The human heart beats, on average, 75 times a minute.
For a person with a 75-year lifespan, that amounts to nearly 3 billion heartbeats. Quite an impressive organ.
Cardiovascular scientist Steven R. Houser, 70, has been intrigued with the heart for decades. Along with the brain, he deems it “the most important organ we have.”
Cut off a finger, and you’ll live. Lose some liver cells, and they’ll grow back. But “if your heart is sick, it has unbelievable consequences on your life.”
Among numerous positions at Temple University’s Lewis Katz School of Medicine, Houser is professor of cardiovascular sciences and medicine and director of the Cardiovascular Research Center.
But he still has time to volunteer. Recently, he was named the 2021 recipient of the American Heart Association’s highest volunteer honor, the Golden Heart Award, for his 35-plus years of volunteering for the association.
He spoke to us recently about how our understanding of the human heart — and our ability to treat it — has evolved.
When you first joined the AHA more than 35 years ago, what was the status of detecting and treating heart disease?
Diseases of our arteries are still very prevalent in our society. They can get clogged. They can get stiff. Blood has trouble going through them.
About 35 years ago, we started to develop new ways to detect problems in these blood vessels. We started to realize that this disease, atherosclerosis, is a disease of lipids.
Usually, detection followed a patient telling the doctor their exercise stamina was down, they had pain in their chest when they were walking. That was the beginning of stress tests. It was one of the first noninvasive tests, and it’s still very accurate.
Cardiac catheterization, which shows if a person’s heart is having trouble with blood flow, was being perfected then. This was when we started to think about bypass surgery. But bypass surgery is invasive. So we started to think about stents. There are also a lot of new medications that can help. But coronary heart disease is still a problem.
When those vessels get clogged, we get what we commonly call a heart attack. The area of the heart that was getting its blood flow from the clogged vessel dies. Often, you literally lose part of your heart. The heart does not regenerate itself. When heart muscle cells die, they are not naturally replaced.
What did we think we knew about heart disease that turned out to be wrong?
I thought we would fix it by now. I thought that 35 years after I started thinking about how you fix a broken heart, if you will, a heart that’s had a heart attack, and make it so the person can get back to normal – not just live, but get back to normal – we would have done that by now. We haven’t.
We can treat the symptoms of heart failure. We’ve extended life by doing that. But we don’t fix it. The real cure, the holy grail of therapies, is to replace the tissue that was killed.
For the last 25 years, there’s been a very, very serious effort to do that. It’s an incredibly difficult field.
Now we have cells that you can get from a patient, put them in a dish and make them into cardiac muscle cells. The question is, when you put those cells in the heart, will they start to interact with the other cells and make a better heart? I don’t know the answer right now. That is where the field is going.
What important things have we learned?
One of the most important things we’ve learned is that vascular disease is largely preventable.
When I first started, we didn’t think much about risk reduction. We thought about treatment. But over the last 35 years, we’ve realized there are factors — aside from genes — that you can do something about. There are phenomenal data that tell us, if we do the right things, we can reduce our risk of cardiovascular disease almost to zero.
If you have hypertension, control it. The same with high cholesterol. We have great drugs for these two, and they are inexpensive. Don’t smoke. If you have type 2 diabetes, treat it. Try to eat healthy. Get some physical activity. Don’t let yourself become obese.
I know it can be difficult. But when I give a talk on heart failure to a lay audience, I tell them that I study the consequences of a disease that is largely preventable.
Tell us about your research.
There’s another type of heart failure, other than a heart attack. In this one, the heart fails to fill properly. Unlike the heart attack heart, the muscle cells are still alive. But if you can’t fill the heart, you can’t eject enough blood and circulate it.
My area of research for 20-some years was to try to figure out how cardiac muscle cells contracted, how they worked. There have been incredible advances. We now know in great detail how cardiac muscle cells work and what changes when they get sick.
When I started, the treatment for heart failure was the same as it had been for 100 years — a drug called digitalis, which makes the heart muscle cell contract more strongly, and diuretics, to get rid of excess fluid that builds if the heart isn’t pumping strongly enough.
Digitalis worked. It still works. It was making patients feel better. But it wasn’t prolonging life.
The mantra at that time was that you never gave a drug that made the heart weaker. But it turns out that when the heart is weak, it sets off the body’s reflex to make the heart stronger. It’s the same reflex as, when you walk up steps, your heart beats faster.
For people with heart failure, that reflex is getting used all the time. There are drugs that can block that reflex. They are called beta blockers. Someone decided to test the idea that maybe part of the problem with heart failure is the constant over-activation of this nervous reflex. They said, maybe if we block it a tiny bit, we can get a beneficial effect.
This was a really gutsy move. And lo and behold, people did better. Beta blockers are now standard of care. How exactly they work, scientists like me have debated for 25 years. But you can’t debate facts. Patients who take these drugs have better cardiac function and they live longer.
Any breakthroughs on the horizon?
I am hoping we can develop new therapies for patients with heart failure resulting from changes that make it difficult to fill the heart with blood. When I first saw patients with this type of heart failure — 35 years ago — they were primarily women, primarily 80-ish, and usually lean. They would say, “I can’t walk up the steps without getting short of breath.”
Now, we’re finding this form of heart failure more often in younger people. People in their 20s and 30s, even. We don’t really understand why it develops. But obesity and diabetes seem to be associated. If you look at people who are morbidly obese — candidates for bariatric surgery — they often have an early stage of this type of heart failure.
What we want to know is, after bariatric surgery, when they lose weight, do they get better? Over the next 20 years, we’ll do the type of science that will help us figure it out.
Another thing about this form of heart failure is that we don’t have any real therapies. This type is now 50% of the heart failure population, and there is no standard of care. New therapies are being tested every day and there is hope.
To me, the exciting thing is that the heart muscle cells are not dead. So if we can figure out how to correct the other things that are making the heart not fill properly, maybe we can get people back to a more normal life. Maybe we can figure out how to treat this form of heart disease and truly reverse it.
The technology we have now is not even on the same planet as it was 35 years ago. I have faith that these new technologies are going to give us the information we need to figure out how to better treat people with cardiovascular disease.