AAS and Cardiovascular/Pulmonary Function

[Michael Scally MD]

[No] Use of Aspirin to Reduce Risk of Initial Vascular Events in Patients at Moderate Risk of Cardiovascular Disease (ARRIVE)

Background - The use of aspirin in the primary prevention of cardiovascular events remains controversial. We aimed to assess the efficacy and safety of aspirin versus placebo in patients with a moderate estimated risk of a first cardiovascular event.

Methods - ARRIVE is a randomised, double-blind, placebo-controlled, multicentre study done in seven countries. Eligible patients were aged 55 years (men) or 60 years (women) and older and had an average cardiovascular risk, deemed to be moderate on the basis of the number of specific risk factors. We excluded patients at high risk of gastrointestinal bleeding or other bleeding, or diabetes.

Patients were randomly assigned (1:1) with a computer-generated randomisation code to receive enteric-coated aspirin tablets (100 mg) or placebo tablets, once daily. Patients, investigators, and others involved in treatment or data analysis were masked to treatment allocation.

The primary efficacy endpoint was a composite outcome of time to first occurrence of cardiovascular death, myocardial infarction, unstable angina, stroke, or transient ischaemic attack.

Safety endpoints were haemorrhagic events and incidence of other adverse events, and were analysed in the intention-to-treat population. This study is registered with ClinicalTrials.gov, number NCT00501059.

Findings - Between July 5, 2007, and Nov 15, 2016, 12 546 patients were enrolled and randomly assigned to receive aspirin (n=6270) or placebo (n=6276) at 501 study sites. Median follow-up was 60 months.

In the intention-to-treat analysis, the primary endpoint occurred in 269 (4·29%) patients in the aspirin group versus 281 (4·48%) patients in the placebo group (hazard ratio

---

0·96; 95% CI 0·81–1·13; p=0·6038).

Gastrointestinal bleeding events (mostly mild) occurred in 61 (0·97%) patients in the aspirin group versus 29 (0·46%) in the placebo group (HR 2·11; 95% CI 1·36–3·28; p=0·0007).

The overall incidence rate of serious adverse events was similar in both treatment groups (n=1266 [20·19%] in the aspirin group vs n=1311 [20·89%] in the placebo group.

The overall incidence of adverse events was similar in both treatment groups (n=5142 [82·01%] vs n=5129 [81·72%] in the placebo group).

The overall incidence of treatment-related adverse events was low (n=1050 [16·75%] vs n=850 [13·54%] in the placebo group; p<0·0001).

There were 321 documented deaths in the intention-to-treat population (n=160 [2·55%] vs n=161 [2·57%] of 6276 patients in the placebo group).

Interpretation - The event rate was much lower than expected, which is probably reflective of contemporary risk management strategies, making the study more representative of a low-risk population. The role of aspirin in primary prevention among patients at moderate risk could therefore not be addressed. Nonetheless, the findings with respect to aspirin's effects are consistent with those observed in the previously published low-risk primary prevention studies.

Gaziano JM, Brotons C, Coppolecchia R, et al. Use of aspirin to reduce risk of initial vascular events in patients at moderate risk of cardiovascular disease (ARRIVE): a randomised, double-blind, placebo-controlled trial. The Lancet. Redirecting

 

[Michael Scally MD]

[OA] [No] Effects of n−3 Fatty Acid Supplements

BACKGROUND - Increased intake of n−3 fatty acids has been associated with a reduced risk of cardiovascular disease in observational studies, but this finding has not been confirmed in randomized trials. It remains unclear whether n−3 (also called omega-3) fatty acid supplementation has cardiovascular benefit in patients with diabetes mellitus.

METHODS - We randomly assigned 15,480 patients with diabetes but without evidence of atherosclerotic cardiovascular disease to receive 1-g capsules containing either n−3 fatty acids (fatty acid group) or matching placebo (olive oil) daily.

The primary outcome was a first serious vascular event (i.e., nonfatal myocardial infarction or stroke, transient ischemic attack, or vascular death, excluding confirmed intracranial hemorrhage). The secondary outcome was a first serious vascular event or any arterial revascularization.

RESULTS - During a mean follow-up of 7.4 years (adherence rate, 76%), a serious vascular event occurred in 689 patients (8.9%) in the fatty acid group and in 712 (9.2%) in the placebo group (rate ratio, 0.97; 95% confidence interval [CI], 0.87 to 1.08; P=0.55).

The composite outcome of a serious vascular event or revascularization occurred in 882 patients (11.4%) and 887 patients (11.5%), respectively (rate ratio, 1.00; 95% CI, 0.91 to 1.09).

Death from any cause occurred in 752 patients (9.7%) in the fatty acid group and in 788 (10.2%) in the placebo group (rate ratio, 0.95; 95% CI, 0.86 to 1.05).

There were no significant between-group differences in the rates of nonfatal serious adverse events.

CONCLUSIONS - Among patients with diabetes without evidence of cardiovascular disease, there was no significant difference in the risk of serious vascular events between those who were assigned to receive n−3 fatty acid supplementation and those who were assigned to receive placebo.

The ASCEND Study Collaborative Group. Effects of n−3 Fatty Acid Supplements in Diabetes Mellitus. New England Journal of Medicine 2018. https://doi.org/10.1056/NEJMoa1804989

 

[bob hughes]

[OA] [No] Effects of n−3 Fatty Acid Supplements

BACKGROUND - Increased intake of n−3 fatty acids has been associated with a reduced risk of cardiovascular disease in observational studies, but this finding has not been confirmed in randomized trials. It remains unclear whether n−3 (also called omega-3) fatty acid supplementation has cardiovascular benefit in patients with diabetes mellitus.

METHODS - We randomly assigned 15,480 patients with diabetes but without evidence of atherosclerotic cardiovascular disease to receive 1-g capsules containing either n−3 fatty acids (fatty acid group) or matching placebo (olive oil) daily.

The primary outcome was a first serious vascular event (i.e., nonfatal myocardial infarction or stroke, transient ischemic attack, or vascular death, excluding confirmed intracranial hemorrhage). The secondary outcome was a first serious vascular event or any arterial revascularization.

RESULTS - During a mean follow-up of 7.4 years (adherence rate, 76%), a serious vascular event occurred in 689 patients (8.9%) in the fatty acid group and in 712 (9.2%) in the placebo group (rate ratio, 0.97; 95% confidence interval [CI], 0.87 to 1.08; P=0.55).

The composite outcome of a serious vascular event or revascularization occurred in 882 patients (11.4%) and 887 patients (11.5%), respectively (rate ratio, 1.00; 95% CI, 0.91 to 1.09).

Death from any cause occurred in 752 patients (9.7%) in the fatty acid group and in 788 (10.2%) in the placebo group (rate ratio, 0.95; 95% CI, 0.86 to 1.05).

There were no significant between-group differences in the rates of nonfatal serious adverse events.

CONCLUSIONS - Among patients with diabetes without evidence of cardiovascular disease, there was no significant difference in the risk of serious vascular events between those who were assigned to receive n−3 fatty acid supplementation and those who were assigned to receive placebo.

The ASCEND Study Collaborative Group. Effects of n−3 Fatty Acid Supplements in Diabetes Mellitus. New England Journal of Medicine 2018. https://doi.org/10.1056/NEJMoa1804989

Not specific to the study but in general, do you think annual physicals and maybe an EKG is enough to monitor heart health and potential warning signs in someone who uses these substances? Or if not, what additional precautions would you recommend thanks

 

[janoshik]

Not specific to the study but in general, do you think annual physicals and maybe an EKG is enough to monitor heart health and potential warning signs in someone who uses these substances? Or if not, what additional precautions would you recommend thanks

EKG + Sono by somebody who does heart sono for living

 

[bob hughes]

EKG + Sono by somebody who does heart sono for living

Thanks good to know. I will ask my doctor for these tests citing TRT and the black box warning about possible heart damage as reasons hopefully that will be enough for him to order them

 

[hurricane]

Thanks good to know. I will ask my doctor for these tests citing TRT and the black box warning about possible heart damage as reasons hopefully that will be enough for him to order them

I myself personally find an EKG a pretty worthless test unless someone is in cardiac arrest at that very moment the test is given.
I have multiple arrythmias and 95% of my EKG's are always fine. It wasn't until an implantable device was inserted into my chest that they found I was having multiple bouts of afib and aflutter.
I'd personally opt for a yearly echocardiogram. It shows everything.
Again just my opinion but at least you're concerned with your cardiac health.

 

[Havah]

I myself personally find an EKG a pretty worthless test unless someone is in cardiac arrest at that very moment the test is given.
I have multiple arrythmias and 95% of my EKG's are always fine. It wasn't until an implantable device was inserted into my chest that they found I was having multiple bouts of afib and aflutter.
I'd personally opt for a yearly echocardiogram. It shows everything.
Again just my opinion but at least you're concerned with your cardiac health.

Do an holter ekg then
Echography doesnt show everything, far from it

 

[hurricane]

[No] Use of Aspirin to Reduce Risk of Initial Vascular Events in Patients at Moderate Risk of Cardiovascular Disease (ARRIVE)

Background - The use of aspirin in the primary prevention of cardiovascular events remains controversial. We aimed to assess the efficacy and safety of aspirin versus placebo in patients with a moderate estimated risk of a first cardiovascular event.

Methods - ARRIVE is a randomised, double-blind, placebo-controlled, multicentre study done in seven countries. Eligible patients were aged 55 years (men) or 60 years (women) and older and had an average cardiovascular risk, deemed to be moderate on the basis of the number of specific risk factors. We excluded patients at high risk of gastrointestinal bleeding or other bleeding, or diabetes.

Patients were randomly assigned (1:1) with a computer-generated randomisation code to receive enteric-coated aspirin tablets (100 mg) or placebo tablets, once daily. Patients, investigators, and others involved in treatment or data analysis were masked to treatment allocation.

The primary efficacy endpoint was a composite outcome of time to first occurrence of cardiovascular death, myocardial infarction, unstable angina, stroke, or transient ischaemic attack.

Safety endpoints were haemorrhagic events and incidence of other adverse events, and were analysed in the intention-to-treat population. This study is registered with ClinicalTrials.gov, number NCT00501059.

Findings - Between July 5, 2007, and Nov 15, 2016, 12 546 patients were enrolled and randomly assigned to receive aspirin (n=6270) or placebo (n=6276) at 501 study sites. Median follow-up was 60 months.

In the intention-to-treat analysis, the primary endpoint occurred in 269 (4·29%) patients in the aspirin group versus 281 (4·48%) patients in the placebo group (hazard ratio

---

0·96; 95% CI 0·81–1·13; p=0·6038).

Gastrointestinal bleeding events (mostly mild) occurred in 61 (0·97%) patients in the aspirin group versus 29 (0·46%) in the placebo group (HR 2·11; 95% CI 1·36–3·28; p=0·0007).

The overall incidence rate of serious adverse events was similar in both treatment groups (n=1266 [20·19%] in the aspirin group vs n=1311 [20·89%] in the placebo group.

The overall incidence of adverse events was similar in both treatment groups (n=5142 [82·01%] vs n=5129 [81·72%] in the placebo group).

The overall incidence of treatment-related adverse events was low (n=1050 [16·75%] vs n=850 [13·54%] in the placebo group; p<0·0001).

There were 321 documented deaths in the intention-to-treat population (n=160 [2·55%] vs n=161 [2·57%] of 6276 patients in the placebo group).

Interpretation - The event rate was much lower than expected, which is probably reflective of contemporary risk management strategies, making the study more representative of a low-risk population. The role of aspirin in primary prevention among patients at moderate risk could therefore not be addressed. Nonetheless, the findings with respect to aspirin's effects are consistent with those observed in the previously published low-risk primary prevention studies.

Gaziano JM, Brotons C, Coppolecchia R, et al. Use of aspirin to reduce risk of initial vascular events in patients at moderate risk of cardiovascular disease (ARRIVE): a randomised, double-blind, placebo-controlled trial. The Lancet. Redirecting

---

Interesting Doc. Just had an angiogram last Friday and they stopped my Coumadin 5 days prior and bridged the gap with Lovenox and aspirin.
I've always been told to chew one or two baby aspirin if I feel something's wrong. Even though I'm on a blood thinner.
Angiogram went fine. They replicated my coronary artery spasms and upped amlodipine to 10mg.
And Lovenox can go fuk itself!! My stomach is almost black!!

 

[hurricane]

Do an holter ekg then
Echography doesnt show everything, far from it

It doesn't show arrythmias you are correct. It shows a shit lot more then an EKG. I started off with a holter over a decade ago.

 

[Michael Scally MD]

 

[Michael Scally MD]

Ference BA, Graham I, Tokgozoglu L, Catapano AL. Impact of Lipids on Cardiovascular Health. Journal of the American College of Cardiology 2018;72:1141. Impact of Lipids on Cardiovascular Health

 

[Michael Scally MD]

 

[hurricane]

Since my LDL is something I try and be conscious of this was a great read.
I'm ashamed to say my weight has exploded back to 296lbs when weighed before angiogram. Although no significant blockages were found I worry that if I keep thinking I have to be huge it will eventually catch up.
Total cholesterol is just barely out of normal range. BP was great at 118/70. HR in mid 50's.
But what do I do last night Doc? I order 3 burgers and fries at Jake's at 8pm. And that was after dinner. Come midnight I'm waking the wife up with horrible chest pain and very light headed. I'm being stupid and need to get a hold of my weight before I drop dead.
Sorry for the pity party of a rant Doc.
Thanks for all you do for us.

 

[Michael Scally MD]

semiglutide

Since my LDL is something I try and be conscious of this was a great read.
I'm ashamed to say my weight has exploded back to 296lbs when weighed before angiogram. Although no significant blockages were found I worry that if I keep thinking I have to be huge it will eventually catch up.
Total cholesterol is just barely out of normal range. BP was great at 118/70. HR in mid 50's.
But what do I do last night Doc? I order 3 burgers and fries at Jake's at 8pm. And that was after dinner. Come midnight I'm waking the wife up with horrible chest pain and very light headed. I'm being stupid and need to get a hold of my weight before I drop dead.
Sorry for the pity party of a rant Doc.
Thanks for all you do for us.

Semaglutide for Weight Loss
https://thinksteroids.com/community/threads/semaglutide-for-weight-loss.134393834/

 

[hurricane]

semiglutide


Semaglutide for Weight Loss
https://thinksteroids.com/community/threads/semaglutide-for-weight-loss.134393834/

I see my EP Dr. Marieb on Friday. I will mention this to him. He's pretty pissed at me. I don't mind some gastrointestinal discomfort if this will work.
Doc I really appreciate you taking the time out of your day to offer help to not just myself but everyone.
I want you to know just how appreciative I am. It truly means alot.
HC.

 

[Michael Scally MD]

Appearance/Image- and Performance-Enhancing Drug Users: A Forensic Approach

Image- and performance-enhancing drugs include a wide range of substances used to promote physical changes to enhance appearance. Anabolic androgen steroids are the most widely used image- and performance-enhancing drugs along with a wide variety of additional substances.

The aim of this study was to identify the pathological changes pertaining to the cardiovascular system possibly involved in the death and characterize the substances associated with steroid use and their possible role in the death.

A series of deaths involving image- and performance-enhancing drug users were selected. Nandrolone and testosterone were the most frequently identified steroids. The most commonly illegal drugs found were tetrahydrocannabinol, cocaine, and methadone. Antidepressants, opioids, benzodiazepines, and barbiturates were also found.

These findings highlight that results obtained from postmortem investigations should be meticulously evaluated to understand the weight that each identified substance may have played in the death process and exclude any alternative causes of death.

Lusetti M, Licata M, Silingardi E, Bonsignore A, Palmiere C. Appearance/Image- and Performance-Enhancing Drug Users: A Forensic Approach. Am J Forensic Med Pathol 2018. Appearance/Image- and Performance-Enhancing Drug Users: A... : The American Journal of Forensic Medicine and Pathology

 

[Michael Scally MD]

[OA] Left Ventricular Assist Device for Ventricular Recovery of Anabolic Steroid-Induced Cardiomyopathy

Herein we report a case of a 26-year-old gentleman with severe cardiomyopathy likely secondary to anabolic-androgenic steroid (AAS) abuse who received a HeartMate II (Abbott Laboratories, Abbott Park, IL) left ventricular assist device (LVAD) for rapidly deteriorating heart failure with hemodynamic compromise.

Following 18 months on LVAD support, excellent recovery of ventricular function was achieved to allow for LVAD discontinuation. Given that active substance abuse is a contraindication to heart transplantation, few options remain for patients with AAS induced heart failure.

Our case demonstrates that LVAD therapy can be an important intervention for bridging to candidacy, recovery or destination therapy.

Luc JGY, Buchholz H, Kim DH, MacArthur RGG. Left ventricular assist device for ventricular recovery of anabolic steroid-induced cardiomyopathy. Journal of surgical case reports 2018;2018:rjy221. Left ventricular assist device for ventricular recovery of anabolic steroid-induced cardiomyopathy | Journal of Surgical Case Reports | Oxford Academic



Chest radiographs (A) on admission, and (B) following implantation of a HeartMate II Left Ventricular Assist Device.

 

[hurricane]

[OA] Left Ventricular Assist Device for Ventricular Recovery of Anabolic Steroid-Induced Cardiomyopathy

Herein we report a case of a 26-year-old gentleman with severe cardiomyopathy likely secondary to anabolic-androgenic steroid (AAS) abuse who received a HeartMate II (Abbott Laboratories, Abbott Park, IL) left ventricular assist device (LVAD) for rapidly deteriorating heart failure with hemodynamic compromise.

Following 18 months on LVAD support, excellent recovery of ventricular function was achieved to allow for LVAD discontinuation. Given that active substance abuse is a contraindication to heart transplantation, few options remain for patients with AAS induced heart failure.

Our case demonstrates that LVAD therapy can be an important intervention for bridging to candidacy, recovery or destination therapy.

Luc JGY, Buchholz H, Kim DH, MacArthur RGG. Left ventricular assist device for ventricular recovery of anabolic steroid-induced cardiomyopathy. Journal of surgical case reports 2018;2018:rjy221. Left ventricular assist device for ventricular recovery of anabolic steroid-induced cardiomyopathy | Journal of Surgical Case Reports | Oxford Academic

View attachment 96760

Chest radiographs (A) on admission, and (B) following implantation of a HeartMate II Left Ventricular Assist Device.

Great article. Less then 10%EF all the way up to what my EP would say is normal at 55%. Never knew this heart device even existed.
I do wonder how much the cocaine and meth use played into his cardiomyopathy. Like I've said before Dr. Marieb has always leaned a little towards my amphetamine use while in the service as being "more" of a culprit then AAS abuse.
I've always wondered what was worse. Most likely will never know.

 

[Michael Scally MD]

Corona GG, Rastrelli G, Di Pasquale G, Sforza A, Mannucci E, Maggi M. Endogenous Testosterone Levels and Cardiovascular Risk: Meta-Analysis of Observational Studies. The Journal of Sexual Medicine. Redirecting

Introduction - The relationship between endogenous testosterone (T) levels and cardiovascular (CV) risk in men is conflicting.

Aim - To verify whether endogenous T levels represent a possible risk factor for CV morbidity and mortality.

Methods - We conducted a random effect meta-analysis considering all the available data from prospective observational studies comparing subjects with baseline reduced endogenous T levels to those with higher T levels as derived from an extensive MEDLINE, Embase, and Cochrane search. The identification of relevant studies was performed independently by 2 of the authors (G.R. and G.G.C.), and conflicts resolved by the third investigator (M.M.).

Main Outcome Measures - CV mortality and morbidity were investigated.

Results - After screening, 37 observational studies, published between 1988 and 2017 including 43,041 subjects with a mean age of 63.5 years and mean follow-up of 333 weeks, were considered.

Low endogenous T at enrollment predicted overall and CV mortality, as well as CV morbidity, when both unadjusted and fully adjusted models were considered (odds ratio = 1.26 [1.17; 1.36], 1.54 [1.25; 1.89], and 1.17 [1.01; 1.36]; all P < .05 when overall mortality, CV mortality, and CV incidence and fully adjusted models were considered, respectively).

The data were confirmed even when non-population-based studies were excluded from the analysis. Meta-regression analysis applied to the fully adjusted model showed that the risk of CV mortality was inversely related to mean age at enrollment (S = –0.014 [–0.017;–0.010] and I = 1.073 [0.806;1.339]; both P < .0001) and directly related to the prevalence of diabetes and to the proportion of active smokers.

Clinical Implications - Low endogenous T levels in aging men can represent a possible CV risk factor.

Strengths & Limitations - The present data demonstrated, for the first time, that low T predicts not only CV mortality but also CV morbidity. Data derived from studies reporting information on CV mortality suggested major publication bias although they were confirmed applying Duval and Tweedie trim and fill method. However, observational studies should be considered with caution due to the lack of complete follow-ups and due to the poor management of missing data.

Conclusion - The present meta-analysis shows that low T in aging men is a marker of CV risk. The possible benefits of T treatment in reducing this risk should be examined in longer-term, specifically designed trials.

 

[Michael Scally MD]

[OA] Testosterone Treatment In Chronic Heart Failure

Mounting evidence suggests that hormonal deficiencies (HD) have an important role in chronic heart failure (CHF). In particular, androgen depletion is common in men with CHF and is associated with increased morbidity and mortality.

This review summarizes the current understanding of the complex relationship between CHF and testosterone, focusing on evidence derived from clinical trials that have investigated the role of testosterone in the treatment of CHF. A greater comprehension of this area will allow researchers and clinicians to plan future studies that improve current strategies to reduce mortality in this high-risk population.

Online databases PubMed (Medline), Web of Science, and Scopus were searched for manuscripts published prior to June 2018 using key words "heart failure" AND "testosterone" OR "anabolism" OR "hormone" OR "replacement treatment". Manuscripts were collated, studied and carried forward for discussion where appropriate.

In summary, findings from the literature demonstrate that testosterone treatment in CHF is a promising topic that requires further investigation.

D'Assante R, Piccioli L, Valente P, et al. Testosterone treatment in chronic heart failure. Review of literature and future perspectives. Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace 2018;88:976. Testosterone treatment in chronic heart failure. Review of literature and future perspectives | D'Assante | Monaldi Archives for Chest Disease