Feature: Arterial disease and cycling
[pullquote align=”right”]Iliac artery endofibrosis — a crippling circulatory condition affecting the legs — is sending more and more cyclists under the knife. Is it actually becoming more widespread, or are doctors just getting better at recognizing it?[/pullquote] SOMETHING WASN’T RIGHT WITH JOE DOMBROWSKI’S LEG. It was July of 2013, and the…
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[pullquote align=”right”]Iliac artery endofibrosis — a crippling circulatory condition affecting the legs — is sending more and more cyclists under the knife. Is it actually becoming more widespread, or are doctors just getting better at recognizing it?[/pullquote]
SOMETHING WASN’T RIGHT WITH JOE DOMBROWSKI’S LEG. It was July of 2013, and the young American was at a Team Sky training camp in his first year with the British super squad. Twenty minutes into a 30-minute climb, Dombrowski’s leg felt like it was about to cramp — quivering, on the verge of seizing. He mentioned it to one of the team coaches, but neither he nor the coach thought much more about it.
For the next several months, the strange feeling intermittently cropped up during rides. It was annoying, but it wasn’t inhibiting his performance. He just thought maybe he wasn’t doing enough core workouts or that perhaps he had some kind of muscular imbalance. He rode on.
That offseason, his symptoms worsened. Before, it might have taken 20 minutes of riding at 400 watts to feel the sensation. Now, if he rode for five minutes at 350, he’d be riding with one good leg and one numb, powerless appendage.
He found ways to compensate during races, desperately trying to squeeze the power out of his malfunctioning limb. But his left leg began to atrophy, eventually becoming almost 3.5 centimeters smaller in circumference. His team prescribed unilateral exercises to try and rebuild his strength. Nothing worked. He mentioned to team doctors that friends had problems with their iliac artery. Much to Dombrowski’s surprise, none of the staff were familiar with the issue. After running rudimentary blood pressure tests, team management dismissed the issue. Another six months passed.
Finally, after Dombrowski persisted, the team sent him to see Dr. Robert Hinchliffe, one of the world’s leading physicians on the mechanics and treatment of vascular issues in athletes. Hincliffe ordered an ankle-brachial index test, which involves taking blood pressure at the wrist and ankle, both at rest and during exercise. A 10 percent or more difference in blood pressure between wrist and ankle indicates some sort of occlusion.
Dombrowski’s left leg showed a nearly 40 percent drop.
It was June of 2014, almost a year after he felt that initial strange sensation, and another professional cyclist was diagnosed with iliac artery endofibrosis (IAE).
ARTERIAL DISEASE USUALLY AFFECTS older individuals who haven’t led healthy lifestyles, people who have damaged their arteries in much the same way coronary arteries are narrowed by plaque — through years of uncontrolled high blood pressure, smoking, and high cholesterol. On the surface, it doesn’t make much sense that young elite athletes would suffer arterial disease and require surgical intervention to continue doing their jobs at a high level. But that’s just what is happening.
“The funny thing about these kinds of diagnoses is, in medicine, [the illnesses] see us for years, but we don’t see them, because we haven’t figured it out,” says Andy Pruitt, founder of the Boulder Center for Sports Medicine, a medical consultant to a number of WorldTour teams and riders, and someone who has likely spent more time working on the bodies of professional cyclists than anyone else. “So this gradual thing happens. There were virtually zero diagnoses in 1995, and then how many in 2016? And then you have to develop the treatment skills to treat it. So there is a time that passes before we figure things out.”
That time seems to be now.
A host of professional riders has been diagnosed with IAE in recent years, including Dombrowski, Bjørn Selander, Jacob Rathe, Mike Friedman, Stuart O’Grady, Bert Grabsch, Ian MacGregor, Derek Bouchard-Hall, Charles Dionne, Stuart Gillespie, Hayden Godfrey, Mari Holden, Bobby Lea, Tony Gallopin, Sally Bigham, Theo Bos, and Travis Meyer. There are undoubtedly others whose diagnoses haven’t been publicized. One research team estimated that among professional cyclists, IAE may account for up to 20 percent of all overuse leg injuries.
Professionals aren’t the only ones who are susceptible to IAE. Given the amount they ride, they are more likely to receive diagnoses. And because it affects their livelihoods, IAE has received more attention amongst pros, relative to the general population. But the average rider can develop the condition.
A 2011 review of the literature on IAE revealed that most patients are younger than 40, but the condition has been identified in subjects as old as 61. The study also reported that the condition is significantly more common in men, with fewer than 12 percent of cases involving women. (However, this may be somewhat biased by the greater number of men taking part in these endurance sports.)
Regardless of age or gender, symptoms vary between individuals and are generally vague. Most sufferers describe it as a cramp, commonly accompanied by swelling, numbness, or pain that develops in the calf, thigh, or buttock on the affected side. The sensation usually hits only one leg and manifests when athletes are pushing near their hardest. Some will also experience weakness in the affected leg. More often than not, people will stop their workout after the onset of the numbness or paralysis. All of these factors contribute to the significant delay that is common in diagnosis. One study indicated a 12- to 41-month delay between the onset of symptoms and a correct diagnosis.
Paradoxically, the delay is often greater in professionals than in amateur athletes. IAE just isn’t the first thing pros or their teams consider when leg problems arise. Given how common musculoskeletal issues are for pro cyclists, they and their doctors generally work through a long list of possible ailments before arriving at IAE, if they get there at all.
In case after case, the story follows a familiar pattern: A professional athlete will see a number of physicians and therapists who will test for myriad possibilities. All of these tests will likely be stabs in the dark. And routine physical exams don’t generally reveal issues that present only under exertion. So those don’t help. Someone will prescribe rest or physical therapy. But the symptoms will worsen. The athlete will start to lose to competitors he or she once routinely beat, forcing questions about whether or not it’s time to quit the sport.
If the athlete persists, eventually they’ll find their way to a specialist — after months or years of increasingly expensive tests — who will diagnose IAE.
But it’s only correct diagnoses that are rare. The truth is that the condition itself is surprisingly common among elite cyclists, triathletes, speed skaters, Nordic skiers, and, to a lesser degree, runners. A 2011 review of the literature at that time revealed that cyclists had cycled an average of 120,000 kilometers (the range was from 30,000 to 500,000 kilometers) prior to the onset of symptoms. Physicians and researchers are still coming to an understanding of the mechanics, causes, and treatment of IAE. There is much yet to be learned.
“You’re really exposing the lack of understanding that we have of the condition,” says Dr. Hinchliffe, a professor of vascular surgery at the University of Bristol, who has conducted more than 30 surgeries and assessed over 100 athletes for the condition. “Our understanding now is pretty basic. There are undoubtedly people who have the condition and their symptoms remain very static for a number of years. There are some people that progress gradually, and there are those who get very rapid progression to complete blockage or occlusion of their iliac artery, which is potentially a limb-threatening emergency. And it’s really difficult to understand which people get those symptoms. We can’t predict who will get endofibrosis at the moment.”
This we know: The aorta, the largest artery in the human body, leaves the heart with oxygen-rich blood and passes behind the lower abdomen. At the level of the fourth lumbar vertebrae — just above the sacrum in the lower back — it splits into two common iliac arteries that head for the legs. Several inches later, right around the sacroiliac joint (where the spine and the pelvic girdle come together), the common iliac arteries split into the internal and external iliac arteries. The former supply blood to the pelvis and buttocks, while the latter continue down the legs, where they become the femoral arteries.
Arteries are composed of three layers: the intima, media, and adventitia. The intima lines the inside of the blood vessel and forms a smooth lining to permit blood flow. The media (middle layer) contains muscle and fibers that expand and contract with each beat. The outer adventitia contains fibroelastic tissue that allows for these changes in volume.
In traditional arterial disease, a cholesterol plaque builds up in the middle layer. In iliac artery endofibrosis, that fibrous tissue starts growing within the intimal layer, which may lead to a loss of elasticity, an inability of the artery to change diameter under a high-blood-flow state, and, eventually, to a constriction (stenosis) of the artery itself.
While IAE in cyclists can surface in the common iliac artery, nearly all cases involve the external iliac artery, because cycling’s forward-leaning body position and repetitive hip flexion place that vessel under constant stress. That repeated strain, under high blood flow, over many years and thousands of miles in an unnatural physiological position is a recipe for a specific, unique pathology.
Interestingly, Team Sky has thoroughly advanced its understanding and awareness of IAE since Dombrowski’s time. The outfit hired Hinchliffe in October 2015 to screen the entire team for symptoms of arterial issues.
SO WHY HAS IT TAKEN SO LONG for the sport and medical community to catch on? “I think there are several possible explanations,” Hinchliffe says. “One, of course, is that we’re more aware of the condition now than we were before. It may be that we’re identifying guys and women who would have previously just soldiered on with the symptoms or stopped cycling.”
The other issue, and one that hasn’t yet been studied, is whether extreme racing positions play a role and how increasing intensity and training and racing mileage might expedite or exacerbate the problem.
“My take is that these guys are doing high miles, under high blood pressure, and the repetitive stretching of the artery and that hemodynamic stress is causing the problem,” Hinchliffe says. “It’s really difficult to say how aggressive positions play a role. My feeling is that it probably doesn’t make a massive difference. I think, like in many medical conditions, it’s a multifactorial problem.”
By that he means it’s likely related to genetic factors, which we probably don’t fully understand. Are your arteries genetically susceptible to damage? What is your blood pressure when you’re exercising? What is the flow rate through the iliac artery? How many hours are you exercising, and at what intensity? While Hinchliffe concedes that a more extreme position might play a role, teasing that out in an epidemiological study would be incredibly difficult.
Even without this academic proof, though, Pruitt, who has spent 43 years studying and writing about how positional changes and anatomical structure can play a massive role in every- thing from cycling comfort to performance, is more willing to make a definitive claim.
“I’m not going to publish a paper on it, but I can tell you that [the development of IAE] is many times positional,” he says. “I can give you examples. There is also anatomical variance that can lead us to it: a wide pelvis with a lot of angulation at the femur, for example. There are things we can see that would impinge it. There are things we create that impinge it.”
In 2012, the Quick-Step team physician asked Pruitt to examine Bert Grabsch, a German former world time trial champion who was facing surgery to correct IAE. The doctor hoped Pruitt could change Grabsch’s position to correct the issue and head off surgery.
Pruitt’s initial exam revealed that Grabsch was mildly duck-footed and slightly bowlegged, with a very wide ischial tuberosity (informally known as the spacing of the sit bones). He was from the East German system, which traditionally fit riders within rigid, often dogmatic constraints: toes in, knees to the top tube, with a narrow saddle.
“All three of those things separately can contribute to iliac artery issues, and he was forced to do all three of those artificially,” Pruitt says.
The reality was that Grabsch had been creating an internal rotation at the hip, then forcing his knees to adapt to it. In the end, Pruitt’s positional changes included elevating the front end of his bike approximately two centimeters, repositioning his cleats, widening his stance, and choosing a saddle that laid him on his pelvis.
“He said he never felt better,” Pruitt says. “And he raced at least one more year, and was a big part of their team time trial.”
The problems in Grabsch’s position — forcing an athlete to fight against his or her anatomy — are common in the professional peloton, as is a lack of appreciation for modern fit principles. The truth is that riders talented enough to make it to the pro ranks are so strong they can excel even with suboptimal positions. So the “if it ain’t broke, don’t fix it” mindset is commonplace. But the science is starting to show us that, for a lot of riders, something does eventually break.
HOW MANY PROFESSIONAL CAREERS HAS IAE CUT SHORT? It’s impossible to know. But the story of Ian MacGregor is a clear example. The former U.S. under-23 national road champion retired from the sport in 2010, after being diagnosed with IAE. He suffered through a year similar to Dombrowski’s, with tests, treatments, and frustration all piling up, but with little resolution. At that time, far fewer surgeries had been performed, and the potential risks were, MacGregor says, enough to make the final decision an easy one. (Ryan Cox, of Barloworld, died in 2007, weeks after undergoing surgery for IAE in France, though it remains unclear whether circumstances surrounding the surgery, or other complications, were to blame.)
“That, to me, wasn’t an option,” MacGregor said at the time. “Cycling is wonderful … but for me, I want to be able to go hiking when I’m 40 and run around with my kids in the future and that kind of stuff, much more than I want to race for another six or seven years.”
But significant advancements in the past five years have made surgical intervention much safer, to the point that it is now rather routine to hear about a rider returning to the professional peloton after going under the knife. In 2015 and 2016 alone, Dombrowski, former Garmin-Sharp rider Rathe (now with Jelly Belly-Maxxis) and former Team RadioShack rider Selander (now with Team Rally) have returned to racing after IAE surgeries.
[pullquote attrib=”Ian MacGregor” align=”left”]
“Surgery, to me, wasn’t an option. Cycling is wonderful … but for me, I want to be able to go hiking when I’m 40 and run around with my kids in the future and that kind of stuff, much more than I want to race for another six or seven years.” [/pullquote]
Each case presents differently, with numerous surgical options to correct the issue. And it’s important to note that though the surgery has become somewhat routine, it isn’t without its risks.
“I would only suggest an operation in those people whose symptoms are clearly progressing or if they are professional or an elite amateur who needs it because it’s their living,” Hinchliffe says. “Most of the people I tend to say, ‘Look, the only known treatment for this is surgery, but surgery comes at some risk. We don’t know in the long term what the risks may be and it may require further surgery, and surgery on arteries is potentially limb- and life-threatening. If anything goes wrong, if you get an infection, then that’s a big, big deal.’ This isn’t like having a cartilage trimmed.”
For Dombrowski, however, there was never any question.
“In terms of the risk, I guess this goes to show you that cyclists are crazy,” he says. “I knew the story about Ryan Cox. That was a lot less scary to me than not racing my bike for a living anymore. I know it sounds ridiculous, but that was the first thing through my head. It was like, ‘How long until I can get back to racing?’”
In August 2015, Dombrowski’s return from surgery became a smashing success when he won the overall title at the Larry H. Miller Tour of Utah.
One of the most common methods of repair is called “endofibrosectomy with patch angioplasty.” If the damage within the artery is well contained, the artery will be clamped, then cut lengthwise; any fibrotic tissue will be removed and the artery freed from any adhesions to the surrounding muscle tissue. Surgeons will then sew in a patch, ideally harvested from the saphenous vein in the calf or groin of the patient (this is known as an autologous graft). The advantage of using the patient’s own vein is that it is very resistant to infection, less likely to have blood clots form on it, and less likely to cause an inflammatory reaction. The artery won’t ever dilate quite the same as a natural one, so it will be made wider than what is normal, effectively allowing it to be dilated all the time.
If an autologous graft isn’t possible (for example, if the veins are scarred, diseased, or very small), surgeons will use a prosthetic patch, usually made of a polyester fabric called Dacron that is commonly used to make sailboat sails.
[pullquote attrib=”Joe Dombrowski” align=”left”] “I knew the story about Ryan Cox. That was a lot less scary to me than not racing my bike for a living anymore. I know it sounds ridiculous, but that was the first thing through my head. It was like, ‘How long until I can get back to racing?’”[/pullquote]
In either case, results from this type of treatment have been excellent, with one study from Saint Joseph’s Hospital in Chicago reporting that 99 percent of individuals were able to return to their sport, including to high-level competition.
In cases where the damaged area is too large to correct with a patch, a full bypass may be the only option. For this procedure, surgeons attach a synthetic surrogate — again, usually made of Dacron and to a lesser extent PTFE (Gore-Tex) — above and below where the artery is damaged, skipping the malfunctioning section altogether. Hinchliffe says future research may determine that not every patient with endofibrosis needs an operation. “We need to be able to target operations to people who really need them,” he says.
He also cautions that angioplasty and stents are particularly bad ideas for treatment of IAE, since symptoms always recur quickly and stents break very easily and quickly. (Most vascular surgeons recommend stents for elderly patients with narrowed arteries — they work well for that application — but not for endofibrosis.)
ACCORDING TO HINCHLIFFE, RESEARCH ON ENDOFIBROSIS is about at the point where sports cardiology was 10 or 15 years ago. That is to say, we are merely on the cusp of a flurry of research and a greater understanding of the issue.
For many, the mysteries can be excruciating. It took Selander three years to figure out his diagnosis. This protracted search for a cause is not atypical. “As cyclists, and just the way I was brought up and learned about racing, you’re told it’s 90 percent mental — you’re going to have pain and you just have to push through,” Selander says. “I think I just took that way too literally. The thing is, you can still ride, and still race to a point — I could race, but I could never throw down, and as soon as the race heated up I’d be out the back. And you don’t want to believe that something’s wrong with you. I just didn’t listen and take care of it when it was happening in the beginning.”
He struggled to understand what was going wrong with his body. He thought, “Oh, I’m just not a good bike racer anymore.” The endless barrage of doctors’ visits was not amounting to any relief.
“After all those times of seeing that nothing was working, you start asking why you should go see the next person, because you’re just going to be let down again,” he says. “I look back now and say, ‘Holy cow, I was miserable.’”
But his wife pushed him on. And finally he figured it out.
He had surgery in September 2015. After spending two months completely off the bike, he slowly returned to riding, 15 minutes at a time, then finally attended team training camps three months after surgery. He’s now back to being a part of the professional peloton.
He rides differently now, conscientious not to allow his knees to collapse to the top tube. He’s also changed his bike fit to better engage his glutes, and he says he feels better than he ever has. Most importantly, he can enjoy riding again.
“The thing I’m happiest about is that when I’m sitting on the bike in the saddle, I just love it again,” he says. “Before I didn’t even want to go train because I knew these sensations were going to happen, and I didn’t want to feel that feeling.”