What is heart disease, and how can it be tackled?

0:00Sonya Babu-Narayan:Therapy's biggest impact doesn't show up in some dramatic breakthrough. It shows up in the smallest moments. You bite your tongue instead of escalating. You put your phone down instead of firing off that text. You say what you actually mean instead of what would hurt someone else the most. Nobody applauds those moments, but they quietly change your life. That's what growing feels like, and that's exactly what Grow Therapy is here for. Grow is therapy that works, covered by insurance. Sessions average$21 with insurance, and some pay as little as$0, depending on their plan. There are no subscriptions, no long-term commitments.

0:37Sonya Babu-Narayan:You just pay per session. Grow connects you with thousands of high-quality, licensed therapists across the U.S., offering both virtual and in-person sessions, nights and weekends. You can search by what matters, like insurance, specialty, identity, or availability. and you can book a therapy session in minutes and begin in as little as two days, not the national 48-day average. See if you could pay as little as$0 for therapy in seconds at growtherapy.com slash ACAST. That's growtherapy.com slash ACAST. growtherapy.com slash ACAST. Availability and coverage vary by state and insurance plan.

1:22Cathy Shanahan:All engine running. Absolute genius. Get this. Welcome. Welcome. This is the show where we bring you... Science. What that essentially means is... Discovery. Advances. Research. Technology. Unbelievable. Without further ado, this is The Naked Scientist. Hello and welcome to The Naked Scientist, the show that brings you the biggest breakthroughs and talks to the major movers and shakers in the worlds of science, technology and medicine. I'm Chris Smith and today we're getting to the heart of the world's biggest killer.

2:02Cathy Shanahan:coronary heart disease is the leading cause of death globally claiming nearly 9 million lives a year 63 000 of them in the uk that's about one person every eight minutes coronary heart disease develops when the coronary arteries supplying the heart itself become narrowed by a build-up of fatty materials in their walls, which makes them prone to developing a blood clot or thrombus that abruptly blocks the vessel, starving the heart of blood and potentially destroying the muscle downstream. This is a heart attack and the ensuing muscle damage often leads later to heart failure, another major medical and quality of life cost.

2:42Cathy Shanahan:In the nearer term though, the electrical disturbance the damage also provokes can throw the heart off rhythm, leading to a lethal cardiac arrest. But before we delve into what's actually happening at the level of the coronary arteries to make this occur and how science is helping us to tackle it, here's Ruth Goss, Senior Cardiac Nurse at the British Heart Foundation, with whom we've partnered for this week's programme, to explain the process in more detail, to tell us who's at risk and what signs and symptoms we should look out for.

3:12Ruth Goss:Coronary heart disease, or CHD, affects your coronary arteries, the blood vessels that supply your heart with blood and oxygen. These vessels become narrowed by fatty material, sometimes called atheromas or plaques in the walls of the vessels. And over time, this can build up inside the artery in a process called atherosclerosis. Eventually, if we don't take steps to sort of help manage this, your arteries can become so narrow that not enough blood can get through them to your heart. So that means the heart muscle is going to be starved of blood and oxygen and nutrients, everything that it needs to work effectively.

3:46Ruth Goss:and then that can increase your risk of having other conditions or other problems. One of those most common conditions or problems that people experience with coronary heart disease is a heart attack. So if a piece of that hardened plaque breaks off, then a clot will form. That clot then blocks your coronary artery and cuts off the supply of blood and oxygen to your heart muscle. So this is what a heart attack is and it's a medical emergency.

4:11Cathy Shanahan:Who is most at risk?

4:13Ruth Goss:Anyone really from any background can develop coronary heart disease. Men do have a higher risk than women at a younger age, but during and after the menopause, women's risk of coronary heart disease will increase. This is because oestrogen falls and then fat builds up in the arteries, causing them to become narrower. Research also suggests that people from different backgrounds, such as South Asian, are more likely to develop CHD and Black, African and African Caribbean communities also have a higher risk of developing conditions like diabetes or high blood pressure which are their own risk factors for CHD so it really is anyone from any background which is why it's so important to raise awareness of it.

4:55Cathy Shanahan:Is that genetics those particular geographical and cultural associations or are there social factors or both?

5:03Ruth Goss:There's a combination of both when we think about the sort of risk factors that can contribute to developing CHD. We have modifiable and non-modifiable risk factors. So your non-modifiable risk factors, these are the ones that you can't change. There are inherited types of high cholesterol, which can then increase your risk of coronary heart disease. This can affect anyone at any age as well. But if you do have a family history or a genetic cause for high cholesterol, you should be getting followed up by your doctor so that they can manage your risk earlier making sure that you're on the right medications so if you've got a parent or a brother or sister who has sort of high cholesterol diet upbringing sometimes that can increase your risk of developing coronary heart disease and also getting older as the body ages that can also increase your risk because they don't have the same sort of protective mechanisms and they don't sort of compensate as well smoking of course being a massive contributor

6:00Cathy Shanahan:the rates of that have gone right down so are we seeing any benefits from the big drop from about half the population of a country like the UK 30-40 years ago smoking down to about 10 % smoking now?

6:14Ruth Goss:Around 90 % of the coronary heart disease burden in the UK is associated with what we would call modifiable risk factors which are often preventable and smoking is one of those so the fact that the smoking rate has come down then yes we would absolutely hope to see that there is like I'd drop. Smoking is also a contributing factor to other factors that can increase your risk, including high blood pressure, having a high cholesterol, type 2 diabetes. You may not take as much exercise, so you might not be doing enough physical activity, or you may be living with excess weight or obesity. So when we see things like the changes in smoking and the interventions that we've done to do that, we are really hopeful and positive that that will have sort of a snowball effect and help bring down the burden of people affected by coronary heart disease.

7:01Ruth Goss:But while we know that smoking is just one factor, we really want to make sure people know all the factors so that they can try and make the changes which are most applicable to them.

7:10Cathy Shanahan:To what extent is this a silent killer and a silent disease in the sense that people don't know they have the problem until it causes really dramatic symptoms, which can even include them dying?

7:23Ruth Goss:Yeah, so some people might not experience any symptoms at all. Coronary heart disease develops really slowly and over time and the symptoms can be different for everyone. Sadly the first time someone knows that they have coronary artery disease or coronary heart disease is when they have a heart attack or a stroke and for some people those can be life-changing or even fatal. One of the more common symptoms is sort of an angina type pain. So angina is a condition and a common symptom of coronary heart disease is the name for the chest pain or an uncomfortable feeling when the blood flow to your heart muscle is reduced.

8:01Ruth Goss:People may experience that in varying degrees of severity. It might get better if they stop or if they sit down. It might get worse when they're exercising or in the cold weather. But if that is a new symptom for them, then that's something we would absolutely want to encourage people to get checked out because that could be a warning sign that there is maybe some coronary heart disease there that needs to be investigated. On the more emergent side, if you think about bigger typical heart attack symptoms, so you might feel just sudden pain, crushing central pain, uncomfortable feeling in your shoulders or your arms, jaw, neck, back or stomach might feel like heartburn.

8:42Ruth Goss:Those are all signs that something might not be right and those should be treated as an emergency. So if you have any of those sorts of symptoms, the best thing to do is to get it checked out by a medical professional.

8:55Cathy Shanahan:Really helpful advice. Ruth Goss, Senior Cardiac Nurse at the British Heart Foundation. As Ruth was just explaining, the disease originates from within the coronary arteries that deliver blood to the heart muscle. So what are the steps that lead to this happening and how? Will Watson is a heart disease specialist at the Royal Papworth Hospital in Cambridge and he invited me over to the Heart and Lung Research Institute to explain the difference between healthy and diseased arteries and, encouragingly, how we can now begin to use non-invasive imaging technology and see, on a CT scan, who might be at risk and in need of treatment.

9:32Will Watson:It starts early on and it starts with cholesterol. So we all think about cholesterol as being something that's bad for us. What happens over time is this cholesterol goes inside the wall of the artery and it starts to get eaten up by cells in the wall of the artery and these cells are called macrophages. And they know this is bad and they start releasing signals that bring in other cells. And over time you get a thickening of the wall of the artery and it fills it with cholesterol, it fills it with inflammatory cells and different things can happen to it over time that manifest in different clinical ways.

10:05Cathy Shanahan:Why does the cholesterol go in the wall of the artery in the first place?

10:09Will Watson:So there are receptors that draw it in. so the cholesterol is encased in these little things called low density lipoprotein or LDL so if you have too much this bad cholesterol low density lipoprotein it gets pulled into the artery and it releases some of this cholesterol inside the arterial wall so that's the difference between the good and bad the high density and the low density but if one looks at arterial disease

10:31Cathy Shanahan:it doesn't happen everywhere uniformly there seem to be hot spots so why do you get hot spots of disease why doesn't it just do that everywhere i don't think it's something we understand terribly

10:44Will Watson:well certainly there are there are factors like what's called shear stress so that's eddies in the blood flow blood flow that's not going in one direction but it's kind of going around the corner and a little bit like an oxbowing river you get pressure on the bank or you get shear stresses along the bank and that causes disruption of the very inner layer of the artery and that can cause an increased uptake of this cholesterol and also cause increases in the inflammatory cells that are going into it. So it's patchy for that reason. There are other things we don't really understand like we know that smokers get really patchy processes of this.

11:17Will Watson:We don't quite understand why you'll get one really nasty lesion in one place and the next bit of the artery can be absolutely fine. So there's still a lot of stuff we're unravelling about this.

11:26Cathy Shanahan:Is it a bit of a self-fulfilling prophecy or a sort of negative feedback loop where once you've damaged the wall of the artery a bit because of the sheer stress blood pressure smoking that becomes a bit more vulnerable to more damage and then if it gets a bit thicker as well that makes more of those eddies and the flow is more turbulent is that possibly a mechanism yeah and i think there's two things

11:51Will Watson:there so one thing is you're talking about the actual initiation what we call a fatty streak so the very first stage of a plaque forming where it's just a bit of cholesterol inside the arterial wall but not a lot else going on so how do you move from normal to having cholesterol in it and then once you've got cholesterol in it how do you move from a fatty streak to atherosclerosis where the which is the technical term where there is thickening of that arterial wall and both of these processes are involved in that and certainly the influx of inflammatory cells is involved as well So I mentioned earlier macrophages.

12:26Will Watson:If you think of a macrophage, it's a white blood cell, it's an inflammatory cell, and it works by gobbling things up. It's like a little kid bringing you what it's done. It'll show you, oh, I've just eaten all of this up. Here are the bits of it. You, rest of the immune system, needs to go and find the other bits of it. So these cells are gobbling it up, and the interplay of arterial stress, blood pressure, et cetera, on that process as well of cells going in there. And then finally, and this is I guess the more recent discovery, what's your immune system doing? So some people's immune systems are going to be much more predisposed to doing this than other people's immune systems as well.

13:02Cathy Shanahan:So you get to a stage where we've deposited this fat in the wall of the artery. It's beginning to build up. It's become inflamed because the macrophages have encouraged all their immune mates to come in. And that's made this lump in the wall of the blood vessel. What happens next? What are the consequences of that? and how does that translate into the symptoms that patients then develop?

13:23Will Watson:So we've got this situation, as you describe, where there's stuff in the wall of the artery and it's thickened it. But then we start to go in two different directions. So these macrophages, as you say, they signal other cells like T cells and that causes changes in the smooth muscle cells in the walls. So they start to deposit fibrous tissue and that thickens the very top, the very inside bit of the wall. So we talk about a fibrous cap to these lesions. And what's fascinating is that you can have some of these lesions which have a really thick fibrous cap. Now those are ones that are growing and growing and growing over time, thickening the artery wall.

14:00Will Watson:There's less space for blood to go through, and that can result in symptoms like angina. But the other thing that can happen is when you have a thinner fibrous cap, and this fibrous cap ruptures, and you get the inside of the plaque talking to the blood vessel, and then you get blood clot forming on top of it and that can block the blood vessel entirely and that's what causes heart attacks that's what causes strokes that's what causes limb ischemia and other bad manifestations of this therefore you've got sort of two different disease processes

14:29Cathy Shanahan:then you've got one where the artery narrows and it produces angina but that might not kill you versus you could be walking around and not know that this is happening to you you won't have any symptoms but you've got one of these very thin walled lumps plaques and that ruptures then you get this blood clot thrombus in the vessel which blocks the vessel and you have a heart attack that

14:51Will Watson:could be lethal exactly so we differentiate between thin capped and thick capped fibroafiroma and unless you put very sensitive imaging on one of those arteries and bear in mind these arteries are often only four or five millimeters across so unless you really sensitive imaging to find these thin capped fibroarthromas. Bear in mind they're thin so they don't protrude very far into the wall of the artery and a lot of our conventional ways of looking for atherosclerosis were just putting dye down an artery and looking to see where it narrows. Well if you've only got a mild narrowing that could easily be missed.

15:26Will Watson:So now we're starting to think about well what's the features of these thin capped lesions that allows us to see them on an imaging test that allows us to, as you say, take someone who has no symptoms but might have risk factors and work out if they're at risk of having an event like a heart attack or a stroke. Can we see them? So we're getting better and better at that. We can do a couple of things where we put an ultrasound probe or an actual imaging probe on a wire not much thicker than a human hair down one of these arteries and we can actually image from the inside of the artery and we can see the different layers that make up the arterial wall and we can see the difference between a thick fibrous cap and a thin fibrous cap but obviously that's quite invasive so more and more recently we're thinking about well what can we see on a ct scan or or similar imaging technique like an mri scan that's going to show up these things and the thing about these thin capped ones is they're inflamed we talked about the role of immune cells earlier didn't we so these guys have got a lot of inflammation going on inside them.

16:30Will Watson:And that can actually be seen on a CT scan. And we can see that one's inflamed, that one's not inflamed. This person needs some treatment, that person's fine.

16:39Cathy Shanahan:It is indeed great to see that progress being made. Will Watson at the Royal Papworth Hospital in Cambridge there.

16:48Sonya Babu-Narayan:Therapy's biggest impact doesn't show up in some dramatic breakthrough. It shows up in the smallest moments. You bite your tongue instead of escalating. You put your phone down instead of firing off that text. You say what you actually mean instead of what would hurt someone else the most. Nobody applauds those moments, but they quietly change your life. That's what growing feels like, and that's exactly what Grow Therapy is here for. Grow is therapy that works, covered by insurance. Sessions average$21 with insurance, and some pay as little as$0 depending on their plan. There are no subscriptions, no long-term commitments.

17:24Sonya Babu-Narayan:you just pay per session. Grow connects you with thousands of high-quality licensed therapists across the U.S., offering both virtual and in-person sessions nights and weekends. You can search by what matters, like insurance, specialty, identity, or availability. And you can book a therapy session in minutes and begin in as little as two days, not the national 48-day average. See if you could pay as little as$0 for therapy in seconds at growtherapy.com slash ACAST. That's growtherapy.com slash ACAST. growtherapy.com slash ACAST. Availability and coverage vary by state and insurance plan.

18:08Cathy Shanahan:The Naked Scientist podcast is produced in association with Spitfire, cost-effective voice, internet, and IP engineering services for UK businesses. Find out how Spitfire can empower your company at spitfire.co.uk.

18:28Cathy Shanahan:This is the Naked Scientist podcast with me, Chris Smith, and today, in partnership with the British Heart Foundation, we're putting the subject of heart disease under our microscope. Still to come, what have we learned in recent years about the best way to manage heart attacks and how can we prevent them in the first place? First though, alongside fatty deposits that build up in the walls of arteries, including the coronary arteries, we also see the accumulation of calcium, which seems to have a stiffening effect. In some blood vessels it can be so pronounced that physical bone forms. While it sounds unusual, this appears to be actually part of the natural ageing process, but it aggravates the progression of arterial disease by pushing up blood pressure.