Welcome to Dr. Warrick's podcast channel. Warrick is a practicing cardiologist and author with a passion for improving care by helping patients understand their heart health through education. Warrick believes educated patients get the best health care. Discover and understand the latest approaches and technology in heart care and how this might apply to you or someone you love. Well, the first thing that I'd like to talk about is a question that came around regarding the influence of blood pressure on cholesterol deposition within the artery wall. And that question, really to a large degree, was asking if you increase the pressure within the artery, within the vessel, and you increase that pressure high enough, does that squeeze cholesterol into the wall of the artery? Well, if you imagine it, it sort of sounds like not a bad idea, and certainly we talk about blood pressure being a problem all the time. Well, to a large degree, that isn't what's happening. Our cholesterol moves around in the body in little capsules, in special transport. These little vehicles, these little transport capsules, are actually protein balls, believe it or not. And these protein balls have little sticky bits on the outside and they're full of cholesterol and troglycerides on the inside. The reason cholesterol moves around in these protein balls is because cholesterol... doesn't dissolve in water and neither do triglycerides. So the free fats that our body tends to use, if they weren't in some sort of protein ball, in some sort of capsule, they would simply float to the surface of the liquid that they're in. And if that's the human body, when we stood up, fat would float up to our heads because it would be lighter. than the density of the serum it's sitting in. So by putting the cholesterol in little balls, little capsules, it can be transported around the body with the blood. So blood pressure within the blood vessel wall doesn't push cholesterol directly into the artery. But where blood pressure is really important is the blood pressure is what drives the flow of blood over blood vessels. And flow can lead to friction. And this is part of fluid hemodynamics. So the friction caused by blood passing over the smooth lining of blood vessels can certainly lead to wear and tear in that blood vessel. And it's localized wear and tear that the body sees as damage and looks to want to repair that damage. Well, because cholesterol is used for membrane construction, because it's a building block for cells, because it's a building block for membranes, then cholesterol particles within the lipoprogen particles, protein capsules are drawn to the areas where there's wear and tear occurring so that the cholesterol can literally be taken out from the protein ball and used where it's needed. So the blood pressure is not driving the cholesterol out of the artery and into the wall. The blood pressure is causing the wear and tear within the artery that subsequently sends off signals to trigger If you like a repair response, and that repair response engages cholesterol, it also draws in inflammatory cells. And so we hear of inflammation included as part of the plaque or atherosclerosis process. So very important, if you want to minimize wear and tear on the inner surface of your arteries, keep your blood pressure low. So that was the first question, and I hope that answers where blood pressure fits in with cholesterol moving into the arterial wall. Another question I received, which I'd like to speak about today, is talking about the effect of stress on the heart. Now, we know that there's good evidence to suggest that depression, depression and anxiety, are poor prognostic indicators, poor things to have if you've got problems with your heart, and certainly they are linked to an increased risk of further event. Well, what's going on? Why is that happening? Well, if you haven't been a bit stressed or uptight yourself, imagine that being the illness of full-blown depression or anxiety, where these things are perpetuated long-term at a high level. There's poor sleep. There's hypervigilance. There's a loss of enjoyment. But things like blood pressure run high because the adrenaline within someone's body is running high, because the cortisol levels are running high. Insulin levels can run high. Food consumption can become a response to depression, and so people can eat badly. Alcohol can be a contributor. Other behaviours such as smoking may contribute. People may stop exercising and may put on weight. So lots of things, hormonal changes, sleep pattern behaviours, nutritional exercise behaviours can all come together such that the person with depression has this internal milieu which is really going to drive a process that we don't want to see, which is wear and tear on the arteries. So we know that depression, depression and anxiety are really significant contributors to coronary artery disease. And it is a multifactorial process that does this. We even know that direct effects of the nervous system on the heart are quite compelling. We see a condition called tachosubo, tachosubo cardiomyopathy. Now that's a heck of a word. But what it means is that the heart is affected by, if you like, a nervous outpouring, generally an emotional nervous outpouring. And that nervous outpouring renders the pumping chamber of the heart ineffective. It looks for all the world like a person's had a heart attack, driven from an emotional state. We call it Takotsubo syndrome, and that's named after a Japanese fishing pot for octopi or octopuses, but octopi. And it's just, it's the shape of a pot. But it's a significant impact on the cardiovascular system driven by emotional outpouring. So stress, gee whiz, try and keep away from it. If you can, it's not. good for your heart. It's not good for your health. So where you can just chill out, relax, have a cup of tea and try and put the stress aside. If you really do think that there may be a major psychiatric illness, whether true depression or true anxiety as a manifest state where it's intruding on your life. in a daily basis and clearly impacting your mood, then please seek help. That's just common sense. Please just seek help. I also have a question from one of the audience, one of the people listening in previously about the aorta and aortic hardening. Well, the aorta is the main blood vessel that comes out of the heart. It's what the left ventricle pumps into it so the aorta comes out of the heart and from the aorta come all the other blood vessels the first blood vessels that come off the aorta are of course the coronary arteries but then the aorta gives off a branch to the shoulder and then up to the carotids to the back of the brain and then off to the spinal cord and the other organs so aorta really important artery and the biggest artery in your body Well, the question was about aortic hardening. Well, we know that as people get older, the aorta gets stiffer. And so let's think about that. If we're thinking about a stiff aorta, let's put that in the context of blood pressure and what happens as people get older. When we think about blood pressure, we're thinking about the heart contracting and squirting blood into the aorta. So in a young, healthy adult, as the heart squeezes blood into the aorta, the aorta is quite supple and has give within it. It is quite elastic. So the pressure within the left ventricle, within the main pumping chamber of the heart, as it squeezes, it squeezes blood into the aorta. Some of that energy... is taken up in the aorta literally dilating, accepting that pump of blood. So, for example, the heart may squeeze at, let's say, 150 millimeters. Let's say the aorta distends substantially so that the pressure... that occurs within the aorta when you measure it is 120. So the aorta is distended in proportion to, say, 30 millimeters of mercury. There's been a pressure drop through the deformation or through the expansion of the aorta because it's stretchy and it's able to absorb some of that energy. Well, that's the top measurement of blood pressure. what we call the systolic or the higher blood pressure measurement. When the heart then relaxes, the aortic valve closes and the aorta and the rest of the vasculature then become a closed system. And so the recoil of that aorta which was stretched during the contraction phase of the heart, that now recoils and comes back and it maintains the blood pressure within the body. So let's say it recoils and it maintains a blood pressure of 80, together with the peripheral blood vessels, which have a certain tone or narrowing to them to maintain. pressure within the system. As the aorta ages, as the body gets older, we lose elastic tissue. And you can see from my face, for example, it sags. As my face gets older, it sags. And so does most other people's faces. We lose elastic tissue from our skin, but we lose elastic tissue also. from our major arteries in the aorta is no different. So that as you age, we see the aorta become less elastic, less compliant, stiffer. So that in older years, when the left ventricle contracts, if it contracts say at 150 millimeters of mercury and the aorta doesn't give at all, then The pressure within the aorta, and this is exaggerating, the pressure in the aorta is the same as the pressure within the left ventricle. It's 150 millimetres. And so there's a direct transfer of that pressure because there's no give in the aortic vessel, no give in the system. Then when the heart's finished contracting and the valve closes, That stiff vessel, that stiff aorta hasn't got any recoil to maintain diastolic pressure. So the diastolic pressure drops substantially because there's none of that secondary pump action from the recoil of that healthy elastic aorta. So the top pressure 150, the bottom pressure down to 50. So a big gap between these... pressure we see while the heart's contracting and the pressure we see when the heart's relaxing. That's a large gap. So the lower pressure, the diastolic pressure drops, the systolic pressure has gone up and that is absolutely a characteristic of what we call isolated systolic hypertension of the elderly. Well the question of course is what can you do about it? Well Probably the single best thing you can try and do is diminish wear and tear on the aorta through life. The single best thing you can do is to try and keep your blood pressure as low as possible for as long as possible. And so it's not using up and wearing out the elastic tissue, the elastin, the elastic tissue that's within the artery wall, the aortic wall. So please do your very best to make sure you are keeping your blood pressure under control, that you're checking in with your doctor and you're making sure that it is well monitored. If we're looking to anything to maybe restore or preserve elastic elastin, the elastic tissue within the arteries, then there is some evidence to suggest that perhaps the... ACE inhibitor medications, the angiotensin-converting enzyme inhibitors, have an effect on reducing the enzymes that break down elastin. So if you can reduce enzymes that break down elastin, you may be able to preserve the elastin. And so there's some evidence to support that. The angiotensin II receptor blockers seem to have a similar action. So there are a class of drugs with a theoretical mechanism that could potentially dampen down or slow down some of that wear and tear that we see with the elastin within the aorta as it ages. So there you go. I've answered a number of... Audience questions? I really hope that makes a bit of sense for you. You have been listening to another podcast from Dr. Warrick. Visit his website at drWarrickbishop.com for the latest news on heart disease. If you love this podcast, feel free to leave us a review.
