November 11th, 2013
Case: An Ironman with a Proximal Circumflex Lesion
John Ryan, MD, JAMES BECKERMAN, M.D. and James Fang, MD
A 48-year-old man who runs 4 to 6 Ironman races per year reports non-exertional chest pain and is referred for a stress echocardiogram. His two sisters suffered MIs and died in their fifties, and his brother underwent CABG at age 49.
The patient goes for 17 minutes on the Bruce stress protocol, with lateral and anterolateral wall hypokinesis at peak stress. He is referred for coronary angiography, which shows a 50% proximal circumflex lesion deemed best treated with medical management.
He is referred to me and asks me how much should he exercise — specifically, whether he should run an Ironman in the Grand Tetons this coming weekend.
What would you advise this patient?
1. Keep running at your current level. (If he has an MI during a marathon, I will obviously feel awful.)
2. Keep running for exercise, but do not compete in marathons.
3. Simply reduce the amount of exercise you do. (It seems strange to tell someone to exercise less.)
4. Reduce your level of exercise, and repeat a stress test in 3 months. If the stress test is normal, you will have a green light to compete again.
5. Something else?
Response (November 11, 2013)
Sometimes I like to think about these situations backwards. A man with very high functional capacity who completes long-distance triathlons is diagnosed with a 50% circumflex lesion. If we assume that an abnormal stress test is generally caused by high-grade lesions, then the 50% circumflex stenosis is potentially not the cause of the positive stress test in this case. The patient could actually have had a false-positive stress test with non-anginal chest pain and an incidental 50% non-culprit lesion. Even if the lesion is causing the positive stress test (FFR would be another consideration), then we still doubt that he is experiencing classic angina because he has been training for hours at a time with no symptoms.
So let’s assume we are diagnosing coronary artery disease that is likely asymptomatic but we still want to recommend that this runner limit his exercise. In that case, it would be a more consistent practice pattern to recommend stress-test screening for CAD before allowing anyone to train for endurance sports — or even to advocate coronary angiography, given the possibility of false-negative stress tests. But that is obviously not how we practice — or how we should practice. In general, when a patient tells you that he or she wants to run a marathon, you take a history and make sure there is no angina, or you might consider an electrocardiogram. Stress testing for asymptomatic patients is generally reserved for those older than 65, or for younger patients who are at significant risk for coronary disease.
This patient likely had the same 50% circumflex lesion during the previous Ironman race he completed 2 months ago and during his 100-km bike ride the weekend before seeing you. I would tell him that his risk goes up in a small but incremental way during these endurance events and that limited evidence suggests that persistent endurance training is associated with arrhythmia and, possibly, myocardial fibrosis.
Fortunately, the event rate during endurance races is low. The 2012 NEJM article from the RACER Study Group showed that the risk for cardiac arrest during marathons is on the order of 1 in 100,000. The risk in triathlons is similar, with the majority of deaths during the swim. ESPN recently published an article, called “Trouble Beneath the Surface,” about deaths during triathlons, especially the swim component. The reasons are unclear, but there are theories about autonomic conflict, when both the sympathetic and parasympathetic systems are activated simultaneously and may provoke arrhythmias. In terms of marathons, note that a higher percentage of events occurs during the last mile, as people have a surge in adrenaline and speed when they are trying to achieve a certain time or beat a personal record.
A big-picture question is whether training more than 15 to 20 hours a week is good for our long-term heart health. I tend to agree with practitioners in this field who suggest that you are not doing multiple long-distance triathlons or marathons primarily for heart health — something else is motivating you. By taking on that additional training, the person must appreciate the possibility of short- or long-term cardiac consequences. And, of course, cardiologists have their own biases. Some who support endurance exercise may be more likely to do it themselves. To be fair, the debate is less about comparing endurance activity to a sedentary lifestyle than about comparing endurance exercise to a lower dose of activity.
Regarding your patient, I would not tell him that he may never participate in an endurance event again. I would be realistic about his risks and recommend that he take any symptoms on the course very seriously. He should also avoid bursts of speed to achieve a certain time. He should do everything he can medically to reduce his risk, such as taking aspirin and a statin. I would empower him with information that is realistic without being alarmist, and help him reach the decision that makes the most sense for him.
Response (November 20, 2013)
Jim Fang, MD
This fit middle-aged man has aggressive atherosclerosis (an obstructive lesion at age 48) and appears to be symptomatic. A 50% angiographic stenosis, corresponding to 70% cross-sectional stenosis, can produce angina. This correlation is why many of the classic angiographic CAD studies have deemed 50% angiographic stenosis to be clinically relevant. FFR (or IVUS to demonstrate true cross-sectional stenosis) may have proven this, but the stress test shows ischemia in the distribution of the lesion, and the patient has typical symptoms. I believe he has probably developed ischemic preconditioning, which likely has allowed him to have this degree of exertional capacity in addition to his peripheral muscle and respiratory conditioning.
Medical therapy would be my first recommendation (aspirin, statin, beta-blocker), but the chronotropic effects of beta-blockade are likely to affect the patient’s athletic performance. I would not be comfortable with prolonged-demand ischemia despite the high workload, given the family history of MI and early death. Although ventricular fibrillation from chronic ischemic heart disease is not common, as noted in the NEJM paper that Dr. Beckerman cites, it may have a familial tendency.
Therefore, I would curtail the patient’s marathon running until he decides what course he wants to elect. I agree that running 4 to 6 Ironman races per year is not of any health benefit to him. Remember, Jim Fixx died of sudden cardiac death.
Wrap-Up (November 25, 2013)
John Ryan, MD
After extensive consultation and discussion, the patient and I opted for aspirin 81 mg, atorvastatin 40 mg, and continued exercise. However, I advised him to take any chest-pain symptoms seriously and also prescribed nitroglycerin for use as needed. He has not had any symptoms while exercising and has reduced his intensity to half marathons for the next 6 months. Since he and I first met, he has successfully run one noncompetitive half marathon, has opted not to run competitively, and is no longer trying to break personal records.
14 Responses to “Case: An Ironman with a Proximal Circumflex Lesion”
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I like the saying “not so much-it applies here: this is a committed high level athlete who is unlikely to listen to such advice. While I find it curious that a 50% stenosis does result in myocardial hemodynamic compromise, nonetheless the wall motion abnormality confirms such. I’d treat the heck out of all his risks (to a nonHDL cholesterol of < 90, TG < 100, A1C <5.5, CRP <1.0…), change him to a very high fiber diet (gladiators like him were called "barley men" & were 90+% (not 100%) vegan diet, and encourage his continuing his exercise after either an absorbable or everolimnus stent. Congrats on doing an echo stress/avoiding radiation. http://www.thepmc.org
“and encourage his continuing his exercise after either an absorbable or everolimnus stent” – That’s it!
I usually perform a CPX stress test in a treadmill, and use a portable CPX machine in a regular exercise training season with this information you can be sure if he is performing a correct treaning, the real functional capacity and pick up very sutile problems, also I look for inflammatory markers, in case he has risk factors modify them. In my experience in an asymtomatic patient, with this caracteristics, with a long history performing exercise they can continue doing it without problems. Is important to explain the ischemic sintomatology, must of this athletes are very good in biofeedback and they are aweare of sutile changes. Most of the patients with cardiac disease benefit of excercice, is a under valuated tool and very effective. Some cases I recomend to the patient to have Nitro just in case, usually they never use it.
Wow. I just a general internist so perhaps I’m taking a risk or being arrogant to weigh in here, but here goes.
So this guy is a mega-athlete but has sx of concern. His stress echo is abnormal and his cath shows an isolated 50% lesion. I guess my question to the cardiologists here is: how often would you stent a 50% lesion and do you actually think THAT lesion is causing his stress abnormalities and sx????
I thought 50% lesions were considered NOT hemodynamically significant. Hard for me to believe that is causing the findings. So, could this be “small vessel disease”, spasm, something else? And, AND, if he gets stented, then he is on antiplatelet rx for year or more which, in this athletic guy, increases his risk of significant bleeds if/when he falls. Scary.
Wouldn’t intensive statin therapy and low dose ASA be a reasonable approach. And let him continue exercising with close monitoring of any sx or more importantly, change in sx. Given his impressive FH,might be reasonable/helpful to do advanced lipid testing as well.
Thanks, fascinating case.
David Kaufman
I personally would not defer stenting in such a patient without at least performing an ffr with high dose adnenosine. something does not fit Either the stress echo is bogus or the lesion is worse than 50% or exercise induced spasm is at play. Lets get a better dx first and then tailor the treatment to the patients wishes if possible
MLC
Poiseuille’s equation establishes that the functional significance of a lesion is proportional to its length. FFRs correlate with the length of the lesion. IVUS may better demonstrate the length, and FFR the hemodynamic significance of the lesion.
Either way, the short- term issues relate to symptoms and Resultant limitations. From the brief presented outline, I would not limit his activity, allowing him to compete as tolerated with aspirin and a statin.
I would recommend limiting the intensity of exercise by avoiding anaerobic threshold and repeat stress echo (or MRI) in 4-6 months, if symptoms should remain stable. Competitions should be avoided.
Statin and aspirin are indicated. The patient should be informed regarding possible influence of statins on exercise capacity.
I think this man is at high risk of MI and death especially considering his horrendous family history. The stability of this lesion is questionable and it could have been tighter at the time of the stress test. Yes, I would suggest a stent with maximal medical therapy and obviously dual antiplatelet regimen and also restrict his exercise and avoid competitions.
Please see articles attached.
Siegel AJ. Siegel AJ. Pheidippides Redux: reducing the acute cardiac risk during marathon running. Am J Med. 2012;125:630-35. Correspondence: Am J Med.2013;126:3,e25-26. http://dx.doi.org/10.1016/j.amjmed.2012.10.026
Siegel AJ. The rationale for pre-race aspirin to protect susceptible runners from sudden cardiac death during marathons: Deconstructing the Pheidippides conundrum. World Jour of Cardiovasc Dis 2013;3,17-20. Published online August 2013 (http://www.scirp.org/journal/wjcd/)
This patient needs to see these as well.
Regards,
Arthur Siegel, M.D.
asiegel@partners.org
How does this patient leave the cath lab without a functional assessment of his lesion? I would take him back and FFR the LCx, stent if significant. Prior, I would have a discussion with the patient re: DAPT duration and stent choice. His lifestyle may be more suited for shorter DAPT. Fixed or not, I have a discussion about his risks with high-intense exercise and allow him to decide what to do.
Thank you Dr. Powell for your comment re: lesion length, as this should answer Dr. Kaufman’s concern, a concern I frequently hear from primary care physicians. Not all 50% lesions are created equal. Especially with the evidence FAMEII provided us, we need to start moving beyond angiographic optical bias and obtain objective data about intermediate lesions.
17 minutes on a standard Bruce protocol!! Even for a highly conditioned endurance athlete, that is no easy feat!
I assume that at 17 minutes — when he was noted to have the segmental wall motion abnormality — he had no chest pain. Why, then, did he terminate exercise? Probably dyspnea (who wouldn’t be dyspneic at 17 minutes of a standard Bruce protocol?). If, in fact, he had no chest pain at peak exercise, I conclude that the nonexertional chest pain that brought him to medical attention in the first place is noncardiac in origin. Hence, from a CARDIAC standpoint, he has no symptoms.
I recommend procedures (medical or nonmedical) in patients for 1 of 2 reasons: (1) to make them feel better and/or (2) to allow them to live longer. In this gentleman, I can’t make him feel better, since he feels great right now on nothing. Could any intervention (medical or nonmedical) cause him to live longer? Not that I know of. I do not medicate or do procedures on patients to prevent MIs, since no data exist to support doing so.
Therefore, I’d send him on his way and wish him the best of luck in his next ironman competition.
Great case with several complexities.
The unequivocal fact(s) are that:
– he has a marked genetic predisposition to coronary atherosclerosis
– he clearly has coronary atherosclerosis based on his angiogram
– he therefore needs aggressive LDL reduction and probably an aspirin
– he has asymptomatic demonstrable PROBABLE ischemia based on stress echo at a very high cardiac workload
– his long term prognosis with non-athlete activity is excellent
The more mirky fact(s) are that:
– it is unclear whether or not that 50% lesion is enough to cause ischemia even at a high workload. Logically should not but “reverse mismatch” (non-obstructive looking lesion but abnormal FFR) is well known
– it is unclear what his risk would be at extremely high activity levels (the 1:100,000 risk equation applies to all comers not to those with known coronary lesions). Overall I suspect it would still be low but is it low enough?
– it is unclear what the medicolegal implications would be, should, heaven forbid, this man collapse on the field
– it is unclear whether stenting the LCx would offer any prognostic benefit in this sort of situation
I would:
– treat with aspirin and statin
– have a clear discussion explaining the lack of clarity on the issues above
– offer him one of these options:
— reconfirm functional significance of LCx lesion with FFR (would make sure we get maximal hyperemia with IV infusion of adenosine perhaps at doses higher than 140 mcg/kg/min)
— in the event of abnormal FFR consider option of beta blockers to reduce ischemic burden (obvious downside is beta blocker side effects) or stenting with the understanding that it would remain UNCLEAR whether the potential risk of an event during a marathon outweighs the procedural risk
need some more data on his BP on stress testing, Lipid profile.
i would recommend ACEI, Aspirin and Statins – nitrates on SOS basis. would stop him from competing but will advise continued training.
the rational is preserving and maintaing the exercise tolerance, improving the hemodynamics (reduction in cardiac work load). repeat stress testing 3 months later ( if remains symptomatic) or on yearly basis, if he remains asymptomatic.
Identified 50% stenosis on angiography may be a subjective findings. I thought if I measure the amount of coronary artery calcification. ıf negative or very low CAC I would say to continue medical treatment.Also, I would say to continue to exercise. Dose of exercise to keep a little low, but I’d say.