It starts innocently. You go for a jog, and you get out of breath a little bit sooner. But it starts getting worse.
Soon, you get winded on a walk to the train station; Then on a walk to the kitchen.
Eventually, your heart pounds away furiously in your chest as you sit idly. Working as hard as it can, your heart simply can’t pump enough blood for your body.
It’s called congestive heart failure, and it affects 5 million people each year in the United States — killing 53,000 of them. It’s one of the most painful diseases you can have and it’s affecting more and more people each year, said Oak Parker Pieter de Tombe.
“Suffering is high, because you’re constantly fatigued,” de Tombe said. “Finally you’ll be sitting on a chair panting, and ultimately, you will die.”
But at the labs of Loyola University in Maywood, de Tombe is working on finding a cure — and he might be close.
The problem during heart failure is that the heart just doesn’t pump as much blood as it should — towards the end, as little as 20 percent of its original capacity.
That’s because the heart’s muscle cells are simply worn out, and don’t compress as much as they used to. So with less blood being pushed out with each pump, the heart works harder and harder. Eventually, it wears out.
The only real treatment right now is a short-term fix via medication or a full-on heart transplant — the latter of which is nearly impossible to come by.
But de Tombe has figured out just why those heart cells stop working, and he’s hoping to create a new solution.
He’s found a group of proteins that appear to be single-handedly responsible for breaking down the cells in sick hearts.
Since failure often happens in weakened hearts after an attack, de Tombe and his team started testing rats. The team gave the rats heart attacks, then monitored them as they developed heart failure.
“They get all the symptoms people have,” de Tombe said. “We found that the same molecule that’s active in the human heart is also in the rat heart.”
Under a microscope, they tried something different with a piece of heart tissue — replacing those damaging proteins from a diseased heart with fresh ones from a healthy heart.
Almost instantly, the heart’s cell was rejuvenated.
So while they have a small-sized solution, there’s no way they’d be able to create enough fresh proteins for that to be an effective cure. Instead, de Tombe’s current goal is to create a drug that can just block those heart-hurting proteins altogether.
“The drugs we use now are not very effective,” de Tombe said. “We’re doing our damndest.”
Scientist of the Year
De Tombe’s groundbreaking work in heart research, as well as his leadership as chair of Loyola’s physiology department, led the university to name him senior scientist of the year last month.
“There’s no more deserving scientist on our campus, anywhere,” said Richard Kennedy, Loyola’s head dean of research. “He’s working in an area where many people suffer and there aren’t really effective treatments. He may have one of the best chances of providing help.”
Kennedy, himself a heart researcher, has been a fan of de Tombe’s for some time.
“I was aware of his research for many, many years before he got here,” Kennedy said. “As soon as I saw his application to be chair of our physiology department, I called him up and interviewed him immediately.”
De Tombe took a long route to Loyola, though. Born in the Netherlands, he started his career as a chemist, and just happened to get his first job in a biochemistry lab working on the heart.
At a lab he was working at in the Netherlands, he caught a break: a colleague was moving to Canada, where he was starting a new lab. Young de Tombe took the opportunity and crossed the ocean to join the new lab at the University of Calgary.
It was there that he found luck and happiness — two things that share the same word in Dutch — in his wife-to-be, Anna Tyberg. As the daughter of an American researcher also working at Calgary, he found the perfect partner.
“I’m married to the daughter of a scientist who isn’t a scientist, which is actually quite nice,” de Tombe said. “She understands how my world functions without actually being a part of it.”
After stints in Baltimore and North Carolina, they moved to Oak Park in 1996 when de Tombe got recruited by the University of Illinois at Chicago.
They bought a home in the Oak Park Arts District near Harrison Street, where de Tombe could just hop on the Blue Line in the morning and go straight to work, and their two sons could walk to Longfellow School. His wife could bike around town, and the family only needed one car.
Today, de Tombe has to drive to work — Loyola’s not quite so simple to get to by public transit — and his sons both attend Oak Park and River Forest High School.
“We moved to Oak Park because we were attracted by all the things that everybody likes: The schools, its progressive nature,” de Tombe said. “But the thing that really got us was the involvement of the community.”
Involvement is something that Kennedy said de Tombe is instrumental in at Loyola, as well.
“He’s just one of the most genuinely nice people that I know,” Kennedy said. “He really takes care of his people. He was a treasure for us to find.”