THURSDAY, Jan. 21, 2016 (HealthDay News) -- A century ago, British explorer Sir Ernest Shackleton was a key figure in the race to explore Antarctica. Now, two expert physicians believe he may have done so while battling a hidden foe: a congenital heart defect.
Shackleton made the first crossing of the mountains and glaciers on the island of South Georgia without any health problems, but suffered repeated bouts of breathlessness and weakness on subsequent Antarctic expeditions.
The physical problems that plagued Shackleton have long been a mystery, however. In an attempt to solve it, retired anesthetist Dr. Ian Calder and consultant cardiologist Dr. Jan Till studied documents held at the Scott Polar Research Institute in Cambridge, England.
The researchers concluded that Shackleton was born with a hole in his heart -- an atrial septal defect. The two experts published their theory online recently in the Journal of the Royal Society of Medicine.
"The evidence rests in diary entries made by Dr. Eric Marshall, the medical officer of Shackleton's second expedition to the Antarctic in 1907-1909," Calder said in a journal news release. "The detection and treatment of an atrial septal defect is now reasonably straightforward, but was not available to Shackleton."
Shackleton likely knew there was something wrong with his heart because he refused to be examined by doctors -- who might have then tried to stop him from going to Antarctica, Calder and Till suggested.
"Some may feel that Sir Ernest was irresponsible in undertaking the leadership of Antarctic expeditions if he suspected a problem, but to paraphrase Dr. [Samuel] Johnson, there is seldom a shortage of prudent people, whilst the great things are done by those who are prepared to take a risk," Calder said.
In the race to be the first to the South Pole, Shackleton lost to Roald Amundsen in December 1911. Shackleton died of a heart attack while on his fourth Antarctic expedition in 1922 at age 47.
The U.S. National Heart, Lung, and Blood Institute has more about "hole in the heart" defects.
SOURCE: Journal of the Royal Society of Medicine, news release, Jan. 18, 2016
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