party.
A forensic autopsy was performed according to the guidelines of the Association for European Cardiovascular Pathology (AECVP). The body showed hypertrophy of skeletal musculature, with low amount of subcutaneous fat and no signs of injury (body mass index, BMI: 26.8 kg/m2).
On internal examination, there were multiorgan congestion, acute pulmonary edema, and cardiomegaly (420 g) with severe coronary atherosclerosis and superimposed acute occlusive thrombosis at the left main trunk and left anterior descendant. Areas of scarring were located at the intersection between the posterior wall and the posterior third of the septum (postero-septal).
At histology, acute myocardial infarction at the anterior third of the septum and the anterior wall, and subacute myocardial infarction at apical septum and apical posterior wall were detected. Other findings were small intramyocardial vessel disease and myocytes hypertrophy.
Chemicotoxicological analysis in blood showed ethanol ((0.90 ± 0.05) g/L), stanazolol (11.31 µg/L), nandrolone (2.05 µg/L) and testosterone (<1.00 µg/L). When confronted with a sudden death in a young athlete we must pay attention to the physical phenotype that may suggest AAS abuse and perform a detailed examination of the heart. Chemicotoxicological analysis is a key to establish the relationship between SCD and AAS abuse.
Hernández-Guerra AI, Tapia J, Menéndez-Quintanal LM, Lucena JS. Sudden cardiac death in anabolic androgenic steroids abuse: case report and literature review. Forensic Sci Res. 2019;4(3):267–273. Sudden cardiac death in anabolic androgenic steroids abuse: case report and literature review
Anabolic androgenic steroids (AAS) have several adverse effects on the cardiovascular system that may lead to a sudden cardiac death (SCD). We herein report a case involving a 24-year-old male, AAS abuser with intramuscular delivery in the 6 months before, who suffered a cardiorespiratory arrest at home’s bathtub when returning from New Year’s party.
A forensic autopsy was performed according to the guidelines of the Association for European Cardiovascular Pathology (AECVP). The body showed hypertrophy of skeletal musculature, with low amount of subcutaneous fat and no signs of injury (body mass index, BMI: 26.8 kg/m2).
On internal examination, there were multiorgan congestion, acute pulmonary edema, and cardiomegaly (420 g) with severe coronary atherosclerosis and superimposed acute occlusive thrombosis at the left main trunk and left anterior descendant. Areas of scarring were located at the intersection between the posterior wall and the posterior third of the septum (postero-septal).
At histology, acute myocardial infarction at the anterior third of the septum and the anterior wall, and subacute myocardial infarction at apical septum and apical posterior wall were detected. Other findings were small intramyocardial vessel disease and myocytes hypertrophy.
Chemicotoxicological analysis in blood showed ethanol ((0.90 ± 0.05) g/L), stanazolol (11.31 µg/L), nandrolone (2.05 µg/L) and testosterone (<1.00 µg/L). When confronted with a sudden death in a young athlete we must pay attention to the physical phenotype that may suggest AAS abuse and perform a detailed examination of the heart. Chemicotoxicological analysis is a key to establish the relationship between SCD and AAS abuse.
Hernández-Guerra AI, Tapia J, Menéndez-Quintanal LM, Lucena JS. Sudden cardiac death in anabolic androgenic steroids abuse: case report and literature review. Forensic Sci Res. 2019;4(3):267–273. Sudden cardiac death in anabolic androgenic steroids abuse: case report and literature review
Safety First
New Member
Good read!
weighted chinup
Well-known Member
Amazing, people can go through their whole life using AAS and not have these issues, but at 24, with 6 months of use, this young man's heart grew probably around 100g and developed severe ASCVD.
weighted chinup
Well-known Member
I don't believe there is a reliable way to estimate.
Notice his BMI? 26? Mine is 33. This cat wasn't a big boy either...
Death After Misuse of Anabolic Substances (Clenbuterol, Stanozolol and Metandienone).
A 34-year old male was found breathless and panting at home by his girlfriend three hours after a gym workout. Minutes later, he collapsed and died. Autopsy, histological and chemical analyses were conducted.
The examination of the heart showed left ventricular hypertrophy, while the right coronary artery showed only a small vascular lumen (3 mm in diameter), due to its anatomical structure.
In femoral blood concentrations of approx. 1 μg/L clenbuterol, approx. 56 μg/L stanozolol and approx. 8 μg/L metandienone, with trenbolone (<limit of quantification (LOQ)) were detected.
Additionally, there were positive results in urine for boldenone, clomiphene, trenbolone, metandienone, stanozolol, clenbuterol and drostanolone, along with indications of testosterone and/or testosterone prohormones having been taken.
In consideration of all aspects of this case, in can be assumed that the long-term consumption of anabolic androgen steroids (AAS) caused apparently pathological changes of the heart.
Over and above, the combination of anatomical (small lumed coronary artery, ventricular hypertrophy) and substance-induced risk factors led to the fatal cardiovascular failure.
Lehmann S, Thomas A, Schiwy-Bochat K-H, et al. Death after misuse of anabolic substances (clenbuterol, stanozolol and metandienone). Forensic science international 2019;303:109925. https://www.sciencedirect.com/science/article/pii/S0379073819303378
A 34-year old male was found breathless and panting at home by his girlfriend three hours after a gym workout. Minutes later, he collapsed and died. Autopsy, histological and chemical analyses were conducted.
The examination of the heart showed left ventricular hypertrophy, while the right coronary artery showed only a small vascular lumen (3 mm in diameter), due to its anatomical structure.
In femoral blood concentrations of approx. 1 μg/L clenbuterol, approx. 56 μg/L stanozolol and approx. 8 μg/L metandienone, with trenbolone (<limit of quantification (LOQ)) were detected.
Additionally, there were positive results in urine for boldenone, clomiphene, trenbolone, metandienone, stanozolol, clenbuterol and drostanolone, along with indications of testosterone and/or testosterone prohormones having been taken.
In consideration of all aspects of this case, in can be assumed that the long-term consumption of anabolic androgen steroids (AAS) caused apparently pathological changes of the heart.
Over and above, the combination of anatomical (small lumed coronary artery, ventricular hypertrophy) and substance-induced risk factors led to the fatal cardiovascular failure.
Lehmann S, Thomas A, Schiwy-Bochat K-H, et al. Death after misuse of anabolic substances (clenbuterol, stanozolol and metandienone). Forensic science international 2019;303:109925. https://www.sciencedirect.com/science/article/pii/S0379073819303378
Similar threads
Sponsors
Latest posts
-
-
-
Giant Semaglutide Thread (and other GLP-1 / GIP agonists)
- Latest: Captainpotatohead
