Cardiac Arrhythmia's in Swimmers - Ignorance is Not Bliss

Reprinted from Sports Medicine Bulletin

For at least one Olympic champion this summer, competing was a matter of life and death. Srijita Sen- Chowdhry and William J McKenna explain how heart arrhythmias can affect young athletes.
Of all the success stories emerging from the memorable return of the Olympics to its birthplace this summer, one of the most remarkable is that of 16- year-old American swimmer Dana Vollmer. At the age of 12 Dana was the youngest participant at the 2000 US Olympic trials. Four years later she won a gold medal in Athens as part of the women’s 4 x 200m relay team, which set a new world record. Dana’s accomplishments, noteworthy in themselves, are made more poignant by reports of her complex cardiac history.

From newspaper articles available at www.danavollmer.com, it appears that Dana’s cardiac problems began two years ago, when she noticed abrupt surges in her heart rate to 250 beats per minute during training. The tachycardia would last up to five minutes before resolving spontaneously. Since the episodes were erratic and relatively infrequent, a wait-and-watch approach was initially adopted. This continued, even when Dana developed symptoms of impaired consciousness while exercising. During one training session, her vision ‘went black’ several times (‘pre-syncope’), although she did not actually pass out (‘syncope’). The pre-syncopal symptoms did not return, but the tachycardias continued, and a cardiac opinion was eventually sought.

The diagnostic work-up at this stage would typically have included a 12-lead electrocardiogram (ECG), two-dimensional echocardiogram (2D echo), exercise testing and ambulatory ECG monitoring. The latter apparently demonstrated QT intervals exceeding 500 milliseconds. The QT interval is a measure of the time it takes for the ventricles of the heart to both depolarise (contract) and repolarise (relax). In normal subjects, the QT interval after correcting for heart rate is usually less than 440 milliseconds. The possibility of ‘long QT syndrome’ was therefore raised.

Her tachycardias, however, appeared to be due to an additional problem: an ‘extra electrical pathway’, to use Dana’s own words, for which she underwent radio-frequency ablation, the same procedure recently performed on Tony Blair, the British prime minister.

Although Dana’s tachycardias have not recurred, the QT prolongation is likely to persist. Long QT syndrome is a recognised cause of sudden cardiac death in young people and Dana was offered an implantable cardioverter-defibrillator (ICD). Her family declined, opting instead to carry a portable defibrillator, which is on hand during all competitive events.

Arrhythmia symptoms

Dana’s story raises a number of issues relevant to sports physicians. The first is the need to investigate symptoms suggestive of arrhythmia. Atypical chest pain and mild breathlessness are common complaints, the significance of which is often difficult to determine in a population engaging in extreme physical exertion.

However, most athletes will be accustomed to the sensation of their heart rates increasing normally during exercise. The perception of palpitation in an athlete therefore merits further investigation, particularly when sudden increases in the heart rate have been noticed, as in Dana’s case.
Exercise-related syncope is the most ominous presentation. It has been suggested that syncope is the same thing as sudden death, except that you wake up⁽¹⁾; an investigative approach based on this premise is recommended in athletes. Further participation in competitive sports should be discouraged until a thorough cardiac evaluation has been performed and the athlete cleared of any possibility of arrhythmia.

Light-headedness, as opposed to blackout, is a less specific symptom. Stimulation of the sympathetic nervous system, muscle activity and decreased intrathoracic pressure all contribute to increased venous return during exercise. An abrupt stop after vigorous exercise may well cause venous pooling, hypotension and a light-headed sensation. Thus, while dizziness and a fall in blood pressure during recovery may be physiological (and ‘normal’), pre-syncopal symptoms during exercise justify concern, particularly in experienced athletes.

Types of arrhythmia

Important causes of palpitation and syncope in athletes include heart muscle diseases, mitral valve prolapse, inherited arrhythmogenic disorders and pre-excitation. Most of these diseases have a genetic basis, reinforcing the importance of obtaining a complete family history. Anomalies in the origin or anatomical course of the coronary arteries should also be considered in an athlete with exertional chest pain and/or collapse.

Notable among the heart muscle diseases are hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC), which frequently present with symptoms of arrhythmia. Sudden death may be the first clinical manifestation of both diseases, leading some authorities to advocate preparticipation screening of all athletes. Dilated cardiomyopathy (DCM) is more characteristically associated with symptoms of heart failure such as breathlessness and reduced exercise capacity; arrhythmia and sudden death are recognised complications, but seldom the mode of presentation.

Long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia fall under the collective term of inherited arrhythmogenic disorders. All have the capacity to produce malignant ventricular tachyarrhythmia (rapid, dangerous disturbances of the heart rhythm) in a structurally normal heart. Disease-causing mutations have been identified in the cellular channels, receptors, and binding proteins that regulate ion flow⁽²⁾.

Finally, pre-excitation arises when there is an extra (‘accessory’) electrical pathway within the heart that bypasses the normal conduction system. The atrial impulse is transmitted along this accessory pathway, and prematurely activates the pumping of the ventricle. The pathway may occur at several possible locations, each producing its own distinctive syndrome. Pre-excitation is associated with supraventricular tachycardia (SVT) and atrial fibrillation with a rapid ventricular response rate.
In Dana’s case the history is suggestive of recurrent SVT secondary to pre-excitation, which is frequently cured by burning off the accessory pathway with radiofrequency ablation. At present there is no established link between preexcitation and the other possible diagnosis of long QT syndrome.
Long QT syndrome is characterised by prolonged repolarisation and a predisposition to ‘torsades de pointes’, a form of polymorphic ventricular tachycardia. There are several subtypes of long QT syndrome, related to the specific gene affected; exercise-induced arrhythmia occurs in LQT1 and to a lesser extent in LQT2⁽³⁾. Swimming and diving are prominent triggers for arrhythmic events in LQT1.
Patients with long QT syndrome are discouraged from participating in competitive sports. However, establishing the diagnosis is far from straightforward, even with molecular genetic analysis. While isolation of a known long QT mutation is confirmatory, at least half of all patients will have defects in genes that have yet to be identified; hence a negative result does not rule out the disease. Clinical diagnosis is challenging because ECG findings may be non-specific and paroxysmal; risk stratification has yet to be fully defined⁽⁴⁾.

The diagnostic difficulties are not confined to long QT syndrome, underscoring the importance of referring athletes with suspected cardiac disease to a cardiologist. Abnormalities are frequently subtle or absent in early ARVC, but patients may nevertheless be at risk of sudden death, particularly during highly strenuous activity⁽⁵⁾. Furthermore, cardiac investigations may be difficult to interpret in elite athletes because of physiological adaptations to training, such as mild left ventricular hypertrophy and ventricular dilation⁽⁶⁾.

However, sustained arrhythmia, frequent ventricular premature beats, and repolarisation abnormalities on the ECG warrant concern^(7,8), in spite of previous controversies regarding their significance^(9,10).

Treatment and management

Management of the athlete with cardiac disease is equally problematic. The clinician is always tempted to play it safe in such instances, discouraging participation in competitive sports and endurance training, and instituting prophylactic treatment whenever there is a perception of increased risk. Athletes are understandably reluctant to relinquish the aspirations and investment of a lifetime. The stakes are even higher for professional sportspeople, in whom a cardiac diagnosis will threaten career and livelihood.
Unfortunately the therapeutic options may be as unpalatable to the athlete as the advice to withdraw from organised sports. Adrenaline appears to precipitate arrhythmia in many of these disorders, notably LQT1, ARVC, and catecholaminergic polymorphic VT. Consequently, the mainstay of medical therapy in these diseases is a class of drug known as betablockers, which counteract the action of adrenaline on the heart. Beta-blockers, however, have the side effect of limiting exercise capacity and performance.

The ICD is the most effective means of preventing sudden death. It has two main components: the pulse generator, containing the battery and complex electrical circuitry; and the wires (‘leads’) that connect it to the heart. The generator is implanted beneath the collarbone, and the leads are inserted through a nearby vein. The device constantly monitors the heart rhythm. On sensing a dangerous arrhythmia, it attempts to pace or shock the heart back into a normal rhythm.

Although ICDs have the potential to be life-saving, their psychosocial impact may be considerable in young patients, and the likelihood of lead-related complications increases over extended treatment periods.

Furthermore, the ICD is incompatible with contact sports because of the potential for blunt trauma and damage to the device. In spite of enhanced sensing algorithms in the new generation of ICDs, the high heart rates attained by athletes increase the likelihood of inappropriate discharge, the delivery of an unnecessary and occasionally dangerous shock to the heart.

Management of athletes with arrhythmia is therefore tailored according to the overall risk profile, tolerance for therapy and individual preference. While the clinician can advise and educate, it is the athlete who must decide whether to undergo evaluation, discontinue high-level activity and accept treatment.

The importance of patient autonomy is perhaps best illustrated by Dana Vollmer’s comment: ‘I basically said that I would rather die swimming than not do it at all.’

This attitude is probably not surprising to marathon and higher level masters swimmers.

Fatal Arrhythmias in Open Water Swimming

Fatal Arrhythmia's in Open Water Swimming: What's the Mechanism?

Reprinted from Lawrence L. Creswell, M.D.

Introduction by Don Macdonald: I recently had a sudden cardiac event, collapsed, received life saving help immediately and found to have arrhythmia problems perhaps brought on by exercise, Well I survived and now find myself with an implanted ICD to prevent such future events. I was running, which I jokingly say was the problem, instead of swimming. I think ICD stands for "I Can't Die".

However my experience now takes me down a path relatively untraveled since only about 1% of such incidents leave survivor's. So onto the next chapter of my swimming journey just One Stroke At A Time.

Cardiac rehab has me exercising already and I am hopeful to return to the pool in the near future.

We've talked previously here at the blog about the general issue of sports-related sudden cardiac death (SCD).  And we've also talked about the specific issue of swimming fatalities during triathlons and open water swims.

But what triggers a sudden, fatal arrhythmia during open water swimming?

The answer isn't known and perhaps it will never be known with certainty.  But a recent report from a group of scientists in the U.K., though, suggests a very plausible mechanism.  Their idea is worth considering.


What's been learned from studies on runners?

As I've mentioned previously here at the blog, sports-related SCD has been best studied in the setting of long-distance running events.  Last year, Dr. Kim and colleagues in Boston reported on a decade-long study of runners with race-related SCD [1].  These investigators found that fatalities during marathons are not distributed uniformly along the race distance.  Instead, they predominate during the final 3 miles or so.  And interestingly, fatalities during half marathon events also predominate during the closing miles.  But why?

In the running population, we know from autopsy studies that the majority of victims have some sort of (often previously unknown) heart disease.  And something happens during the closing miles of the race.  In the words of the investigators, their "findings suggest that demand ischemia (i.e., ischemia due to an imbalance between oxygen supply and demand) may be operative in exercise-related acute coronary events during long-distance running races."  The leading hypothesis is that this mismatch in blood (or oxygen) supply and demand in the heart occurs when the runner picks up the pace, producing an adrenaline surge and increased physiologic demands on the heart, once the finish line is mentally within sight.

Based on this hypothesis, the International Marathon Medical Directors Association issued an advisory in March, 2010 that recommended, among other things, that athletes "not sprint the last part of the race unless you have practiced this in your training."

The concept here is that a susceptible heart (in a susceptible athlete) is triggered at a particular moment in the race to have a fatal arrhythmia because of a specific trigger.  The surge hypothesis might not explain all running race-related deaths, but is a plausible explanation for the physiology behind the majority of the deaths that occur late in a race.

It's very likely that the same concept is in play in triathlon-related sudden cardiac death.


What's going on in triathlon?

In triathlon, athletes have died at any point during the race--from the first few strokes of the swim through the final strides of the run.  And a couple athletes have collapsed with SCD even a few hours after the finish.  But the majority of deaths have occurred during the swim.  USA Triathlon issued a report last year that summarizes these facts.

What might be the trigger for sudden cardiac arrest during the swim portion of a triathlon?

Recently, two researchers in the U.K.--Michael Shattock and Michael Tipton--have offered a new hypothesis that they have labeled autonomic conflict [2,3]

To understand their hypothesis, we first need to talk for a moment about some features of the heart's physiology.


Sympathetic and Parasympathetic Influences

One component of our nervous system is called the autonomic system.  This portion of the nervous system is involuntary, responding to internal and external stimuli below the level of our consciousness.  The autonomic nervous system has 2 different divisions--the sympathetic and parasympathetic systems.  Each of these divisions can operate independently, often with opposite effects on the body's organs, including the heart.

We often think of the sympathetic nervous system as being excitatory--providing the so-called "fight or flight" response.  When activated, the sympathetic nervous system has several effects on the heart:  an increase in heart rate, vasodilation of the coronary arteries (leading to more blood flow), and increased contractility (contraction strength) of the heart muscle.  And importantly for athletes, activation of the sympathetic nervous system also increases the blood flow to the skeletal muscles, decreases blood flow to the abdominal organs, and opens up the airways of the lungs.

In contrast, the parasympathetic nervous system has an inhibitory effect on the heart, acting to restore a baseline heart rate after sympathetic activation and by slowing electrical conduction in the specialized areas of the heart's electrical system known as the sino-atrial (SA) node and the atrio-ventricular (AV) node.  In well-trained endurance athletes, the parasympathetic nervous system is often highly developed, and is one cause of a very low resting heart rate.


A Hypothesis

Drs. Shattock and Tipton have proposed a mechanism where sudden activation or sudden increase in activation of both the sympathetic and parasympathetic nervous systems can produce a fatal arrhythmia.  This idea is supported by studies in isolated hearts as well as in healthy volunteers.

Let's say that an athlete's heart might be predisposed to an arrhythmia because of one or more anatomic or physiologic conditions such as:  congenital or inherited long QT syndrome, coronary artery disease, myocardial hypertrophy, ischemic heart disease, or pathologic hypertrophy (eg, hypertrophic cardiomyopathy).

During an open water swim, an athlete's sympathetic nervous system is activated because of physical exertion, (relatively) cold water temperature, anxiety, or even anxiety or overcompetitiveness.  The parasympathetic nervous system is activated because of facial wetting, water entering the mouth, nose, and pharynx, and extended breath holding--and particularly so, just at the moment of breaking a breath hold.  At that very moment, there can be maximal parasympathetic activation.

These scientists suggest that this autonomic conflict--between the sympathetic and parasympathetic nervous systems--is what triggers a sudden, potentially fatal arrhythmia.


It's Plausible

This is a plausible hypothesis.  It fits with the observations that have been made on victims of sudden cardiac death during open water swimming.  And it fits with the general concept of a susceptible heart and an arrhythmia trigger that seems to be in play in victims of SCD in other sports.



References

1.  Kim JH et al.  Cardiac arrest during long-distance running races.  N Engl J Med 2012;366:130-140.

2. Shattock MJ, Tipton MJ.  'Autonomic conflict':  a different way todiedu  ring cold water immersion?  J Physiol 2012;590:3219-3230.

3.  Tipton MJ.  Sudden cardiac death during openwater  swimming.  Br J Sports Med 2013. Online in advance.


Related Posts

1. Sports-relatd sudden cardiac death in the general population

2. Athletes, sudden death, and CPR

Stop Seeking and Start Finding: Create a Near-Perfect Life

“What could I say to you that would change your beliefs, except that perhaps you seek too much, that as a result of your seeking you cannot find. Simply put your asking the wrong questions."

'Don Macdonald - motivational speaker, open water marathon swimmer, and cardiac and resilience health advocate'.

I have a confession: I hate slowing down. When I finally let myself stop—being alone with my thoughts, vulnerable and open to the world—I become afraid.

I have another confession: There was a specific time in my life when went through a painful and scary situation. It almost broke me. And the only way I knew how to cope was to get back up. I didn't learn how to do this without years of practice, many failures and successes and good family and friends. 

Although not quite my circumstances, the story below hits the mark dead on.

Simply put: If times were hard, I ran.

I changed schools, moved to different cities, traveled to different countries, and found solace in running, a sport that calls for constant movement. I began seeking specifically for happiness: for the people, the place, and the situation that would help me find the “perfect life.”

I was a seeker who kept looking for happiness and different ways to “become a better person.” I was searching for a new life that would be “perfect” like the lives I saw on college campuses, TV shows, and Facebook feeds.

I believed my old life and my old self weren’t good enough, so I had to create a new life that would allow me to start over.

I pondered getting a Masters in global health, joining a rock band, writing a bestseller, running marathons, making music in West Africa, climbing mountains, and learning how to build lean-to’s.

I was convinced accomplishing any of these things would make me happy, make me feel deserving, and make me whole again.

A couple years passed by, and I slowly began to realize that no matter where I went, what I sought out, and the situations I was in, I was still the same exact person inside.

That’s when I realized if I wanted to find happiness, I had to first understand that the perfect life did not exist, and the acceptance of my past and my imperfections is what creates the near-perfect life. 

Most importantly, I had to find myself again, which meant I had to stop feverishly seeking.

We should all go after the things we want; we should be driven to chase after our dreams, embrace new challenges, and go on new adventures. But seeking often means deliberately searching for something that isn’t always meant to be there, or to simply run away from something that can truthfully never escape you.

By being too tunnel-visioned and too set on a goal—landing the “perfect” job, finding the “perfect partner,” or making the “perfect” group of friends—you may miss out on the less-obvious scenarios that are intended to fill your near-perfect life.

When on your journey to stop seeking, start finding, and create a life where you are whole-hearted, fulfilled, and accepting, take note of these tips:

Accept who you are. 

Know that your core self, and your emotions, outlook, and attitude, will follow you everywhere, no matter what situation you are in. Recognizing the beautiful and imperfect person you are is the first step towards accepting new challenges and allowing new experiences into your life.

Give yourself options. 

You may really want one thing—a specific job, a house in a certain part of the country, or certain fame or fortune. But if one of your dreams doesn’t come into fruition, maybe this means that another bigger and better dream is waiting for you. Don’t get discouraged, and allow yourself to be open.

Be vulnerable. 

Invite fear, uncertainty, and imperfection into your life. Once you fully open yourself up to the universe, it will allow you to see the incredible number of options for you, and let you try new things to help create the near-perfect life.

Meditate.  

Use meditation as a way to be with nothing but your present self. This helps you to slow down and stop seeking, to really get to know your true self and what you feel, want, and need.

Try again.  

Things don’t fall into place right away. There will be ten hardships before one celebration. Don’t give up. Be patient.

Don’t be stagnant.  

None of these tips mean you should stop moving completely and wait for life to work itself out on its own. Rather, it’s about finding a balance between learning what you want and inviting new opportunities, while recognizing that how you react to life’s situations is in your hands.

After nearly ten years of seeking, I found my near-perfect life in New York City, the one place I had once swore I’d never move to. I found an apartment with an old friend, and we rekindled a friendship from nearly five years prior. I discovered a support system of friends and family who were always there for me, and one company of hundreds I applied to hired me.

My time in New York has helped me uncover the happy spirit that was always within me—the spirit that once was simply too tired from my constant seeking to spread its light.

I’m still not very good at slowing down. I’m happiest when moving, when constantly trying to reach that next tier. But I’m also trying to slow down and breathe—to stop seeking for “better” and start finding myself, allowing my near-perfect life to meet me halfway.

Reprinted from Laura Schwecherl

Endurance Athletes - Nutrition Matters and corn products are not healthy for you long term

Corn is not a vegetable

Reprinted from The natural nutritionist

Endurance Athletes, pay attention to what you are eating as 'false' energy from corn products can adversely affect your cardiovascular system, causing inflammation long term. As an endurance athlete we eat lots of food but processed foods such as GU gels, snack bars, Gatorade, smoothies, the list goes on and on...carry very poor nutritrients and for some of us with genetic family traits, this can be harmful long term.

Parents, with kids in school and athletics. Please engage with your school and coaches to learn exactly what your kids are being fed. 

Just like peanuts are legumes and not nuts, corn is a grain, not a vegetable. But (whole)grains are good for me aren’t they? No. 

The truth is that we’ve been fed that lie to support industry. (Just like how the food pyramid was created by the agricultural industry!) Corn in particular, is the perfect industrial crop. According to Toby A.A. Heaps, author of The Killer Kernel, it has an abundant source of cheap interchangeable calories, and with a large amount of fertilizer, can be grown rapidly and predictably often on a one-person, one-machine farm enterprise.

Before I continue, let me get one thing straight. I’m not talking about the occasional corn on the cob at your family barbecue, but rather the reliance on corn as an every day food. Cornflakes for breakfast. Corn cakes and Vegemite as your afternoon snack. Cornbread. Corn starch, a common gluten free substitution; often found in low-fat products. ANYTHING containing high fructose corn syrup (HFCS). It’s simply not real food. All you are doing is jumping on the blood sugar-insulin roller coaster, which leads to chronic hunger, energy peaks and troughs, and the all-too-common 3.30-it is. Significantly, chronically elevated insulin levels are the enemy to sustainable weight loss, lean muscle mass development and weight maintenance.

Why corn is not part of my daily food pyramid

1. Corn is a sugary, starchy, low-nutrient grain.
2. While gluten is by far the worst culprit, grains can still be inflammatory and are high in phytic acid, substances that can inhibit nutrient absorption. The problem with high levels of phytate is mostly relevant when gut health is sub-optimal, and the overall nutrition is deficient in micro nutrients and essential food sources. Something you will definitely need to consider if you have been following our traditional food pyramid.
3. The over consumption of grains decreases the release of our major digestive and satiety hormone cholecystokinin, or CCK.  This is known to be one of the major causes of insulin resistance, the precursor to obesity.
4. There is not a single nutrient, vitamin or mineral present in grains that you cannot obtain from natural, wholefoods.
5. Corn is used to fatten pigs, cows and other livestock, and is the key ingredient in HFCS, the leading cause of obesity in America. Enough said?

Is corn GMO?

Overseas, corn, otherwise known as maize, is genetically modified (GM) for greater resistance to pests and viruses, higher nutritional value and longer shelf life. In Australia, imported GM corn is predominately used as cattle feed and thankfully, has not been approved for farming. 

However, GM corn may have entered our market through imported foods like bread and cereals, corn chips, gravy mixes and sports drinks. Avoid these products like the plague.

On a positive note, before any of these products are sold in Australia, they are checked for safety by Food Standards Australia and New Zealand (FSANZ). According to Australia’s Chief Scientist, the law in Australia requires that food labels must show if food has been GM, or contains GM ingredients, or whether GM additives or processing aids remain in the final food product. Please avoid GM foods, but that’s another story all together.

The moral of the story?

There are far better choices than corn. Focus on nutrient dense, real food. And if you do buy food products with a label, read them carefully. 

References

Genetically Modified Foods. Food Standards Australia and New Zealand. Available: http://www.foodstandards.gov.au/consumerinformation/gmfoods/.

Genetically modified food explained. Australia’s Chief Scientist. Available: http://www.chiefscientist.gov.au/2011/11/genetically-modified-food-explained/.

Haros M, Bielecka M, Honke J, & Sanz Y. (2007). Myo-inositol hexakisphosphate degradation by Bifidobacterium infantis ATCC 15697. International Journal of Food Microbiology, 117(1), 76-84.

Heaps TAA. The Killer Kernal. Corporate Knights. Available: http://www.corporateknights.com/article/killer-kernel.