Ascending Aortic Aneurysm & Silver Lining

[Survived03]

Besides the obvious fact that if you are reading this as a patient who survived an ATAA, there is another silver lining. Enjoy.

https://www.medscape.com/viewarticl...240104_etid6219891&uac=459029HG&impID=6219891

 

[pellicle]

Besides the obvious fact that if you are reading this as a patient who survived an ATAA, there is another silver lining. Enjoy.

Very interesting

We noticed in the operating room that many patients we worked on who had an ATAA had pristine arteries, like a teenager's," John Elefteriades,..., told theheart.org | Medscape Cardiology. "The same was true of the femoral artery, which we use to hook up to the heart-lung machine."​

because when I was on the slab getting my angiogram the cardiologist doing it remarked (I assume he was recording) that my coronary artery was in perfect condition.

Nice correlation, maybe should form the basis of the question of "why is it so"

 

[Survived03]

Nice correlation, maybe should form the basis of the question of "why is it so"

I'm familiar with Dr E and was fortunate enough to consult with him when my aneurysm was newly discovered. He is very active in the genetics behind ATAA's so I'm certain he will dig deeper from that standpoint.

Pretty fascinating. Possibly TGF-beta?? If I recall correctly, TGF-beta is one of the numerous markers with a pretty high association with ATAA's.

"The ligamentum arteriosum separates the ascending from the descending (thoracoabdominal) aorta. ATAAs, located above the ligamentum, tend to be pro-aneurysmal but anti-atherosclerotic. In the descending aorta, below the ligamentum, atherosclerotic aneurysms develop.

The differences between the two sections of the aorta originate in the germ layer in the embryo, Elefteriades said. "The fundamental difference in tissue of origin translates into marked differences in the character of aneurysms in the different aortic segments."

"What specifically underlies the reduced cardiovascular risk? "We don't really know, but we think that there may be two possible etiologies," Mukherjee said. One hypothesis involves transforming growth factor–beta (TGF-beta), which is overexpressed in patients with ATAA and seems to increase their vulnerability to aneurysms while also conferring protection from coronary disease risk."

Second hypothesis

"Another hypothesis involves matrix metalloproteinases (MMPs), which are dysregulated in patients with ATAA and may confer some protection, Mukherjee said. Several studies have shown higher plasma levels of certain MMPs in patients with ATAAs. MMPs also were found to be elevated in the thoracic aortic walls of patients with ATAA who had an aortic dissection, as well as in the aortic smooth muscle cells in the intima and media.

In addition, some studies have shown increased levels of MMP-2 in the aortas of patients with ATAAs compared with patients with coronary artery disease."

 

[pellicle]

Morning

What specifically underlies the reduced cardiovascular risk? "We don't really know, but we think that there may be two possible etiologies," Mukherjee said.

very interesting

Another hypothesis involves matrix metalloproteinases (MMPs), which are dysregulated in patients with ATAA and may confer some protection, Mukherjee said. Several studies have shown higher plasma levels of certain MMPs in patients with ATAAs.

I'll watch this space, but if you're following this as well, please allow me to be a bit lazy and post up what you find ongoingly (here or new thread works for me) ... its quite interesting (even if of no benefit to me, I always like to know why).

Best Wishes

 

[Dano64]

I had my ascending aortic aneurysm replaced two years ago, and I too was told after my angiogram that my arteries were in great shape. So your saying I am low risk for heart attack? At least I've got that going for me? Cheers to that!

 

[Survived03]

So your saying I am low risk for heart attack? At least I've got that going for me? Cheers to that!

@Dano64 well, to be certain I am not saying that you have low risk for an MI. I'm just passing along the interesting and intriguing publication. But regardless, we both survived what could have been a medical tragedy. Definitely Cheers To That!

 

[Croooser]

Interesting info that I had not heard before. Thanks for posting.

My story, just for an informal data point:

My family history is dismal: Paternal GF died late 60s from long-term cardio disease. Father died from long term cardio disease early 80s. Both had multiple MIs before it killed them and my Father had a quintuple bypass along the way. Father's brother also had >1 MI, stents, etc.

I seem to have a fair amount (or more) of the family DNA judging by other physical features. I was first diagnosed with high cholesterol in my early 40s and started on Statins. Since starting them, my blood work has been good to very good. So, they seem to be performing well for me. I also won the lottery with hypertension in my early 30s - from my maternal side only.

I knew (or so I thought) that it was inevitable that I would have the "family heart attacks" at some point - just not sure when. I was diagnosed with BAV and AA in my early 50s. I was fortunate in that the BAV and AA progressed slower than some until surgery was indicated at .9 AVA and 5.0 AA. That was 2 1/2 years ago at age 71.

2 days before my OHS at CC they performed a cardiac cath to see what the condition of the arteries was. Much to my surprise and relief, the test showed 20% blockage in the LAD and virtually all clear in the rest. The carotid arteries showed minor blockage as well. CC's standard for intervention at that time IIRC was >80% blockage. My comment to the Dr. who performed the cath was "Thank goodness for statins." I was convinced that they saved me for what I thought was inevitable.

Could it be that the AA and the statins combined to save me from an MI? I wonder.