Published by Communications and Public Affairs (519) 824-4120, Ext. 56982 or 53338
July 25, 2003
U of G prof seeking clues to causes of sudden cardiac death
Research by a University of Guelph professor may one day help scientists better understand the mystery of sudden cardiac death, which recently claimed the life of a young Guelph athlete.
John Dawson of the Department of Chemistry and Biochemistry is studying abnormalities in genes for actin – the most abundant protein in the body – which have been directly linked to hypertrophic cardiomyopathy (HCM). HCM causes excessive thickening of the heart muscle without obvious cause and, in rare cases, can lead to sudden cardiac death. “If the heart wall is thickened, it’s not going to pump as much blood, it’s not going to relax as easily, and there is a greater chance of obstruction,” Dawson said.
About one in 500 people has the genetic condition, which is hard to diagnose. For most people, it doesn’t affect duration or quality of life, Dawson said, but in a minority of cases, symptoms can be severe. “It’s the most common heart condition that causes sudden death in athletes.”
Boston Celtic basketball star Reggie Lewis died of a cardiomyopathy heart attack during a pick-up basketball game, and Olympic figure skater Sergei Grinkov collapsed and later died during a routine practice. Most recently, a 22-year-old Guelph man died July 19 while playing in a volleyball tournament. “Athletes’ hearts are already enlarged due to their training, so HCM often isn’t diagnosed until it’s too late,” Dawson said, adding that it’s still unknown whether athletes are at greater risk. “Our research may help lead to better understanding of HCM and, eventually, to the development of ways to treat it in the early stages.”
Dawson is looking at the mutations in actin, trying to find out the deficiencies and how the deficiencies are connected to HCM. The abnormalities have also been linked to dilated cardiomyopathy, one of the other three forms of cardiomyopathy. “Actin is a must in the body, so a mutation can be lethal,” he said.
Actin and myosin – the other protein Dawson studies – are involved in almost every vital process in the body, he said. In muscle cells, they allow contraction and extension through their molecular-scale interactions. In the body, actin assembles into long filaments, forming a track on which myosin runs in muscles. “If actin is the track and myosin the train, if there is something wrong with the track, the amount of force generated by the locomotive is not going to be right.”
As a Natural Sciences and Engineering Research Council (NSERC) post-doctoral fellow at Stanford University, Dawson was the lead author of a study published in the Journal of Biological Chemistry that was the first to reveal the crystal structure of actin filaments. At U of G, his work has been supported by an NSERC Discovery Grant and the Canada Foundation for Innovation’s New Opportunities program, and he is applying for a grant from the Canadian Institutes for Health Research and the Heart and Stroke Foundation for his work on actin mutations in cardiac diseases.
“I hope my research generates knowledge about how different forms of cardiomyopathy develop,” he said. “Understanding the molecular basis behind it could one day lead to the development of drugs that will allow the ‘track-and-train’ interactions to return to normal levels.”
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