Don't Have a Coronary

Welcome to Pulse Check, the Cardiology podcast designed for junior doctors who's appreciation for work-life balance transcends waiting through up-to-date articles and 400 page guidelines. I'm James Faye, a cardiology advanced trainee based in Melbourne, Australia. This is where I empty my brain of all the practical, exam-relevant cardiology I wish someone had just told me straight when I was a BPT. The first four episodes are deliberately dense. They're aimed at second and third-year basic physician trainees staring down the REC P-written exam. Expect heavy doses of coronary disease, heart failure, vascular disease and arrhythmias. All taught the way you'll use it on the ward or in the exam room tomorrow. I've skipped a lot of the rabbit holes on physiology and trial minutiae so we can keep this clinical, memorable and reasonably useful. So whether you're cramming on the tram, doing night shifts or just trying not to piss anyone off by ordering a troponan, you're in the right place. Let's get into it. This is Pulse Check, episode one. There are four standard modifiable cardiac respectors. These are the smearfs. Hypertension, hypercholestrolemia, diabetes malitis and smoking. Firstly, regarding hypercholestrolemia. We look at LDL cholesterol. We don't tend to look at the other aspects of the lipid panel, like HDL. We target LDL and we target based on cardiovascular risk. So a patient who is low risk, we generally target an LDL of less than 3.0. Moderate risk, less than about 2.6. High risk, less than 1.8. And then very high risk, i.e. secondary prevention. i.e. patients that have had, say a non-stimmy, stemmy stroke. We target less than 1.4. The guidelines are quite clear on that 1.4 target. The stepwise management. First, we initiate a statin and uptodrate to maximally tolerated dose of either bristurver statin, so 40 mg or retorted per statin, 80 mg. There are other statins, and regarding equivalence, bristurver statin 5 mg is equivalent to a torver statin, 10 mg, bristurver statin, 20 mg and bristurver statin, 40 mg. So I remember, rasp, r-a-s-p for equivalence. I generally prescribe bristurver statin, and that's largely because bristurver statin at 40 mg is a physically smaller pill to swallow than a torver statin 80 mg. You should see an 80 mg of torver statin tablet. It is quite large. Once you're at maxedose statin and your LDL is still above target, we would add a zetamib, 10 mg, so it's just a single dose. And generally, it comes in combination pill with bristurver or retorted statin. zetamib inhibits the Neem and Pick C1 like one protein, thus inhibiting cholesterol absorption in the small intestine. If your cholesterol is still above target, you would initiate a PCS-K9 inhibitor, like Evalocumab or Repetha, or an anti-PCS-K9 silencing RNA, which is in Clisoran, if your patient meets PBS criteria. The PBS criteria is an LDL cholesterol of greater than 1.8, despite 12 weeks of maximally tolerated, statin and zetamib. And the patient has symptomatic ASCVD, a thoracic cardiovascular disease with a risk factor, or they meet the criteria for heterosigous familial hyperclistralemia. When I say symptomatic ASCVD, I mean that had a non-stemmy, stemmy stroke, signiving at peripheral arterial disease with clodication. PBS includes diabetes malitis with age greater than 60, obstructive coronary artery disease in two vessels, and by obstructive coronary artery disease we mean 50% stenosis or more, i.e. moderate in two different vessels. ASCVD in two vascular territories, that might be, say, stroke and non-stemmy, or non-stemmy and some significant peripheral arterial disease, or two major cardiovascular events in five years, like two non-stemmy and five years. Heterosigous familial hyperclistralemia is defined by a Dutch lipid clinic network score, DLCNS of six or greater, and you can look that up on MD-Calk. For the medical science as examines, worth knowing that PCSK9 degrades the LDL receptor. So PCSK9 inhibitor leads to less degradation of the LDL receptor, and so you have more LDL receptors on your hepatocytes to remove LDL from the circulation. FH familial hyperclistralemia, the genes that are largely implicated are the LDL receptor, APOB and PCSK9. LPL gene is implicated in familial hypertricleceridemia. Sometimes we use further risk-stratifying tools to help us determine a reasonable LDL target for our patients, and these include LP-little A and the coronary artery calcium score. LP-little A, I would often use if I had a young patient and we just wanted a bit more information on whether we should treat hyperclistralemia. Let's say for example you've got a patient, they're 30, they don't have that many cardiovascular risks, and the LDL is say 3.5. I mean it's kind of borderline of whether we start a ludo-stata or not, well we could check a LP-little A if that's very elevated, then that might just be that extra push to start a statin or if the patient has a family history of premature ASCVD, let's say non-stemmies and the 40s, then it's worth checking LP-little A on that index patient, and then if that's significantly elevated, checking it on first degree relatives, and then you just have that greater inclination to target a lower LDL cholesterol in patients with a high LP-little A. Statins do not lower the LP-little A, nor does a Z-tomib, only PCSK9 inhibitors lower LP-little A. It's regarding coronary artery calcium score, and this is just a non-contrast CT. It will quantify the amount of calcium in the coronary arteries and expresses it in a gatsden unit. This can be useful in, let's say, middle aged patients who have risk factors to determine a reasonable LDL target, a lot of middle aged patients, particularly those who aren't on many medications. Don't really want to start a statin, so often request a calcium score, and then if it's significantly elevated, then you kind of have greater inclination to start a statin and lower the LDL and cardiovascular risk. So statins work part of their mechanism is that they stabilize plaque and convert soft plaque to calcified plaque. So if you've started a statin on a patient, you probably shouldn't do or repeat a coronary artery calcium score, because it will become elevated if they start a statin. Moving on to hypertension. I would say an anti-hypertensive, if a patient has a blood pressure consistently of greater than 140 or 90. Some patients get white coat high-potension, and in those I would suggest that they get a home blood pressure cuff and record it regularly at home or do 24-hour blood pressure monitoring. I would start with a single-pill combination tablet, like TwinStar, which is telmosatin and lot of pain. The other indication to start an anti-hypertensive is if the systolic blood pressure is more than 130, and the patient has either diabetes malitis, age greater than 55 with clinical ASCVD, like they have had a non-stemmy or stroke, or age greater than 55 and their ASCVD 10-year risk is greater than 10%. We got that data from the Sprint trial in 2015. The first agent I would start would be either an ACE inhibitor or an ARB, or a dihydroperidine calcium phenoblocker, like amlotyping, or hydrochlorothyazide. I generally prefer ARBs over ACE inhibitors. The cost of the patient is the same, based on PBS, they've both been around a long time, but with an ARB you're not going to have to worry about a cough, which patients with ACE inhibitors can get. And still a pub target, you did two of the three. For example, twin-star telmysatin and amlotyping. I would generate for primary hypertension start with a single pill combination of the two. Telmysatin is the most commonly prescribed anti-hypertensive bi-GPs. I think it's better to prescribe something that GPs are more familiar with. So a reasonable starting dose would be telmysatin 40, with amlotyping 5 milligram. It's hard to predict the patient to patient, but if a patient's got a blood pressure of about 140 and you start that regime, you would expect it to go down to around 120, give or take. If blood pressure is still above target, you would add a third agent. So all three of ASAR, DHP, goes from Toneblok and HCT. I would probably then switch them from the twin-star to a triple combination pill, like X-Forge, HCT, which is Val-Saden and amlotyping and HCT. Or you could just add HCT to the twin-star that they're already taking. And then uptightrate that to macstose. If you're still above target, the fourth agent is Spurnalactone and guidelines are reasonably clear with that. If it's still above target, the fifth agent tends to be either one of Prazason, Moxonodin, Beta-Blocker, like Carvetolol, which is an alpha-1 antagonist as well. And then you would choose the agent based on the patient in front of you. Moving on to Anjyna. By definition, anjonal chest pain has all three of the following. Constricting chest pain, provoked by exercise, relieved by wrist and nitrates. So I remember that I'm on XCPR. And then I'm on XCPR. A typical Anjyna, by definition, has two out of the three. And then non-anginal chest pain has zero or one out of the three. When patients present the ED with chest pain, it's not generally with anjonal chest pain. Sometimes they present with crescendo Anjyna, which is anjonal chest pain that over the last few weeks is becoming more frequent and lasting longer sometimes at rest. Merit's admission and an angiogram, because that's essentially unstable Anjyna. But patients with chest pain, when they put it to ED, it's usually acute chest pain. When I think about cardiac chest pain, I think acute central crushing chest pain. Sometimes they describe it as a tightness or a pressure. And sometimes it's just dull and non-specific. Plus minus radiation to the jaw and arms. Plus minus associated dysnia and nausea. Chest pain that's less. likely to be cardiac and I say less likely sometimes we're fooled is pain that is positional, pleuritic, palpable, prolonged for more than 30 minutes with negative triponans and pain that is very brief less than 15 seconds. You can think about the peas. The reason why prolonged chest pain more than 30 minutes with that negative triponans is unlikely to be cardiac is because if you're having ongoing cardiac chest pain, the chest pain implies a schemia to myocardium. So it's going on more than 30 minutes if it truly is a schemia by that time you're going to have a triponan rise. So if you've had more than 30 minutes of chest pain and you've got negative triponans then it's probably not a schemic or cardiac chest pain. When a patient presents ED with chest pain you should stratify as either low intermediate or high risk. So high risk is that cardiac sanding chest pain with triponan rise with ECG changes with respecters. These patients merit admission in angiogram. Low risk chest pain would meet a number of those criteria for non cardiac sanding chest pain. They don't really have risk factors. They look well, no ECG changes negative triponans. These patients can either be discharged or if there's an aspect of uncertainty can be referred for rapid access chest pain clinic. Intermediate risk are those patients falling somewhere in between? You're not confident enough that it's non cardiac to just discharge them but they don't really mirror it any angiogram. So if for these patients, intermediate risk patients you would do a non-invasive coronary assessment. And we divide those into functional tests including stress echo which can be exercise stress echo, debutamine stress echo, myocardial perfusion scan or an anatomical test like a CT coronary angiogram. This is a non-invasive coronary assessments. The two main ones are stress echo and CTCA. Different hospital networks will have different access to these two tests. Trials like the promise study in 2015 have shown no significant difference in outcomes, whichever of the two you choose. Your treatise is based on what your institution offers. So some institutions will have a stress echo waiting list a week or less while CTCA wait lists can be you know two, three months and then some institutions will have the opposite availability. So a stress echo involves patient having a baseline echo looking at left ventricle in a number of different views. Often they also look at some diastolic parameters as well and cursorally look at the valves. And then the patient goes on a treadmill. It follows what's called the Bruce protocol in every three minutes. It becomes faster with a greater incline until the patient hits what we target as 85% of their maximal predicted heart rate. And then they stop when they've hit their limit. They lie back down the bed and get another targeted echo looking for regional wall motion abnormality. A positive stress echo is when you've got exercise induced regional wall motion abnormality or they've got horizontal or down sloping ST depression associated with chest pain. If a patient doesn't get to 85% maximum predicted heart rate it can be a non diagnostic test and in which case you might need either a CTCA or a myocardial perfusion skin. As a rule of thumb a positive stress echo suggests that there is at least 70% stenosis in some coronary artery. So a stress echo is preferred over a CTCA if there is a high pre-test probability of the patient having some coronary disease. For example the patient has risk factors like diabetes, significant CKD, hypertension they've had prior MI because the information you can gain is if the patient functionally has a significant stenosis I use 70% or more. And you know they have coronary disease they'll probably do. You just want to know if something 70% or more are you doing it to think about stenting or optimizing anti-enginals. In contrast a CTCA it's a contrast CT scan of the coronary arteries. It's a very good rule out test. It is preferred if the patient has very few comorbidities. For example let's say you've got a patient in their 40s or 50s with very few cardiovascular risk factors and they're getting some chest pain. You can do a CTCA and then you might see just smooth coronaries or just very minor plaque. In which case you can provide that information to them and you also obtain a calcium score. You can give that to the patient as well. You can very reliably rule out significant coronary disease as the chords for their chest pain and also use the calcium score to guide statter initiation and LDL target. Why do we don't like CTCA's over stress echo in someone who has significant risk factors and likely has significant coronary diseases because when you have heavily calcified vessels it can be difficult to decide is there some aspect of the coronary arteries that is you know 70% or more. Some patients have diffusally calcified vessels really hard to interpret the CTCA and they'll just go on to get an angiogram anyway whereas the stress echo may have been a better choice than those because a negative stress echo would mean that they don't have anything that say severe enough 70% or more. Alternatively a myocardial fusion scan and this is generally used if the patient has an equivocal stress echo or if they're just unable to exercise. The alternative here if they were unable to exercise and you wanted a functional test would be a debutamine stress echo myocardial fusion debutamine stress echo you could consider them as reasonably interchangeable. Some institutions will have a better myocardial fusion reporting service say or someone might have better access to the debutamine stress echo so it really depends. Myocardial fusion is also might be better if they have a left bundle branch block because it's really hard to interpret regional war-motion abnormality in the septum patients that have a bundle branch block. So with a myocardial fusion scan we use the radio tracer like Technician 99M system maybe that's almost universally used the other option is Stallium 201 and they get a stress agent so this includes simple exercise on a treadmill that's actually the preferred stress option or a pharmacological agent like diaper remol this is Percentin adenosine or debutamine. So diaper remol and adenosine are both vasodilators they work because stenosed coronary arteries won't dilate the non-sternosed ones will so you get signs of inducible oschemia and differential radio tracer uptake. These two can cause bronchoconstriction so avoid them in severe asthma or CPD and can worsen high-grade AV block. diaper remol has a slower onset of action but has less intense adversifix. Both diaper remol and adenosine are inactivated by caffeine and aminophilin. diaper remol and adenosine won't significantly increase the heart rate whereas debutamine will you'd still need to get that 85% maximum predicted heart rate with the debutamine. Diaperidomol works by inhibiting cellular uptake of adenosine which is then free to act on coronary smooth muscle. Regarding management of stable angina the ischemia trial in 2020 randomised patients with stable angina with moderate to severe ischemia on stress testing to an initial medical management with optimal anti-inginal initiation and uptitration so patients got to an average of two to three anti-inginals versus an initial invasive approach with PCI and this study showed no difference in major adverse cardiac events and all caused mortality at five years. The caveat is that most enrolled patients had a CTCA to rule out left-means stenosis severe left-means stenosis merits cags. When I talk about the anti-inginals my general stepwise regime would be first you would initiate one of three of a die-hard repeating calcium chino blocker like amlotapine which causes coronary vasodilation reduces the afterload the main adverse effect with that one would be swollen ankles a beta blocker which works by increasing the diastolic time to increase the blood flow through the coronaries which occurs during diastole the main adverse effects of that one would be exercising tolerance a rectile dysfunction as well as bronchospasm which is actually quite minimal and a nitrate. This can be isolated by mononitrate which is tablet or a GTN patch. Sometimes we refer to GTN patches as five milligrams which is five milligrams per 24 hour or we refer to it as like a nitro 25 which is 25 microg per minute which is equivalent to five milligrams per hour so GTN patch also comes in 10 milligrams which is 50 microg per minute. The nitrates caused coronary vasodilation and they reduce preloading afterload reduces my cardiovascular stress the main adverse effect with nitrates is headache. So generally with anti-inginals you would initiate one two and then three of those three agents. The fourth thing you would introduce would be nickerandle which has dual properties of a nitrate stimulates guanolate cyclase and a potassium channel agonist. It's main adverse effects include headache but tends to be less significant than with nitrates and there's also a risk of GI ulcers with nickerandle. The fifth agent that we would use in refractory angina would be perhexaline. We don't use that a lot it really is not that effective and it can cause hepatotoxicity and preferl neuropathy but the mechanism of action is that it is a mitochondrial carnitine parmatoil transferase inhibitor which thus reduces cardiac fatty acid oxidation and it switches the fuel source of the myocardium to glucose. Another trial worth knowing is the orbiter study in 2017 in patients with stable angina on optimal medical therapy patients were randomized to PCI versus sham PCI. These patients had no difference in symptoms. Moving on to myocardial infarction. The fourth universal definition of myocardial infarction is a tropone elevation greater than equal to the 99th percentile upper limit of normal i.e. a height sense to be tropone of t of greater than 14 with a rise in fall pattern and we generally quote about 20% as the threshold for a rise in fall and a feature of ischemia. For example ischemic chest pain ischemic ECG changes or regional wall motion abnormality on a neco. You need both of these things to define myocardial infarction. Tropone elevation without a feature of ischemia with a rise in fall pattern is a cute myocardial injury. This could be triggered by takeeridmya like fast AF, acute dick compensated heart failure or sepsis. But if they don't have that feature of a Schemier, it's not by definition a myocardial infarction. So we call it acute myocardial injury. Sometimes I'll refer to this as non- ischemic myocardial injury to avoid confusion because acute myocardial injury, some people think, oh, that's AMI, but it's not, it's injury. Sustained treatment and elevation with the outer rise and fall pattern with no feature of a Schemia would be chronic myocardial injury. And you can see this in CKD, LVH. And in chronic myocardial injury, even though the patient's not infarcting, these CKD, LVH patients with the static troponins of, you know, the 90s, hundreds, the higher the troponin, the worse prognostic sign. Patients with end stage CKD, the most common cause of death is cardiovascular disease. Then myocardium is sustaining chronic myocardial injury. There are five types of MI. Type one is intracoronory thrombus or plaque rupture. This is traditionally what I refer to as a myocardial infarction. Type two is demand a Schemier. This could be due to fast AF, think I'm saying a half-halleus sepsis severe anemia. There needs to be some feature of a Schemia to refer to it as a type two MI. Otherwise, it's just acute myocardial injury. We never refer to it as type two non-Stemmy. So a non-Stemmy is, by definition, a type one MI. Demand a Schemier is type two MI. That these patients don't generally benefit from any anti-cogulation. Like therapeutic clixine, we can ask this all the time. Should we deform it, it has therapeutic clixine for these type two MIs. There's no evidence to suggest any benefit. When you think about clixine and heparin for plaque ruptured mechanistically, you're thinking about stabilizing the rupture and reducing the risk of further thrombosis and blocking off the vessel. It's a demand a Schemier. That's not happening. They haven't had any plaque rupture. The treatment is treat to the underlying cause. Same with type two MI and acute myocardial injury. The higher the trapponin goes, the more likely they have underlying significant coronary disease. Sometimes in type two MI or acute myocardial injury, it the trapponin rises to a very high level. Sometimes after the offending disease process has resolved and went safe to do so. Sometimes we will do coronary assessment and sometimes that is an angiogram. Type three MI is death where biomarker values are unavailable. Type four MI is related to either PCI. That's four A or stent thrombosis. That's four B. And now criteria that the prenat has to go greater than five times up in the middle of normal with ST, QA's, echo or NGO findings. Type five MI is related to CAHG's coronary artery graft surgery. That requires trapponin more than 10 times up with an abnormal with QA's or echo findings. Trapponin is more sensitive than CK for myocardial infarction. So that is generally used by default in the emergency department. However, CK returns to the normal range much quicker than trapponin, which can stay elevated for weeks after an infarction. So it's more useful if there's concern for re-infarction in the month post MI, where trapponin will remain elevated. CKMB, most labs no longer perform it. Cardiomyocytes express trapponin T and trapponin I whilst skeletal muscle cells express trapponin C. Sometimes we see trapponin elevation in ribdomylicis and myocytis. This is because injured or in an acrotic skeletal muscle cells can have transient re-expression of trapponin T in the skeletal muscle. And that's because the degenerating and regenerating in the have immature forms when they're regenerating. And so they produce some trapponin T. With stemmy and non-stemmy, what we don't want to miss is an occluded vessel. There are two main features that a coronary artery is occluded and needs urgent angiography and PCI. And those are ST elevation and refractory pain. There are schools of thought to change the name of stemmy to OME, occlusion MI, because it's just better than the ment glitcha. And there's thoughts from some ED practitioners that there's delayed to care in non-stemmies with occluded vessels. So generally, if we have a non-stemmy, if they have refractory pain, despite their best efforts with GTN and fentanyl, we would take them to lab. Because what we don't want to miss is occluded vessel, because that's just myocardium that is dying. But a non-stemmy that is pain-free and stable, generally, when we do an endogram, the vessel is open. You might see some severe stenosis with some evidence of thrombus. But as long as the vessel's open, no infarction is actively occurring or ischemia. When we receive a call about a stemmy, or a stemmy comes to ED, they're in the ambulance, the general advice we give is they should have aspirin through 100 milligrams. They should have hepron at 4,000 to 5,000 units. It's about 60 units per kilo, bolus, IV, and sublingual GTN and fentanyl, aiming pain-free, if possible. When we activate the lab, it's about 30 minutes before all members of the team are present. So that includes interventionalists, registrar or fellow two nurses, a scrub nurse, and a scout nurse, a radiographer, and a cardiac tech. If the patient is hypertensive, they'll be sudden on either noradrenaline or adrenaline. If they're hypertensive and they have an inferior MI and RV failure, they should be given IV fluids. RV failure is the triad of hypertension, raised JVP, and a clear chest. The acute marginal branch of the right coronary artery comes off the junction between proximal to mid-RCA, that's the defining portion between proximal and mid, and that supplies the right ventricle. So a proximal RCA occlusion can lead to RV failure, and RV failure is preload dependent, so they should be given fluids and avoid GTN. You can do a right-sided ECG, and you might see ST elevation in V3R to V6R to suggest RV infarction, but rarely is this done in practice. In a STEMI, if there is high grade or complete AV block, and there's severely bradycardic or unstable, they should be given atropine. This is more common in an inferior MI, because the AV nodal branch comes off the PDA, and 85% of people are right dominant, so the PDA comes off the right, 15% left dominance, the PDA comes off the left circumflex. If they complete AV blockies for fructory, and they're severe brady arrhythmia, they need transcutaneous pacing, until a temporary transvenous pacing wire can be inserted in the cath lab. Regarding initial non-STEMI care, so let's say they've had a bit of atropine and rise, they've got some ECG changes, but they're currently pain-free and unstable. We would advise aspirin, therapeutic clixane, PRN, sublingual GTN, and fentanyl, if they have pain, and we would do an angiogram on the next available list. If there was concern that they may have ongoing pain, we'd probably hold off the therapeutic clixane for now, and advise hepron infusion again. We would prefer not to do an angiogram within 12 hours of giving therapeutic clixane. You still can, but it's just greater risk because it's less reversible than hepron. With a non-STEMI and a STEMI, we generally don't give the second anti-plaitlets until after they've finished in the cath lab. Giving the second anti-plaitlet, I eat the P2Y12 inhibitor, tachygrilore, clopidogrel, before taking them to lab is referred to as the upstream approach, and the guidelines suggest that routine upstream P2Y12 inhibitor confers no added benefit. It increases the bleeding risk, and it can delay cardiac surgery if the patient is needing urgent cags compared to just giving it downstream, i.e. after you've stinted the vessel. There are three main causes of ST elevation. These are STEMI, pericarditis, and benign early repolarization. So a patient has ST elevation. It's probably going to be one of these. There are other causes. ST elevation confined to a coronary territory with reciprocal ST depression is generally slam dunk STEMI. We get a lot of calls ST elevation ECG. What do you think do you want to have to meet the lab? And sometimes it is a tough call. ST elevation and T-wave inversion are both specific for coronary territories. Whilst ST depression is not specific for any coronary territory. An ST elevation in AVR with global ST depression makes you think of either left main stenosis, triple vessel disease, or a global demand ischemia. It's also worth knowing the scarbosis criteria for myocardial infarction in left bundle branch block. I like to regard as the rule of concordance. So if you've got concordant ST elevation or ST depression more than one millimeter with the QRS, then that's scarbosis positive. And what do I mean by that? Well, a left bundle is negative in V1 to 3. So concordant ST change would be ST depression in that lead. I, it's going in the same direction as the overall QRS. So ST depression more than one millimeter in V1 to 3 would be scarbosis positive. Or if you've got significant discordant ST elevation. So more than 25% of the QRS height would be scarbosis positive. Scarbosis criteria is to try to not miss occluded vessels in left bundle branch block where you can't really interpret ST elevation. But also if you've got a patient with a left bundle with refractory cardiac xanin chest pain, we would consider that as a oomy equivalent and would take them to labs. Any non-stemmy with refractory pain should go to lab. When the patient arrives in lab, we establish access and that's radial offemoral. We take a diagnostic catheter to image the likely non-coupled coronary territory. And then we take a guide catheter to the culprit coronary territory to image and intervene on the culprit. Routine radial approach, bed offemoral has a low major avas cutoff events and mortality due to less bleeding complications largely. And that was from the matrix 2015 study. Sometimes we'll find multiple significant stenoses and what do I mean by significant? By visual estimate on angiography or luminography when you just inject contrast into the coronary arteries, if it visually looks 70% or greater, instantosis, that would be considered a significant stenosis. Or if it's 50% to 69% and it's FFR positive. So FFR is when we put a pressure wire across the surface. stenosis and we check the ratio of pressure distal to proximal of the stenosis, which is adenosine and GTN to induce maximum hyperemia. If the FFR is less than 0.8, that is a significant stenosis. That was from FAME 2009. So the FFR guided PCI had better outcomes than angiore, just visual guided PCI in multivessel coronary disease. So if you find multiple significance stenosis, if the patient is in shock, you should stand just a culprit vessel only and that reduces the total procedural time, the total contrast load, get some off the table quicker and to ICU quicker when their ion tropes can be tutrated easier. Whereas if the patient is not in shock, you should stand all significant stenosis and that can be either immediate or staged PCI and the staged can be impatient or can be outpatient staged PCI. So generally you're sent the culprate lesion first if they have no shock and then often you would do inpatient or outpatient staged PCI on the non culprate lesions. And that all comes from the complete revascular trial in 2019. It's also multi-stars AMI in 2023. Furthermore, routine thrombor aspiration is not performed as twice the stroke risk compared to PCI with no benefit to major berschatic events. That was the total trial in 2015. We do still use thrombor aspiration in heavily thrombotic lesions, particularly in right coronary arteries. Sometimes you'll get a plaque rupture and there'll just be thrombus and plot throughout the vessel. You might be able to wire it, but you simply, you don't know where you're going, you don't know where to stand. And so in these cases we might take an aspiration catheter and to thrombus aspiration in these vessels. In these cases often we can't stand anything. If we were to stand we would just fill with clot and be useless. We put these patients on dual interplay with therapy, hiprin infusion, bring them back in a few days and have another look and often we can find something to intervene on them. After PCI we would give the second anti-platelet. Clipeter growl, it's mechanism of action is that irreversibly inhibits the P2R12 subtype of the ADP receptor, thus reducing platelet activation. Clipeter grow is metabolized by SIP2C19. Whilst Ticagrullol is a irreversible P2R12 inhibitor and we regard it as a potent P2R12 inhibitor. A small portion of people get Ticagrullol induced dysnia, which is thought to be a denocene mediated. And in these patients, if it persists for more than a few days or prior to discharge, most people would change them across to Clipeter growl. If a patient has high thrombus or thrombur symbolic burden, sometimes you'll stent a vessel and you'll get a distal symbolic shower that reduces flow in the distal vessels. In these patients you can give a 12 to 18 hour tyrophyban infusion. Tyrophyban is a reversible glycoprotein 2B3A receptor inhibitor. Ab6CMab is an irreversible inhibitor. We don't use it at our institution. If a patient has an indication for intercregulation, for example, they have a true fibrillation, an ov thrombus, or a histriff PE, and they're long term dog or intercregulation. We would generally give 1 to 4 weeks of triple therapy. So that's aspirin clipeter growl and the intercregulant, whether it be dog or wolf or whatever. And then you would give the intercregulant plus clipeter growl for 12 months and then just the intercregulant monotherapy. We generally give dual antiplate with therapy for 12 months after ACS and 3 to 6 months after elective PCI. After a stemmy, you would stay in hospital for somewhere between 3 and 5 days, a shorter duration for a lesser infact as guided by the CK rise and the echo findings, and also just hematonomics in general, and a longer stay for a more significant infact, so like a big LED infact with LV dysfunction, CK of 10,000. During this time, we initiate some other therapies. ACS, inhibitor, and ARB are routinely used post-MI, regardless of the ejection fraction, definitely in reduced ejection fraction. In preserved ejection fraction, there is some evidence to suggest that reduces cardiovascular events and remodeling, particularly in high-risk patients. It's class 2B to initiate routine ACS ARB in preserved ejection fractions, is based on the hope 2000 and Europa 2003 trials. Regarding beta blockers, these were previously used routinely, but most are switching away from routine use in preserved ejection fraction, because there's no evidence of benefit in routine use post-MI with preserved ejection fraction. It's based on recent trials like the reduced AMI 2024, the reboot CNIC in 2025 and the Abyss 2024 studies. There are four scenarios where surgery, like Cags or Cabbage, has better outcomes than Multivessel PCI. These are triple vessel disease with decreased LV function. This was the Stitch Study 2011. Triple vessel disease with type 2 diabetes. This was Freedom 2012. Left main stenosis. The main study there was Noble in 2019, and in complex Multivessel disease with a syntax score of 22 or greater. This was the syntax study in 2009, and the syntax score is a scoring system based on complexity of coronary disease essentially. Regarding Cags, Gen. 4-5 hours, depending on how many grafts, and the patients will stay in hospital for usually 5-7 days. Regarding grafts, the Lima left internal mammary artery, or Lita left internal thoracic artery, has a very high 10-year graft potency. The Lima will generally go to the LAD. The Lima never dies, and it is highly effective. The next best will be the Lima right internal mammary artery, 10-year graft potency, 97%. The next best will be the radial arteries, 90-2% 10-year potency, and the next best will be a saffonous vein graft. About 82% 10-year if the patient is on aspirin and statin. Generally, you would put the Lima onto the LAD, you might put a radial onto the next most severe lesion, and you would put a vein on the other less significant lesion or lesions. Regarding delayed presentation myocardial infarction, the open artery trial or OAT trial showed that in late presentation, a clusive MI, so 3 days or more delayed presentation before you've done the inggram. With poor absente flow of the culprit artery, there's no difference in PCI versus medical management if they're stable, particularly if they're pain free. In these patients, if we think the occlusion has been there for 3 days, they've probably infarcted all, if not most, of that coronary territory, and whatever is remaining has been salvaged or picked up by collaterals that have formed from the other arteries. As a general rule, there's no significant benefit in opening up that occluded artery. That is, you know, you can see Q waves are present, the ECHO shows it's a kinetic and the patient's pain for it is probably no more, you know, myocardium left to infart. However, if they have ongoing pain, it implies there is still myocardium left to infart, and they should probably have PCI to salvage that remaining myocardium. In patients that have persistent ST elevation days, two weeks, or longer post their event, this can be due to alveanurism or dyskinesis. A CTO or chronic total occlusion is defined by 100% occlusion for three months or more. In these patients, you can set a PCI if they're symptomatic, and there's been two RCTs that have shown symptomatic and quality of life improvement compared to ocular medical therapies. It's a Uricitio and impact the CTO. After an infart, if the patient has regional hypo or acinesis, there are three main possibilities. Firstly, they could have infacted myocardium. This myocardium will not recover. If you did a cardiac MRI, it would show that territory is non-viable. Greater than 50% transmural lake-gan enhancement. IE scar in that territory. It is infacted. It would not get better. Second possibility, it could be stunned myocardium. Even after a transient occlusion, let's say to an LED, 10 minutes of chest pain, then they've become pain-free, done an angiogram, you've found a lesion, there's good flow, you've stunted it, and they've only had a small trooperized. They might still have hypochinesis in that LED territory, and it's just because the myocardium is stunned, and you would expect resolution or improvement in days to weeks. The third possibility is they might have hibernating myocardium. This is where your post-dyschemic territory remains at least partly alive, but it has adapted to a low-flow state by denregulating metabolic and contractual activity. This is common in myocardium that is supplied by a chronic totaly occluded vessel that has had collaterals form from elsewhere, and let's say not the briskest of flow is getting through to that myocardium from the collaterals. They've got some hypo or even a canesis there. If you did a cardiac MRI, you might see that there's less than 50% transmiral late-gadolineum enhancement i.e. that is still viable myocardium, and that patient might actually benefit from opening up the CTO or putting the graft to the area that is supplied by collaterals. So that's where cardiac MRI is very helpful for what's called viability testing. Debuted in stress echo and myocardic perfusion scanner alternative options, but this cardiac MRI is best. Lastly, regarding fibrolysis or thrombolysis, TPA altoplae's give if it is within 12 hours of the onset of chest pain, and it's anticipated to be two hours, 120 minutes, door to balloon time. The criteria for success is resolution of chest pain and the ST elevation reducing by 50% or more. If the patient has accelerated idioventricular rhythm, this is highly specific for re-proficion. This is like slow VT. After you've performed fibrolysis, and you know you've given the agent, they should be transferred emergentally to a center that can do PCI. Instant re-sternosis refers to gradual narrowing of the stentolumine over time due to near-into-more proliferation, resulting in angina, usually years after stenting. This was a common issue in bare metal stents. Bare metal stents are generally not used anymore. Our cathode doesn't stock them, almost universally, drug-eluding stents are used these days. In drug-eluding stents, compared to bare metal stents, stent thrombosis is more of an issue, particularly in the first year, before the stent struts have had time to end a thelialized, because those stent struts are pro-collegialable, hence the period of dual anti-platelet therapy and the importance of adhering to them. Stent thrombosis is acute occlusion of the stent judoclott, it generally presents as stemmy. Minoka refers to myocardial infarction with non-obstructed coronary arteries. So this would be your patient's presence with cardiac chest pain, got a truponan rise, they may have easy due changes, you're taking to cath lab, doing an angiogram, and they've got no obstructed coronary artery. We can't see a culprit lesion, this is minoka, it's usually one of four things. Myocarditis, vasospasm, tacatubo, cardiomyopathy, or recanalyzed or overlooked plaque rupture. A cardiac MRI will establish the diagnosis in about 75% of cases. It has an ESC Class I recommendation for use in minoka. Vaisospasm can be provoked with intracuronary acetylcholine, this is called vasospasm testing, and then when you give intracuronary GTN, this improves. Spontaneous coronary artery dissection was scad, typically it occurs females aged 50s or less, it's associated with fibromuscular dysplasia, and so we generally screen these patients with abdominal and head neck contrast CT to look for FMD, like renal artery stenosis, as well as aneurysms. This is generally managed with aspirin, beta blockers, and cancelling to avoid heavy lifting and devalcellver. There are several mechanical complications of myocardial infarction. The three main ones are ventricular septal rupture, this is like a VSD, and this is a harsh pan systolic murmur. Papillary muscle rupture, this is pan systolic MR like murmur, usually it's actually quite soft. This is more common in inferior myocardial infarction because the postero medial pap muscle has a single supply from the PDA, whilst the anterolateral pap muscle has dual supplies from LED and circumflex. And the third mechanical complication is LV free wall rupture. All three of these are surgical emergencies and merit urgent transfer to a surgical centre. Finally, there are a number of cardiac driving restrictions based on VicRoad's guidelines. A PCI can't drive for two days, AMI is two weeks, so it's non-stemmy or stemmy, or SCAD or monocard, we generally lump into there, two weeks, pacemaker is two weeks, cardiac syncopy is four weeks, Cags is four weeks, cardiac arrest is six months, if there's nothing clearly reversible with no revascularisation, so like an out of hospital via for rest, that is taken to the lab and has an occluded LED and we stand to that and open it. That's still just two weeks, so even though the phaticardic arrest, it was clearly reversible and we fixed the offending reason for the arrest. Unexplained syncopies, six months as well. That's it for this episode of Pulse Check. Perhaps you'll feel less terrified about calling the cardiology red overnight about that non-stemmy with ongoing pain, just don't go giving them click saying it for I am or you will feel their wrath. Thanks for listening, look after yourselves and I'll catch you in the next one.