Cardiovascular disease is the leading cause of death in the U.S — more than 800,000 people die from it each year. A new report by the Pharmaceutical Research and Manufacturers of America, or PhRMA, finds that 200 new medicines are currently in development to help prevent and treat heart disease, and nearly two dozen of these are in the works in Massachusetts. Dr. Jennifer Allport-Anderson, a cell biologist at Novartis, discusses these developments and their potential impact.

This transcript has been edited for clarity.

Joe Mathieu: Heart disease remains the leading cause of death in the U.S., the American Heart Association estimating that one out of three deaths is, in fact, related to cardiovascular disease. That's one person dying every 40 seconds. But researchers are working to fix that.

A new report out by the biopharmaceutical research company PhRMA lists about 200 new medicines in development to cure cardiovascular disease. Nearly two dozen of them are being developed here in Massachusetts, and here to explain some of these breakthroughs is Dr. Jennifer Allport, a cell biologist at Novartis in Cambridge. Good morning, and welcome to WGBH's Morning Edition.

Jennifer Allport-Anderson: Good morning.

JM: We're talking about some pretty important stuff here in terms of medical advancements. Tell us about some of the different forms, for starters, of cardiovascular disease that we're trying to target.

JA: Right. So, I mean, a lot of people have heard of, you know, having a heart attack. And the underlying cause of a heart attack is a disease called atherosclerosis, and that's what clogs the arteries, basically. But there are many other aspects of the disease besides lowering cholesterol that currently being investigated, and new drugs are being developed in those areas.

JM: When we talk about heart disease, though, this can be any number of things?

JA: Yes. I mean the other area that I'm researching a lot is in heart failure. So this is something that, many members of the public don't really understand what heart failure is. It's a syndrome. It's a characterization of patients where their heart just really can't meet the needs of the body, and people who have had a heart attack particularly at risk for going into heart failure. Basically after some time, the heart because it's damaged from the heart attack, will then go into failure, it's not able to pump as well.

JA: There's another form of heart failure and patients that haven't had a prior heart attack, where basically the heart gets stiffer and stiffer and stiffer and is not able to take in enough blood with each heartbeat to then pump it around the body. These patients typically tend to have, suffer from obesity, diabetes, high blood pressure, that puts a lot of strain on the heart.

JM: So when we have 200 new medicines in development, do you envision a day when you can get ahead of all of these?

JA: That's what we're hoping. I mean, we're really hoping that we can stop more people from having a heart attack in the first place. That's sort of the sentinel event by which all these other things happen, for many people. 50 percent of the population of heart failure are patients who've had a prior heart attack. And then for patients who have heart failure, aside from treating their other risk factors like diabetes, their blood pressure, trying to get that body weight down, if we could improve the heart function, or in patients that have had a heart attack, if we could regenerate the heart, this is sort of the Holy Grail in cardiovascular research. For patients who have had a heart attack and the heart is damaged, if we could replace that or repair that, regrow that area of the heart, then these patients would do a lot better.

JM: So, doctor, what kind of breakthroughs then are you hoping for or waiting for?

JA: So, some of the therapies that are in development are now, things like cell-based therapy, stem cell replacement of the heart, for example, to regenerate that heart tissue that's damaged. This is not a new idea. This has been worked on for some time, but it's always been met with challenges. Now we're taking actually cells from the patient themselves, taking a normal cell, turning it into a stem cell and then turning that stem cell into a cardiomyocyte, which is the cell of the heart.

JM: And that eliminates the controversy?

JA: That eliminates all the controversy around stem cells, it also eliminates the need for the patient to have drugs ... immunosuppressant drugs, if that was a donor situation, and so now we're at this stage of really trying to integrate those cells into the heart so that they work in concert with the rest of the heart, and not at odds with the rest of the heart, which causes an arrhythmia.

The other thing, of course, is to use drugs to cause the heart itself to regenerate, and that's an area that we're looking into. Some of the challenges with that is that you give a drug to the whole patient and you don't want all sorts of bits of the body growing, you only want the bit of the heart growing. And so we're [in] experimental development now really in drug delivery. How do we get that drug to that site only and keep it there so it can regrow the heart but not cause cancer or other complications in the patient?

JM: Or have a bunch of mutants.

JA: Yes, exactly. I would say for preventing heart attacks from happening in the first place, the other main, sort of, new breakthrough is in inflammation. So inflammation is something that's really important to your body in fighting disease, fighting infection. If you get strep throat, for example, you mount an immune response that fights off the infection. But we can also have an immune response to things that are endogenous to us. You've heard of autoimmune diseases like lupus and things like that. Well the same autoimmune responses can happen in cardiovascular disease as well. And so we've discovered through recent clinical trials that if we can inhibit the inflammatory process we can improve outcomes for patients. We can lower the incidence of a second heart attack. So now the question is, can we prevent a first heart attack using the same methods of inhibiting inflammation?

JM: Because you see that inflammation before an initial heart attack?

JA: Exactly.

JM: We're talking with Dr. Jennifer Allport, a cell biologist at Novartis in Cambridge. Doctor, if we all took great care of ourselves, if we were in perfect health, would any of these still be necessary?

JA: Yes they would. I can give you a very clear example from the sort of popular TV, which many of your listeners would know. Bob Harper, he was a trainer on The Biggest Loser, fabulous shape. I'm sure many of your listeners know him by sight and watch The Biggest Loser. He was in great shape, ate extremely healthy, had a massive heart attack last year. And it was discovered that he had high levels of something called lipoprotein, little A. It's another risk factor for cardiovascular disease that we've really only come to understand in recent years. There's no treatment to reduce the levels of that protein at this point in time.

So he was doing everything right and he still had a problem. So there are still genetic contributions to cardiovascular disease, that no matter what we do with our lifestyle we can't overcome. That's not saying I'm advocating to your listeners, don't care about your lifestyle. I think you need to get out and walk, you need to eat healthy most of the time, they need to go to their physicians they need to get these their cholesterol and blood pressure checked and make sure that those are under control. But there will still be a need for therapies, that is a great target. We need to lower that level of lipoprotein, little A, so we can treat people like Bob Harper.

JM: That's why you're here. Dr. Jennifer Allport from Novartis in Cambridge, thank you for coming across the river to talk to us and sharing your expertise on WGBH Radio.

JA: My pleasure, thank you.