Having stepped out of his ride due to the discovery of blood clots – very unusual for an otherwise healthy 26-year old – Brian Vickers’ future in racing has been a big question mark. Brian is one of the smartest (and kindest) drivers I’ve met. He is one of the few drivers that could have his choice of a wide range of careers if racing were on the list of permanently prohibited activities. Luckily, as we found out Saturday, it’s not.
The heart is a pump that circulates blood throughout the body. The adult heart has four chambers: two atria and two ventricles. Ventricles send oxygenated blood through the arteries to muscles and organs. The right ventricle discharges into the lungs, where the blood picks up oxygen molecules. The left ventricle discharges its blood toward the rest of the body via the aorta. Veins carry the de-oxygenated blood back to the atria (plural of atrium). The picture is from wikipedia.
That’s the adult heart – you don’t start out with four chambers: you start out with one ventricle and one atrium. The septum primum starts growing downward, which divides the single atrium into a left and right side, as I’ve tried to show schematically below . (The word “septum” almost always denotes a flexible division, whether it is chambers of a heart or between a vial and air. The cartilage that separates your nostrils is a nasal septum.) The septum primum (literally “first septum”) that divides your atrium isn’t entirely continuous – there is a hole in this septum.
Somewhere around the third to fourth week of gestation, a second septum (the septum secundum) grows on the right side of the first septum. This second septum, which is parallel to the first one, covers most of the original opening, but not all of it. This opening, called the foramen ovale, is not a hole – a hole would allow blood to flow in either direction. The foramen ovale is a one-way flap that allows blood to flow only from the right atrium to the left and not vice-versa. In the womb, a baby gets oxygenated blood via the placenta through the umbilical cord. Blood doesn’t need to make the trip to the lungs to gather up oxygen because the baby isn’t breathing air. Bypassing the lungs isn’t a big deal for a baby in utero.
In 75% of the population, this one-way path closes within three months after birth. The blood pressure in the left atrium becomes greater than that in the right, pressing the foramen ovale against the septum, which allows the tissue to grow together and seal the flap. In about a quarter of people, the flap doesn’t seal over the hole completely, which is called a PFO – a patent foramen ovale. The PFO is a shunt, which means a shortcut, in this case between the right and left atrium. In most cases, the hole is a few millimeters in diameter – large enough to present a problem because it allows blood shortcut the circulatory system.
The symptoms of PFO are: well, none. You’re unlikely to know if you have a PFO unless something dramatic happens, like extreme pain in your extremities, or (the worst case situation) a stroke. The first medical report of undiagnosed PFO related to stroke was in 1877. A young woman had an embolic stroke – blockage of an artery, usually by a blood clot, but blockages can also be caused by air bubbles, cancer cells, clumps of bacteria from an infection or even fat. Brian noted that they found a blood clot in his left pinkie (I think it was his pinkie – I was driving and not taking notes.), which was an indication that there was someplace in his circulatory system that was allowing blood (and clots) to go where it shouldn’t.
As Brian mentioned during his press conference, diagnosing PFO (or any other kind of heart defect) requires invasive procedures, such as transesophageal echocardiography – an ultrasound device is threaded through the mouth, down the esophegous to allow better images of the heart that you could get from outside the body. Other means of diagnosis include threading an ultrasound probe into the heart, or heart catheterization. Although many people successfully undergo these diagnostic processes, there is an inherent risk anytime you start poking around the inside someone’s body. Once a PFO is found in an otherwise healthy person, most doctors advise having the hole fixed.
It used to be that open-heart surgery was the only way to fix these types of heart problems – I think Brian telling us he was doing 30-60 miles of cycling in Denver within a month after the surgery is pretty strong evidence he didn’t go that way. I have no inside knowledge as to the particular type of repair Brian had, but the most likely surgery would be catheter introduction of a device that seals the hole.
How do you fix a hole in the heart? It’s actually a little like fixing a hole in drywall. Most of the devices for fixing holes in adult hearts deploy through catheters (thin tubes that can be fished through your arteries and veins much like wire is fished through a wall when you’re wiring a stereo system). Sorry for all the home repair analogies. I spent a lot of time at Lowe’s this week. The catheter is inserted into a vein in the groin and slowly threaded up to the heart.
Although there are a number of different types of devices, most work on the same principle – two discs designed to sit on either side of the hole. The devices are usually made of Nitinol (an alloy of nickel and titanium) which forms a mesh frame onto which fabric is adhered. Nitinol is popularly called ‘memory wire’. You can form a material into a shape at high temperature, for example. Let’s say we make a disk from a hot piece of nitinol. Then we cool it down and deform it like an umbrella. That allows us to stuff the device into the catheter (which is really just a tube). (Here’s a YouTube video showing the effect with a spring shape.)
When the catheter reaches where it needs to be, it can be heated (by thermal conduction or current) and recovers its original, disk-like shape. An alternative method is simply to coil the device up inside the catheter and push it out once it reaches the target area. One disk is inserted on either side of the hole and the two patches are pulled together. The implant provides a scaffold for heart tissue to grow and cover the hole. The tissue might not be able to span the hole by itself, but the implant gives it a path to do so.
Nitinol not only has a good memory, it is also biocompatible – the body doesn’t mind having it in there. Some new eyeglass frames are made from nitinol – if you step on them (as long as you don’t actually break them) they can be heated and spring right back into shape. We haven’t finished working on the self-healing materials problem. Nitinol got its name from the elements from which it is made and the place it was discovered: Nickel Titanium Naval Ordnance Laboratory.
A typical type of implant — and again, I do not know what Brian and his doctors chose – is GORE HELEX – the nitinol is spiral shaped and uncoils when pushed from the tube, as shown in the picture at left. The wispy white stuff is a polyer fabric. The green tube in the picture is the catheter – you can see how small the device has to be to get in there and then how large it can expand. There is a tether between the two disks that can be tightened to place the device so that it is entirely covering the hole on either side, and then locked in place. I don’t know whether the shape-memory properties of Nitinol are being used here, or whether the superelasticity properties are the important thing. I’m thinking it is the latter. The primary competition is the Amplatzer septal occluder. These are relatively new devices, earning FDA approval in 2001 and 2006. Both have outstanding success rates in fixing holes in the heart.
Such a device shouldn’t set off metal detectors in the airport and, yes, you can have MRIs done after having such a device implanted. The danger of the MRI is that metal heats up in the radio-frequency field of the MRI. Also, MRI magnet strength is increasing – higher fields means better resolution – and there is always some concern that very high magnetic fields might cause a device to migrate. The device could also blur MRI images in the region. When you have such a device implanted, they give you a card with all these notices on it that you need to have and present anytime you get tests done.
The other issue Brian was facing is May-Thurner syndrome, which is when the left common iliac vein (which runs from the left leg to the large vein in the abdomen that leads to the heart) is compressed by the right common iliac artery. The right common iliac artery runs to the right leg and normally travels over the left common iliac vein. May-Thurner syndrome significantly increases the risk of deep vein thrombosis, which is forming blood clots in veins deep inside the body as opposed to surface veins.
Three primary components contribute to blot clot formation, a triad that is called “Virchow’s triad” after the German physician Rudolf Virchow, even though Virchow did not propose these elements, nor was he the one to suggest that there were three primary components for blood clot formation. Those three components (in medical-ese and regular English) are:
- Hypercoagulability (the blood likes to form clots more than it should);
- Hemodynamic changes (the motion of the blood changes: it slows down, lingers too long in one area, or becomes more turbulent); and
- Endothelial injury/dysfunction (the blood vessels are damaged in some way)
The first factor is the reason why people with blood clots are put on Coumadin, Plavix or other blood thinners/anticoagulents. These medications decrease the ability of the blot to clot.
The second and third factors are affected by May-Thurner syndrome affects: If the blood slows down, or has to move around an obstruction, clots are more likely. The iliac artery crosses over the iliac vein: In May-Thurner syndrome, the artery actually presses the vein against the spine, squishing the vein and preventing blood flow, as shown in the picture.
Your arteries and veins normally are pretty strong; however, your blood pulses with your heart contractions, so if the artery is too close, it doesn’t just rest on the vein, it actually rubs against the vein and causes the vein to rub against the spine. All this rubbing can damage the vein, leading to compression and blood pooling. Symptoms can include swelling and pain in the left-side extremities.
The solution to this problem is the same one you would use if you had an artery or vein that had collapsed due to other types of injury: a stent. A stent is a hollow tube, also often made of nitinol mesh, that is collapsed to fit in a catheter, then inserted into an artery or vein to help keep it open and allow blood flow. A balloon is usually inserted through the target site (again using a catheter) to ensure that the area is clear before the stent is inserted. (They use a balloon to measure how large the hole in the heart is, too.) Stents can be impregnated with drugs to aid in healing the artery or vein, or even to discourage clots.
The prognosis for both these conditions is excellent, although frequent checks with the doctors are necessary to make sure that nothing unexpected happens. Both conditions really needed to be addressed to minimize the likelihood of something happening in the future. Although these types of surgery are inherently risky, the probability of success in a healthy young person is very high.
The main reason keeping Brian out of the car for the remainder of this season is the need to be on blood thinners: blood thinners decrease the ability of the blood to clot, so what would normally be a minor injury could be major due to loss of blood. A six-month course of blood thinners is recommended – the surgery was July 12th, so that puts mid-January as a perfectly reasonable time to return.
Here’s looking forward to seeing Brian back in the 83 at Daytona next year.