Do We Need A Better Abdominal Aortic Aneurysm Risk Equation?

RE: good<5cm<bad

Hi folks, welcome!

Remarkable scientist, but AAA got him apparently.

I was looking around at the literature on AAA and I came across this interesting snippet from Chez Ollie, and I learned that we people with AAA are in distinguished company:

“Vesalius described the first abdominal aortic aneurysm (AAA) in the 16th century. Before the development of a surgical intervention for the process, attempts at medical management failed. The initial attempts at control used ligation of the aorta, with the expected consequences [bad idea, but you’ve got to start somewhere!].

In 1923, Matas performed the first successful aortic ligation on a patient. Attempts were made to induce thrombosis by inserting intraluminal wires. In 1948, Rea wrapped reactive cellophane around the aneurysm in order to induce fibrosis and limit expansion. This technique was used on Albert Einstein in 1949, and he survived 6 years before succumbing to rupture. In 1951, Charles Dubost performed the first AAA repair using a homograft.”

Here is a recent medical quote concerning AAA:

“The likelihood of rupture increases as the aneurysm increases in size, and treatment is generally indicated for asymptomatic AAAs over 5 cm in diameter.”

This was lifted from the MDGuidelines Website. I hear of cases where an AAA was ‘watched’ for several years, never achieved the magic 5 cm diameter that might trigger surgery, and the patient died of aortic rupture anyway. Other people have AAAs that fill a significant volume of their abdominal cavity and they survive. Clearly size matters, but it is not the only significant variable when it comes to AAA-induced mortality. So I wondered where this magic 5 cm comes from, and why should it apply to men and women of all sizes, races and backgrounds. Does it apply to aneurysms of all shapes too, I wonder? For instance, if a bike tire starts to swell evenly in one region I am less worried about it than a focused bulge in one small spot.

There is one rather odd thing about AAA, general lack of awareness of the problem.  I had never heard of it as a significant human syndrome before I found mine. In spite of having veterinary medical training and working extensively in biological research related to human risk assessment, my awareness of my risk of AAA was essentially zero. Yep! Big fat zero. My ignorance of the issue even empresses me! There is a message there.

In my brief research today (I’m blogging, not writing a PhD dissertation) I came across an interesting article, which appears to be very thorough. It was written by Mike Poullis.This gentleman is highly qualified, and I certainly appreciate his thoughtful article, which I enjoyed a lot. But does anyone really understand aortic fluid mechanics, the role of aortic compliance in distal aortic pressure waves and local boundary conditions, the role of the distal aortic elastic laminae in distal aortic aneurysm development, or the proximal aortic laminae for that matter, and so forth? I sure don’t! I know that there is some good work going on out there, and I’ve read some of it.

Here are a few salient quotes from the above article:

• “As opposed to absolute size criteria, some surgeons prefer the use of ratios of measured to expected size. The expected size is based on the body surface area and age of the patient.” [This is at least encouraging and implies some thinking behind the decision-making process, but the calculation hasn’t come to my attention previously]
• “The rate of expansion is also an important consideration.” [That’s true of bike tires, too, especially when going down a steep hill].
• “And they generated an interesting formula to help predict the risk of rupture, as follows Estimate Rate of Rupture post CT Scan  Ln Lamda = -21.055 + 0.093 x age + 0.841 x pain + 1.282 x COPD + 0.643 x descending aortic diameter in cm + 0.405 x abdominal aortic diameter in cm .Pain and COPD are 1 if present 0 if absent Probability of rupture within 1 year = 1- e ^-Lamda(365) ” [I have to confess that ‘e’ is one of my favorite numbers, but it wasn’t mentioned by my surgeon as I was a nice clear 7 cm. Boy, this reminds me of quantitative human risk assessment – lots of equations and most of the data missing].

It seems that a number of things are needed, in the following order of priority (for the general case, not the specific case):

1. Improved levels of public awareness.
2. A screening program, such as that in the UK, but including women.
3. Improved approaches to therapy, including non-surgical methods designed to improve growth of the ‘weak link’ tissue (elastic laminae?).
4. Understanding of the underlying genetic factors to guide research on laboratory tests for high-risk individuals, who would then be screened more aggressively.
5. Determination of behaviors that actually do exacerbate the condition, in order to provide guidelines for people wishing to continue enjoying sports.
6. A solution to the 5 cm dilemma.