So this means that an increase in cardiovascular activity can ameliorate the damage otherwise caused by regular use of AAS? (Sorry, medspeak is never quite clear to me.)
Respects,
Solo
MESO-Rx
Anabolic Steroids
AAS and Cardiovascular/Pulmonary Function
- Thread starter Michael Scally MD
- Start date
So this means that an increase in cardiovascular activity can ameliorate the damage otherwise caused by regular use of AAS? (Sorry, medspeak is never quite clear to me.)
Respects,
Solo
cazper
New Member
Everyday I'm on this forum I learn so many new things.
I'll definately be sticking around.
I'll definately be sticking around.
Lacunar infarction is traditionally ascribed to lipohyalinosis or microatheroma.
We report the case of 40-year-old man, without traditional risk factors for ischemic stroke, who presented to the Emergency Department with recurrent episodes of transient right-sided weakness and paresthesia.
A 40-year-old bodybuilder presented to the Emergency Department following 2 episodes of right-sided weakness and paresthesia on the same day, each lasting 10 min. The patient admitted regular use of AAS for bodybuilding (2a-17a-dimethyl-17b-hydroxy-5a-androstan-3-one, stanozolol, testosterone and trenbolone). Past medical history was significant for steroid-induced cholestasis 6 years previously.
Of note, he was not hypertensive at the time of that presentation. Outside of a 5 pack-year history of tobacco smoking, there was no history of traditional cardiovascular risk factors. There was no history of erythropoietin use. He denied other drug use, including cocaine.
Lacunar infarction was confirmed on diffusion-weighted MRI and blood tests showed a marked polycythemia. Quantitative magnetic resonance perfusion imaging demonstrated dramatically abnormal perfusion throughout both cerebral hemispheres, and transcranial Doppler revealed reduced cerebral artery velocities, both consistent with the proposed mechanism of hyperviscosity.
His symptoms settled with treatment of the polycythemia and workup did not find another cause of ischemic stroke.
We propose that hyperviscosity secondary to steroid-induced polycythemia caused ischemia in this case and not lipohyalinosis or microatheroma, to which lacunar disease is commonly attributed.
Harston GW, Batt F, Fan L, et al. Lacunar infarction associated with anabolic steroids and polycythemia: a case report. Case Rep Neurol 2014;6(1):34-7. http://www.karger.com/Article/FullText/360076
We report the case of 40-year-old man, without traditional risk factors for ischemic stroke, who presented to the Emergency Department with recurrent episodes of transient right-sided weakness and paresthesia.
A 40-year-old bodybuilder presented to the Emergency Department following 2 episodes of right-sided weakness and paresthesia on the same day, each lasting 10 min. The patient admitted regular use of AAS for bodybuilding (2a-17a-dimethyl-17b-hydroxy-5a-androstan-3-one, stanozolol, testosterone and trenbolone). Past medical history was significant for steroid-induced cholestasis 6 years previously.
Of note, he was not hypertensive at the time of that presentation. Outside of a 5 pack-year history of tobacco smoking, there was no history of traditional cardiovascular risk factors. There was no history of erythropoietin use. He denied other drug use, including cocaine.
Lacunar infarction was confirmed on diffusion-weighted MRI and blood tests showed a marked polycythemia. Quantitative magnetic resonance perfusion imaging demonstrated dramatically abnormal perfusion throughout both cerebral hemispheres, and transcranial Doppler revealed reduced cerebral artery velocities, both consistent with the proposed mechanism of hyperviscosity.
His symptoms settled with treatment of the polycythemia and workup did not find another cause of ischemic stroke.
We propose that hyperviscosity secondary to steroid-induced polycythemia caused ischemia in this case and not lipohyalinosis or microatheroma, to which lacunar disease is commonly attributed.
Harston GW, Batt F, Fan L, et al. Lacunar infarction associated with anabolic steroids and polycythemia: a case report. Case Rep Neurol 2014;6(1):34-7. http://www.karger.com/Article/FullText/360076
OhNoYo
New Member
I've speculated this before in previous posts. Nice to see a study may actually show this to occur. Hopefully, if this is indeed the case, then other more rigorous & detailed studies will follow.
Ilic I, Djordjevic V, Stankovic I, 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/img/doi/0042-8450/2014/0042-84501300046I.pdf
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.
Quite incredible really, as the findings go against almost all the information that reaches the public. Thanks Doc Scally.
Respects,
Solo
Wickramatilake CM, Mohideen MR, Withanawasam BPS, Pathirana C. Testosterone and high-sensitive C-reactive protein in coronary artery disease patients awaiting coronary artery bypass graft. Andrologia. Testosterone and high-sensitive C-reactive protein in coronary artery disease patients awaiting coronary artery bypass graft - Wickramatilake - 2014 - Andrologia - Wiley Online Library
Natural androgens inhibit atherosclerosis in men.
This study aimed to examine whether testosterone and high-sensitive C-reactive protein differ between patients with coronary artery disease and those without coronary artery disease and to determine the association with the severity of coronary artery disease.
Two hundred and six male subjects were recruited. Serum total testosterone and high-sensitive C-reactive protein were estimated. Severity of coronary artery disease was assessed by angiographic scores.
Total testosterone level in patients was significantly different from controls (11.4 ± 2.7 vs. 18.1 ± 7.2 nmP = 0.001) and high-sensitive protein level in cases was significantly higher compared to controls (3.37 ± 1.62 mg l?1 vs. 1.71 ± 0.60 mg l?1, P = 0.001).
Testosterone levels were not significantly different with vessel (P = 0.592), Leaman (P = 0.694) and Gensini (P = 0.329) score groups, but high-sensitive C-reactive protein showed significant positive correlation among the respective groups (P = 0.005, P = 0.028, P = 0.015).
Testosterone was lower, while high-sensitive C-reactive protein was higher in patients compared to controls. Testosterone showed no correlation with the severity of atherosclerosis, but high-sensitive C-reactive protein showed significant positive correlation.
Natural androgens inhibit atherosclerosis in men.
This study aimed to examine whether testosterone and high-sensitive C-reactive protein differ between patients with coronary artery disease and those without coronary artery disease and to determine the association with the severity of coronary artery disease.
Two hundred and six male subjects were recruited. Serum total testosterone and high-sensitive C-reactive protein were estimated. Severity of coronary artery disease was assessed by angiographic scores.
Total testosterone level in patients was significantly different from controls (11.4 ± 2.7 vs. 18.1 ± 7.2 nmP = 0.001) and high-sensitive protein level in cases was significantly higher compared to controls (3.37 ± 1.62 mg l?1 vs. 1.71 ± 0.60 mg l?1, P = 0.001).
Testosterone levels were not significantly different with vessel (P = 0.592), Leaman (P = 0.694) and Gensini (P = 0.329) score groups, but high-sensitive C-reactive protein showed significant positive correlation among the respective groups (P = 0.005, P = 0.028, P = 0.015).
Testosterone was lower, while high-sensitive C-reactive protein was higher in patients compared to controls. Testosterone showed no correlation with the severity of atherosclerosis, but high-sensitive C-reactive protein showed significant positive correlation.
Akcakoyun M, Alizade E, Gundogdu R, et al. Long-term anabolic androgenic steroid use is associated with increased atrial electromechanical delay in male bodybuilders. Biomed Res Int. 2014:451520. http://www.hindawi.com/journals/bmri/2014/451520/
We investigated the effect of long-term supraphysiologic doses of anabolic androgenic steroids (AAS) on atrial electromechanical delay (AEMD) in male bodybuilders.
We clearly demonstrated that long-term consumption of supraphysiologic doses of AAS is associated with higher values of inter- and intra-AEMD in healthy young bodybuilders.
We investigated the effect of long-term supraphysiologic doses of anabolic androgenic steroids (AAS) on atrial electromechanical delay (AEMD) in male bodybuilders.
We clearly demonstrated that long-term consumption of supraphysiologic doses of AAS is associated with higher values of inter- and intra-AEMD in healthy young bodybuilders.
Thanks, Dr Scally. But what, exactly, is "atrial electromechanical delay (AEMD)". Through blood donations, I no longer suffer from Polycythemia, but now on cycle again, by BP is rising (nothing dangerous). However, only the systolic is high (157), while pulse and diastolic remain normal, even good. Is this AEMD? (My left ventricle is just fine.)
Respects,
Solo
I was diagnosed with severe LV Dilated Cardiomyopathy 8 years ago. I had been an infrequent user of steroids for the 10 years previous to diagnosis. However I was also a binge drinker and very fond of ephedrine. Did Steroids alone cause my cardiomyopathy? I don't think so. But they may have very well contributed to my condition. My ejection fraction is 30.
However I can definitely testify that my continued use light use of steroids and peptides has certainly improved my quality of life. I am much fitter than the average 40 year old and with a heart as busted as mine, that's a miracle in my book.
However I can definitely testify that my continued use light use of steroids and peptides has certainly improved my quality of life. I am much fitter than the average 40 year old and with a heart as busted as mine, that's a miracle in my book.
Hartgens F, Rietjens G, Keizer HA, Kuipers H, Wolffenbuttel BHR. Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). British Journal of Sports Medicine 2004;38(3):253-9. http://bjsm.bmj.com/content/38/3/253.full
Objectives: To investigate the effects of two different regimens of androgenic-anabolic steroid (AAS) administration on serum lipid and lipoproteins, and recovery of these variables after drug cessation, as indicators of the risk for cardiovascular disease in healthy male strength athletes.
Methods: In a non-blinded study (study 1) serum lipoproteins and lipids were assessed in 19 subjects who self administered AASs for eight or 14 weeks, and in 16 non-using volunteers. In a randomised double blind, placebo controlled design, the effects of intramuscular administration of nandrolone decanoate (200 mg/week) for eight weeks on the same variables in 16 bodybuilders were studied (study 2). Fasting serum concentrations of total cholesterol, triglycerides, HDL-cholesterol (HDL-C), HDL2-cholesterol (HDL2-C), HDL3-cholesterol (HDL3-C), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), and lipoprotein (a) (Lp(a)) were determined.
Results: In study 1 AAS administration led to decreases in serum concentrations of HDL-C (from 1.08 (0.30) to 0.43 (0.22) mmol/l), HDL2-C (from 0.21 (0.18) to 0.05 (0.03) mmol/l), HDL3-C (from 0.87 (0.24) to 0.40 (0.20) mmol/l, and Apo-A1 (from 1.41 (0.27) to 0.71 (0.34) g/l), whereas Apo-B increased from 0.96 (0.13) to 1.32 (0.28) g/l. Serum Lp(a) declined from 189 (315) to 32 (63) U/l. Total cholesterol and triglycerides did not change significantly. Alterations after eight and 14 weeks of AAS administration were comparable. No changes occurred in the controls. Six weeks after AAS cessation, serum HDL-C, HDL2-C, Apo-A1, Apo-B, and Lp(a) had still not returned to baseline concentrations. Administration of AAS for 14 weeks was associated with slower recovery to pretreatment concentrations than administration for eight weeks.
In study 2, nandrolone decanoate did not influence serum triglycerides, total cholesterol, HDL-C, HDL2-C, HDL3-C, Apo-A1, and Apo-B concentrations after four and eight weeks of intervention, nor six weeks after withdrawal. However, Lp(a) concentrations decreased significantly from 103 (68) to 65 (44) U/l in the nandrolone decanoate group, and in the placebo group a smaller reduction from 245 (245) to 201 (194) U/l was observed. Six weeks after the intervention period, Lp(a) concentrations had returned to baseline values in both groups.
Conclusions: Self administration of several AASs simultaneously for eight or 14 weeks produces comparable profound unfavourable effects on lipids and lipoproteins, leading to an increased atherogenic lipid profile, despite a beneficial effect on Lp(a) concentration.
The changes persist after AAS withdrawal, and normalisation depends on the duration of the drug abuse. Eight weeks of administration of nandrolone decanoate does not affect lipid and lipoprotein concentrations, although it may selectively reduce Lp(a) concentrations. The effect of this on atherogenesis remains to be established.
Objectives: To investigate the effects of two different regimens of androgenic-anabolic steroid (AAS) administration on serum lipid and lipoproteins, and recovery of these variables after drug cessation, as indicators of the risk for cardiovascular disease in healthy male strength athletes.
Methods: In a non-blinded study (study 1) serum lipoproteins and lipids were assessed in 19 subjects who self administered AASs for eight or 14 weeks, and in 16 non-using volunteers. In a randomised double blind, placebo controlled design, the effects of intramuscular administration of nandrolone decanoate (200 mg/week) for eight weeks on the same variables in 16 bodybuilders were studied (study 2). Fasting serum concentrations of total cholesterol, triglycerides, HDL-cholesterol (HDL-C), HDL2-cholesterol (HDL2-C), HDL3-cholesterol (HDL3-C), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), and lipoprotein (a) (Lp(a)) were determined.
Results: In study 1 AAS administration led to decreases in serum concentrations of HDL-C (from 1.08 (0.30) to 0.43 (0.22) mmol/l), HDL2-C (from 0.21 (0.18) to 0.05 (0.03) mmol/l), HDL3-C (from 0.87 (0.24) to 0.40 (0.20) mmol/l, and Apo-A1 (from 1.41 (0.27) to 0.71 (0.34) g/l), whereas Apo-B increased from 0.96 (0.13) to 1.32 (0.28) g/l. Serum Lp(a) declined from 189 (315) to 32 (63) U/l. Total cholesterol and triglycerides did not change significantly. Alterations after eight and 14 weeks of AAS administration were comparable. No changes occurred in the controls. Six weeks after AAS cessation, serum HDL-C, HDL2-C, Apo-A1, Apo-B, and Lp(a) had still not returned to baseline concentrations. Administration of AAS for 14 weeks was associated with slower recovery to pretreatment concentrations than administration for eight weeks.
In study 2, nandrolone decanoate did not influence serum triglycerides, total cholesterol, HDL-C, HDL2-C, HDL3-C, Apo-A1, and Apo-B concentrations after four and eight weeks of intervention, nor six weeks after withdrawal. However, Lp(a) concentrations decreased significantly from 103 (68) to 65 (44) U/l in the nandrolone decanoate group, and in the placebo group a smaller reduction from 245 (245) to 201 (194) U/l was observed. Six weeks after the intervention period, Lp(a) concentrations had returned to baseline values in both groups.
Conclusions: Self administration of several AASs simultaneously for eight or 14 weeks produces comparable profound unfavourable effects on lipids and lipoproteins, leading to an increased atherogenic lipid profile, despite a beneficial effect on Lp(a) concentration.
The changes persist after AAS withdrawal, and normalisation depends on the duration of the drug abuse. Eight weeks of administration of nandrolone decanoate does not affect lipid and lipoprotein concentrations, although it may selectively reduce Lp(a) concentrations. The effect of this on atherogenesis remains to be established.
Kunnas T, Solakivi T, Huuskonen K, Kalela A, Renko J, Nikkari ST. Hematocrit and the risk of coronary heart disease mortality in the TAMRISK study, a 28-year follow-up. Prev Med 2009;49(1):45-7. https://www.sciencedirect.com/science/article/pii/S0091743509002163
OBJECTIVE: To evaluate whether hematocrit (HCT) is associated with coronary heart disease (CHD) mortality in men over 55 years of age in Finland.
METHODS: Health survey data were recorded in 1980 from 670 men, aged 55 years. The causes of deaths during a 28-year follow-up were obtained from official records. Statistical comparisons were done by Cox proportional hazard regression model after dividing the men into two groups, one with HCT<50% and the other, HCT> or =50%.
RESULTS: There were altogether 412 deaths of all causes, including 140 from CHD. In men having HCT<50%, the crude CHD mortality rate per 10,000 population was 2203, while in men with HCT> or =50%, the corresponding figure was 4255. Men with HCT> or =50% were 2.4 times (95% CI 1.6-3.5) more likely to die from CHD than were men with HCT<50%. After adjusting for established coronary risk factors, the increased risk remained 1.8-fold (95 % CI, 1.1-2.7).
CONCLUSIONS: Borderline polycythemia was associated with increased CHD mortality. The cut-off value in our study was > or =50%, proposing that for men over 55 years of age such HCT levels might be an additional risk factor.
Boffetta P, Islami F, Vedanthan R, et al. A U-shaped relationship between haematocrit and mortality in a large prospective cohort study. International Journal of Epidemiology 2013;42(2):601-15. http://ije.oxfordjournals.org/content/42/2/601.full
Background Only a limited number of studies have investigated the correlation between haematocrit (HCT) and mortality in the general population, and few of those studies have had data on a wide range of low and high levels of HCT. We investigated the association between baseline HCT and mortality in a prospective cohort study of 49 983 adult subjects in Iran with a broad spectrum of HCT values.
Methods Data on socio-demographic and life-style factors, past medical history, and levels of HCT were collected at enrollment. During a mean follow-up of 5 years (follow-up success rate ∼99%), 2262 deaths were reported. Cox proportional hazards regression models were used to estimate hazard ratios and corresponding 95% confidence intervals.
Results There was a U-shaped relationship between categories of HCT and mortality in both sexes: both low and high levels of HCT were associated with increased overall mortality and mortality from cardiovascular disease.
The U-shaped relationship persisted after several sensitivity analyses were done, including analyses restricted to non-smokers and non-users of opium; analyses excluding deaths from accidents and other external causes as well as deaths of persons with self-reported ischemic heart disease at the baseline interview for the study; and analyses excluding the first 2 years of follow-up.
Self-reported past medical history and lack of data about lipids and other cellular blood components were the major limitations of the study.
Conclusions Low and high levels of HCT are associated with increased mortality in the general population. The findings in the present study can be of particular importance for low- and middle-income countries in which a substantial proportion of the population lives with suboptimal levels of HCT.
OBJECTIVE: To evaluate whether hematocrit (HCT) is associated with coronary heart disease (CHD) mortality in men over 55 years of age in Finland.
METHODS: Health survey data were recorded in 1980 from 670 men, aged 55 years. The causes of deaths during a 28-year follow-up were obtained from official records. Statistical comparisons were done by Cox proportional hazard regression model after dividing the men into two groups, one with HCT<50% and the other, HCT> or =50%.
RESULTS: There were altogether 412 deaths of all causes, including 140 from CHD. In men having HCT<50%, the crude CHD mortality rate per 10,000 population was 2203, while in men with HCT> or =50%, the corresponding figure was 4255. Men with HCT> or =50% were 2.4 times (95% CI 1.6-3.5) more likely to die from CHD than were men with HCT<50%. After adjusting for established coronary risk factors, the increased risk remained 1.8-fold (95 % CI, 1.1-2.7).
CONCLUSIONS: Borderline polycythemia was associated with increased CHD mortality. The cut-off value in our study was > or =50%, proposing that for men over 55 years of age such HCT levels might be an additional risk factor.
Boffetta P, Islami F, Vedanthan R, et al. A U-shaped relationship between haematocrit and mortality in a large prospective cohort study. International Journal of Epidemiology 2013;42(2):601-15. http://ije.oxfordjournals.org/content/42/2/601.full
Background Only a limited number of studies have investigated the correlation between haematocrit (HCT) and mortality in the general population, and few of those studies have had data on a wide range of low and high levels of HCT. We investigated the association between baseline HCT and mortality in a prospective cohort study of 49 983 adult subjects in Iran with a broad spectrum of HCT values.
Methods Data on socio-demographic and life-style factors, past medical history, and levels of HCT were collected at enrollment. During a mean follow-up of 5 years (follow-up success rate ∼99%), 2262 deaths were reported. Cox proportional hazards regression models were used to estimate hazard ratios and corresponding 95% confidence intervals.
Results There was a U-shaped relationship between categories of HCT and mortality in both sexes: both low and high levels of HCT were associated with increased overall mortality and mortality from cardiovascular disease.
The U-shaped relationship persisted after several sensitivity analyses were done, including analyses restricted to non-smokers and non-users of opium; analyses excluding deaths from accidents and other external causes as well as deaths of persons with self-reported ischemic heart disease at the baseline interview for the study; and analyses excluding the first 2 years of follow-up.
Self-reported past medical history and lack of data about lipids and other cellular blood components were the major limitations of the study.
Conclusions Low and high levels of HCT are associated with increased mortality in the general population. The findings in the present study can be of particular importance for low- and middle-income countries in which a substantial proportion of the population lives with suboptimal levels of HCT.
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This mega-thread on anabolic steroids and cardiovascular function is an amazing resource - thanks @Michael Scally MD
I recommend that all long-term AAS users bookmark it as a reference for recent and future research in this area.
I recommend that all long-term AAS users bookmark it as a reference for recent and future research in this area.
Juice n Goose
New Member
I have used AAS on and off since I was 19( that is 29 years.) A couple of years ago, I was hospitalized for respiratory distress and my chest was xrayed.
It was discovered that I had severe cardiomegaly. Upon further inspection I was diagnosed with dilated cardiomyopathy and was at a late stage in that as well as CHF. My ejection fraction was around 20 as shown by 2D echocardiography and other invasive tests. I was fully worked up and told I would not survive more than 18 months.
During this time I struggleded with left venticular disorders and it was discovered that I was having one arrythmia after another.
Once several blood clots were discovered in my heart they revised my prognosis and told me Id be "checking out" real soon. I could bareky sweep the floors etc without damn near collapsing.
Eventuallyt they decided to install an implantable cardioversion defibrillator in my chest to help stop the constant rythm issues and low ejection fraction. I was also put on 50mg/day of carvedilol.25mg/day of lisinopril and 40+mg/day of furosemide,spironolactone,simvastanton(I dont know why) and low-dose aspirin.
During the install of the ICD it had to be tested by sending a scrambled signal to my heart to see if the ICD could fix it..it couldnt and I spent the next several hours on various pressor therapy. I damn near died a couple of times..Two years later,my ICD goes off about 3-5 times a year and sometimes I get damn scared. My life-expectancy remains very low and I often feel as if my cardiologist has given up.
He claims,as does the rest of the team that I did this to myself with AAS use over about 30 years.
I dont know and never will.
I would,however not rule this out.
Friend of a friend
It was discovered that I had severe cardiomegaly. Upon further inspection I was diagnosed with dilated cardiomyopathy and was at a late stage in that as well as CHF. My ejection fraction was around 20 as shown by 2D echocardiography and other invasive tests. I was fully worked up and told I would not survive more than 18 months.
During this time I struggleded with left venticular disorders and it was discovered that I was having one arrythmia after another.
Once several blood clots were discovered in my heart they revised my prognosis and told me Id be "checking out" real soon. I could bareky sweep the floors etc without damn near collapsing.
Eventuallyt they decided to install an implantable cardioversion defibrillator in my chest to help stop the constant rythm issues and low ejection fraction. I was also put on 50mg/day of carvedilol.25mg/day of lisinopril and 40+mg/day of furosemide,spironolactone,simvastanton(I dont know why) and low-dose aspirin.
During the install of the ICD it had to be tested by sending a scrambled signal to my heart to see if the ICD could fix it..it couldnt and I spent the next several hours on various pressor therapy. I damn near died a couple of times..Two years later,my ICD goes off about 3-5 times a year and sometimes I get damn scared. My life-expectancy remains very low and I often feel as if my cardiologist has given up.
He claims,as does the rest of the team that I did this to myself with AAS use over about 30 years.
I dont know and never will.
I would,however not rule this out.
Friend of a friend
BIGMESC
New Member
Wow, that sure brings it home. Stay safe fellas, and be wise in your choices.
Long time AAS user,started in 1980 and done over 30 cycles.Im getting a complete cardio work up,So far it looks good,i had a sonogram done so far and asked the tech if my heart was enlarged and she it was not.Done the stress test and wore a monitor for 24 hours.will get the results next month so we'll see what long term AAS use had on me........I have led a pretty healthy life style,never smoked,havnt really drank much hardly ever now and if i do its only a couple beers,no rec drugs in a long time,did pot when i was younger.
3 Things to Know About Niacin and Heart Health
http://well.blogs.nytimes.com/2014/07/16/3-things-to-know-about-niacin-and-heart-health/
[The use of Niacin to thwart the effects of AAS does not work and is a waste.]
Recent studies are adding to concerns about the safety and effectiveness of niacin, a popular drug for the prevention of cardiovascular disease.
The studies reveal that although this B vitamin can reduce triglyceride levels, raise “good” cholesterol levels (HDL) and reduce “bad” cholesterol levels (LDL), it does not produce the benefits that patients and their doctors might expect.
And the studies are revealing serious harms.
Here are three things you need to know about niacin.
First, these new studies failed to show that niacin reduced the risk of heart disease and stroke.
Second, niacin causes multiple side effects, many of which are serious.
Third, there are still experts who say that the recent studies do not provide adequate evidence to stop recommending niacin.
http://well.blogs.nytimes.com/2014/07/16/3-things-to-know-about-niacin-and-heart-health/
[The use of Niacin to thwart the effects of AAS does not work and is a waste.]
Recent studies are adding to concerns about the safety and effectiveness of niacin, a popular drug for the prevention of cardiovascular disease.
The studies reveal that although this B vitamin can reduce triglyceride levels, raise “good” cholesterol levels (HDL) and reduce “bad” cholesterol levels (LDL), it does not produce the benefits that patients and their doctors might expect.
And the studies are revealing serious harms.
Here are three things you need to know about niacin.
First, these new studies failed to show that niacin reduced the risk of heart disease and stroke.
Second, niacin causes multiple side effects, many of which are serious.
Third, there are still experts who say that the recent studies do not provide adequate evidence to stop recommending niacin.
graniteman
New Member
^^^Good to know! My HrT clinic had me supplementing niacin, I didnt like it and quit. I feel vindicated now
This is pretty much my regiment on or off:
http://www.livestrong.com/article/122416-herbs-clear-arteries-plaque/
http://www.livestrong.com/article/122416-herbs-clear-arteries-plaque/
Josiak K, Jankowska E, Piepoli M, Banasiak W, Ponikowski P. Skeletal myopathy in patients with chronic heart failure: significance of anabolic-androgenic hormones. Journal of Cachexia, Sarcopenia and Muscle 2014:1-10. http://link.springer.com/article/10.1007/s13539-014-0152-z
In heart failure, impairment of cardiac muscle function leads to numerous neurohormonal and metabolic disorders, including an imbalance between anabolic and catabolic processes, in favour of the latter.
These disorders cause loss of muscle mass with structural and functional changes within the skeletal muscles, known as skeletal myopathy.
This phenomenon constitutes an important mechanism that participates in the pathogenesis of chronic heart failure. both its clinical symptoms and the progression of the disease.
Attempts to reverse the above-mentioned pathologic processes by exploiting the anabolic action of androgenic hormones could provide a potentially attractive treatment option.
The current concepts of anabolic androgen deficiency and resultant skeletal myopathy in patients with heart failure are reviewed, and the potential role of anabolic-androgenic hormones as an emerging therapeutic option for targeting heart failure is discussed.
The Muscle Hypothesis in Heart Failure: Pathogenesis of Skeletal Myopathy
Mechanisms of Action of Anabolic Hormones on Skeletal Muscles
AR - Androgen Receptor, UPS - Ubiquitin-Proteasome System
In heart failure, impairment of cardiac muscle function leads to numerous neurohormonal and metabolic disorders, including an imbalance between anabolic and catabolic processes, in favour of the latter.
These disorders cause loss of muscle mass with structural and functional changes within the skeletal muscles, known as skeletal myopathy.
This phenomenon constitutes an important mechanism that participates in the pathogenesis of chronic heart failure. both its clinical symptoms and the progression of the disease.
Attempts to reverse the above-mentioned pathologic processes by exploiting the anabolic action of androgenic hormones could provide a potentially attractive treatment option.
The current concepts of anabolic androgen deficiency and resultant skeletal myopathy in patients with heart failure are reviewed, and the potential role of anabolic-androgenic hormones as an emerging therapeutic option for targeting heart failure is discussed.
The Muscle Hypothesis in Heart Failure: Pathogenesis of Skeletal Myopathy
Mechanisms of Action of Anabolic Hormones on Skeletal Muscles
AR - Androgen Receptor, UPS - Ubiquitin-Proteasome System
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