Regression of aortic dilation?

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S

Susan BAV

I have wondered...

Is there anything known specifically about the possibility of an aortic dilation regressing? Particularly post-AVR?

Do you have any knowledge or thoughts about this? Any studies you can post or cite?

A few simultaneous threads on the site have me wondering about this again.
 
"aortic dilation...seems mainly due to the fragility of the aortic wall...

"aortic dilation...seems mainly due to the fragility of the aortic wall...

Failure to Prevent Progressive Dilation of Ascending Aorta by Aortic Valve Replacement in Patients With Bicuspid Aortic Valve: Comparison With Tricuspid Aortic Valve
Hisayo Yasuda, MD; Satoshi Nakatani, MD, PhD; Marie Stugaard, MD, PhD; Yuko Tsujita-Kuroda, MD, PhD; Ko Bando, MD, PhD; Junjiro Kobayashi, MD, PhD; Masakazu Yamagishi, MD, PhD; Masafumi Kitakaze, MD, PhD; Soichiro Kitamura, MD, PhD; Kunio Miyatake, MD, PhD
From the Departments of Cardiology and Cardiothoracic Surgery, National Cardiovascular Center, Osaka, Japan...

"...Background— Patients with bicuspid aortic valve (BAV) have been frequently complicated with ascending aortic dilation possibly because of hemodynamic burdens by aortic stenosis (AS) or regurgitation (AR) or congenital fragility of the aortic wall.

Methods and Results— To clarify if the aortic dilation could be prevented by aortic valve replacement (AVR) in BAV patients, we studied 13 BAV (8 AR dominant, 5 AS dominant) and 14 tricuspid aortic valve (TAV) patients (7 AR, 7 AS) by echocardiography before and after AVR (9.7±4.8 years). We also studied 18 BAV (11 AR, 7 AS) without AVR. Diameters of the sinuses of Valsalva, sinotubular junction and the proximal aorta were measured. The annual dilation rate was calculated by dividing changes of diameters during the follow-up period by the body surface area and the observation interval. We found that aortic dilation in BAV patients tended to be faster than that in TAV patients, although a significant difference was found only at the proximal aorta (0.18±0.08 versus -0.08±0.08 mm/(m2/year), P=0.03). BAV patients with and without AVR showed similar progressive dilation. AR dominant group showed tendency of more progressive dilation than AS dominant group in BAV, although it did not reach statistical significance. TAV patients did not show further aortic dilation after AVR.

Conclusions— AVR could not prevent progressive aortic dilation in BAV. Since the aorta did not dilate in TAV, progressive aortic dilation in BAV seems mainly due to the fragility of the aortic wall rather than hemodynamic factors.
"

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I just found this [above], an excerpt from ahajournals.org
(Circulation. 2003;108:II-291.) © 2003 American Heart Association, Inc.
 
AlanG said:
Hi Susan Thanks very much for finding and posting this. I have more questions about aortic dilatation - apart from can it be reversed? can it happen over the whole aorta evenly, so that it goes undetected? - or is it always in a small area, an obvious swelling? How often should we have a check-up to keep an eye on the aorta?

I thought I'd reply because I know what it feels like to post a really good question and get no response! :D (Have a look at my post on MR and CT scans ...)

After I was told (see post started by Momohio) by a Sports Cardiologist in London that I had a slightly less than 50% chance of my aorta decreasing from 4.4cm to under 4cm after BP treatment, I began to research this to my bemusement and disappointment. It seems that that whilst it is possible to slow down the growth, there is no evidence to sugest that aortic dilatation can be regressed.
After emailing a cardiologist in NY about the subject, he spoke of a study being carried out on RATS which indicated this was possible, with some particular drug (cannot remember what it was). But whether it was suitable/effective for humans was unclear, but interesting nonehteless. I've deleted the email, but will ask him again what the details of the study were, and post the info here.

There are many far wiser people on here who will be able to give their tupence worth about how often you should get checked out. Suppose it depends on:
1. Average growth of aorta each year 2. Any symptons?? 3. BP readings


For what it's worth: if there is evidence to suggest that your aorta is growing more than 1mm per year (average) I would be want to be monitored closely and often. (maybe every 3 months) If it is growing on average of 1mm per year then once per year is probably ok. Having said that I think it depends very much on it's current size (in relation to your own BMI), your BP readings and how active you are.
Personally, my ascending aorta is currently 4.4mm (at last check up), my valve (homograft) is also coming within its last couple of years. I have no symptons, but my BP is quite high when I exercise. Even though my Cardiologist said he was happy to see me in a years time, I have since requested that I be reviewed every 6 months from now until I need the whole shebang fixed!!

BM
 
The drug is an angiotensin II receptor antagonist called Losartin

The drug is an angiotensin II receptor antagonist called Losartin

Researchers at Johns Hopkins published a study last year in which they gave the drug to "teenage" mice with dialated aortas and rechecked their aortas later to find their aortas were of normal size. The study is specific to mice with Marfan Syndrome, which is caused by a fibrillin-1 genetic mutation. As far as I know, it is not known if it has the same effect in humans with MFS or other conditions.

http://www.hopkinsmedicine.org/Press_releases/2006/04_06_06.html
 
AlanG said:
...I thought I'd reply because I know what it feels like to post a really good question and get no response! :D (Have a look at my latest post on MR and CT scans ...)
Thanks, Alan:); I was wondering last evening if I should bump the thread up or not. You solved my problem!

Very interesting, about the teenage mice study, also. And then you wonder what such a potentially powerful med like that might do to other connective tissue throughout the body.

Regarding the study I posted, it brings to my mind so many other questions, particularly in connection to the possibility of degrees of the condition of BAV, like Marfans [which also has degrees of condition].

And why does the fragility of the aorta occur when it does and how it does? What possible catalysts? Why for some with BAV and not for others? I posted a question about smoking/nicotine some time ago and there seemed to be a strong connection there.

And speaking of Marfans, I have wondered also if BAV people tend to have other common characteristics, as Marfans people do. Does anyone know if that has been studied?
 
Our personal experience with ACE Inhibitors (Lisinopril)... Aorta dimensions have remained the same, unaffected by the medication. BUT LV growth, which had been on the rise, seems to be stabilized by it--no increase in size over the last year. In that way at least, it seems to be a very effective drug from our experience!

I know that Arlyss has been interested in other manifestations of BAVD besides in the heart and aorta... I remember her asking about us about eyes and teeth, etc... Though I don't think it was a formal study, she noticed common features frequently among BAVers.
 
Our personal experience with ACE Inhibitors (Lisinopril)... Aorta dimensions have remained the same, unaffected by the medication. BUT LV growth, which had been on the rise, seems to be stabilized by it--no increase in size over the last year. In that way at least, it seems to be a very effective drug from our experience!

Francie, I'm not sure if you meant this in reference to the "teenage mouse study's" use of Angiotensin II Receptor Antagonists. ACE inhibitors are a different class of drugs.
 
Susan BAV said:
Thanks, Alan
And speaking of Marfans, I have wondered also if BAV people tend to have other common characteristics, as Marfans people do. Does anyone know if that has been studied?

Hi Susan,
Cedars Sinai has a good discussion of the complex of characteristics that can go along with what they call Biscuspid Aortic Disease at this link -

http://www.csmc.edu/3893.html

The ones they mention include hiatal hernias, cysts of the liver and kidneys, poor eye sight and other aneurysms.

This topic is of interest to me as I have nieces and a nephew diagnosed with Marfans and wonder about my having the bicuspid valve and aortic aneurysm. Do I have a partial expression of their Marfans or has their inheritance of what I have been misdiagnosed as Marfans? Or is it all just a coincidence? There doesn't seem to be great information on this. Best, Kate
 
PJmomrunner said:
Researchers at Johns Hopkins published a study last year in which they gave the drug to "teenage" mice with dialated aortas and rechecked their aortas later to find their aortas were of normal size. The study is specific to mice with Marfan Syndrome, which is caused by a fibrillin-1 genetic mutation. As far as I know, it is not known if it has the same effect in humans with MFS or other conditions.

http://www.hopkinsmedicine.org/Press_releases/2006/04_06_06.html

This is great news for all mice suffering from Marfan Syndrome and will greatly reduce the need for surgery. Also this will benefit the surgeons who have to order those tiny little instruments to do the surgery. :D

Sorry...I couldn't resist. Lots of "promising" studies have been done on mice that didn't pan out in humans. I'm not trying to discourage anyone, but until clinical trials are conducted on humans I wouldn't count on this new drug to shrink dilated aortas back to normal. Right now I think the best course of action is to take ace inhibitors and have your dialated aorta checked on a regular basis (every 6 months IMO) for any increases in dialation. Knowing whether or not the dialation is stable or growing is important when considering if and when surgical intervention is required.

My aortic root is mildly dialated and was measured at 3.3cm at my first annual checkup. My next two checkups have shown no progression. Since I had a Ross Procedure this is something they like to keep an eye on, but so far it appears that my pulmonary valve and root (which is now my aortic valve and root) is holding up well. For the record...I did not have a BAV or any history of connective tissue disease. I had a large VSD that got smaller but never closed. This caused a "suction" at my aortic valve causing aortic valve prolapse, which in turn caused aortic insuffiencency. Contracting bacterial endocarditis was the catalyst that prompted the need for my aortic valve to be replaced.

I feel lucky that they made improvements to the Ross Procedure before I had mine done...which included replacing the aortic valve and root with my pulmonary valve and root. In earlier RP's replacing the valve and root was not a routine part of the RP.
 
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