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Enlarged Hearts May Be To Blame For Triathlon Swim Deaths

New research sheds light on drownings.

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New research sheds light on drownings

Deaths at triathlons are extremely rare. In 2012, USAT produced an incidents study that calculated the fatality rate at about one in every 76,000 participants. (A similar study found the rate at marathons is about one per 100,000 finishers.) What’s remarkable about triathlon fatalities is more than 72 percent of them happen in the swim, and until now we had little idea why.

Enter new research. At the end of August, Duke University researchers published a study in the journal BMJ Open Sport & Exercise Medicine that suggests left ventricular hypertrophy (LVH), a condition that occurs when the muscle in the heart’s left chamber thickens, ultimately may be to blame because it can predispose those who have it to immersion pulmonary edema.

“IPE is the rapid build-up of fluid and sometimes blood in the lungs during either swimming or scuba diving, in the absence of ingestion of water,” says Dr. Richard Moon, who led the Duke research team. Sometimes described as drowning from the inside, IPE occurs during heavy exertion in cold water, when the body diverts blood from the extremities and moves it towards the core. This can cause high blood pressure in the small capillaries of the lungs, resulting in abnormal leakage of fluid into the alveoli, or air sacs, of the lungs. When IPE occurs, a person experiences difficulty breathing, blood-tinged sputum, confusion, and—in extreme cases—death.

To come to the conclusion that LVH may have caused IPE-related swim deaths, Moon and his team analyzed the autopsy reports from 23 of the 46 swim deaths taking place at triathlon events between 2008 and 2015. They found many of the athletes whose deaths were originally attributed to simple cardiac arrest had LVH.

“We deduced that individuals with cardiac disease, particularly enlargement of the left ventricle (left ventricular hypertrophy, or LVH), are at increased risk of IPE,” says Moon, taking care to point out that LVH is vastly different from athlete’s heart, a mild expansion of the left ventricle caused by training. In other words, the triathletes who died from IPE had significantly enlarged hearts, a structural abnormality not usually associated with exercise.

Moon says a lot more research must be done to firmly establish a link between LVH, IPE, and triathlon swim deaths. If they do, it may ultimately change how doctors screen athletes planning to participate in triathlons. Moon and his team suggest doctors screen for LVH and conditions that may co-occur with LVH, such as hypertension and sleep apnea.

Measures such as Ironman’s SwimSmart, which encourages athletes to take a “proper warm-up prior to the start, preferably in the water” in order to increase circulation is good advice for preventing cardiac arrest, says Moon, but not IPE. “I don’t believe any warm-up strategy will prevent IPE.”

What could: “There is evidence that certain medications can prevent IPE, when taken before a race by susceptible individuals,” Moon says. Viagra and hypertension trug nifedipine might help, but they need more testing before being prescribed for that purpose.

Finally, Moon says, it’s important to note that even LVH screening won’t be able to prevent all swim deaths. “We have observed in our lab that some individuals susceptible to IPE may have completely normal blood pressure and heart function under normal conditions but experience severe blood pressure elevation and heart valve abnormality when exercising in cold water. Methods of identifying such people need to be developed.”