athlete

A Conversation with Cyclist and Heart Transplant Recipient, Paul Langlois

December 10, 2015 By Larry Creswell, MD 8 Comments

I recently met Paul Langlois–online, at least. Many thanks to Joe Friel for making the kind introduction.

I’ve had a chance to chat with Paul and thought I’d share his interesting story here at the blog. Paul is a long-time recreational and competitive cyclist who developed a rare medical condition called amyloidosis. His heart was particularly affected. He developed life-threatening heart failure and required a heart transplant as the only effective treatment. He has now made a great recovery and has returned to his passion of cycling.

I know that heart transplantation remains a bit of a mystery for most non-medical folks. In part, it’s just a rather uncommon operation. Last year in the United States, for example, 2,655 individuals underwent heart transplant operations. Here at the University of Mississippi, I’m involved in about 10-12 heart transplant operations each year. For the patients who need the transplant operation, the results are usually quite remarkable.

It’s very unusual, though, for lifelong athletes to need a heart transplant operation. And that’s why Paul’s story is so very intriguing. He kindly agreed to answer my questions about his experience….

Thinking back to before your heart transplant, can you tell us a little about your interest in cycling? When did you get started? Were you involved in team cycling? Or competitions, of various sorts?

Yes, I had been actively involved in competitive Masters cycling since the age of 30, attaining Category 2 status on the Road, Track, and Cyclocross. Before I became a cyclist, I competed in collegiate rowing at the Coast Guard Academy, winning three national titles. After college, I got hooked on the running boom and completed four marathons (qualified for Boston), ran many shorter events, and did some medium distance triathlons. Problems with my right knee resulted in two surgeries when I was 30, when I switched my competitive focus entirely to cycling, which was became part of a long rehab process for the knee. Only a few years later at age 34, I won the All-Military National Cycling Championships stage race in Colorado Springs. Over the years, I had competed at over 20 various Masters National Championship events for road, track, and cyclocross. Somewhat surprisingly, some of my best performances on the bike were attained in my early 50s, when I won two consecutive years as Best All Around Rider 50+ in the Mid-Atlantic District, and rode a Personal Best 40K Time Trial in 54 minutes. I raced with numerous amateur teams in different parts of the country, as the Coast Guard typically relocated me to a new duty station every three years. I served for 30 years in the Coast Guard, primarily as a helicopter rescue pilot, and retired as a Captain in 2006. After retirement, and settling in Santa Rosa, California, I continued non-stop racing, until a year before my diagnosis at age 56, mentioned below.

I understand that you were diagnosed with cardiac amyloidosis, a rare cause of heart failure. How did you and your doctors discover this problem?

It took me a bit more than one year of frustration before I was properly diagnosed. I attribute my eventual diagnosis in large part through my own keen awareness of my slow, but steady deterioration in fitness level. Initially, I noticed that I was having trouble keeping up with my teammates on training rides, especially when climbing. And then, soon thereafter, I had to pull out of a criterium race after two laps, experiencing almost no aerobic capacity, in the same race I had nearly won the year prior. I first checked with my primary care physician, who commented “I was simply getting older”, which I refused to believe was the problem. I was later referred to a cardiologist and a pulmonologist for stress tests and neither test came back with any abnormality. Over the next six months, I progressed into becoming short of breath when climbing one flight of stairs, and nearly fainting when I quickly rose out of a chair. I noticed my legs and ankles were swelling in a way which I had never seen. Finally, I checked myself into my local ER, and by a stroke of luck, a talented cardiologist was on duty who performed an Echocardiogram, an EKG, a chest xray, and did some lab work. He noticed I had very high protein in my urine, and suspected I might have Amyloidosis. The following week, I had a heart biopsy, and a special test revealed I was positive for Amyloidosis. This was the cause of my heart failing, and it readily became apparent to me that it was a life and death situation. I was referred to Stanford Hospital for further evaluation, as they have one of the few clinics in the USA with significant experience treating this rare blood disease.

Once heart transplantation was recommended, how long did you spend on the waiting list? And during the waiting period, were you able to exercise? What was your fitness level right before the transplant operation?

My first consultation at Stanford was with their Cardiology Dept, which recommended heart transplant, as no other option was available to keep me alive. I went through the pre-qualifying tests successfully over a period of six weeks, until I was allowed to be listed for transplant. I have Blood Type AB, and was listed as Priority 1B, and I was extremely fortunate to only have to wait for eight days until a good match was found for me. Leading up to the transplant, my fitness level had diminished considerably over the past year due to the onset of heart failure, although I still attempted to get exercise, primarily through cycling. As an example, in the months just before transplant, I was not able to get my heart rate over 130, when giving it my hardest effort, whereas the previous year before I became ill, I could easily exceed 165 during a hard effort.

Tell us a little bit about your early recovery after the transplant operation. How long were you in the hospital? When did you begin walking, afterwards? How long did it take to get healed up?

Heart Transplant is obviously a very traumatic surgery, including the need to separate the center of the rib cage to perform the transplant. And so the body needs many weeks to heal and rest afterward. I spent only one week in the hospital. I was up and walking slowly around the ward within three days. After discharge, I was required to live nearby Stanford for many weeks with a Caregiver (my wife Linda), to allow for frequent clinical check ups at Stanford, including many heart biopsies, Echos, and labwork, with a focus on ensuring no organ rejection might be taking place. I began exercising very gently at first, and then with steadily increasing intensity and distance as the weeks went by. Within one month and much to my surprise, I completed a six mile hilly walk around the Stanford Campus. I had to wear a protective mask whenever I was outside or around people to minimize any chance of catching an infection or virus. I finally got to go home at almost two months after the transplant which was a wonderful day.

I understand that you’re back to cycling now. What’s your routine? Are you still competing?

Yes, I have been able to get back into cycling, but have not been able to develop the required fitness to race competitively. Having said that, I still have the mental mindset to someday be competitive, and so I keep training with the belief that I may attain that level again. Unlike many who have heart transplant, my case is much more complex and challenging, as I still have the underlying blood disease to deal with, which required a stem cell transplant just six months after the heart transplant. As I approach the five year mark, I have endured almost nonstop chemotherapy treatments, and clinical trial drugs. Amyloidosis has no known cause, and still has no proven cure. My kidneys have become involved with Amyloid damage (Stage 3 failure), and I have to battle fatigue with anemia. As a result, my ability to train hard and go for long endurance is diminished compared to my earlier success. But, as an example, I was able to complete two 75 mile charity rides within two years after my transplant, and still routinely cycle 3-4 times per week, typically between 1-3 hours each session. I also spend lots of time in the gym with weight training and physical rehab, as I also elected to have a total right knee replacement two years ago, which set me back for awhile. Despite the pain, side effects from medication, and lesser ability to push myself, I enjoy getting out and riding the bike frequently. In the past few months, I have begun to challenge myself on much steeper and longer climbs, and have started to incorporate various interval sessions and sprint workouts. I am getting back into group riding with my teammates again. I have a goal to try and enter some low key racing next year in my 60+ age group, provided my health remains stable.

As you know, the autonomic nerves (from the “involuntary” nervous system) that supply the heart are cut during the transplant operation. As a result, some of the usual mechanisms that influence the heart rate during exertion aren’t available after heart transplant operation. Have you noticed this? And, if so, how has this situation affected your exercise routine or training?

Yes, without any question, I have noticed significant changes in how my heart beats and reacts to demands. Since denervation takes place after transplant, my new heart has a resting heart beat of about 85, whereas it used to be about 44. In the first year after transplant, I noticed during exercise that it would take me about 20 minutes to get my heart rate to a maximum of 120-125. And then, once I eased off the intensity and started to rest, the heart rate would not drop down very quickly. But as the years have gone by, and I have trained consistently, my new heart responds to effort much quicker, and so I can get my heart to rise up over 120 in less than five minutes, and my maximum heart rate after climbing a long hill is about 155. And when I slow down, the heart rate drops much quicker than the first year, but not nearly as fast as when I was in great shape with my original heart. My resting heart rate has not dropped with time, and it remains just above 80 at its lowest resting rate, which I am told is quite normal for heart transplant patients. When I ride, I try to warm up gradually for the first 15 minutes, before applying much intensity, and I have found that I tend to really feel much better after about one hour on the bike. But, I also can report that I do not recover nearly as fast as I used to after a long workout, and so I typically do not ride on consecutive days, to ensure I get sufficient rest and recovery.

Recipients of organ transplants must take anti-rejection medications, usually forever. These medications sometimes hinder the body from dealing effectively with infection. Has this issue affected your cycling? Do you have strategies to prevent illness?

Yes, I definitely have concerns about having to take two different immuno-suppressant medications every day, supposedly for the rest of my life. On one hand, they serve to prevent organ rejection, but on the flip side, my body is much more prone to catching virus and various illnesses. As an example, I had a very difficult year last year (2015), when after the total knee replacement, I came down with shingles all over my body, which took over a month to clear, including hospitalization for a week. Following that episode, I came down with pneumonia, which had me inpatient in isolation for two weeks, and didn’t clear until two months later. If that wasn’t bad enough, this past April, my spleen ruptured due to Amyloid involvement, requiring an emergency splenectomy. While not all of these may be attributable to the anti-rejection drugs, I believe these medications make my body very fragile and less able to fight infections and germs. As a result, I try to be very careful to minimize exposure, especially in public places around large gatherings. I constantly wash my hands and avoid people who appear to be sick. My predicament sometimes means I have to avoid certain social situations in order to lessen my exposure. I wear a protective mask whenever going into hospitals or clinics. I have learned that winter time is a very high risk time for me, so I ensure extra precautions, especially during the Holidays.

Related Posts:

1. Another Heart Transplant Triathlete

2. Ironheart Racing Team

Updated 2015 ACC/AHA Guidelines on Competitive Athletes with Cardiovascular Abnormalities

December 9, 2015 By Larry Creswell, MD 1 Comment

The American College of Cardiology (ACC) and American Heart Association (AHA) have recently released a Scientific Statement on “Eligibility and Disqualification Recommendations for Competitive Athletes with Cardiovascular Abnormalities: Preamble, Principles, and General Considerations.” This 2015 edition is an update for the previous guidelines that were published as Proceedings from the 36th Bethesda Conference in 2005.

The new Guidelines were assembled by a large group of experts who were organized into 15 task forces. Each of these task forces considered the current scientific evidence, graded the evidence, and reached consensus conclusions about recommendations that could be supported. As such, this collection of recommendations represents the best available consensus expert opinion today in the United States.

It’s important to know that there is also a similar set of guidelines developed by the cardiology community in Europe. There are differences between the ACC/AHA and European recommendations that often stem from legitimate differences of opinion.

It is also important to remember that the new ACC/AHA guidelines are targeted toward the young “competitive athlete.” The authors define such an athlete as one “who participates in an organized team or individual sport that requires regular competition against others as a central component, places a high premium on excellence and achievement, and requires some form of systematic (and usually intense) training.” As such, these guidelines are targeted primarily at student athletes of high school and college age (up through 25 years). That said, the various recommendations may well be applicable to other athletes, including: young but non-competitive athletes; older competitive athletes; and adult recreational athletes or exercisers. Particular judgment must be used by physicians and athletes when extending the recommendations beyond the intended target population.

The new guidelines are some 115 pages long. It’s not my intention to summarize things succinctly here in a blog post, but I thought it would be useful to point out what’s new….and what caught my attention in each of the 15 sections….

Task Force 1: Classification of Sport–Dynamic, Static, and Impact

There is now a refinement of the former categorization of sports according to their “static” and “dynamic” components. A new summary chart still uses the former I-II-III (static) and A-B-C (dynamic) scheme, but recognizes that there is actually a continuum along each axis. In addition, a new table provides a useful categorization of sports according to their risk of impact, both at the junior high school and high school/college levels. New recommendations for athletes taking various forms of anticoagulant medications caution against activities where impact injuries may be expected.

Task Force 2: Preparticipation Screening

Preparticipation screening is widely applied in the United States for school-based athletic programs. Controversy remains, though, about the effectiveness of history and physical examination alone for identifying serious cardiovascular abnormalities. This Task Force continues to endorse the AHA 14-point screening guidelines or those of the American Academy of Pediatrics Preparticipation Physical Examination, suggesting particular value in standardization of questionnaire forms used. The new guidelines suggest that the use of ECG in addition to history and physical examination may be appropriate in “relatively small cohorts” of young athletes, where physician expertise is available for counseling and follow-up of test results. Mandatory screening with ECG is not recommended in young athletes or non-athletes.

Task Force 3: Hypertrophic Cardiomyopathy (HCM), Arrhythmogenic Right Venricular Cardiomyopathy (ARVC), and Other Cardiomyopathies

The Task Force recognizes the heterogeneity of disease among athletes with hypertrophic cardiomyopathy (HCM) and advises that judgment is needed in the application of the recommendations in specific situations. New from 2005, the guidelines now recognize that athletes with genotype-positive, phenotype-negative HCM (ie, carrying a gene but no overt manifestation[s] of the disease [yet]), and particularly if there is no family history of HCM-related sudden cardiac death, may participate in athletics. The new guidelines advise against the use of pharmacologic agents or an implantable cardioverter-defibrillator (ICD) solely to facilitate participation in sports. There are no major changes in the recommendations regarding ARVC, other cardiomyopathies, myocarditis, or pericarditis.

Task Force 4: Congenital Heart Disease

There is a very long list of conditions that, together, constitute “congenital heart disease.” These are inherited conditions that usually manifest during childhood, but sometimes these conditions may remain unrecognized until adulthood. Exercise prescriptions are very specific to the particular condition, but the Task Force recognizes that many athletes with “corrected” congenital heart disease may participate fully. Compared with 2005, the new recommendations remain similar or unchanged for: atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), pulmonary valve stenosis, aortic valve stenosis, coarctation of the aorta, elevated pulmonary vascular resistance (PVR), ventricular dysfunction after surgery for congenital heart disease, cyanotic heart disease including Tetralogy of Fallot, and Ebstein’s anomaly. The new guidelines now provide greater detail in the recommendations for patients with transposition of the great arteries (TGA) treated by either atrial switch (eg, Mustard procedure, Senning procedure) or by more contemporary arterial switch operations. In the area of coronary artery anomalies, additional evidence and experience now allows for recommendations for various subsets of patients, including those who have had surgical correction.

Task Force 5: Valvular Heart Disease

The 4 most common valve problems are aortic stenosis (AS), aortic regurgitation (AR), mitral stenosis (MS), and mitral regurgitation (MR). In many respects, the new guidelines parallel the former guidelines. The new guidelines specifically recommend that athletes with these conditions, even if mild, should be evaluated yearly to determine whether sports participation can continue safely. A new recommendation is offered for athletes with severe AR and normal left ventricular dimensions and function; it may be reasonable for these athletes to participate fully if they have normal exercise tolerance and echocardiography shows no progression of ventricular size or dysfunction. MS is probably the least common of these valve conditions. The new recommendations suggest that exercise testing to the anticipated level of sports activity may be useful in patients with MS to ensure that no symptoms develop. The recommendations specifically recommend only low-intensity activities for those with severe MS, but most of these individuals would probably best be treated with valve repair or replacement. Exercise testing is also recommended for asymptomatic patients with MR, again to the anticipated level of sports activity.

For those patients who have undergone operative procedures for valve repair or replacement, the guidelines make the important point that decisions about future participation in sports activities be made together, by both athlete and physician(s).

Task Force 6: Hypertension

The new guidelines recommend that athletes with sustained hypertension undergo screening echocardiography. For those with left ventricular hypertrophy (LVH) beyond what might be expected from “athlete’s heart,” activities should be curtailed until the hypertension is controlled. The guidelines also remind athletes and treating physicians that some medications used for the treatment of hypertension (eg, beta-blockers, diuretics) are considered banned substances by some sports governing bodies. Athletes should be aware that a therapeutic use exemption (TUE) may be required for participation, both outside and during competition.

Task Force 7: Aortic Diseases, including Marfan Syndrome

There was a separate Task Force that reported on the collection of aortic diseases in the new guidelines. In the previous version of the guidelines, these conditions were parceled out among the other task forces. The new organization is helpful because all of the pertinent recommendations can easily be found in one place. Particular mention is made of the importance that aortic size (eg, diameter) be considered in the context of the athlete’s size (eg, age, gender, body surface area). In many circumstances, use of a z-score–the number of standard deviations above/below the mean for a size- or age-specific population–may be more appropriate than absolute measurements alone.

Athletes with Marfan syndrome or any of the other connective tissue disorders that affect the aorta (eg, Loeys-Dietz syndrome, Ehlers-Danlos syndrome, familial thoracic aortic aneurysm and dissection [TAAD] syndrome) should receive frequent reevaluation with echocardiogram, computed tomography (CT), and/or magnetic resonance imaging (MRI). The recommendations regarding safe levels of activity parallel the previous guidelines.

For athletes with bicuspid aortic valve (BAV), the new guidelines focus on z-scores to define the degree of aortic enlargement: not enlarged, z-score < 2; mild enlargement, z-score 2 to 2.5; moderate enlargement, z-score 2.5 to 3.5; severe enlargement, z-score >3.5. Athletes with mild enlargement of the aorta should be confined to low-and moderate-intensity static and dynamic sports that do not have a likelihood of bodily injury. In this group, intense weight training should be avoided. Athletes with moderate enlargement of the aorta should participate in only low-intensity sports that do not have a likelihood of bodily injury. And finally, those with a severely enlarged aorta should not participate in competitive sports.

Task Force 8: Coronary Artery Disease

We think of coronary artery disease (CAD) as a disease of older individuals, but there are sometimes young athletes with acquired diseases of the coronary arteries.

One important aspect of the new guidelines in the area of coronary artery disease is the recommendation that athletes should participate in decisions about safe exercise with their physician(s), taking into consideration the health and psychological benefits of exercise as well as any potential risks. The new guidelines are explicit that asymptomatic athletes with known CAD but with normal LV function and no inducible problems with stress testing should be able to participate fully in their sports. For those who have had myocardial infarction (MI) or coronary revascularization procedure (eg, coronary artery bypass grafting [CABG] or coronary stenting), participation in sports activities should be curtailed for a period of 3 months.

A new section is devoted to the problem of spontaneous coronary artery dissection, a condition where a tear develops in the inner wall of the coronary artery itself, without warning and seemingly without explanation. The new guidelines recognize that there is not yet sufficient experience and evidence with this problem to formulate specific recommendations, but that it may be reasonable to restrict affected athletes from high-intensity sports.

Also new in these guidelines is a section devoted to heart transplant recipients. The guidelines recognize that for many such patients, participation in sports activities can be safe, especially if there is annual stress testing designed to demonstrate the safety of exercise up to the level of exertion that is anticipated during sports activities.

Task Force 9: Arrhythmias

The section on athletes with arrhythmias is the longest and most complicated section of the new guidelines, in part because there are many different arrhythmias to consider. This is an area where particular expertise on the part of the physician is required to make sound judgments about participation.

The recommendations suggest that athletes with permanent pacemakers can participate fully in sports if there is no limiting underlying heart condition or symptoms. Those who are pacemaker-dependent (ie, require the pacemaker continuously to generate the heartbeat) should avoid sports in which a risk of collision might result in damage to the pacemaker system. All others with a pacemaker should recognize the inherent risks of bodily injury that might also damage the pacemaker.

Atrial fibrillation (AF) deserves special mention because it is so common. For athletes with AF, the new guidelines recommend evaluation that includes thyroid function tests, queries for drug use, an ECG, and an echocardiogram. The new guidelines remind us that athletes with well-tolerated and low-risk AF may participate fully. Those who are taking anticoagulants other than aspirin alone should consider the bleeding risk in deciding which sports activities may be safe. Finally, the new guidelines recognize that catheter ablation for AF might eliminate the need for medications and should be considered in athlete patients.

The new guidelines suggest a similar evaluation for patient with atrial flutter. For this condition, catheter ablation has a high likelihood of success and should be considered.

For athletes with SVT (eg, AV nodal reentry tachycardia, AV reciprocating tachycardia, atrial tachycardia), catheter ablation should be considered.

For athletes with ventricular arrhythmias (eg, premature ventricular contractions [PVC’s], non-sustained ventricular tachycardia [VT], sustained VT, or ventricular fibrillation), careful evaluation for underlying structural heart disease. The algorithms for determining safe levels of exercise are complex and athletes should seek expert guidance.

The new guidelines have a new section on syncope, the problem of blacking out unexpectedly. Athletes with exercise-induced syncope should be excluded from sports activities until a full evaluation is completed. Cardiac causes of syncope can sometimes be life-threatening. If the cause of syncope is determined to be neurally mediated, athletes can resume all sports activities once treatment measures are shown to be effective. If no cause for the syncope can be determined, athletes should not participate in sports activities in which a transient loss of consciousness might result in serious bodily injury.

The final new section relates to athletes who have an implanted internal cardioverter-defibrillator (ICD). The guidelines recommend that the indications for ICD implantation be no different for athletes and non-athletes. In particular, an ICD should not be implanted solely to allow participation in sports. For athletes with an ICD who have no episodes of ventricular arrhythmias that necessitate device defibrillation for a period of 3 months, participation in low-intensity sports activities may be reasonable. Decisions about participation in sports activities with higher degrees of intensity, though, should consider the possibilities of greater likelihood of inappropriate shocks or device dislodgement with contact sports.

Task Force 10: Cardiac Channelopathies

The new guidelines include the recommendations from a new Task Force devoted to the cardiac channelopathies. These disorders are typically characterized by a structurally normal heart but a predisposition to develop syncope, seizures, or cardiac arrest from VT or VF. At a cellular level, these disorders are caused by abnormalities in various ion channels in cardiac muscle cells that ordinarily permit the coordinated ebb and flow of charged ions with each heartbeat. Approximately 1 per 1,000 individuals is affected by such conditions. The most common types are long QT syndrome (LQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT), Brugada syndrome (BrS), early repolarization syndrome, short QT syndrome, and possibly idiopathic VF.

Historically, athletes with any channelopathy have been restricted from sports activities of all types because of the potential risk of sudden death. Since the 2005 guidelines, though, much has been learned about the genetics, clinical manifestations, and course of these disorders. It is now thought that some affected athletes may participate safely in sports activities. The key, though, is careful evaluation by a cardiologist who specializes in heart rhythm disorders or by a genetic cardiologist.

Task Force 11: Drugs and Performance Enhancing Substances

Not surprisingly, the guidelines contain the recommendation that athletes meet their nutritional needs through a healthy, balanced diet without dietary supplements. The guidelines further recommend that the use of performance-enhancing drugs (PEDs) and supplements be prohibited by schools, universities, and other sponsoring organizations as a condition for participation. The guidelines suggest the use of the principle of “unreasonable risk” (the potential for risk in the absence of defined benefit) as the standard for banning or recommending avoidance of substances being evaluated for use by athletes.

Importantly, the guidelines recommend that athletes receive formal education about the potential risks of PEDs and supplements, including the specific risks of sudden death and acute myocardial infarction.

Task Force 12: Emergency Action Plans, CPR, AED’s

The new guidelines include the recommendation that schools and other organizations that host athletic events have an emergency action plan that includes provision of basic life support (BLS), the use of an automatic external defibrillator (AED), and activation of the emergency medical system (EMS). Coaches and athletic trainers should be trained in CPR and the use of an AED and the AED should be available within 5 minutes, if needed.

Task Force 13: Commotio Cordis

Commotio cordis is an unusual event, but t is important for coaches, athletes, and officials to be aware of this possibility and be prepared to respond to a lifeless victim. Prompt initiation of bystander CPR and early defibrillation are the keys to survival.

Task Force 14: Sickle Cell Trait

A section devoted to sickle cell trait (SCT) is included in the new guidelines. Although athletes with SCT may participate fully in their sports, the guidelines recommend strategies such as adequate rest and hydration to reduce the likelihood of an event occurring during sports participation. This risk is greatest during periods of high environmental temperature or extreme altitude.

Task Force 15: Legal Aspects

The section of the new guidelines devoted to legal aspects considers the various conflicts that may arise when the guidelines are put into practice.

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Laurent Vidal, Elite Triathlete 1984-2015

November 15, 2015 By Larry Creswell, MD Leave a Comment

The very sad news came this week that retired French elite triathlete, Laurent Vidal, died in his sleep at his home in southern France.

There has been a worldwide outpouring of emotion. I particularly enjoyed this video.

Life-threatening heart problems are unusual in Olympic-caliber athletes, but Vidal suffered an episode of cardiac arrest at the swimming pool last spring. I wrote about that episode and his remarkable recovery in a blog post that focused on cardiac arrest, more generally.

After his recovery, Vidal shared very little about his diagnostic evaluation, any conditions that were discovered, and any implications regarding his prognosis. He immediately retired from the sport of triathlon, though, and I suspect that he was advised that continued participation posed some danger. He remained physically active over these past months, though, and often shared pictures of himself bicycling or hiking. Media reports this week mention a pacemaker and I wonder if he actually received an internal cardioverter-defibrillator (ICD) for “secondary prevention” in case of a repeat episode of cardiac arrest. Unfortunately, even an ICD doesn’t guarantee long-term survival in situations like this. It’s worth reflecting that Vidal’s first indication of a potential problem was a couple years earlier, when he had an episode of syncope, or fainting. That’s an important problem to get sorted out.

Vidal’s story surely reminds us that life is sometimes too short. The remembrances on social media this week speak to the way that Vidal embraced life. I wish I’d had the chance to meet Vidal. I’ll always remember his smiling face.

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Thoughts on the Recent VeloNews Article

September 1, 2015 By Larry Creswell, MD 3 Comments

I enjoyed reading a recent article in VeloNews by Chris Case, entitled “Cycling to Extremes: Are endurance athletes hurting their hearts by repeatedly pushing beyond what is normal?” The article is good reading.

First, I give a lot of credit to Chris Case and the editors at VeloNews. It’s great that a publication with such a broad audience would devote time and space to the issue of heart health and endurance sport. In recent months, they’ve also brought attention to the heart problems of pro cyclists, Robert Gesink, Olivier Kaisen, and Eddy Merckx. I wish that other writers and publications would do the same.

I also thank Lennard Zinn and Mike Endicott for sharing their personal stories with their heart problems. It would be very easy to keep quiet. I very much enjoy reading personal accounts such as these. Their stories are real and also familiar. This is how we learn.

Since the article was published, I’ve gotten a bunch of inquiries asking my opinion about the article in general or about specific information that was presented. Let me share a few thoughts that may be helpful to readers here at the blog….

Don’t be scared (too much)! For most people, cycling is a healthy pursuit. In general, exercise is healthy and provides a myriad of benefits. So don’t stop cycling! It’s important to keep in mind that the stories of Zinn and Endicott are not the norm, even among veteran endurance athletes. Zinn’s multifocal atrial tachycardia (MAT) is one of the least common atrial arrhythmias and Endicott’s sudden cardiac death is rare. As you absorb their stories, focus not on the particular arrhythmias but rather on the possibility that an arrhythmia–any arrhythmia–can cause significant problems or be an indication that things are amiss with the heart. In that sense, their stories should cause you to put on your thinking cap.

My favorite quote from the article? “But fit for racing doesn’t necessarily equal healthy.” Readers here at the blog will know that I’ve said this repeatedly. It’s easy for seemingly healthy endurance athletes, particularly men, to believe that fitness is the same thing as healthiness. This isn’t necessarily true. To dispel the myth, I’ve shared the stories of many elite endurance athletes who’ve struggled with heart problems of various sorts. We can add Zinn and Endicott to these lists. Heart problems are common….and athletes aren’t exempt. This is the most important take-home message from the article.

Arrhythmias are common–in athletes and non-athletes, alike. All athletes experience arrhythmias. Infrequent premature beats, originating in either the atrium (premature atrial contractions, or PAC’s) or in the ventricles (premature ventricular contractions, or PVC’s) most likely have no consequence. Sustained arrhythmias, on the other hand, deserve attention and evaluation. There are far too many varieties of arrhythmias to consider here, other than to mention some of their names: SVT, or supraventricular tachycardia; WPW, or Wolff-Parkinson-White syndrome; atrioventricular (AV) nodal re-entry tachycardia; atrial or ventricular bigeminy; sick sinus syndrome; sinus bradycardia; atrial fibrillation (AF); atrial tachycardia; MAT; ventricular tachycardia (VT); and ventricular fibrillation (VF).

The last part of the VeloNews article alludes to AF. Other than sinus bradycardia (simply a heart rate slower than 60 beats per minute, which may be very healthy in athletes) or innocuous premature beats, AF is probably the most common arrhythmia in athletes. We know from longitudinal studies that the lifetime risk of having AF is approximately 25% in the general population. The question of whether athletes–and endurance athletes, specifically–are more prone to AF is a current controversy, with important implications for long-term endurance athletes. I’ll try to finish up a separate blog post that summarizes the accumulated evidence on this issue. For men, there may be an association with long-term exercise and the prevalence of AF, but there is certainly no consensus among experts. For women, the evidence does not suggest an association between long-term exercise and AF.

Pay attention to warning signs. I particularly like the last section of the article, written by Dr. John Mandrola. He’s a cardiologist who specializes in arrhythmias and who is also a (former?) triathlete and current avid cyclist. He provides good advice in the Q&A. I like to talk about 5 important warning signs of possible heart disease: chest pain or discomfort, especially during exercise; unexplained shortness of breath; light-headedness or blacking out (syncope), especially during exercise; unexplained fatigue; and palpitations–the sense of a rapid or irregular heartbeat. Any of these warning signs may be due to an arrhythmia. All deserve investigation. Dr. John makes the apt point that, very often, heart rhythm problems start off small and get worse with time. Not surprisingly, it’s best to get things sorted out earlier rather than later.

Less may be more. Lastly, I would encourage athletes with identified arrhythmias to be open to the idea that less exercise may be helpful. In fact, this may be the most appropriate prescription. For the long-term endurance athlete, this can be difficult to accept. In this regard, the stories of Zinn and Endicott are particularly poignant.

2. Atrial Fibrillation in Athletes (in a Nutshell)

3. Too Much Exercise, Revisited

4. Don’t Stop Running Yet!

Triathlon, Open Water Swimming, and the Heart: What Can We Learn From Dolphins and Seals?

March 16, 2015 By Larry Creswell, MD Leave a Comment

A recent study about marine mammals caught my eye. I don’t know much about non-human biology and physiology, but this study on dolphins and seals may shed some light on the problem of fatalities during open water swimming or triathlon events.

The Study

A group of investigators headed by Terrie Williams from the University of California at Santa Cruz shared their report, “Exercise at depth alters bradycardia and incidence of cardiac anomalies in deep-diving marine mammals” in the January 16th edition of Nature Communications (1).

This group of investigators has been interested in the physiology of the so-called “dive response” in marine mammals. This is a response that is governed by the involuntary, or autonomic, nervous system, which has two antagonistic components: the parasympathetic nervous system and the sympathetic nervous system. As a group, the marine mammals depend on feeding by chasing pray to depths that can range up to 3,000 m. Even at lesser depths, these mammals must maintain a breath-hold under large hydrostatic pressures while they undergo extreme exertion to catch their pray. During a dive, breath-holding stimulates the parasympathetic nervous system to slow the heart rate (producing bradycardia). At the same time, the exertion required to chase pray stimulates the sympathetic nervous system, producing an increase in the heart rate. The current study offers the first detailed study of the interplay between the components of the autonomic nervous system during routine diving and feeding activity in these animals.

The investigators created an electrocardiograph-accelerometer depth monitor that was deployed on 10 Atlantic bottle-nosed dolphins and 3 Weddell seals. This device allowed high-fidelity recording of the heart rate, ECG, water depth, and swimming stroke frequency (a measure of exertion) during dives. For the dolphins, measurements were made for 74 dives to depths of up to 210 m. For the seals, measurements were made for 91 dives to depths of up to 390 m.

The Results

As expected, there was a strong relationship between diving depth and heart rate for both species, with heart rates falling during descent and reaching a minimum at the lowest depth of the dive. Superimposed on this effect was an additional effect of exertion. For the dolphins, the maximum heart rate was 1.7 to 3.7 times greater during periods of extreme exercise compared to gliding alone. For the seals, the maximum heart rate was 1.5 to 1.8 times greater during periods of extreme exercise compared to gliding alone.

The surprising finding was that cardiac arrhythmias occurred in more than 73% of the dives. The investigators defined arrhythmias to include ectopic beats or significantly increased variability in the interbeat interval (IBI). There were apparently no sustained or fatal arrhythmias., but there were discrete examples of “wandering pacemaker” and ventricular premature beats. In the Weddell seals, there were often patterns of alternating periods of tachycardia (fast heart rate) and bradycardia (low heart rate) during periods of constant, intense exertion.

The presence of cardiac arrhythmias was strongly correlated with increased depth of dive (parasympathetic activation) and increased exertion (sympathetic activation). As an example, cardiac arrhythmias occurred in 81% of the dolphin dives to >210 m but in only 26% of dives to <100 m.

The authors concluded that our previous understanding of the dive reflex in marine mammals was not totally correct. Given that these animals depend on diving for their food sources, the development of cardiac arrhythmias during feeding appears to be mal-adaptive. In fact, feeding might actually be dangerous.

My Thoughts

At first glance, the physiology of the diving response of dolphins and seals during feeding seems far afield from open water swimming and triathlon. And moreover, we already know about the development of cardiac arrhythmias during submersion in breath-holding humans as well as other marine species. The important observation here, though, is what I might call “irritability” or “instability” in the heart rhythm during periods of intense parasympathetic and intense sympathetic activation….and that’s the possible link to human fatalities during open water swimming or triathlon.

We know from autopsy reports of triathletes who’ve died during the swim portion of an event that there are sometimes only subtle abnormalities of the heart, and often nothing that seems explanatory. That leaves us in a difficult position to explain such deaths. In a previous blog post, I wrote about one very plausible hypothesis. Two UK physiologist,s X and X, proposed the concept of “autonomic conflict,” where a surge in both the parasympathetic and sympathetic stimulation of the heart might lead to a fatal arrhythmia. I’ve been intrigued with this hypothesis because it seems to fit many of the observations made about the swim victims. It is easy to see where exertion, cold water, anxiety, etc. might lead to strong sympathetic activation. And it’s equally easy to see where facial wetting, water entering the mouth/hypopharynx/nasopharynx, and breath-holding, even without diving, might lead to strong parasympathetic activation. In that instant, in an athlete with some sort of susceptible heart, a fatal arrhythmia might occur.

The new observations about the dolphins and seals seem to play into this hypothesis.

2. Triathlon Fatalities: 2013 in Review

Reference:

1. Williams TM, Fuirman LA, Kendall T, et al. Exercise at depth alters bradycardia and incidence of cardiac anomalies in deep-diving marine mammals. Nature Communications 2015;6:6055.