I went from a 4.3 cm CTA measurement of an aortic root and ascending aortic
aneurysm to a 4.1 cm measurement after a seven month time separation.
According to the radiologist it is not shrinkage, but rather natural differences like variation in aorta in systole and diastole phases. The radiology report stated there was no change, and this additional information resulted from my inquiry about the difference between the original 4.3 and the 2nd CTA result of 4.1cm. I have been on atenolol and recently switched, perhaps unwisely at my own request, to metoprolol. THe above information about valsartan and losartan seems contrary to the literature describing size as irreversible.
Daily variations in measurements may occur, but actual shrinkage seems
out of the question, according to what I have read. I am very curious if any further study on rats or otherwise has shown shrinkage. This is my first post here. I was diagnosed in November 2009 with ascending aortic aneurysm and at aortic root, with guess that valves are all right based on
normal echo. Echo of course showed root aneurysm, as did CTA, but echo was normal as to heart function and otherwise.
QUOTE "Anyway, my aortic root shrunk from 3.9cm to 3.7cm (ie, "normal") and has remained stable there for several years now!"
Has a study with patients concluded that valsartan is effective in preventing the progression of AA. "Overall, the present study demonstrated that treatment with valsartan, significantly prevented of AAA? There are positive results with progression on of experimental AAA in a rat model. These data suggest that blockade of Ang II has an inhibitory effect on the development of AAA".
Are you differentiating BAV and Marfin Syndrome from the results you have experienced and posssible not applicable to those conditions? Also, could the different measurements for your condition be within the margin of error? There are theoretical reasons why ACE inhibitors might work better in Marfan's than ARBs alone. The key defects in arterial structure are mediated through both angiotensin-2 type-1 (AT1) and angiotensin-2 type-2 receptor pathways, both of which are downregulated by ACE inhibition; ARBs directly inhibit only the AT1 receptor.
Marfan syndrome (MS) is a genetic disorder caused by a mutation in the fibrillin gene FBN1. Bicuspid aortic valve (BAV) is a congenital heart malformation of unknown cause. But statin and ARB might have inhibitory effects on the formation of aneurysms via hrough the suppression of NADH/NADPH oxidase.
Also, has size of AAA been considered...you have a measurement of AA that does not fit into the AA range (>4.0 cm).
We don't know, but it is strongly suspected that this medication must be taken for life. If you stop, it will probably grow again.
Do trials show that once the medication is stopped that the aorta remains the correct size? or is it too early to tell yet?
I haven't posted on this thread in awhile, and since CynNS asked, I will:
since my first post up above, I increased my valsartan dosage up to 320mg/day. Really, if you are my size or bigger (6' 200lb), you need to be taking the FDA maximum dose or higher (if your doc will prescribe it). This aneurysm/ARB therapy really is dose dependent.
Anyway, my aortic root shrunk from 3.9cm to 3.7cm (ie, "normal") and has remained stable there for several years now!
Thank the Lord.
Nick
Of course you are absolutely correct, there is no guarantee that any aneurysm will not rupture. Unlikely or low risk are the terms which doctors usually use, or should, not it will not rupture. My brother in law had his head scanned in November last year because he was suffering headaches. They found nothing except a small aneurysm and they put it at low risk. In January this year he suddenly had severe headaches and collapsed, because it ruptured. Yes it shocked the doctors, but it just proves things happen unexpectedly.
They put around 5 or 6 platinum coils into the aneurysm and then stented it. Thankfully he has nearly fully recovered but it was a big scare.