RIP Daniel Alexander

[Bio]

How do people make claims that someone had an undiagnosed/genetic Hart condition after they have died? If something is undiagnosed than it's never been confirmed, especially if you say it was genetic. Did someone test this guys DNA after he died and got the results back in record time?

Genetic or not, this guy likely died from cardiac arrest after a lethal arrhythmia was triggered. For example, most people talk about Dallas McCarver having a heart attack and bring up his family history. Problem there is that Dallas never had a heart attack. Yeah he had a family history and yeah autopsy showed his cardiovascular system had significant signs of congestive heart failure due to the size of his heart and his large amount of atherosclerosis. However, in that same autopsy report it states that he did not have any signs of myocardial infarction. Same goes for Rich Piana, mild plaque in his arteries and an inlarged heart, but zero damage present to his heart in regards to signs of myocardial infarction. Both guys went into cardiac arrest than died.

Take away point, If you work out or use drugs of any kind, go get an EKG. If you have not had an EKG done and you do things that put stress on your heart, you are playing a moronic game of Russian Roulette. 1 EKG, (a patient that takes his doctors advice) and 1 non invasive surgery implanting a pacemaker, and all these guys would likely still be alive.

The person would be the coroner and the diagnosis would come from the autopsy. It's undiagnosed if medical records and information from the family and the individual's PCP don't confirm a prior diagnosis or knowledge of any heart issue(s). As far as it being genetic, family history would play a role in that.

EKG is good for any arrhythmia. Getting a coronary calcium scan and knowing your coronary calcium score is very important.

 

[Anabolic_Beast]

The person would be the coroner and the diagnosis would come from the autopsy. It's undiagnosed if medical records and information from the family and the individual's PCP don't confirm a prior diagnosis or knowledge of any heart issue(s). As far as it being genetic, family history would play a role in that.

EKG is good for any arrhythmia. Getting a coronary calcium scan and knowing your coronary calcium score is very important.

Thank you for that information. I have never had an EKG or a coronary calcium scan in my life but to be honest with you...I think I'm going to schedule a test with my doctor to make sure that everything is up to date.
Hearing about all of these brothers (who look perfectly healthy and fine) passing away so suddenly..makes me want to be more vigilant in making sure everything is okay..even though there are no symptoms of any problems.you never know..right guys?

 

[Getnbiggger]

Thank you for that information. I have never had an EKG or a coronary calcium scan in my life but to be honest with you...I think I'm going to schedule a test with my doctor to make sure that everything is up to date.
Hearing about all of these brothers (who look perfectly healthy and fine) passing away so suddenly..makes me want to be more vigilant in making sure everything is okay..even though there are no symptoms of any problems.you never know..right guys?

I dont understand why cardiac testing is not part of routine physicals. It is relatively inexpensive and would save a lot of lives and reduce the burden on the system.

 

[Rex Feral]

I dont understand why cardiac testing is not part of routine physicals. It is relatively inexpensive and would save a lot of lives and reduce the burden on the system.

"However, screening of athletes is still not universally accepted due to concerns primarily related to the lack of randomised control evidence for its efficacy, reliability issue and cost." Cardiac Screening of Young Athletes: a Practical Approach to Sudden Cardiac Death Prevention

Well, it's not quite so simple unfortunately. Basically you're asking how do we identify those at risk for sudden cardiac death and what intervention do we make to prevent the outcome. This is a decades old conundrum.

As someone else mentioned, Dallas and Piana we know pretty much without a doubt that they experienced sudden cardiac death due to a fatal arrhythmia secondary to cardiomyopathy/LVH. More than likely this kid and Matt Porter also experienced sudden cardiac death. Sudden cardiac death is the leading medical cause of death in athletes. So we shouldn't be that surprised when we see it. The incidence varies widely depending on which study you look at. The highest I've seen is 1:3000, the latest meta analysis that I've seen, will post below, puts it at 1:50,000 per year. The sub set athlete population of bodybuilders/strength athletes is obviusly probably a little higher than this due to the nature of the exercise and exogenous hormones exacerbating LVH.

So you perform a 12 lead ECG, ECG states LVH. But LVH is common in athletes. What do you do then? It's a normal adaptation to exercise. Tell the person to stop participating in physical activity? The vast majority of sudden cardiac death occurs at rest. But assuming the athlete doesn't have hypertension, what other intervention can you perform to decrease LVH?

Okay so send them for echo let's measure LVH. I have LVH on 12 lead, some machines even say "marked LVH." "Over 4 decades ago the Framingham Heart Study reported that electrocardiographic evidence of LVH (ECG LVH) was associated with 3 to 4-fold increase in cardiovascular and all-cause mortality, with a disproportionately high risk of sudden cardiac death (SCD). Subsequently, multiple studies in different population samples have confirmed these associations."

But on echo and CT (coronary calcium) follow up I do not have LVH. Josh Wade recently posted his coronary calcium results that show no LVH as well, it would be interesting to see his 12 lead. At least 4 people come to mind, 2 of them physicians, who like me do not have LVH on echo or CT but we do have it on 12 lead. How can that be? "Among patients who suffered SCD, there was a relatively low level of agreement between ECG and echocardiography for diagnosis of LVH. 57% of patients with ECG LVH did not have evidence of echo LVH, and conversely, 84% of patients with echo LVH did not have ECG LVH. More recently however, we are learning that ECG LVH and echo LVH may be clinically distinct entities. In fact, there are now data to suggest that while these two entities can often overlap, each may provide distinct prognostic and potentially, mechanistic information, especially in the context of cardiac arrhythmias."

Hmmm, so now what was "relatively inexpensive" is not so much anymore and we still don't know what to do with this asymptomatic normotensive athlete. I know people don't like to accept the idea that there really is nothing you can do as an athlete to keep yourself from dropping dead from a fatal arrhythmia but it is a risk if you have any form of LVH whether it be electrical or structural.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6132782/#CR5

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4807859/

https://www.ncbi.nlm.nih.gov/pubmed/25977310

Rex.

 

[maldorf]

I dont understand why cardiac testing is not part of routine physicals. It is relatively inexpensive and would save a lot of lives and reduce the burden on the system.

The problem with a lot of arrhythmias is that your heart can be just fine when you get the ekg done, but just an hour later when youre at home it can go haywire. Different things can trigger it. The best ekg would be a stress test where it is done while you are running on a treadmill at a progressively faster rate and increasing inclination.

Things like alcohol, food, nicotine, and drugs in general can stir it up too. So you can have a normal ekg at the doctor and still have a problem brewing. I don't think having a standard ekg done while you are lying down or sitting is too good to rely on, but its better than nothing.

 

[Beti ona]

I don't think having a standard ekg done while you are lying down or sitting is too good to rely on, but its better than nothing.

Well, it's the one they use for before any surgery.

 

[RoyHobbs]

"However, screening of athletes is still not universally accepted due to concerns primarily related to the lack of randomised control evidence for its efficacy, reliability issue and cost." Cardiac Screening of Young Athletes: a Practical Approach to Sudden Cardiac Death Prevention

Well, it's not quite so simple unfortunately. Basically you're asking how do we identify those at risk for sudden cardiac death and what intervention do we make to prevent the outcome. This is a decades old conundrum.

As someone else mentioned, Dallas and Piana we know pretty much without a doubt that they experienced sudden cardiac death due to a fatal arrhythmia secondary to cardiomyopathy/LVH. More than likely this kid and Matt Porter also experienced sudden cardiac death. Sudden cardiac death is the leading medical cause of death in athletes. So we shouldn't be that surprised when we see it. The incidence varies widely depending on which study you look at. The highest I've seen is 1:3000, the latest meta analysis that I've seen, will post below, puts it at 1:50,000 per year. The sub set athlete population of bodybuilders/strength athletes is obviusly probably a little higher than this due to the nature of the exercise and exogenous hormones exacerbating LVH.

So you perform a 12 lead ECG, ECG states LVH. But LVH is common in athletes. What do you do then? It's a normal adaptation to exercise. Tell the person to stop participating in physical activity? The vast majority of sudden cardiac death occurs at rest. But assuming the athlete doesn't have hypertension, what other intervention can you perform to decrease LVH?

Okay so send them for echo let's measure LVH. I have LVH on 12 lead, some machines even say "marked LVH." "Over 4 decades ago the Framingham Heart Study reported that electrocardiographic evidence of LVH (ECG LVH) was associated with 3 to 4-fold increase in cardiovascular and all-cause mortality, with a disproportionately high risk of sudden cardiac death (SCD). Subsequently, multiple studies in different population samples have confirmed these associations."

But on echo and CT (coronary calcium) follow up I do not have LVH. Josh Wade recently posted his coronary calcium results that show no LVH as well, it would be interesting to see his 12 lead. At least 4 people come to mind, 2 of them physicians, who like me do not have LVH on echo or CT but we do have it on 12 lead. How can that be? "Among patients who suffered SCD, there was a relatively low level of agreement between ECG and echocardiography for diagnosis of LVH. 57% of patients with ECG LVH did not have evidence of echo LVH, and conversely, 84% of patients with echo LVH did not have ECG LVH. More recently however, we are learning that ECG LVH and echo LVH may be clinically distinct entities. In fact, there are now data to suggest that while these two entities can often overlap, each may provide distinct prognostic and potentially, mechanistic information, especially in the context of cardiac arrhythmias."

Hmmm, so now what was "relatively inexpensive" is not so much anymore and we still don't know what to do with this asymptomatic normotensive athlete. I know people don't like to accept the idea that there really is nothing you can do as an athlete to keep yourself from dropping dead from a fatal arrhythmia but it is a risk if you have any form of LVH whether it be electrical or structural.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6132782/#CR5

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4807859/

https://www.ncbi.nlm.nih.gov/pubmed/25977310

Rex.

Could this not be at least in part because EKG is primarily measuring electrical conductivity and LVH is a muscular/contractility issue thus imaging (echo/CT) would better show LVH issues? I mean we dont do CT to check for dysrhythmia's so why use EKG to check for contractile issues right?

 

[Rex Feral]

Could this not be at least in part because EKG is primarily measuring electrical conductivity and LVH is a muscular/contractility issue thus imaging (echo/CT) would better show LVH issues? I mean we dont do CT to check for dysrhythmia's so why use EKG to check for contractile issues right?

The thought has been if you have LVH on EKG then on follow up imaging you don't have LVH then the EKG was seen as false, right? I believe this is what you are saying and for contractility/muscular issues as you call them I would say this is correct. But now we are seeing that EKG LVH and echo LVH appear to be completely separate entities that may or may not overlap. In the majority of cases surprisingly enough they do not, 57% vs 85% disagreement. In one of the studies I posted they corrected for echo LVH and still found a 2.9 fold increase of sudden cardiac death in EKG LVH. So EKG LVH is a predictor of arrhythmia/sudden cardiac death risk regardless of the presence of structural LVH. So both imaging and EKG would need to be performed to fully assess risk for sudden cardiac death. All 3 conditions confer greater risk for SCD, EKG LVH, echo LVH & EKG + echo LVH.

Rex.

 

[Rex Feral]

Well, it's the one they use for before any surgery.

This is primarily to detect long QT syndrome which could affect the anesthesia and other meds used as it places you at risk for the potentially fatal ventricular arrhythmia Torsades de pointes. Long QT also predisposes to sudden cardiac death. QTc > 450 ms is prolonged and is probably worse than EKG LVH in terms of risk.

Rex.

 

[RoyHobbs]

The thought has been if you have LVH on EKG then on follow up imaging you don't have LVH then the EKG was seen as false, right? I believe this is what you are saying and for contractility/muscular issues as you call them I would say this is correct. But now we are seeing that EKG LVH and echo LVH appear to be completely separate entities that may or may not overlap. In the majority of cases surprisingly enough they do not, 57% vs 85% disagreement. In one of the studies I posted they corrected for echo LVH and still found a 2.9 fold increase of sudden cardiac death in EKG LVH. So EKG LVH is a predictor of arrhythmia/sudden cardiac death risk regardless of the presence of structural LVH. So both imaging and EKG would need to be performed to fully assess risk for sudden cardiac death. All 3 conditions confer greater risk for SCD, EKG LVH, echo LVH & EKG + echo LVH.

Rex.

Yes that is what I was saying. I guess my question (rhetorically) is, in each of these testing scenarios what degree, if any, Left Ventricular Hypertrophy is present? Ventricular enlargement either is or is not present in the body regardless of which test(s) are used or say. Perhaps this is only 100% confirmable with open heart surgery or autopsy. I read the studies and understand what they are saying regarding risk of SCD but it just seems to say there is "ekg ventricular hypertrophy" and also "echo ventricular hypertrophy" just doesn't make 100% sense to me as there either IS or IS NOT ventricular hypertrophy/growth/enlargement.... or I am misunderstanding the wording.

 

[maldorf]

Well, it's the one they use for before any surgery.

Yeah, its fast and easy to carry out. Just about anyone can do one, so the cost is cheap too.

Another great test to do is have a Holter Monitor, that runs for like 10 days or more. If something is wrong there is a much bigger chance it will happen in a time span that long rather than just 1 minute in the doctor's office.

 

[Rex Feral]

Yes that is what I was saying. I guess my question (rhetorically) is, in each of these testing scenarios what degree, if any, Left Ventricular Hypertrophy is present? Ventricular enlargement either is or is not present in the body regardless of which test(s) are used or say. Perhaps this is only 100% confirmable with open heart surgery or autopsy. I read the studies and understand what they are saying regarding risk of SCD but it just seems to say there is "ekg ventricular hypertrophy" and also "echo ventricular hypertrophy" just doesn't make 100% sense to me as there either IS or IS NOT ventricular hypertrophy/growth/enlargement.... or I am misunderstanding the wording.

I think very few people actually know this is a thing. I actually know this guy from when I worked at Cedars-Sinai he has the Chugh Lab that is part of the Oregon Sudden Unexpected Death Study and he runs the Heart Institute there. He is the world's top expert on sudden cardiac death.

In lone EKG LVH there is no actual LVH. There is only electrical remodeling. We have known for a while that electrical remodeling precedes structural/anatomic remodeling. But this doesn't explain why some develop anatomic LVH and some do not. One explanation that he had is that they could have dropped dead before LVH could develop but this doesn't seem plausible to me. I'm 49, some of these people with lone EKG LVH were in their 70s, when is this structural remodeling going to occur if not yet? In people with lone echo LVH it is thought that structural remodeling has already occurred thus the voltage amplitudes that are set to detect LVH on EKG no longer meet criteria for LVH. This would explain why 85% of echo LVH do not have EKG LVH. I haven't looked at the history of development oif EKG voltage formulas for LVH, but it begs the question of who these were developed on given the incongruence between EKG and echo LVH.

He says "These altered electrophysiological properties of the myocardium seem to be somewhat independent from the morphological transformations in LVH." Which then begs the question why even call it LVH if there is no LVH present and it is independent of the structural/morphological changes? He then goes on to explain "However, these factors would not explain the existence of ECG LVH in the absence of anatomic LVH." Hypertension is not the cause as in structural LVH, so basically they don't know what is causing this. So the wording of EKG LVH is really a misnomer, unless perhaps you know the history of the development of these voltage formulas, which is what I think you mean when you say you're not understanding the wording.

Rex.

 

[Bio]

I think very few people actually know this is a thing. I actually know this guy from when I worked at Cedars-Sinai he has the Chugh Lab that is part of the Oregon Sudden Unexpected Death Study and he runs the Heart Institute there. He is the world's top expert on sudden cardiac death.

In lone EKG LVH there is no actual LVH. There is only electrical remodeling. We have known for a while that electrical remodeling precedes structural/anatomic remodeling. But this doesn't explain why some develop anatomic LVH and some do not. One explanation that he had is that they could have dropped dead before LVH could develop but this doesn't seem plausible to me. I'm 49, some of these people with lone EKG LVH were in their 70s, when is this structural remodeling going to occur if not yet? In people with lone echo LVH it is thought that structural remodeling has already occurred thus the voltage amplitudes that are set to detect LVH on EKG no longer meet criteria for LVH. This would explain why 85% of echo LVH do not have EKG LVH. I haven't looked at the history of development oif EKG voltage formulas for LVH, but it begs the question of who these were developed on given the incongruence between EKG and echo LVH.

He says "These altered electrophysiological properties of the myocardium seem to be somewhat independent from the morphological transformations in LVH." Which then begs the question why even call it LVH if there is no LVH present and it is independent of the structural/morphological changes? He then goes on to explain "However, these factors would not explain the existence of ECG LVH in the absence of anatomic LVH." Hypertension is not the cause as in structural LVH, so basically they don't know what is causing this. So the wording of EKG LVH is really a misnomer, unless perhaps you know the history of the development of these voltage formulas, which is what I think you mean when you say you're not understanding the wording.

Rex.

Are you aware of any theories they're working on or headway they've made? Something you can't even see via any type of scan because it has to do with electrical remodeling. This is fascinating stuff!

 

[Rex Feral]

Are you aware of any theories they're working on or headway they've made? Something you can't even see via any type of scan because it has to do with electrical remodeling. This is fascinating stuff!

No, he mentioned a possible genetic component. Like long QT has a genetic component but there is no evidence of this yet. If it hadn't happened to me I wouldn't know about it. Then it happened to a close friend of mine same age who is a physiatrist now who started competing as a teenager as I did. Long history of steroid and GH use, multi decade. He said he remembers clearly the EKG LVH from when he was in med school and they performed EKGs on themselves which was obviously some time back now like 25 years. I can remember maybe 16 years ago now when I started in research and I'd have to certify on various machines it always said LVH. So when we both had our first echo that showed no LVH like a year and a half - 2 years ago not too far apart we were both kind of shocked. I asked the echo tech over and over and he said no here let me show you the measurements. Then I saw my friend's report and I've since seen two other people. It's dismissed when you have a normal echo, no one gives a shit about your 12 lead when your echo is literally perfectly normal. But come to find out this is not quite so uncommon and I have a 2.9x greater risk of dropping dead from a fatal arrhythmia. We are both very normotensive < 110/70. We can't have been developing LVH for more than 1-2 decades with no structural changes it seems. Perhaps there is a genetic component that is preventing the structural remodeling, maybe I had it and a pharm intervention like metformin reversed it. But none of this fully explains why 57% of people with EKG LVH do not have LVH.

Rex.

 

[thethinker48]

No, he mentioned a possible genetic component. Like long QT has a genetic component but there is no evidence of this yet. If it hadn't happened to me I wouldn't know about it. Then it happened to a close friend of mine same age who is a physiatrist now who started competing as a teenager as I did. Long history of steroid and GH use, multi decade. He said he remembers clearly the EKG LVH from when he was in med school and they performed EKGs on themselves which was obviously some time back now like 25 years. I can remember maybe 16 years ago now when I started in research and I'd have to certify on various machines it always said LVH. So when we both had our first echo that showed no LVH like a year and a half - 2 years ago not too far apart we were both kind of shocked. I asked the echo tech over and over and he said no here let me show you the measurements. Then I saw my friend's report and I've since seen two other people. It's dismissed when you have a normal echo, no one gives a shit about your 12 lead when your echo is literally perfectly normal. But come to find out this is not quite so uncommon and I have a 2.9x greater risk of dropping dead from a fatal arrhythmia. We are both very normotensive < 110/70. We can't have been developing LVH for more than 1-2 decades with no structural changes it seems. Perhaps there is a genetic component that is preventing the structural remodeling, maybe I had it and a pharm intervention like metformin reversed it. But none of this fully explains why 57% of people with EKG LVH do not have LVH.



Rex.

I wonder what role an ace inhibitor or arb plays long term in preventing cardiac remodeling.

I always thought physiological changes were more due to BP than anything; and then secondary igf mediated changes from long term GH use. So a BP drug would work directly from that front in preventing remodeling.

Maybe the high systolic load from heavy training plays some role in an otherwise normal tensive individual?


Sent from my iPhone using Tapatalk

 

[Marvin Martian]

Cardiac arrest isn't that big of a deal

It’s not the arrest that’s so bad - it’s the incarceration that gets ya.

 

[RoyHobbs]

Very interesting information Rex. Thank you.

 

[maldorf]

Are you aware of any theories they're working on or headway they've made? Something you can't even see via any type of scan because it has to do with electrical remodeling. This is fascinating stuff!

Before I had my ventricular ablation done they did a PET scan on my heart, and it shows abnormal areas where the conduction would get screwed up. Not sure though if it would be of as much use in a relatively healthy heart though.

 

[nothuman]

I wonder what role an ace inhibitor or arb plays long term in preventing cardiac remodeling.

I always thought physiological changes were more due to BP than anything; and then secondary igf mediated changes from long term GH use. So a BP drug would work directly from that front in preventing remodeling.

Maybe the high systolic load from heavy training plays some role in an otherwise normal tensive individual?


Sent from my iPhone using Tapatalk

GotGame used to say an ARB directly prevented cardiac remodeling