Welcome, my name is Dr. Warrick Bishop. I'm a cardiologist, an author and a keynote speaker. I'm CEO of the Healthy Heart Network. I'm all about trying to help people live as well as possible for as long as possible. Heart disease is huge in Australia. Every 20 minutes someone suffers a heart attack. Most of these could probably have been avoided if only we knew what to do. This podcast is all about helping you understand blood pressure, weight, cholesterol for better health. If you enjoy this podcast, I would be honoured for a five-star review. You can share it with your family and friends. It may well save someone you love. Hi, my name is Warrick Bishop and welcome to my podcast and videocast station. I really do appreciate you tuning in and I hope you find the information valuable. I'm going to let you know that I've got the door open here at the moment to let in some cool air. My office is hot and that noise in the background, it's not interference. It is the soothing sound of the ocean and the waves. Well, if you listen to the podcast immediately before this, then this is part two of the conference I went to where they spoke about predominantly heart failure. and cholesterol management so it was a fantastic conference and that's why i'm pretty keen to share it with you lots and lots of information was available i've already told you about the first half where we talked about heart failure with professor zeroth associate professor john amarina josephine harris and then went to some workshops where there was a j ramanathan talking about the young patient who was on a paleo diet with very raised cholesterol levels. No family history. Interesting case and certainly led to lots of debate. I also spoke about the role of close supervision and management and keeping a close eye in regard to surveillance for patients who have gone through chemotherapy as some chemotherapeutic agents can be detrimental to heart function. Well, let's move on to the next bits of this fantastic conference. The next thing that was discussed was a lipid particle called lipoprotein A or lipoprotein little a. Now, most of you will have heard of such things as triglycerides. You will have heard of such things as high-density lipoprotein, the so-called good cholesterol, and you will have heard of low-density lipoprotein, the so-called bad cholesterol. But you probably haven't heard of lipoprotein A. Now, the reason why it's important and the reason why it's interesting is several-fold. Firstly, what we've observed clinically is... In spite of us lowering cholesterol in certain individuals, there continues to remain what we call residual risk. So try as we may, we're not able to make the risk of someone after we commence therapy zero. It still exists. We reduce the risk substantially and generally in proportion to the cholesterol or LDL lowering. but we don't reduce it to zero. And so there's a lot of debate around what other factors could be contributing to this observation that we can't get risk down as low as we would ideally like to, because if you've had an event, we really do want to stop you having another one. Well, one of the players in this particular space is this lipoprotein called lipoprotein. little a or lowercase a. Well, what is it? Well, when we think of lipoprotein particles, when we think of LDL or HDL, the way I often describe these particles to people is they're the way that cholesterol and fats move around in the body. Because cholesterol and fat doesn't just float around in the body. If it floated around in the body without some sort of transport particle, then if we stood up upright for long enough, all that fat would simply float to the highest part, which is our brains, and we'd look like a bottle of milk with cream on top. Well, of course, that doesn't happen. Fat within our body is carried in little particles, vesicles, balls, if you like, carriage vehicles. These little carrier vehicles look a little bit like a Ferrero Rocher, which have irregular and bumpy external outsides, have a particular outer structure, and then a core, which is slightly different. In these lipoproteins, in these particles that I'm talking about, that internal core is the fatty bit, the outside bit, which is a bit rough and bumpy. Well, that's the external lining, the external cover. Lethison, phospholipid, it's also made up of ApoA and ApoB. These are lipoproteins. So these fantastic protein balls, which can dissolve or at least be carried around in water without floating to the surface, hold the cholesterol and fat that moves around in our body. Lipoprotein little a is one form of one of these lipoprotein particles. It's particularly notable because its structure has a mischievous tail on the end of it and we don't see that with all the lipoproteins. Most of them are like a Ferrero Rocher but lipoprotein little a is like a Ferrero Rocher with a bit of a sticky tail hanging off the end of it so that as it rolls along that sticky tail could get caught on something. And you guessed it, that's something that we're concerned about it being caught on is the inside of the artery wall where these particles can be accumulated and lead to plaque. Well, an amazingly intelligent thought leader called Professor Brian Ferencz spoke about lipoprotein delay and... its distribution within the population and the sort of expectation we might have from it being elevated within individuals and the sort of results we might expect from lowering lipoprotein little a in these potential high-risk individuals as well. It turns out that lipoprotein little a not only can end up in the arteries and increase the chance of having coronary artery disease and in fact is probably the most common. hereditary marker for premature coronary artery disease, but it also seems to have a role in increasing the possibility of aortic stenosis. And interestingly, there's even trials looking at that. We then had Dr. Natalie Ward all the way from WA present our current Australian position paper on lipoprotein little a. because it's fairly new, a group of interested parties got together and created some guidelines and recommendations on who should be tested and when they should be tested and what would be considered reasonable therapy for these people. We also had Ms. Natalie Rafool from the Heart Foundation speak about cardiovascular risk assessment and tried to incorporate not only the current state of play with risk assessment within the community, but dovetail that with where lipoprotein A might fit. Well, that was the end of that day. We had a fantastic Q&A session, which was presided over by Professor Karam Kostner, a personal friend who you will have heard on this podcast already if you've listened previously. And we wrapped up there. for the end of day one. Day two saw more around the space of lipid lowering and in this situation Brian Ferencz, Professor Brian Ferencz was presenting again and on this occasion he was introducing concepts around using causal AI, artificial intelligence, to help us best guide our understanding of risk in an individual. Now, this is absolute cutting-edge stuff, and what it is about is using our current risk factor. tools or instruments and recognizing that these tools or instruments can be refined by adding in the results of the randomized control trials that are available to us. Now some of those randomized control trials are set by research, they're specific studies, but one group of randomized control observational data is from what we call Mendelian randomization. Or the situation where, for whatever reason, a particular group, through a genetic predisposition, have a particular characteristic. And we can match those people up with people who don't have that characteristic. And lo and behold, we've got what's called Mendelian randomization. A quick example to make sense of that. If we could identify a large group of people who have very high cholesterol and... then compare those people to the average population with normal cholesterol levels, then our Mendelian randomization would simply say all factors are similar, except for one group has very high cholesterol, the other group has average cholesterol. And then when we look at the outcome, we can use that as an indicator of the causal impact of raised cholesterol. So Professor Brian Ferencz was talking about incorporating this information using artificial intelligence risk calculation in a way that gives causal information in regard to risk factors that we're trying to manage, be it cholesterol or blood pressure. Now, this is absolutely fascinating. Watch this space. This could be present and in our practices within months to years. This is not science fiction. And it's very close, I think, to being something that's incorporated on a regular basis. We then had a Dr. Mazhar Haig talk about fatty liver. And really, the take-home message with fatty liver was that these individuals really benefit from weight reduction any way you can. And that's really important because... Obesity leading to non-alcoholic fatty liver disease is now becoming a major cause of cirrhosis. Also, Dr Haik demonstrated to us that these same individuals are likely to carry the risk factors that would mean not only do they have fatty liver, but they're likely to be carrying significant risk factors for coronary artery disease as well. Professor Jerry Greenfield then picked up the baton and told us about adipose tissue. And is it safe anywhere? Well, as you're probably aware, there are different types of fatty tissue. There's white fat, if you like, and brown fat. Brown fat being the sort of more metabolically active fat that you might see more commonly in children. But white fat also moves. The conversation was around visceral versus subcutaneous fat. And one of the most striking images was that of sumo wrestlers who, when they're exercising and active, although they're eating almost their body weight a day in food, all their fat is subcutaneous. And we believe that that subcutaneous fat is less problematic for cardiovascular risk. People have done research on sumo wrestlers who stop exercising but keep eating. And Professor Greenfield showed a fantastic comparative set of CT scans, which is a cross-sectional view of the abdomen and chest, showing the difference between before and after for a sumo wrestler who had been eating and exercising versus continued to eat. but stopped exercising and it was compelling there was no question you could see this migration of fat from the subcutaneous tissue to surrounding the organs and this is where it drives inflammation and this is where it drives impact on the micro vessels a real problem and a fascinating bit of medicine to be more aware of and a great presentation from dr greenfield Our last session for the conference was, again, featuring Professor Shelley Zeroth, who did a fantastic job. And she talked about what's outdated in left ventricular ejection fraction in 2023. And this was really about how we measure it and what might end up being the best ways for us to reproducibly measure. how the heart's pumping. There's certainly a feeling that looking at how the heart contracts in isolation is probably not going to inform us as well as looking at how the heart moves in both relaxation and contraction. And one of the ways that we can do that is looking at the strain within the muscle. How is that muscle looking under load? So going from a visual of how the Overall, pump is going to a more finessed evaluation of the actual muscle structure and how's that behaving. That's called strain therapy and we're going to see more and more of that. In fact, I mentioned surveillance during chemotherapy in the last podcast. In fact, we're using strain evaluation in that space already. fascinating discussion from a professor diane fatkin who shared with us where the future looks in terms of understanding the intersection of genetics and heart failure trying to identify those genes that could well be the markers for people who are prone to developing cardiac failure either de novo or subsequent to some sort of external trigger That external trigger could be chemotherapy, as we touched on before. It could be alcohol. It could be an infective process. Lastly, we finished off, as you might expect, with a bit on COVID-19 by Dr. Louise McCormack, and that was a lovely way to tie up an absolutely fascinating, enjoyable, and educational conference. From my own perspective, the opportunity to not only attend and listen and learn from some of these great experts, It was so appreciated. But one of the other things I really appreciate from these conferences are the conversations in the corridor, the chances to catch up with friends over a cup of coffee, and even catch up with friends over a meal or dinner at night. So a great way to connect, a great way to learn, a very satisfying experience all around. I hope you've found this podcast interesting. If you haven't, you might wish to keep that to yourself. If you have, I'd love you to leave a positive review somewhere. I'd love you to subscribe if you'd be so kind. And if you think of someone who might find these podcasts interesting, please share it with them. If you've got any ideas on future podcasts, drop us a note at info at drWarrickbishop.online. I'd love to hear from you. If you've got any queries or questions, drop us a note on the same email. For now, though, until next time. I wish you the very best. Please live as well as possible for as long as possible. Take care and bye for now. Ever wonder what your risk of heart attack is? After all, it is the single biggest killer in the Western world. It accounts for 9 million deaths globally. And the scary thing is it seems to be able to affect anyone. Well, if you're interested in knowing more about your risk. and understanding more about precision around that please check out a free risk check at www.virtualheartcheck.com.au
