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. Hi, my name is Dr Warrick Bishop and I'd like to welcome you to my podcast and videocast station. Today I'd like to talk about the concept of deprescribing. Deprescribing and what does it mean to individuals. Deprescribing is the idea of trying to make an individual patient's medication list more accessible easier to deal with less medications on it and therefore reducing the possibility of medication side effects which sounds like a really good idea because the concept is that people can end up on medications and maybe don't need them or maybe are over treated and no one really reviews those medications and so deprescribing is having a close look at an individual's medication list and adjusting it to simplify it, reduce the risk of interactions and complications. Makes perfect sense. So I'm going to share with you a patient story that I had just recently. This is about a man who I know extremely well. He's about 65 odd years of age or thereabouts. And in fact, I know him well enough that I used to play soccer with him a number of years ago. So we actually played in the same team. Now I saw this particular patient around about four or five years ago when he was near 60 odd years of age. And he came to see me for risk evaluation in regard to his cardiovascular health. As you would be aware from my interest in imaging, I proceeded to recommend that cardiac CT imaging might be a really good way to see what's going on with his arteries. At the time, the individual was asymptomatic. We put him through CT imaging and lo and behold, he had really significant plaque. at the distal left main running into the left anterior descending and into the circumflex artery. So that means that at the main artery that breaks into two other important arteries he had significant build up of plaque and it looked narrowed on the CT scan. It was a very high risk feature and right back then I elected to put this gentleman through stress testing to see if I could demonstrate significant lack of blood flow to the heart. I put him through stress testing and indeed his stress test showed features of lack of blood flow. His ST segments or the part of the ECG that we look at to try and ascertain whether there's a problem with blood flow had flattened out and gone down. suggestive diagnostic of what we call lack of blood flow the word we use is inducible ischemia well because of the location of where his plaque was and because of that inducible ischemia I took him to the cath lab and did an invasive coronary angiogram to get more detail well it turned out in this particular case that the invasive coronary angiogram correlated very closely to the CT coronary angiogram So the non-invasive and the invasive tests really lined up pretty well. When we looked at the plaque, at the distal left main running into the left anterior descending and into the circumflex arteries, this was complex lesion. There was no question that trying to stent it was going to be difficult because opening one artery would squeeze the other artery if you like, snow plow and close off the other artery and vice versa. So very tricky. Looking at the images on invasive angiography, it was clear that it wasn't critical, but it was pretty narrowed. At that time, I made the decision to manage this guy maximally, to reduce his risks as much as possible and to put him under very close surveillance because if there were any change whatsoever, I would have an incredibly low threshold to intervene. So, I commenced him on aspirin because I believed that although he was in a primary prevention setting, that if he did have any problems with his arteries, that aspirin would be protective for him. And I looked to drive his cholesterol levels down as hard as I possibly could. Because all the data at that time was telling us that bringing cholesterol levels down really low continues to offer a benefit down to extraordinarily low levels. Well, this particular patient went on to that therapeutic regime, basically was asymptomatic and felt well. We monitored. sugars we monitored blood pressure kept that under control and i made an arrangement for surveillance stress testing to keep a close eye on him and make sure nothing untoward changed well that was four or five years ago and he's been coming back every year we've driven his cholesterol levels down to low levels we've maintained his blood pressure we've kept him on aspirin and we've had fantastic lipid panels which the data now available would suggest that there's every chance we may have seen plaque regression. So the plaque may have got less based on how low his cholesterol levels were. And we were using high-dose statins and azetamib and getting his cholesterol level at approximately 0.9 millimoles per liter, so less than 1 millimole per liter. Well, I had my... yearly catch up with this patient only a week or two ago. And when he came in, how are you going? Feeling perfectly well, thank you, no worries at all. Any problems? No, no, none at all. My new GP has made some changes to my medication. Well, interested of course, as I would be, I said, well, what sort of changes did your GP make to your medication? Well, he said, first of all, the GP told me that because I'm primary prevention and haven't had a problem with my heart, that aspirin is not recommended. And he said, because my cholesterol levels were so low that I didn't really need all the cholesterol lowering therapy that I was on. I'll give you a moment to think about how you think I may have responded to that. Okay, there's your time. i was overwhelmed actually i was struck by the disconnect between what i know was going on with this patient's arteries and what the gp well-intentioned had done in an effort to de-prescribe and simplify this patient's life so a couple of points um what I knew of this patient was that he had terrible, high-risk disease. And what I know is that the current literature for aspirin in primary prevention has really been defined by three major trials that came out probably in the last 18 months or even less. And those three trials are called ASCEND, ARRIVE, and ASPRI. The third of those, in fact, was Australian-led. There's some local flavor to it. These three trials represent a substantial number of patients. The first trial, the Ascend trial, looked at about 15,000 patients. These were people with diabetes who didn't have any previous coronary disease. And so they took people who they perceived to be at high risk because they were diabetic, put them on aspirin, followed them for a number of years, 15,000 people. And at the end of the time, figured out who was living Which group had more people living in it? The group taking aspirin or the group not? Well, it turned out that aspirin didn't keep more people alive. And that's because aspirin had a side effect and the aspirin side effect was bleeding from the gut and that potentially ran risks of its own. However, close analysis of the same data would suggest that aspirin actually reduced risk of heart attack. So it reduced risk of heart attack, but it caused problems. So it's interesting thought, maybe it did have a role, but not broadly to all those people. The ARRIVE trial looked at individuals who were intermediate risk of heart attack, somewhere between 10 and 20% over the next 10 years. These people had not had any previous problem. They were randomised, these 39,000 people. I think it was four to six years. Don't quote me on that. But long enough for it to be statistically significant, there was no clear-cut benefit to the group assigned aspirin. However, there was a reduction seen in heart attacks in the group allocated aspirin. It's just that. The side effects... outweighed the benefits. And this tells us again, just giving aspirin to people randomly is probably not the best idea. And lastly, the ESPRE trial, a really neat trial done locally, took individuals who were said to be elderly or older, we're talking individuals about 70 years of age or above, who were generally fit and well. Now these people were also randomized to aspirin or not and followed up and it turns out again aspirin wasn't particularly helpful. But remember this was a group of people who'd got to 70 years of age and had defined themselves as fit and well so they hadn't had a problem with anything else. Which is really interesting and sort of tells us that this was a group of individuals who probably weren't at increased risk anyway because they'd already survived seven decades without a problem. Anyway, the long and the short of it is that those three trials have now created a situation where we believe in the literature and in guidelines that we don't give aspirin to people in a primary preventative setting. Now the irony with that of course is that none of those trials actually used imaging to look at the arteries or to look at the carotid arteries in the heart or the carotid arteries in the neck going to the brain so that those trials simply took people, didn't really look at who had bad arteries or not within those cohorts and then drilled down as to whether those individuals would do better or not. Let's balance that off against what we know about aspirin, and that goes back over 20-odd years, somewhere around 25 years, when we had the ISIS-2 trial demonstrate to us that individuals who have had a heart attack, if given aspirin, have a reduced risk of subsequent event and a better outcome. Multiple studies since ICIS-2 have demonstrated to us over and over people at high risk do better on aspirin than not. So what does this tell us? This is telling us that if you've clearly got bad plaque in your arteries you will do better if you're on aspirin. But our three aspirin studies none of them actually look specifically within their groups to find the people who have bad arteries by using imaging. So my take on that is if I find someone like this patient I'm talking about who's at really high risk because of very adverse plaque features then I believe those people will do better from being on aspirin because The difference between primary prevention, i.e. stopping someone having an event, versus secondary prevention, i.e. stopping someone having a second event, is really minutes. And so if we think of someone having a heart attack at 12 midnight, then at 12 midnight they become secondary prevention patients. At 11.59 and 45 seconds they're primary prevention patients. aspirin is beneficial for secondary prevention patients does it make sense to maybe get that aspirin on board just before they have their heart attack well i think it does and i think that the interpretation of the data without imaging in there needs to be considered in the context of trying to isolate or identify the true high-risk individuals because we know you can't put aspirin in the water and expect it to be beneficial for everyone. It's like any tablet or any medication. So I explained this to my patient and said, I really want you back on aspirin. And I said it almost calmly, considering how wound up I was. The second bit that really surprised me was deprescribing and reducing cholesterol medication. Now, cholesterol happens to be an area that I'm really interested in. I would like to think I keep up with the most recent studies. It is an area where I even offer input at a national level. So it's an area that's dear and important to me. And we have had in the last couple of years, particularly with the advent of new cholesterol lowering agents, very clear data that the lower, the better. And if we can get cholesterol levels below. about 1.6 1.7 millimoles per liter and 1.6 1.7 millimoles per liter is around about 70 milligrams per deciliter if you use the grams per deciliter scale so if you can get cholesterol levels down around that that level or below we know we can get plaque regression. So knowing what this patient's arteries looked like, knowing how difficult it would be to put a stent in there, knowing that he would only need surgery for two arteries because the third artery was okay and I wanted to avoid stenting, sorry, wanted to avoid surgery for this gentleman for two vessel disease, I was driving his cholesterol levels down as low as possible. in the hope that we could get plaque regression interestingly that position has been supported just in the last couple of months by the european society of cardiology our position statement on cholesterol management which for very high risk patients supports an ldl cholesterol of less than one millimole per liter so why am i telling you all this i'm letting you know all this because i'd made very clear very specific decisions regarding this gentleman based on his clinical situation the clinical interpretation of his coronary anatomy both on ct imaging on invasive angiography and on stress testing based on what I understand to be the best interpretation of the data in regard to aspirin usage and cholesterol lowering for him. And I'd like to think that that's an area where I have some expertise and experience in. What I want to let you know is that the GP, who I've written back to politely and explained that I think we really need to have him on these agents, the GP, well-intentioned, with all the right reasoning, looked to try and de-prescribe for the sake of the patient. But honestly, he nearly killed him, in my opinion. The take-home message is if you have a specialist who specifically puts you on a therapeutic regime, then that specialist may well have done it for a reason. Now, I'm not going to say that all specialists are right and I'm not going to say that I'm beyond reproach or beyond questioning. But what I am going to say is if someone who really should know their game recommends a certain or specific therapeutic regime for you and someone else wants to change it, then my strong recommendation is you ask the question, can we go back to who put me on it? Or put me on this regime and ask why they've done that. And is this okay? Because I would have been very happy to have shared and educated the GP with regard to this particular individual's situation. And he wouldn't have had his medication changed. The flip side is, what if he had been deprescribed only a week or two after me seeing him and had gone a whole year? missing out on the best possible therapy for his care. So please, de-prescribing, great idea. But if someone, a specialist in a particular area, in regard to your specific situation has commenced a certain therapy, before you change it, please check. I hope you have found this podcast to be interesting and informative as always if you have any queries or questions please let us know that would be at info at drWarrickbishop.com if you've got any suggestions for future podcasts again please feel free to drop us a line on the same email address as always i do wish you the very best stay well take care Thank you for your attention and please don't die from a heart attack. Goodbye. 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.
