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In September, 2002, Candian singer-songwriter Gordon Lightfoot (Sundown, The Wreck of the Edmund Fitzgerald) had such severe abdominal pains that he was airlifted to a hospital. After emergency surgery, he was put in intensive care. He had four more surgeries, a tracheotomy, and spent 6 weeks in a coma. He had another followup surgery in 2003. He was lucky.

He was lucky because he eventually returned to performing and touring - he might have lost a limb or had severe kidney damage. He was lucky just to survive - the same thing killed Albert Einstein. He was also lucky to be Canadian - in the US his medical bill would have easily topped $1 million dollars.

There's a chance the same thing could happen to me. There's a chance the same thing could happen to you - Lightfoot's condition is the 13th leading cause of death in the US, 10th for men over 55. And if you need one more thing to worry about - the condition has no symptoms. It's often diagnosed by a pathologist - during the autopsy.

The mystery condition is an abdominal aortic aneurysm (AAA). It's an increase in size of part of the aorta, the largest artery in the body - picture what it would look like if you stuffed a golf ball into a garden hose. The increase in size is due to the degradation of the artery walls.

What enables your arteries to dilate and contract and retain their structural integrity is a framework or "extracellular matrix" made up of elastin and collagen. The most accepted explanation is that your body's immune system, via some complex biochemistry, produces enzymes at the aneurysm site that consume the elastin and collagen faster than your body replaces it. A similar mechanism causes old-age wrinkles.

Enzymes that eat protein are called proteases, and the likely culprits in this case are the matrix metalloproteases (MMP), of which there are several - especially implicated are MMP-2 and MMP-9. But there are dozens of chemicals involved, all naturally produced by your body and its immune system.

What triggers the destruction of the extracellular matrix isn't known for sure, but there are a number of risk factors. Being Caucasian is one, so is being 65 or over and male. So this is largely a disease of old white men, but not entirely - my sister had her AAA repaired 4 or 5 years ago. AAA does occur among non-Caucasians (especially given racial purity being largely mythical), although with much lower frequency. Having smoked, ever - more than 5 packs lifetime - is an additional risk factor, as is atherosclerosis and high blood pressure.

Aneurysms are possible anywhere over the course of the aorta, which leaves the top of your heart, makes a U-turn (the aortic arch), descends through your chest (thoracic aorta) and then through your abdomen (where the renal arteries that supply your kidneys branch off), and finally divides at the iliac bifurcation into the two iliac arteries which feed each leg via the leg's femoral and popliteal arteries.  A similar condition is an aortic dissection, where the interior layer of the aorta separates from the artery wall, creating either a pocket that traps blood, or a second pathway for blood flow inside the aorta. Aneurysms outside the abdomen and dissections are not rare, but are much less common than AAA, which this discussion will stick to.

The typical AAA is located somewhere between the bottom of your breastbone (sternum) and your navel, usually below the renal arteries. If you can detect it, it's usually described as a "pulsatile mass". If you have throbbing lump in your abdomen, and you're not pregnant, it would be wise to get it checked.

There are almost no symptoms for an AAA, until it's gotten so large as to be extremely dangerous. There are also, so far, no treatments likely to have a huge degree of success, short of surgical intervention. A normal aorta is around 1.5 cm in women and about 1.7 cm in men (about 2/3s of an inch). A definite diagnosis of AAA is at 3cm. Repair is indicated at 5 cm to 5.5 cm. The probability of rupture at around 5.5 cm is about 10%. Aneurysms can grow much larger - grapefruit size - and the probability of rupture increases with size.

There are basically three ways AAA is first diagnosed: by accident, for example, noticed on a chest X-ray or other imaging procedure; rupture, usually followed closely by death; looking for it. Mine was found by looking because of one other risk factor: genetics.

If you have a close relative with an AAA, your risk increases. As mentioned above, my sister had one. My father died in surgery getting his fixed. My uncle died sitting in his car in a parking lot when his ruptured. It's likely my grandfather and another uncle went the same way. That would suggest some genetic component.

I had a very good family practitioner who, during a routine checkup about 30 years ago, actually looked at my family history and suggested checking for an aneurysm. Aneurysms already developing can be detected by a physician palpating your abdomen less than 1/3 of the time. The best test is a simple ultrasound - I had one this morning that took about 10 minutes. I've had several over the years, as recommended by that doctor, until diagnosed with a AAA about 3 years ago.

Sometimes I've had to argue with family practitioners about the need to get an ultrasound (it's been the only reason for me to see a doctor). Some doctors probably spend years in practice without ever seeing a AAA and consequently don't know much about it. There are cases of even ruptured aneurysms being misdiagnosed in emergency rooms as gas pains. My current doctor, who I first saw Monday, is a family practitioner, but is either well up-to-speed on the subject, or brushed up before the appointment. It was refreshing to have a doctor who understands the condition, some of the possible approaches to care, and is willing to be aggressive in treatment. I feel better already.

The usual course of treatment for an aneurysm is called "watchful waiting", which means "wait til it gets big enough that the risk of surgery is less than the risk of rupture" - around 5 cm to 5.5 cm. While you wait, your aneurysm continues to grow at an average rate of 0.4 cm per year. Mine has grown at about half that rate, which makes me happy. Of course quitting smoking and getting blood pressure under control are important adjuncts to aneurysm care - important for anyone, but both impact the rate of aneurysm growth.

“There is no disease more conducive to clinical humility than aneurysm of the aorta,”  according to Sir William Osler, and founder of Johns Hopkins and sometimes called the "father of modern medicine". The possibility of treating aneurysms pharmacologically still exists in the future, unless you're a mouse. Mice have had aneurysms induced and then completely eliminated chemically. However there are some things to consider. Since hypertension often accompanies AAA, lowering blood pressure is indicated to reduce risk of rupture. It turns out that one of the most common blood pressure medication families - ACE inhibitors - was also shown in a large Canadian population study to reduce the risk of rupture.

There is also a Danish study that shows that low-dose aspirin slowed the rate of aneurysm growth by about 0.2 cm over the course of the trial. There are a number of studies that show similar results using the antibiotic doxycycline (and some studies that show no benefit). A study of tissue from aneurysms also shows an accumulation of the same biochemicals that trigger asthma, suggesting something like Singulair (monolukast) might be beneficial, but no clinical trials have been done. Other possible medications to slow growth include statins (anti-cholesterol drug), COX-2 inhibitors (several of which have been taken off the market), immuno-suppressive drugs (hugely expensive), renin inhibitors and beta-blockers.

For any of these drugs, treatment of AAA is an off-label use, and the benefits usually come from something other than what the drug is designed to do. For example, doxycycline is an antibiotic, but it has anti-inflammatory properties as well, which are probably what works (if it does) on AAA. Similarly ACE inhibitors are intended to lower blood pressure by reducing the production of angiotensin II, which causes arteries to contract and neutralizes bradykinin - bradykinin is a vasodilator. But it appears that the chemistry around angiotensin II is part of the elastin-eating chemistry that causes the aneurysm in the first place.

Einstein's surgeon in the 1950s attempted to repair the physicist's aneurysm using a method roughly equivalent to wrapping the bulge in the artery with duct tape. A couple years later, the surgeon wanted to try again, but Einstein basically said "Let it bleed" and died. Since then, things have improved.

From the 1950s through the 1990s, the method of treating a dangerous aneurysm was something now called "open repair". The surgeon opens the abdomen, locates the aneurysm and then clamps off the aorta, cutting blood flow above and below the damaged area. He then slices open the aorta length-wise, inserts a dacron tube and sutures it to be leak free above and below the aneurysm. He sutures the aorta shut around the dacron tube and closes the incision. Depending on the amount of artery damage, the repair, and incision, may extend into the patient's thigh. (A rupture repair would use the same procedure, but a little more frantically). There is a small mortality rate with this procedure, but generally the outcomes are very good and lasting. It's accompanied by a 5-7 day hospital stay, including some time in intensive care.

Since the 1990s, some vascular surgeons have gone to laprascopic methods to perform the surgery, which is less stressful than traditional open repair. However, in the 1990s endovascular aneurysm repair (EVAR) was developed and eventually received FDA approval.

With EVAR, the vascular surgeon makes two small incisions in the groin or one in each thigh to access the femoral or iliac arteries. A radiologist then threads a control wire into one artery, and pushes a stent through the other incision until it reaches the aneurysm. The stent is then expanded, somewhat like opening an umbrella, and seals off the aorta above and below the aneurysm.

EVAR has a much lower operative mortality rate than open repair, and usually requires only one or two nights of hospitalization. The long term results are also comparable to open repair, although a small percentage of procedures eventually requires correction with open repair. EVAR also requires periodic CAT scans to insure the stent is functioning correctly. The location of the aneurysm and individual anatomy determine whether EVAR is a possible alternative to open repair, but it's become common enough that the town of 50,000 south of me has a vascular surgeon/radiologist team that does EVAR.

If you are 65 or over, or near that age, and have a risk factor like smoking or a relative with AAA, your socialist government will provide a free ultrasound as part of your "Welcome to Medicare" exam. If you have any of the risk factors, it might be worth getting an exam earlier - my aneurysm was already 3.3cm at age 58. My last ultrasound cost $300, which I pay out of pocket. Even cheaper is a for-profit organization called Lifeline, which will perform the ultrasound and some other probably unnecessary but simple tests for about $130 (which is how mine was found).

Early detection is probably better than a rupture bleeding into your abdomen. Some EMTs have said that AAA rupture victims actually slosh when they move them.

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