In this episode of PodMD, cardiac imaging specialist Dr Jason Kaplan will be discussing the practical advice you can provide to your patients for living a heart healthy lifestyle, including the main factors that can impact heart disease, what advice we can give to patients to reduce their risk, when medication is required, what a GP can do to assess their patients and more.
Please note this is a machine generated transcription and may contain some errors.
*As always, all in this PODMD podcast is intended for health professionals and the comments are of a general nature. Information given is not intended as specific medical advice pertaining to any given patient. If you have a clinical issue with one of your patients please seek appropriate advice from a colleague with expertise in the area.
Today I’d like to welcome to the PodMD studio Dr Jason Kaplan
Dr Jason Kaplan is a cardiac imaging specialist who studied Medicine at UNSW and graduated with Honours in 1999, completing his Internal Medicine Training at St George and Prince of Wales hospitals and Adult Cardiology training at Royal Prince Alfred Hospital.
Dr Kaplan has done additional training in all aspects of echocardiography at international centres including the Mayo Clinic and has been involved in training echo sonographers for the last 10 years. He is currently a senior clinical lecturer in Medicine in the Faculty of Medicine and Health Sciences at Macquarie University teaching undergraduate and postgraduate students.
Today, we’ll be discussing the early development of atherosclerosis and the impact choices made earlier in life can have on the heart.
*We do hope you enjoy this podcast but please remember that the advice here is of a general nature and is not intended as specific advice about a given patient. The views and opinions expressed in this podcast are those of the doctor, not PodMD.
If you do have a patient on whom you require specific advice, then please seek advice from a colleague with appropriate expertise in that area.
Jason, thanks for talking with us on PodMD today.
Jason : Thank you for having me.
The topic of today’s discussion is atherosclerosis build up. Jason, can you give us a brief overview about the build up of atherosclerosis?
Jason: Thank you. So atherosclerosis is the most common cause are, well the most common manifestations of heart disease we see in Western society, and I think the important factors are that it starts to occur early in life in Western society and we know that we know from some of this we’ve done autopsy studies on young soldiers, when we see early fatty streaks in the in the aorta. But I think the other important thing to know, it’s not inevitable, because there’s a study published in Lancet in 2017 that looked at a Hunter Gatherer tribe in the Amazon called the Chimane and Chimane to do a lot of physical exercise. They hunt for their own food. They gather their own food. And they have a very low rate of atherosclerosis, and in fact some of their, you know, some of their 75 year olds who have no plaque build up in their artery or healthier than some of the 50-year-olds we see in in West in Western society.
However, our concept of atherosclerosis is slowly changing. The cause of atherosclerosis is not just purely fatty, fibrous plaque or cholesterol build up in the walls of arteries, and that’s one of the key factors that I try communicate to patients when I talk about talk about plaque. Atherosclerosis is actually a complex interplay between the build up of plaque, the role of chronic inflammation in plaque, and actually more and more we are finding the link between bone marrow cells, inflammation and plaque buildup. So it is not as straightforward as just thinking about the higher your cholesterol, the more the more plaque buildup you’re going to have and that’s why over the last few years there’s been a big focus on inflammation and we know we like to think about a patient, you know, So what is both a vulnerable patient? And the second thing is what is vulnerable plaque.
And we know that vulnerable atherosclerosis plaque in in coronary arteries includes plaque that is inflamed with lots of inflammatory cells. That is quite lipid. That is quite, quite lipid rich, lipid rich. And then that is compounded by injury to the plaque. And in fact, that’s what happens when someone has a heart attack on acute thrombotic event in your coronary artery, you have a vulnerable plaque that is that then gets a further insult or injury and lots of things cause insult injury from poor dietary choices, high fat meals, high amounts of, you know, nicotine consumption. Poor dietary choices, lack of exercise. All of these contribute towards an inciting event in a vulnerable plaque. So atherosclerosis, I think we’re learning is a much more complex mechanism than just the accumulation of cholesterol plaque in arterial walls and also it’s a it’s a dynamic process.
So there is lots of activity going on in plaques and there’s work being done to try and try and look at that activity and we’re starting to image on when my area of interest is cardiac CT, we’re starting to look for factors in part build up in coronary arteries that may make patient more vulnerable. And also the mind, eventual cardiology colleagues are looking at ways looking at vulnerable plaque using intravascular ultrasound. So the message I try get to my patients is that at first chlorosis starts early, it’s a dynamic, it’s a dynamic process. There’s a very strong association with inflammation. And there have been some recent trials in the last few years that have looked at treatment using anti inflammatory to reduce atherosclerotic risk. Some of these were included the use of hypostasis and patients with elevated CRP, leaving the use of some novel anti anti-inflammatory medications and more recently there’s been a trial of a culture scene as well and chronic coronary syndromes or acute coronary syndromes.
So more and more we are thinking about what are the residual risks we need to address in atherosclerosis. And this brings need for the patient in front of you with atherosclerotic vascular disease. One of the key pearls I learned from this year from Paul [inaudible], who was one of the Chiefs chief authors on and he’s done a lot of the seminal work about inflammation in coronary artery disease is what is the residual risks of the patient in front of you with atherosclerosis? What is their residual lipid risk? Are there early LDLCs to target? Was the residual LPA level risk? What is their residual inflammatory risk? Have you measured HSRP, and the last part is what is the residual thrombotic risk?
Is aspirin and well, there’s been a lot of talk about whether aspirin is enough to prevent atherothrombosis or clot formation of coronary arteries and in some people it is actually not enough and we have to think about stronger blood daily medication such as such as [inaudible] or [inaudible] or there was a very nice under publicised study called the Compass trial that use low dose anticoagulants, low dose [inaudible] at 2.5 BD. You know with the with an anti-platelet agent. So it’s an exciting
At what age does a build up of atherosclerosis usually present?
Jason: So we know that atherosclerosis starts early early in life and interestingly in some of the work done by [inaudible] and his team used in a study called the Pisa Study and in some of the work called the Cardia study as well is. We’ve seen the early buildup of atherosclerosis in femoral arteries interestingly enough, using femoral artery ultrasound in people in people in, in their 30s. And that has been strongly associated with lifestyle habits and has been in the in the Cardia study, which looked at atherosclerosis in young people and then followed them for event rates later in life, the group that had they divided the group into 4 into 4 four groups, the highest level of of LDLC and the lowest. And if you had a higher level of LDLC or more atherogenic or more atherogenic cholesterol and sometimes we call it non HDLC. You had an over 10% increase in subsequent event rate event later, later in life.
So just like we talked about with I’ve we talked to people about smoking pack years the amount of time they’ve been exposed to nicotine. We can think about how many years has the patient in front of us been exposed to higher levels of more atherogenic lipoproteins and that exposure will be directly for most people will directly than proportional to the future risk of developing atherosclerosis. So, we know that atherosclerosis starts in the young. It may not always occur first in the coronary circulation. That’s where in my area where we often see it, where people come to see me for heart disease. But it can occur in peripheral arteries. And so such as the femoral artery. Earlier than the than the coronary circulation, and I think it found. That there is. A greater opportunity for prevention earlier in life.
What are the risks of the build up?
Jason: The risk of build, there are a few different fold risk of build up the risk in and when we talk about you know heart disease, we talk about the coronary arteries, but you know atherosclerosis is not just confined to the coronary arteries. We often see in the carotid vessels the intracranial vessels and also the peripheral vessels, so. Build up of atherosclerosis may cause you know, as it gets severe build up, it may cause stenosis or narrowing, and then we get end organ dysfunction, whether it be claudication in legs, angina, angina manifestation in the heart or, you know, the brain. Sometimes there isn’t a warning, but sometimes presents with a stroke, a stroke, or a TIA.
But it’s not just, especially in cardiology we need to move away from just the percentage stenosis, because sometimes a 50% or 60% narrowing in someone’s LAD may be causing the functional significance, while a 70 or 80% and a smaller in a smaller blood vessel may not be causing any symptoms. And as mentioned earlier, we know that atherosclerosis is a complex interplay between, you know, between inflammation, and bone marrow cells and lipids, and sometimes even a narrowing of around 50%, may be vulnerable for that particular patient. And with that, there’s been studies that have analysed men who have had heart attacks and what the what the pre-event narrowing was and mostly they’re in the range of 50 to 70%.
Now that is really important because. These men would not have had these men and women would not have had symptoms with the coronary stenosis of 50-70%. If you needed greater than 70 percent, 75% reduction in cross-sectional luminal area for people to develop angina or anginal equivalent, such as such as shortness of breath. However, these plaques of vulnerable plaques that can rupture or and we talked about the vulnerable part when these plants, fissure or rupture, you get an acute platelet thrombus forming on top of the plaque and suddenly you’re 50% narrowing goes from 50 to 100% fairly quickly. And that is your classic pathophysiology of a myocardial infarction. And that’s when we rush people to the cath lab and try to open up the artery. There’s open up the artery with the stents in a balloon as soon as possible.
How would a patient usually present and what are the treatment options?
Jason: So patients present with atherosclerotic vascular disease anywhere from being asymptomatic to being picking up a high burden of coronary atheroma and it gives me great pleasure to that more and more coronary artery calcium scores are being used by primary care doctors to assess someone’s risk and once again they are best used in the intermediate risk asymptomatic person. They’re not for symptomatic people when intermediate risk asymptomatic person that can be most useful in either upgrading their risk or placing them into a low-risk category. And there’s a great risk score calculator called the Multiethnic Study of atherosclerosis calcium score tool calculator. Where you can incorporate patients’ calcium score with a more traditional Framingham risk factors and it gives you an idea of their global risk that we know very clearly that when patients have a calcium score above 100 or even 400 that they stand to benefit from the use of statin medication of the course of their lifetime.
However, low risk ptients, often it also is a great point of discussion, cause low risk patients do not necessarily benefit from statins. And then lifestyle and diet and exercise habits become even more important. And so patients present on the spectrum they present from acute stroke, acute myocardial infarction, angina. Think about the organ and think about what are the down, what are the down the downstream, the downstream effects as my role as a preventative cardiologist. I try to pick up the risks or the development of risks before someone presents before someone presents with an event, and that’s where we use low non-invasive you know not non-invasive imaging in our in our rooms we also use a lot of functional testing you know stress echocardiography and there are certain, we know that there are certain features on stress, echo and stress, ECG that are associated with worse with worse prognosis. So, there are multiple different presentations that I think the goal in primary care is to pick up the higher risk patient with a higher burden of athersclerosis using non-invasive imaging techniques.
Have there been any developments in treatment in the last years or are there any in trials or development now?
Jason: So one of the newer therapies that we are currently trialling in in Australia is another version of another treatment of the monoclonal antibodies for PCSK 9 lowering and this is a molecule called PCSK 9 small interfering RNA molecules and these offer quite profound lowering of intra and extracellular PCSK 9 and the really interesting thing is, is you have a lower dose frequency, so initially patients may need to be injected once every three months, but then ultimately it will change to once every six months. Importantly, we know they are safe and efficacious at lowering LDL, but we are awaiting outcome studies of these and outcome studies in cardiovascular medicine. You know can take anywhere from 5 minimum of 4 to 8 or even longer of the course, the more we follow, the more we follow patients.
Now these therapies are exciting, including the PCSK9 inhibitors, because we’ve shown regression of atherosclerosis and reduction in the volume of the volume of plaque. And we have shown this with statin therapy as well. But I think a lot of us taking care of patients know that it often is very difficult to achieve LDLC levels of under you know 1.8. What the really interesting thing, one of the things I think I’d like to bring to your attention, is that the European Society of Cardiology have have suggested a much more stringent levels of LDLC in secondary prevention, which we’ve been adopting across our via our heart care network for many years. So any patient wit a stent in our network our goal LDLC is 1.3. And because we have a unified medical record, we are able to track this and we know that reduction, lower you get the LDC, the lower the chance of subsequent events. So for high-risk patients, I would say we need to be pushing harder for lower LDL C targets. And these novel therapies will be very helpful in achieving these goals in higher risk patients.
Are there any warning signs a GP or their patient can look out for?
Simon: So depending on the territory, the territory involved the two organs that I get, we worry most about is the effects of, you know, atherosclerosis on the brain. To anyone, a TIA should be thought of as you know a medical emergency because the the next event could be a stroke and unfortunately the brain tissue is not as forgiving as heart tissue to ischemia. So, I think warning sign and people getting chest pain at rest that seems typical for angina in an appropriate patient should people should also be very concerned and get into appropriate medical care as soon as possible.
One of the strongest interventions that we can do is ensure that you if someone you think is at risk having a Tia or unstable angina is to is that getting some aspirin on board as soon as soon as possible because some of the pathophysiology often involves, you know, platelet aggregation on an atherosclerotic plaque. But presentations are varied and I think some people, its also we all know that patients don’t always present like the textbooks, so I like to think about is an event happening. If it is this an at risk patient and a possible at risk event and that may need more urgent. Medical attention.
What practical advice can we give patients?
Jason: So look the practical advice to give patients is that. And I think this has been a key message in some of this podcast series is that earlier intervention and earlier lifestyle and diet and if necessary medication changes earlier in life will help prevent the build-up of atherosclerosis. I think it’s important that patients understand that atherosclerosis, or the plaque build up in arteries is not just due to cholesterol and the risk factors for subsequent event is not purely just mediated by the cholesterol level, though it will certainly help, but their dietary and lifestyle patterns, their levels of inflammation in their body from either from either food or lifestyle habits or other diseases are important.
I think it’s important the patients know that it’s possible to regress or reduce the volume of atherosclerosis and also turn what may be high risk plaque and stabilise it with the medical therapies we know that work and reduce their risk of a sudden cardiovascular event. I really would try, I really try and encourage patients to be proactive in their care and not just accept that the medication is not going to do all the work.
What role does the GP play in the treatment of the condition?
Jason: So I think the. Important role that GP’s play is identifying asymptomatic people that may be at risk. With their high burden of atherosclerosis, even the peripheral circulation in the coronary circulation or in the in the carotid or the CNS circulation, and being able to get those patients to get an appropriate preventative therapy. Now, not all those patients will need intervention. However, for the higher risk patients, I think it’s important to risk stratify them and get them on to the best possible best possible medical therapy for them.
You know, we can’t see, we can’t help patients that don’t, don’t get to us for more advanced cardiovascular test, but I think it’s important to use non-invasive cardiac testing and especially coronary artery calcium scoring to identify those patients at risk and then get them on appropriate you know guideline directed medical therapy especially with those patients with the calcium score greater than 100. Who would stand to benefit most from statin or other lipid lowering therapies?
Thank you for your time here today in the PodMD studio. To sum up for us, could you please identify the three key take home messages from today’s podcast on atherosclerosis build up?
Jason: So some of the take home messages. Atherosclerosis is complex. Lipid metabolism is complex. It’s one of the key message is not just all about your cholesterol level. Atherosclerosis is a dynamic disease with contributions from inflammatory cells and bone marrow cells. And also we are learning more and more about the types of plaques. And which plaques may be vulnerable and put patients at risk for subsequent cardiovascular events? Know that the buildup of atherosclerosis is gradual over the course of time and may be directly proportional to the years of exposure to more atherogenic lipoproteins. And also to know that lifestyle habits are mostly plant centred, diet regular aerobic exercise are all very healthy for endothelial function and can significantly someone’s subsequent risk of a heart event.
Thanks for your time and the insights you’ve provided.
Jason: Thank you