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Well hoped to not ever have to post this, heart problems help

maldorf

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If maldorf's physicians had performed the appropriate blood tests at about the time of his initial muga stress test (including testing for his prothrombin mutation), his massive, catastrophic heart attack would likely have been prevented.

Yeah, I think you are right. The heart attack would have been avoided if I knew I had the clotting factor because I would have stopped taking steroids. I wouldn't have stopped lifting hard though, doing heavy squats etc.
 

nothuman

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Nothuman what are your doses of both Telmisartan and Nebivolol daily? My Doc switched me from Amlodipine to Telmisartan 80mg/day a few months back. If my resting HR is in the 70's do I even need Nebivolol? Also of the above heart "supplements" you listed which do you think makes the biggest impact on lowering BP and improving heart health in general?

Getting my BP down has been a frickin battle. My PCP just seems apathetic and will say 140's/90's is ok. I'd like to get it down in the 110's/70's and keep it there!

On TRT, 40mg Telmsartan and actually no Nebivolol anymore since my RHR hit the high 50s thanks to my conditioning. But personally if it were 70, I would use Nebivolol at 5mg every night. I think it's much safer to keep the pulse no higher than low 60s while using it than 70s and not using it at all. It really appears to be low risk if you tolerate it well. I'd go up to 10mg if I had to. But try to get in better cardio shape too so you wouldn't even need to use it. That should be the first priority.

If you are really struggling to get BP down, I still think carditone has a more profound effect, but there are concerns with long term use regarding neurotransmitters so only use it as a last resort if the ARB/beta-blocker combo don't work well enough.

As far as normal legal supps go (besides carditone), I always refer to examine to see which supplements give at least two arrows down on their human effect matrix. Olive Leaf, garlic, magnesium and spirulina all do. I'd hop on those for sure.
 

mementomori515

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On TRT, 40mg Telmsartan and actually no Nebivolol anymore since my RHR hit the high 50s thanks to my conditioning. But personally if it were 70, I would use Nebivolol at 5mg every night. I think it's much safer to keep the pulse no higher than low 60s while using it than 70s and not using it at all. It really appears to be low risk if you tolerate it well. I'd go up to 10mg if I had to. But try to get in better cardio shape too so you wouldn't even need to use it. That should be the first priority.

If you are really struggling to get BP down, I still think carditone has a more profound effect, but there are concerns with long term use regarding neurotransmitters so only use it as a last resort if the ARB/beta-blocker combo don't work well enough.

As far as normal legal supps go (besides carditone), I always refer to examine to see which supplements give at least two arrows down on their human effect matrix. Olive Leaf, garlic, magnesium and spirulina all do. I'd hop on those for sure.

would you mine expanding on how carditone affects neurotransmitters? Also, beet root powder is amazing for BP
 

maldorf

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The massive spike in blood pressure from heavy squatting placed you at great risk for a blood clot, given your genetic disorder, irrespective of gear use.

Lets keep the thread dedicated to the member on this board that started this thread asking for help. No use in arguing back and forth about what caused my heart attack.
 

MethodAir

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Lets keep the thread dedicated to the member on this board that started this thread asking for help. No use in arguing back and forth about what caused my heart attack.

It's not an argument. The information is relevant, objectively speaking, with respect to risk factors. The other member might also want to consider refraining from heavy exertion right now.
 
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nothuman

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would you mine expanding on how carditone affects neurotransmitters? Also, beet root powder is amazing for BP

Don't feel like spending my morning looking for the exact link but I had this sentence saved

"Reserpine depletes stores of catecholamines and 5-hydroxytryptamine in many organs, including the brain and adrenal medulla"

But if you need to get BP down, you should still absolutely use it if an ARB and natural supps don't work well enough.
 

Black Beard

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Not sure how heavy squatting would increase the risk of blood clots...
 

MethodAir

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Keywords being "critically hypotensive" and "cardiogenic shock" ie. an acute problem. We are talking about prevention and chronic issues. What you mention is an acute problem.

You can use things like BNP to look for signs of CHF but as studies have shown, it's not a definitive test for the condition. You need to look at the actual ejection fraction.

Contrary to what you suggest, the BNP blood test can be an accurate indicator of the extent of chronic coronary artery disease, for stable patients with normal ejection fractions.

Again, as mentioned, unlike ejection fraction, severe, chronic coronary artery disease won't be detected/imaged by echocardiogram.

That's why cardiac blood tests are also used. The level of BNP is correlated with the severity of coronary lesions with stable/non-acute patients:

https://www.ncbi.nlm.nih.gov/pubmed/15915074/

CONCLUSION: Plasma levels of BNP were higher in patients who have stable coronary artery disease with preserved left ventricular systolic function. The level of increase in plasma BNP concentration was positively correlated with the extent of lesion and LAD involvement on coronary angiography.

https://www.uscjournal.com/articles/nt-bnp-stable-coronary-artery-disease

Conclusions

This review of the literature clearly indicates the remarkable ability of NT-BNP to predict adverse clinical events, particularly death in a large spectrum of patients. It appears to be effective in patients with an ACS, in stable CAD and in populations at risk from CAD. Its value appears to be incremental to that obtained from standard clinical variables. In addition, it seems to integrate risk from an array of clinical variables that may be relatively easy to comprehend.

Hopefully this clarifies some of the misinformation which has been floating around here.
 
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Black Beard

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MethodAir is a troll?


First he goes after Maldorf for no reason, now he's bringing up a random old post from page 2 in the thread and ignores my question asking how heavy squats increase clot risk.


Just gonna ignore this guy moving forward. I suggest everyone else do the same.
 
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MethodAir

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Not sure how heavy squatting would increase the risk of blood clots...

If you understood the mechanics of increased LV afterload from heavy squatting, risk factors for blood clots (eg spikes in blood pressure, genetic clotting disorder), and you were as you claim, 'a clinician', it's unlikely you would make that statement.
 
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emeric delczeg

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Well all finally went to the Dr because of some chest pains and my fear confirmed.. looks like there are some heart abnormalities from the EKG.

So this is a long story, but having some symptoms and after lethargy n shortness of breath so need to know what are next steps from others who have had this issue.

Dr says I have left ventricle issues this far. They are going to do a chemical stress test and another test that I am waiting for. They pulled labs which I do every 6months anyway. Dont have them back yet. Here is some info below....

42 years old 5ft 10 244pounds 18%BF.
Always had high BP ,but lately its averaged 160-180 over 100/130. Very very high stress job. Also family history.
Cholesterol is total 205, but HDL n LDL always been bad.
Just started high BP meds n a statin.

Gear- 600mg test cyp/500mg Primo/ 50mg proviron daily.
Been cutting past 8weeks.

This year have run test up to 900mg and 8 weeks tren at 150mg per week.

I used to cycle 20 years ago, only started back when I started TRT at 40. Only ran test at high doses up to 900mg nothing else except arimidex 3times a week Nolva 3 times a week.

I dont know if gear has caused any of this. I am worried about blockage in the arteries. BP has been a concern.

So is there any tests I should ask for? Can i check for Heart health? Can they run dye in the arteries to check for plaque buildup?

Just not sure what to ask for or what to do next. I am droppin test to my TRT dose of 300mg. Primo i stopped not sure if it affects heart at all. Proviron same dont know whether to start back.

Any help would be appreciated. Will report labs when I get them.

Thanks

I know you will not follow my suggestion, so one more time, start by injecting only 10mg every other day for 8 weeks, then have a blood work, and take natural anti oxidants, including fresh fruits and veggies, consume healthy fats (raw egg yolk included) and start cardio every day minimum 35 minutes.
 

warlock

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I know you will not follow my suggestion, so one more time, start by injecting only 10mg every other day for 8 weeks, then have a blood work, and take natural anti oxidants, including fresh fruits and veggies, consume healthy fats (raw egg yolk included) and start cardio every day minimum 35 minutes.

Emeric,

What other antioxidants would you recommend?
 

maldorf

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Clotting factors

Emeric has factor 5 and has managed to remain healthy for a long time now.
 

maldorf

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Good Article here on a successful bodybuilder/strongman

https://www.mja.com.au/journal/2015/203/5/steroid-induced-cardiomyopathy


"The patient was a successful bodybuilder and strongman. Over the past 12 months, he had taken testosterone 1.5 g per week, trenbolone 500 mg per week, methandrostenolone 40 mg daily, anastrozole 0.5 mg daily and naproxen 1.1 g daily in preparation for a national championship competition. The products were obtained through other users at the gym where the patient trained. He had ceased all the above supplements about 6 weeks before his admission. He was 141 kg at the time of presentation."

"Cardiomyopathy, including ventricular hypertrophy and dilatation, is a complication of anabolic steroid use that has previously been described.3,4 Anabolic steroids are thought to cause changes in heart muscle structure through their effect on androgen receptors expressed on cardiac myocytes.3" Our case highlights an interesting presentation of a dilated cardiomyopathy with acute decompensated heart failure 6 weeks after cessation of anabolic steroids in a patient who had performed physically at an elite level only 2 weeks before admission. Further inhospital decompensation may have been precipitated by the acute effect of β-blocker therapy on cardiac output in this context, reducing the heart rate when stroke volume was extremely low. Definitive management involved cessation of the offending agents, exclusion of other reversible causes of heart failure, and initiation of conventional heart failure therapy. Awareness of the harmful cardiac effects of anabolic steroid use must be promoted within the medical profession and among potential users so that such cases can be prevented."

Looks like this study took place in Australia.
 
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maldorf

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Coronary thrombosis in a young lifter, aged 23 years

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1767361/

I was 38 when I had mine. Dallas was I think 26 years old.

"There have been several case reports of acute myocardial infarction in young male athletes using anabolic steroids. The mechanism is unclear but may involve the adverse effects on thrombosis and lipid profile. Some reports suggest thrombosis in “normal” coronary arteries, but underlying atheroma cannot be excluded without IVUS. This case supports the concept that both atheroma and the thrombogenic effects of anabolic steroids may be necessary for vessel occlusion." Can be deadly, as we have seen.
 
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maldorf

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AAS and increased hematocrit, risk of thrombosis

"The association between testosterone-replacement therapy and cardiovascular risk remains unclear with most reports suggesting a neutral or possibly beneficial effect of the hormone in men and women. However, several cardiovascular complications including hypertension, cardiomyopathy, stroke, pulmonary embolism, fatal and nonfatal arrhythmias, and myocardial infarction have been reported with supraphysiologic doses of anabolic steroids. We report a case of an acute ST-segment elevation myocardial infarction in a patient with traditional cardiac risk factors using supraphysiologic doses of supplemental, intramuscular testosterone. In addition, this patient also had polycythemia, likely secondary to high-dose testosterone. The patient underwent successful percutaneous intervention of the right coronary artery. Phlebotomy was used to treat the polycythemia acutely. We suggest that the chronic and recent “stacked” use of intramuscular testosterone as well as the resultant polycythemia and likely increased plasma viscosity may have been contributing factors to this cardiovascular event, in addition to traditional coronary risk factors. Physicians and patients should be aware of the clinical consequences of anabolic steroid abuse."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663437/


About this subject in the study:

" His physical examination was remarkable for his muscular appearance and a blood pressure of 190/100. He was in mild distress with no signs of heart failure. His blood chemistry revealed a creatinine of 1.3 mg/dl and elevated liver enzymes (aspartate aminotranferease 86 units/L, and alanine aminotransferase 79 units/L). Hematologic studies noted an hemoglobin of 22 g/dl and hematocrit of 63%. The ejection fraction was 35%. The patient was phlebotomized until his resultant hematocrit was 45%."

"Several case reports describe the deleterious cardiac effects of anabolic steroids including its potentially atherogenic and thrombotic properties. These range from lipid disorders to acute myocardial infarction and sudden cardiac death (Kennedy and Lawrence 1993; Hourigan et al 1998; Fineschi et al 2001; Wysoczanski et al 2008). Thromboembolic phenomenoma, intracardiac and peripherally, have been described (McCarthy et al 2000). Cardiomyopathy, cardiomegaly and biventricular dilatation have been associated with AAS use. Mewis and colleagues (1996) demonstrate a case report of a young bodybuilder with severe coronary artery disease with a two-year history of chronic anabolic steroid use. A case control study of 62 male competitive powerlifters notes a possible increase in premature mortality compared with controls (12.9% versus 3.1%) Parssinen et al 2000). Although difficult to quantitate, the increased risk of cardiac disease may be as high 3-fold among individuals who use AAS (Melchert and Welder 1995; Sullivan et al 1998)."

"Development of an atheromatous plaque perpetuates endothelial dysfunction and promotes platelet aggregation and intracoronary thrombus formation (Ajayi et al 1995; Nieminen et al 1996). AAS may cause a hypercoagulable state, by an increase in production of thromboxane A2 and platelet thromboxane A2 receptor density as well as aggregation responses and a decrease in production of prostaglandins (Ajayi et al 1995). Moreover, a component of endothelial dysfunction has been proposed, which may contribute to abnormal vessel reactivity. However, testosterone in physiologic doses may even be beneficial in patients with angina (English et al 2000), have higher ischemic thresholds and improved quality of life (Malkin et al 2004). Short-term intracoronary administration of testosterone induces coronary artery dilation and increases coronary blood flow in men with established coronary artery disease (Webb et al 1999). Therefore, an interplay of endogenous factors of the patient’s risk profile as well as the testosterone dosing may be issues of whether adverse events occur."
 
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MethodAir

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https://www.mja.com.au/journal/2015/203/5/steroid-induced-cardiomyopathy

"The patient was a successful bodybuilder and strongman. Over the past 12 months, he had taken testosterone 1.5 g per week, trenbolone 500 mg per week, methandrostenolone 40 mg daily, anastrozole 0.5 mg daily and naproxen 1.1 g daily in preparation for a national championship competition. The products were obtained through other users at the gym where the patient trained. He had ceased all the above supplements about 6 weeks before his admission. He was 141 kg at the time of presentation."

"Cardiomyopathy, including ventricular hypertrophy and dilatation, is a complication of anabolic steroid use that has previously been described.3,4 Anabolic steroids are thought to cause changes in heart muscle structure through their effect on androgen receptors expressed on cardiac myocytes.3" Our case highlights an interesting presentation of a dilated cardiomyopathy with acute decompensated heart failure 6 weeks after cessation of anabolic steroids in a patient who had performed physically at an elite level only 2 weeks before admission. Further inhospital decompensation may have been precipitated by the acute effect of β-blocker therapy on cardiac output in this context, reducing the heart rate when stroke volume was extremely low. Definitive management involved cessation of the offending agents, exclusion of other reversible causes of heart failure, and initiation of conventional heart failure therapy. Awareness of the harmful cardiac effects of anabolic steroid use must be promoted within the medical profession and among potential users so that such cases can be prevented."

Looks like this study took place in Australia.

You omitted many key facts, thus creating a very misleading picture of what actually transpired.

The grossly overweight strongman's first echocardiogram showed NORMAL heart/valve function and largely unremarkable cardiac blood markers, while (presumably) using large amounts of AAS.

The athlete incurred a serious mitral valve injury during the 15 month period that followed, thus predisposing him to acute heart failure. He became symptomatic 6 weeks after ceasing AAS use, and ended up in hospital.

Our case highlights an interesting presentation of a dilated cardiomyopathy with acute decompensated heart failure 6 weeks after cessation of anabolic steroids in a patient who had performed physically at an elite level only 2 weeks before admission...Fifteen months before presentation, he had a transthoracic echocardiogram for hypertension, which revealed normal biventricular size and systolic function, normal biatrial size, normal diastolic function and normal valve function.

Approximately 15 months later, and after ceasing AAS use:

The patient underwent transoesophageal echocardiography on Day 3 of his admission. This showed severe global biventricular dysfunction, moderate to severe mitral regurgitation as a result of annular dilatation

The athlete then went into cardiogenic shock after receiving an ace inhibitor, as per the cardiac lab readings:

he deteriorated on Day 4, developing hypotension (blood pressure, 80/50 mmHg) and renal dysfunction (creatinine level, 267 μmol/L), and a worsening of his liver function (ALT, 1857 U/L; AST, 1697 U/L). Low-dose dobutamine infusion was started and continued for 72 hours, resulting in excellent diuresis and improvement in his clinical condition with recovery of liver and kidney function.

The athlete weighed 141 kg, with serious valve dysfunction, and predictably went into decompensated heart failure (irrespective of gear use). And again, extreme weightlifting is correlated with the heart valve damage:

Athletes involved in mainly static or isometric exercise (e.g., weight lifting, power lifting, and bodybuilding) develop pressure overloads due to the high systemic arterial pressure found in this type of exercise. It is hypothesized that chronically elevated aortic wall tension in strength-trained athletes is associated with aortic dilatation and regurgitation.

As stated, the suggestion that the onset of his heart failure was solely the product of steroids, is highly misleading and inflammatory.
 
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