Coronary Artery Disease (ABIM Review)

I'm Dr. Griffin. And I'm Dr. Taylor. Welcome, everyone. You are joining us for Evidence at the Bedside Board Review Edition. Yeah, so glad to have you all here. If you are tuning in, you are likely preparing for the ABIM exam, or perhaps you are just looking to solidify your clinical reasoning. Either way, you are in the exact right place. Today, you are joining a dedicated board review session focused entirely on coronary artery disease, or CAT. Which is just, I mean, it's a massive topic. We are pulling from a huge stack of sources today. Oh, definitely. We have the latest ASAIE guidelines on the management of chronic coronary disease. We are looking at landmark literature, like the SYNTAX trial and the ISCHEMIA trial. And crucially, we have the most recent ABIM exam blueprints. Right, which is what we all really care about, honestly. Exactly. And our mission today is very clear. Coronary artery disease is the absolute cornerstone of the board exam. Yeah, it is inescapable. It really is. But the boards. They do not just test rote memorization. They are not simply asking you to identify a drug class or recite a normal lab value. No, they're testing your diagnostic branching logic. I mean, they want to see your understanding of long-term management nuance. They're designing questions specifically to see if you can navigate the algorithms when the clinical picture is deliberately blurry. Deliberately blurry is a great way to put it. The exam specifically preys on the gray areas. Yeah. And those critical. And those critical algorithmic decision points. They want to know if you understand not just what to do, but what to do next. And honestly, just as importantly, what absolutely not to do. Right, the contraindications. Yeah. But before we get into the material, we want to invite you to like, subscribe, and share this show with your colleagues who are also preparing for the boards. Yes, please do. Our goal is to help elevate the standard of care across the clinical community. And, well, sharing this resource helps us do exactly that. Definitely. Okay. So let's unpack this. Okay. So let's talk about the board. and we decide the patient is firmly in that intermediate zone, greater than 15%. So if Bayes' theorem tells us this patient is in the danger zone, how do we look inside the heart without causing unnecessary harm? That brings us to the great debate. The great debate, coronary CT angiography versus functional stress testing. The ABIM exam loves to make you choose between visualizing the anatomy with a CT scan and testing the physiology with a stress test. Oh, this is a major area of focus for the modern exam, reflecting recent shifts in the clinical guidelines. You have an intermediate risk patient. How do you decide? Yeah, what's the rule? The core rule the guidelines rely on is largely based on the patient's age and the clinical suspicion of the type of obstructive disease present. Let's use an analogy here because visualizing this makes it so much easier to remember. I love analogies. Imagine the coronary arteries are the plumbing system of a house. A very fitting way to look at it, especially when we talk about plaque buildup. Right, so coronary CT angiography or CCTA is essentially like sending a tiny high-definition camera down into the pipes of this house. Okay. You are looking directly at the walls of the pipes. You are looking for early buildup, the soft grime that hasn't hardened yet. This camera is absolutely fantastic at ruling out disease if the pipes are clean. It has a phenomenal negative predictive value. Exactly. Therefore, CCTA is the preferred test for patients younger than 65 years old or those with a lower suspicion of severe, established obstructive CAD. You are looking for soft, non-calcified plaque. The key word there is non-calcified. But you know what happens to the pipes in a house as it gets very old? They get nasty. Or in a patient with long-standing diabetes and renal disease, the pipes calcify. The plaque gets covered in hard, dense mineral deposits. Right, so if you send a camera into an 80-year-old heavily calcified pipe, the glare from all that hard calcium completely blinds the camera. You literally cannot see the actual lumen where the blood flows. Yeah. The technical term for this on the boards is calcium blooming artifact. Glooming artifact, right. The calcium scatters the beams of the CT scanner, making the plaque look much larger and more obstructive than it actually might be. So the anatomical camera becomes useless for determining true stenosis. So what do you do? Instead of a camera, you need a functional test. You need to turn all the faucets in the house on full blast and see if the actual water pressure drops at the end of the line. I love that. Turning the faucets on full blast, that functional test is the stress test. Exactly. You're stressing the system to see if the physiological flow is compromised when demand goes up. And that is why stress testing is preferred for patients 65 and older or those with a higher clinical suspicion of widespread obstructive CAD. Because their vessels are more likely to be heavily calcified, making the CCTA unreliable. Right. The stress test does not care about the calcium scatter. It only cares about one thing. Can the blood flow adequately when the heart muscle demands it? Precisely. Okay. So if we decide to go with the functional route, we're turning the faucets on full blast, we still have a massive decision to make. Yes, we do. We have to choose which stress test to use. The boards will give you a multiple choice list. Exercise EKG, stress echocardiogram, or a nuclear spec scan. Let's break this down because you cannot just pick one at random. No, you absolutely cannot. The absolute primary distinction here revolves around the patient's baseline resting EKG. Okay. A standard exercise treadmill EKG is the cheapest, most accessible, and honestly most physiological test. But it relies entirely on your ability to read ST segment changes, specifically ST depressions, during the peak of exercise. Right. Therefore, you can only use an exercise EKG if the patient has a perfectly normal baseline EKG and crucially is physically capable of walking briskly on a treadmill. That's a huge trap. If the baseline EKG is already abnormal, the exercise EKG becomes completely uninterpretable. For example, if they have left ventricular hypertrophy with repolarization strain patterns. Or if they have a paced ventricular rhythm from a pacemaker. Right. Or if they just have more than one millimeter of ST depression at baseline, you cannot read the test. The baseline is already skewed. Exactly. You won't know if the ST changes during exercise are due to new ischemia or just, you know, an exaggeration of their baseline. Abnormality. So what's the move when the EKG is unreadable? In those cases where the EKG is uninterpretable or if the patient is at a higher risk of false positives, you must add imaging to the stress test. Okay. Imaging. You do the stress portion either by having them exercise or by giving them a pharmacologic agent if they have bad knees and can't walk. And then you physically image the heart. Like with an echo. Yes. You can use echocardiography to look for stress-induced regional wall motion abnormalities. Essentially, you are looking to see if a segment of the left ventricle stops squeezing when it gets starved of oxygen. Or you can use a nuclear SPECT scan, which stands for single photon emission computed tomography. Yes. Myocardial perfusion imaging. Right. You inject a radioactive tracer, like technetium 99 meters, at peak stress. The tracer flows where the blood flows. If there is a blockage, the tissue downstream won't get the tracer and it will show up as a dark defect or cold spot on the scan. Exactly. Then you compare it to a resting scan. If the defect is there during stress, but fills in during rest, that is reversible ischemia. That's the one we worry about. But if the defect is there during both stress and rest, that is a dead zone, a prior myocardial infarction, scar tissue. Understanding that distinction between anatomy and function and knowing exactly when to deploy imaging over a simple EKG is fundamental to passing the CAD section of the exam. It really is. So we have navigated the diagnostic maze. We have confirmed the diagnosis of stable core coronary artery disease. What's the next step? Yeah, we have to manage it. We have to manage it. This brings us to the bedrock of chronic care, guideline directed medical therapy or GDMT. The Holy Grail. The boards will test you on the nuances of every single class of medication here. Let's start with the foundational layers, antiplatelets and statins. Right. For a stable chronic CAD, the antiplatelet therapy is generally straightforward. Low dose aspirin, typically 75 to 162 milligrams daily with 81 milligrams being the standard in the U.S. Baby aspirin. Exactly. The mechanism here is the irreversible acetylation and inhibition of the COX-1 enzyme in platelets. Which prevents them from synthesizing thromboxane A2, right? Yes, which is a potent inducer of platelet aggregation. We use low dose because it is sufficient to inhibit the platelets in the portal circulation before the aspirin is sparing enough of the COX enzymes in the systemic circulation to maintain the protective prostaglandins in the stomach lining. That's such a neat physiological trick. It really is. And if they have a true aspirin allergy like actual anaphylaxis or severe bronchospasm, what is the move? Clopidogrel is your acceptable alternative. It is an ADP receptor inhibitor, specifically blocking the P2Y12 receptor on the platelet surface. But a massive point to remember, you do not use the newer, more potent P2Y12 inhibitors like Prashagrel or Ticagrel for stable chronic CAD. Why not? Those agents are strictly reserved for acute coronary syndromes or the immediate post-stent management phase. Because a bleeding risk of those potent agents massively outweighs the ischemic benefit in a stable outpatient. Exactly. You're just asking for bleeding complications. Okay, now what about the statin? This is a place where old school clinical habits often clash with modern board answers. Yes, they do. High intensity statin therapy is absolutely required. Required. That means atorvastatin 40 to 80 milligrams or rosavastatin 20 to 40 milligrams. Here's the pearl. High intensity statins are required in established CAD regardless of the baseline LDL cholesterol level. I cannot emphasize that enough for you listening. The question stem will deliberately try to trick you. They absolutely will. They will present a 60-year-old man with known CAD who has a beautifully controlled LDL of 65 on a moderate intensity statin like simvastatin 20 milligram. They'll ask what the next best step is. And you want to say continue current management. Right. The instinct is to say that because the LDL looks great. But the answer is to switch to a high intensity statin. Period. Why? Because it is not just about the lipid lowering numbers. It is about the pleiotropic effects of the high intensity statin. Ah, the pleiotropic effects. Yes. They stabilize the fibrous cap of the atherosclerotic plaque, physically preventing it from rupturing. They dramatically reduce inflammation within the arterial wall by lowering CRP levels. And they upregulate endothelial nitric oxide synthase, which improves the blood sugar level. And they upregulate the blood sugar level. And they upregulate the vasodilation of the coronary arteries. So they're doing a lot more than just lowering cholesterol. Exactly. The mortality benefit of high intensity statins in secondary prevention is proven, irrespective of the starting LDL. Okay. Now let's talk about symptom control. A patient is having angina. What is the anti-anginal of choice? Beta blockers are the definitive first-line agents for anti-anginal therapy. The pathophysiology here is so elegant. It is. Angina is fundamentally a supply and demand mismatch. Beta blockers specifically beta-1 selective agents like metoprolol or bisoprolol decrease myocardial oxygen demand by lowering the heart rate and reducing the force of contractility. Right. But the crucial secondary benefit is that by slowing the heart rate, you prolong diastole. A coronary perfusion occurs almost entirely during diastole. Exactly. When the heart muscle relaxes, blood can actually flow through the coronaries. If the heart is racing at 100 beats per minute, diastole is incredibly short. And the sabendocardium just starves. It does. And the clinical goal, which you absolutely will see tested, is to titrate the beta blocker to achieve a resting heart rate. rate of 55 to 60 beats per minute 55 to 60 yes if the vignette shows a patient with angina on metaprolol but their heart rate is 75 they are not fully optimized precisely you must optimize the first line agent before adding a second line agent like a calcium channel blocker or a long acting nitrate right don't jump to adding drugs when the first one isn't maxed out so what does this all mean for ace inhibitors and arbs arbs of course being angiotensin the secret receptor blockers i feel like in the hospital every single patient with any history of heart disease is automatically placed on lisinopril or lusartan right in the real world it often seems that way but on the abin exam you must be incredibly precise with your indications okay ace inhibitors and arbs are not automatically indicated for every single patient with stable cad they have specific heavily tested indications centered around the need to prevent negative cardiac remodeling remodeling so if the patient just has stable angina completely normal kidney function no diabetes and the normal ejection fraction of 60 percent the renin angiotensin aldosterone system isn't the primary driver of their pathology exactly you add an ace inhibitor or an a or b if the cad patient also has concomitant diabetes chronic kidney disease an ejection fraction of 40 or less or clinical heart failure got it in those specific scenarios blocking the raa's pathway prevents the left ventricle from dilating and failing over time and it protects the nephrons but for uncomplicated stable angina and aca inhibitors not going to improve their survival and it is the wrong answer on the test good to know so we've covered the medical foundation let's look at risk stratification we briefly mentioned the coronary artery calcium score or cac score earlier yeah very useful test this is a non-contrast ct scan that just looks for the presence of calcium in the coronaries it's used to refine that pre-test likelihood we talked about if a patient is in that low to intermediate gray zone a cac score of zero can powerfully downgrade their risk absolutely it suggests a near zero event rate over the next few years often allowing you to skip further testing entirely but what about the other end of the spectrum when do we abandon all the non-invasive tests the cts the treadmills the echo and send the patient straight to invasive coronary angiography in the cath lab you bypass the non-invasive workup and go straight to invasive angiography when the patient is exhibiting high-risk features that suggest impending catastrophic failure like what this can be determined clinically for example a patient who has refractory angina despite being on maximal gdmt right if there are already taking an optimized beta blocker a calcium channel blocker and a long-acting nitrate and they still cannot walk from their bedroom to the kitchen without severe chest pain you do not need a treadmill test to tell you they have severe flow limiting disease yeah that's pretty obvious you go straight to the cath lab for potential revascularization the boards will also give you scenarios where a patient had a prior non-invasive test that showed terrifying high-risk findings yes if a prior echocardiogram or nuclear scan showed a resting left ventricular ejection fraction less than 45 in the setting of known cad that is a high-risk feature right or if a stress test shows large fixed perfusion defects or stress-induced transient lv cavity dilatation which is a fascinating phenomenon oh i love the physiology of transient ischemic dilation it implies that the ischemia during stress is so globally severe across the subendocardial system that the left ventricle temporarily fails to squeeze and the cavity actually balloons outward filling with blood yes the heart literally dilates acutely under stress if you see that on a report in the question stem do not order another test that is an automatic trigger for invasive angiography to define the anatomy for possible bypass surgery exactly do not pass go okay we have covered the deep theory the pre-test probabilities the diagnostic branching and the medical therapy but theory only goes so far until you apply it true so let's take all of this theoretical pattern physiology and put it on the wards imagine you're rounding we're going to simulate a rapid fire teaching session sounds fun we're going to test your application of these algorithms with eight specific abim style board vignettes let's dive right in case one the conduction defect you are evaluating a 68 year old woman who is presenting with stable exertional chest pain you get a baseline resting ekg in the clinic and it shows a classic left bundle branch block an lbb okay lbb you calculate her risk and you decide she needs a functional evaluation for ischemia what is the next best step the correct answer here is a pharmacologic vasodilator stress test using an agent like adenosine regedinosin or dipyridamol paired with myocardial perfusion imaging like a spec scan let's unpack the logic here why do they absolutely need a vasodilator stress test and not an exercise ekg the distractors on the test will definitely offer exercise ekg and dibutamine stress echo as options they always do let's dismantle the exercise ekg first exercise ekg is completely incorrect because of the electrophysiology of the left bundle branch block in an lbb the left ventricle depolarizes late and abnormally which fundamentally alters the repolarization phase the st segment and the t wave right it's already a mess it completely obscures the st segment depressions that you rely on to diagnose sebendocardial ischemia during exercise you literally cannot read the ischemic changes because the baseline repolarization is so wildly abnormal okay so we need imaging but why not a dibutamine stress echo or just putting her on a treadmill with imaging why must it be a vasodilator this is a massive physiological trap this comes down to the mechanics of the interventricular septum if you elevate the heart rate significantly in a patient with an lbb whether by having them run on a treadmill or by giving them dibutamine which is an inotrope and chronotrope that mimics exercise uncoordinated contraction of the ventricles causes the septum to move paradoxically the septal bounce exactly instead of thickening and moving inward during systole it bulges abnormally on a nuclear perfusion scan this abnormal rapid septal motion actually creates a false positive perfusion defect in the septum oh wow yeah it looks exactly like an ischemic blockage in the lad but it's just an artifact of the heart rate and the bundle branch block to avoid this artifact you must use a vasodilator like a denna scene a denna scene works directly on the a2a receptors in the coronary vasculature causing profound dilation of the normal coronary arteries which steals blood flow away from the diseased already maximally dilated arteries right crucially adenosine does this without significantly raising the heart rate by keeping the heart weight low the septum doesn't bounce around as violently allowing you to accurately image the true perfusion without the artifact it is a beautiful interception of electrophysiology mechanics and pharmacology absolutely moving to case two the maxed out patient okay a 72 year old man with known established cad complains of ongoing stable angina it has happened a few times a week severely limiting his ability to work in his garden poor guy you look at his medication list he is already on maximal tolerated doses of a beta blocker let's say metaprolol sussanine 200 milligrams and a calcium channel blocker amlodipine 10 milligrams you check his vitals in the clinic his blood pressure is soft let's say 105 over 65 and his resting heart rate is a perfectly optimized 58 beats per minute what is the next best step in his medical management the correct answer is to add ranolazine let's break down why ranolazine is the specific key that unlocks this question the distractors will offer things like titrate the beta blocker higher add a long-acting nitrate or add an ace inhibitor titrating the traditional medications up or adding a nitrate is entirely incorrect here because of the patient's hemodynamics yeah his numbers are low his blood pressure is already soft at 105 over 65 and his heart rate is perfectly at goal at 58. if you give him more beta blocker he becomes bradycardic and symptomatic right if you give him a long-acting nitrate which is a potent venu dilator his preload drops his blood pressure tanks and he passes out in his garden we need an anti-anginal that does not touch the hemodynamics enter ranolazine the mechanism of ranolazine is utterly unique it really is it does not lower heart rate it does not dilate blood vessels it works at the cellular level by inhibiting the late inward sodium current in the myocardium right during ischemia the myocytes get starved of oxygen and this late sodium current stays open too long leading to a massive intracellular buildup of sodium the cell tries to pump this sodium out using the sodium calcium exchanger but in doing so it pulls massive amounts of calcium into the cell which is bad news terrible news this calcium overload prevents the heart muscle from relaxing during diastole increasing wall tension which compresses the microvasculature and worsens the ischemia ranolazine blocks that late sodium current preventing the calcium overload and allowing the muscle to relax the beautiful thing is that it does this without affecting blood pressure or heart rate at all it is the perfect add-on for the hemodynamically maxed out patient but there is a major caveat you must watch out for in the question stem regarding ranolazine yes the side effects and interactions you must watch the ekg for qt prolongation ranolazine blocks the rapid delayed rectifier potassium current which stretches the qt interval increasing the risk of torsades of point furthermore ranolazine is heavily metabolized by the liver via the cyp3a4 enzyme system so drug interactions are huge you must strictly avoid ranolazine in patients taking strong cyp3a4 inhibitors the boards love to test drug drug interactions if the patient is taking clarithromycin for an infection or certain azole antifungals like ketoconazole or protease in inhibitors for HIV, those drugs will block the CYP3A4 enzyme, which causes ranolazine levels in the blood to spike dangerously high, leading to massive QT prolongation and potentially fatal arrhythmias. The phenomenal integration of pharmacology and clinical management. Let's keep the momentum going. Case three, the syntax logic. Okay, this is a big one. A 64-year-old man with a long-standing history of type 2 diabetes presents with worsening angina. He undergoes invasive coronary angiography in the cath lab, which reveals severe, complex three-vessel disease. Three vessels got it. Specifically, the blockages include the proximal left anterior descending artery, the LAD, often called the widowmaker. The question asked for the most appropriate revascularization strategy for this specific patient. The correct answer is coronary artery bypass grafting, or CAVG. The distractor here will absolutely be PCI percutaneous coronary intervention, which means going in with wires and balloons, deploying multiple drug-eluting treatments. Why is PCI the wrong choice for this patient? PCI with stents is incorrect because in this specific population, the historical trial data, specifically the landmark syntax trial and the freedom trial, is incredibly clear. Undeniably clear. CAVG is proven to significantly lower the rates of repeat revascularization, and crucially, it improves overall survival. We are talking about reducing the composite endpoints of death, myocardial infarction, and stroke. This survival benefit is seen specifically in diabetic patients with multi-vessel disease. Why does diabetes change the arithmetic so drastically? It comes down to the nature of the plaque. Diabetic patients do not just have discrete focal blockages that are easy to stent. They have diffuse, incredibly calcified atherosclerotic disease that runs the entire length of the vessel. If you try to stent that, you are just laying metal across long segments of diseased endothelium, which has a very high rate of instant restenosis and failure. Exactly. CAVG bypasses the entire disease segment entirely by attaching a clean conduit, like the internal mammary artery, distal to the blockages. The boards want you to recognize this algorithm immediately. Multi-vessel disease plus diabetes equals CAVG. It is one of the most reliable algorithmic rules on the exam. Okay, let's look at case four, the tricky ACS timing. This is a classic trap that catches even seasoned residents. Yeah, I've seen this happen. A 55-year-old woman presents in the emergency department with severe crushing chest pain, radiating to her jaw. Her ECG shows significant ST-segment depressions in the anterior leads, and her high-sensitivity troponin is markedly elevated. Okay, so NSTEMI. Exactly. She is diagnosed with a non-ST-elevation myocardial infarction and NSTEMI. Despite being given the standard medical therapy aspirin, a P2Y12 inhibitor, a heparin drip, and intravenous nitroglycerin, her chest pain is completely refractory, and her blood pressure is starting to drop to 85 over 50. She's crashing. What is the next best step? The correct answer is urgent invasive coronary angiography in the cath lab, typically mandated within two hours for this level of hemodynamic instability. The distractor answer that catches so many people is administer thrombolytics, like TPA, tissue plasminogen activator. Yes. Let's explore why that is so dangerously wrong. It feels like an emergency. The patient is crashing. They're having a heart attack. Why not give the powerful clot-busting drug right now? This is an absolute red line rule in cardiology. Systemic thrombolytics are strictly contraindicated and have zero benefit in non-ST elevation acute coronary syndrome. Zero benefit. It comes down to the microscopic architecture of the clot. In an NSTEMI, the coronary artery is usually only partially occluded. The obstruction is typically a platelet-rich white thrombus. Thrombolytics like TPA are designed to break down fibrin-rich red thrombi, which are what cause total occlusions in a STEMI. Right. If you give systemic TPA to a patient with a partially occlusive platelet-rich and STEMI clot, you not only fail to dissolve the blockage, but you also paradoxically increase the risk of plaque hemorrhage. Which is terrifying. You can actually cause the plaque to rupture further, converting a partial occlusion into a catastrophic total occlusion. And that is on top of exposing the patient to a massive risk of intracranial hemorrhage for absolutely no benefit. Right. You only use thrombolytics in a full-blown STEMI when a cath lab is geographically unavailable within 120 minutes. Right. For a crashing, unstable, and STEMI, you must push them directly to the cath lab for mechanical intervention with wires and stents. Exactly the kind of mechanistic understanding the boards require. Moving on to case five, the post-MI complication. Let's do it. A 68-year-old man is admitted with a large inferior STEMI. He is taken to the cath lab, treated with PCI, and a stent is successfully placed in his right coronary artery. Okay. Successful stent. Four days later, while he is recovering on the telemetry floor and doing well, he suddenly develops profound hypotension, tachycardia, and signs of cardiogenic shock. Uh-oh. You rush to the room and listen to his chest. His lungs are clear, but you hear a loud, harsh, new, holosystolic murmur at the left lower sternal border, accompanied by a palpable thrill. This murmur was absolutely not there yesterday. You need to obtain an urgent echocardiogram at the bedside, followed by an immediate surgical evaluation for a ventricular septal defect, a VSD. The distractors will offer medical management with aggressive actor load reduction and intravenous diuretics. Why is conservative medical management the wrong path here? The timeline and the physical exam are the massive clues. This is a mechanical complication of a myocardial infarction. When the myocardium dies, it undergoes coagulative necrosis. Right. The tissue dies. Around days three to five post-infarct, macrophages infiltrate the area to clear out the dead tissue. This process dramatically softens the ventricular wall, before strong, fibrotic scar tissue has a chance to form. It turns to mush. Exactly. If the infarct involved the interventricular septum, that softened tissue can literally tear open under the high pressure of the left ventricle. And that tear creates an acquired ventricular septal defect. The left ventricle is now pumping high-pressure blood directly across the septum into the low-pressure right ventricle during every systole, which creates that incredible turbulence, resulting in the loud, harsh, holosystolic murmur. This is the cause of the myocardial infarction. Right. Medical management alone is deeply incorrect, because the mortality of a medically managed post-infarct VSD approaches 100%. The fundamental problem is not neurohormonal; it is mechanical. The pump has a hole in it. You cannot fix a physical hole in the heart with a pill. They need structural repair, usually open-heart surgery, to patch the defect, to have any chance of survival. Recognizing the timeline day three to five and matching it with a specific murmur is a guaranteed board point. Let's stick with complications for case six. The right ventricular infarct. Oh, this one is tricky. A 60-year-old man presents to the emergency room with an inferior MI. His EKG shows ST elevations and leads to three in AVF. His blood pressure in the ER is dangerously low, 80 over 50. Okay. You examine him. His jugular veins are massively distended, with the JVD visible all the way up to his earlobes while sitting at 45 degrees. But, crucially, you listen to his lungs and they are completely clear, no crackles, no fluid. What is the next best step in his acute management? The correct answer is intravenous volume resuscitation, giving him a rapid bolus of normal saline. The classic fatal distractor here is administer sublingual nitroglycerin, or start an wavy nitroglycerin drip. Most chest pain protocols include nitroglycerin. Why is giving nitro to this specific patient a terrible, potentially lethal idea? Because the presentation hypotension, massively elevated JVD, and clear lungs in the setting of an inferior MI is the classic triad for a right ventricular infarct. The right coronary artery often supplies the right ventricle. When it occludes, the right ventricle becomes ischemic, severely stunned, and fails to pump blood forward into the lungs. So, if the right ventricle can't squeeze, how does blood get to the left side of the heart to maintain cardiac output? It becomes entirely dependent on venous return preload. Preload? Yes. The pressure of the venous blood returning from the body physically pushes the blood through the stunned right ventricle. Sublingual nitroglycerin is a potent venodilator. If you give it, you drastically expand the venous capacitance vessels. Oh, boy. You will pool all of their blood in their legs and splanchnik system, completely wiping out the preload that the right ventricle is desperately relying on. You will cause profound, potentially fatal cardiovascular collapse. That is wild. Instead, you do the opposite. You give IV fluids to increase the preload and physically force blood through that failing right side. It's all the same. It's all about recognizing that the right ventricle operates on completely different hemodynamic principles than the left ventricle during an infarct. Case 7. The atypical STEMI presentation. Okay. A 32-year-old woman, who is two weeks postpartum, presents to the emergency department with sudden, severe tearing chest pain. Her ECG shows classic ST elevation in the anterior leads, and her high sensitivity troponins are sky high. She is rushed emergently to the cath lab, assuming it is a standard plaque rupture. Because why wouldn't you? What is the most likely diagnosis, and what is the appropriate management once the anatomy is visualized? Given her demographics, you must immediately suspect spontaneous coronary artery dissection, or SCAD. SCAD. When the angiogram confirms it, crucially, unless she has incredibly high-risk anatomy like left main involvement or is hemodynamically crashing, the correct management is conservative: medical therapy, beta blockers to reduce shear stress, and close observation. Hey, hold on. She is having a STEMI? The ECG? Yes, STEMI. The EKG shows ST elevation. The distractor on the test is going to be immediate aggressive stenting with PCI. Everything we learned says STEMI equals immediate PCI. to open the vessel. Why is Stenning the wrong answer here? Because the underlying pathophysiology is entirely different from a standard heart attack. This is not an atherosclerotic plaque rupture filled with cholesterol and platelets. In SCAD, an intimal tear occurs in the wall of the artery, often related to the extreme hormonal changes and vascular stress of pregnancy or underlying conditions like fibromuscular dysplasia. Blood dissects into the arterial wall, creating a massive intramural hematoma that bulges inward, compressing the true lumen and starving the heart muscle. If you go into that fragile, torn vessel with stiff wires and high-pressure balloons to place a stent, that acute vascular manipulation can easily propagate the tear. You can extend the hematoma and the dissection further down the artery, turning a localized problem into a catastrophic full vessel occlusion. Which is the exact opposite of what you want to do. Exactly. The data shows that these vessels are incredibly friable, but they also have a remarkable capacity to heal on their own once the acute stress passes. So, counter-intuitively, doing less is often more in SCAD. You manage them conservatively unless they are actively dying in front of you. That is a phenomenal board pearl that perfectly illustrates how pathophysiology dictates management. It really does. Last case, case eight, the supply-demand mismatch. Let's hear it. You were consulted by the intensivist in the ICU. An 80-year-old patient is admitted with severe urosepsis. His blood pressure is 85/40. His heart rate is 140 beats per minute and he has a fever of 103 Fahrenheit. Sick patient. Very sick. The primary team checked a routine troponin and it is elevated. They are panicking about a heart attack. However, you look at his EKG and it shows only sinus tachycardia, no ST depressions, no T wave inversions. When he is lucid, he denies any chest pain whatsoever. The correct answer is to ignore the heart for a moment and vigorously treat the underlying heart. This patient has underlined urosepsis with IV fluids, pressors, and broad-spectrum antibiotics. This patient is experiencing a type 2 myocardial infarction. The aggressive distractor will be transferred to the cath lab for emergent coronary angiography or start a heparin drip for NSTEMI. Why do we leave his heart alone and focus on the infection? Because there is no acute atherothrombotic event here. There is no unstable plaque that has suddenly ruptured. A type 2 MI is entirely a supply and demand mismatch. Okay, explain that. Think about the hemodynamics. His heart is racing at 140 beats per minute to try and compensate for the sepsis, which dramatically increases the myocardial oxygen demand. At the same time, his blood pressure is 85 over 40, which means his diastolic pressure is terribly low. And coronary perfusion happens in diastole. Exactly. Since coronary perfusion happens in diastole, his oxygen supply is drastically reduced. The myocardium is simply starving for oxygen because of the extreme physiological stress of the sepsis. That is the leak of troponin from the stressed myocytes. Going to the cath lab does absolutely nothing to fix the sepsis, there is no clot to stent, and you are only exposing a critically ill, unstable patient to the immense risks of contrast dye and invasive procedures. Fix the supply and demand mismatch by treating the root cause: infection. That perfectly encapsulates the concept of treating the patient, not just the lab value. Wow. We just ran an incredible gauntlet. If you can navigate the underlying logic of those eight cases, you are in phenomenal shape for the clinical vignettes on test day. Now, let's pivot and distill this even further. Let's look at the absolute highest yield testable facts, the isolated pearls, that can get you a quick point. Here's something the boards love to ask. They love to test your understanding of the difference between the best initial test and the gold standard. Oh, yes. We spent a lot of time talking about CCTA and functional stress testing. Those are your best initial non-invasive tests for the functional or anatomic workup. We're going to talk about the most common test for the functional or anatomic workup of stable disease in an outpatient setting. But do not forget, if the question asks for the gold standard or the definitive test, invasive coronary angiography remains the gold standard for defining coronary anatomy, especially if the patient is high risk. Let's talk about contraindications. The never do this list. We already covered the legal combination of nitroglycerin and right ventricular infarcts. What else makes the list? Never give nitrates of any kind to a patient who has used a PDE5 inhibitor like sildenafil or tadalafil in the last 24 to 48 hours. The Viagra trap. Exactly. Both of these drugs work by dramatically increasing intracellular CGMP levels in the vascular smooth muscle, causing profound relaxation. If you combine them, the synergistic effect causes catastrophic, completely refractory hypotension that is incredibly difficult to reverse. What about the classic toxicology crossover? Cocaine. Never give pure unopposed beta blockers in a patient with acute cocaine-induced vasospasm and chest pain. Right. Cocaine stimulates both alpha-1 and beta-2 receptors. The beta-2 receptors normally provide some degree of vasodilation to counteract the alpha-1 vasoconstriction. If you give a pure beta blocker, you block that protective vasodilation, leaving the alpha-adrenergic receptors completely unopposed. Which is bad. Very bad. This leads to massive paradoxical coronary vasoconstriction, severely worsening the hypertensive crisis and the myocardial ischemia. If you must lower the heart rate, you use a mixed alpha-1. Or better yet, benzodiazepines to calm the central nervous system. And what about our heart failure patients who have angina? Never use non-dihydropyridine calcium channel blockers, specifically verapamil and diltiazem in patients with known left ventricular dysfunction or heart failure with reduced ejection fraction. Why is that? These specific drugs are potent negative inotropes. They directly weaken the mechanical squeeze of the heart muscle. In a patient whose squeeze is already failing, giving verapamil can push them straight into acute decompensated heart failure or cardiogenic shock. Those are absolute lifesavers on the exam. Let's look at mortality predictors and high-risk ECG signs. When you are looking at a stress test report in a vignette, what findings should make you stop in your tracks? A drop in blood pressure during a stress test is a massive red flag. Normally, as you exercise and your sympathetic nervous system kicks in, your blood pressure shouldn't actually rise. Right. If it drops during exertion, it means the ischemia is soaked. It's so globally profound across the myocardium that the left ventricle is acutely failing to maintain cardiac output under stress. That almost always points to severe left main disease or critical multivessel disease. And on the EKG, the boards love showing visual exhibits and asking for the next step. There are two eponymous signs to burn into your brain. First, the de Winter sign. This presents as tall, prominent, symmetric T waves arising directly from upsloping ST depression at the J point in the precordial leads. It looks a bit like the peaked T waves of hyperkalemia, but in the clinical setting of chest pain, it is a stealthy indicator of a critical proximal LAD occlusion. It is a STEMI equivalent. And the second. Wellens sign. This is characterized by deep, symmetrical T wave inversions, or sometimes biphasic T waves, in the anterior leads, primarily V2 and V3. Wellens. The major catch here is that the patient may be completely pain-free at the exact moment the EKG is taken. The ST segment. The ST segment's might be perfectly isoelectric. But that specific T wave pattern means the proximal LAD has a highly unstable lesion that is critically stenosed and is intermittently occluding and reperfusing. Wow. Both de Winter and Wellens are massive red flags for impending catastrophic anterior wall myocardial infarction, and they warrant urgent cath lab evaluation. Unbelievably high yield. Hmm. Okay, we are entering the final stretch of our session. We are going to bring the energy up for a rapid board review summary. We are going to deliver five precise, concise. Takeaways to lock in your memory for test day. These are fast pattern recognition facts. Ready? Let's do it. If you see a patient with severe reactive airway disease, like poorly controlled asthma, who has stable CAD and requires a stress test. Think exercise stress or adalbutamine over adenosine or regadanosine. The pharmacologic vasodilators can trigger severe, life-threatening bronchospasm in asthmatic patients. If you see a diabetic patient with severe three-vessel disease on angiography. The answer for revascularization is almost always positive. Most always, coronary artery bypass grafting, CIBG, not PCI with stents, to improve long-term survival. The absolute first-line agent for symptom control and stable ischemic heart disease is. Always a beta blocker. And remember the goal. Titrate to a resting heart rate of 55 to 60 beats per minute. If you see a rise and fall of troponins with absolutely no clinical signs of ischemia, no pain, no EKG changes, no echo wall motion abnormalities. Think acute myocardial injury due to supplied man mismatch. Perhaps related to. Renal failure, heart failure or sepsis focus on treating the underlying systemic cause, not an acute plaque rupture. If an older adult presents with sudden syncope and pulseless electrical activity, four days after a large anterior MI suspect left ventricular free wall rupture leading to catastrophic cardiac tamponade. Phenomenal to close out our board review session today. I want to summarize the single most important concept we have covered regarding stable CAD. It is a concept that governs everything from the outpatient. Clinic to the cath lab guideline directed medical therapy or GDMT must be fully optimized before you consider revascularization in stable disease crucial point you must internalize this unless a patient has specific high risk anatomic criteria like critical left main disease or multivessel disease with a significantly reduced ejection fraction putting a stent in a stable patient does not prevent heart attacks and it does not extend their life PCI does not improve survival over maximal medical therapy and stable heart attacks and it does not extend their life. angina. It only helps relieve symptoms. Optimize the medication first. That is the rule. That is the cornerstone of modern cardiology guidelines proven by trials like courage and ischemia. Now, I want to leave you with a provocative thought, something that is right on the cutting edge of where the guidelines are heading and something you might see creeping into future board exam iterations. We talked about how the guidelines currently do not recommend routine stress testing or CAC scoring in asymptomatic diabetics. Right. We generally don't go looking for trouble if they don't have symptoms. But with the massive rise in high resolution chest CT scans for lung cancer screening and other pulmonary reasons, we're stumbling upon an incidental finding all the time. Silent myocardial ischemia. Yeah, we see it a lot now. We are seeing incredibly heavy calcification and severe coronary disease on imaging before the patient ever feels a single cringe of chest pain. How will this change the definition of asymptomatic in the future? If we can literally see the advanced disease on a scan, should we be aggressively putting these patients on high intensity statins, aspirin and perhaps even beta blockers before they ever complain of angina? It is a fascinating question that challenges our current strict algorithmic boundaries. It absolutely challenges the paradigm. It completely blurs the traditional line between primary prevention and secondary prevention. It certainly does. Well, that is all the time we have. Thanks for joining us for this board review edition. Don't forget to like, subscribe, and share for the benefit of your peers. Good luck with your studying. See you at the bedside.