Management of Angina and Myocardial Infarction

by Carlo Raj, MD

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    00:01 Let us take a look at the management of your patient who has stable angina, acute coronary syndrome. Let us go back to quickly our discussion. If it is stable, exertion, angina, pain. If it is acute coronary syndrome, then the plaque has gotten so big that the pain is going to be at rest. Myocardial infarction, acute, we've walked through in great detail in our previous lectures. What is the two immediate goals? Let us go back to the physiology that we talked about where we are addressing the demand and we are addressing the supply.

    00:36 What do you want to do? If you know that your heart is compromised due to whatever reason, in this case the atherosclerosis, then would that make sense to try to decrease the demand of the heart. So, therefore, what kind of receptor does the heart have in which its activity is pretty much controlled or influenced? Beta-1 receptor. When I try to control the beta receptors, why not administer some calcium channel blockers? Those are the thing that you pay attention, now be careful though because if you administer too much or if you have your patient going into massive MI, then the heart has no chance of recovering, you’re going to kill your patient so be careful when you are giving such drugs. Or what about the supply? We know that the supply has already been compromised when I try to get in there and try to remove that clot and by doing so, aren’t you addressing both goals? By decreasing myocardial oxygen demand, we have beta-blockers, slows down the heart rate. Remember the two major factors or components or constituents of your work of the heart demand depended on heart rate and the ability to pump. The heart rate when I try to give a beta-blocker decrease heart rate. Nitrates what they do? Well, we talked about how you could have vascular resistance, which has increased, which it does because of sympathetic activity and so, therefore, nitrates might cause vasodilation. Now you tell me, be careful, how do you decrease your afterload? It is about working on the arteries, arterial side or is about working on the venous side? And you will tell me correctly working on the arterial side. Good. By doing that, you are then relieving some of the resistance, aren’t you? And what about morphine? It decreases the pain and produce the adrenergic drive with morphine.

    02:24 What about the supply? Let us give oxygen. I have to give oxygen. What about that clot? It is already too big, so when I try to get in there, get rid of it. You've bust that clot. You call this as a blood thinner and how important is that concept, vary in hemodynamics, all the different ways in which you can bust that clot. Aspirin or aspirin alternatives including clopidogrel or "Plavix".

    02:48 A clopidogrel enables your ADP and if your ADP is not released from your platelet, then you can't express what? Remember this from pharmacology, pay attention, you can't express your glycoprotein IIb, IIIa.

    03:01 You do not have that, you do not have proper aggregation, do you? Or else might you want to use something like cilostazol and a couple of others as well. IV heparin, anticoagulant, prevents thrombus formation. At some point, let us say that you want to use a blood thinner in which you try to bust that clotting and you have coags or coagulation factors, important options here including heparin. Heparin works to antithrombin III as you should know and antithrombin III is going to do exactly that, knock out thrombin. Or you have direct thrombin inhibitors, don't you? And this then brings you to important topics in drugs such as dabigatran, direct thrombin inhibitor or apixaban. We have got a couple of these that you want to pay attention to. Why? Because you want to try to increase the supply of oxygen to your dying heart so that you can then shift over into aerobic glycolysis and proper ATP production.

    04:05 Continuing our discussion, nitrates. Now rapid reperfusion could be an issue. You want to be careful here. Pay attention. So you had this clot. How could this clot develop? A clot was developing and over years and years and years, and at some point in time, the tissue distally, so if this is my clot and my tissue distally became accustomed to that decreased perfusion, didn't it? And then all of a sudden that clot became so big and you are going to go in there and use something like a plasminogen analog, some type of plasminogen activator and you gave a tissue plasminogen activator such as alteplase or what have you, and you bust that clot. My goodness, gracious. Water is good for you. But you are doing kind of a fire hydrant, it will kill you. Now that tissue distal to the stenosis, drinking all this oxygen all of a sudden, oh! My goodness, this excess oxygen that has been introduced into the tissue, you think there may be perhaps some of their oxygen might lose electron and become a free radical? Exactly.

    05:10 What's that called? Reactive oxygen species. Welcome to rapid reperfusion, but we're specific referring to reperfusion injury. And calcium play a huge role. We will talk about that. All this is to come while you are trying to do that. You are trying to induce rapid reperfusion. Here are some of your drugs such as your thrombolytics, your tPAs and also you try to go in there and say that the drugs aren’t working well enough or you want to go in there and really make sure that you prevent further thrombi formation and so, therefore, you will think about using percutaneous intervention and you either have angioplasty in which you will try to balloon in and while you're in there, you'll try to place a stent as well. Worst case scenario, you can't go in and place a stent, then you have to do bypass surgery.

    05:59 Using thrombolytics, there is some absolute relative type of contraindications, but keep in mind, before we move on here, if your patient is already in a state of bleeding why would you want to use a thrombolytic? That is just going to exacerbate the issue. It might actually kill your patient. Who are my patients? Hemorrhagic strokes, non-hemorrhagic stroke past three months, intracranial neoplasia, active internal bleeding, aortic dissection, closed head or facial trauma, once again for three months. Now take a look at some of these. If the patient is already at risk for severe bleeding, by adding a thrombolytic, these are absolute contraindications for then using a thrombolytic now. This is absolute for any licensing exam. In clinical practice, you might always find that attending who might be extremely confident in his or her ability to still give a thrombolytic in such situations, but that is not being asked here nor is it going to be asked on your boards. Relative, severe hypertension, proliferative diabetic retinopathy, what does that mean to you? You are thinking about the eye and when undergoes proliferation, you want to be careful though because what might you do? By thrombolytic, you might then cause bleeding take place. Known bleeding diathesis, for example von Willebrand disease, prolonged CPR, allergic reactions, pregnancy, blood pressure, ulcers be careful there, please. Very careful actually, for example, when you use a thrombolytic at some point with that ulcer, there might be so much bleeding that you might actually bring about perforations.

    07:38 So please be careful when using such drugs. Contraindication for thrombolytics, absolute versus relative. Now, management continues. All patients with AMI should undergo intensive treatment for modifiable risk factors. What were they again? Aspirin, ACE, beta-blockers, secondary prevention. So you want to continue taking baby aspirin, ACE inhibitors always a good thing, beta-blockers all these are then for secondary prevention. Treatment of hyperlipidemia, statins. I had another drug in there for you that is very relevant. That's your, once again proprotein convertase subtilisin kexin 9 inhibitor, and those of some of your monoclonal antibodies, we have referred to that earlier known as alirocumab or your evolocumab, locumab is their suffix you pay attention to please. diabetic control, smoking, and diet and exercise. If you are able to do this and if you are able to educate your patient properly where you are exercising prevention is not the best medicine. Mechanical complications that we are worried about. Weakened infarcted cardiac tissue. Remember the timeline that we walked through with myocardial infarction and at some point with that scar formation, it might become weak and may result in a ventricle aneurysm or rupture. Oh my goodness we have either septal or wall rupture may result in papillary muscle might have a new type of murmur that has been introduced. A mitral valve regurg or if you had a septal rupture, it kind behaves like a VSD. What kind of murmurs are these please? Close your eyes. You got theses. Systolic murmurs that are being introduced newly. If it is a wall rupture, you're worried about death from what? Sudden accumulation of blood within your pericardial cavity and say that you have tachycardia and have hypertension, you have what is known as kussmaul sign mean to say positive JVD and you have muffled heart sounds. Worried about pericardial tamponade, don't you? What is your next step in management? My goodness gracious get in there, do a pericardiocentesis and get that fluid out. Mechanical complications require emergency type of surgical issues. Papillary muscle rupture can present with acute hypotension, acute pulmonary edema. Understand that everything is being backed up. Here is our mitral valve.

    10:08 Are you with me? And you have regurg back into where? Left atrium. Back into where? Pulmonary veins.

    10:17 Pulmonary edema acutely, new systolic murmur. Chronically what kind of issues are you worried about? Conduction system big time and if that is the case my goodness gracious you plant a pacemaker, arrhythmias due to scar formation. That's what we'd talk about over and over again and major complication that you are worried about resulting in sudden death is the fact that you are messing up the conduction chronically. Mechanical failure, your left systole or should I say your left ventricle is dying. So, therefore, the systolic function on the left side is also not working. And so therefore, now I want you to pay attention to this statement, there is a lot of clinical importance for this particular stanza. When I walk you through this, if your heart dies on the left side and that is which you focus upon here, please.

    11:10 If the heart dies on the left side, it cannot pump forward. What is the active process of your heart phase? Systolic. What kind of dysfunction would you call this if the left ventricle is not functioning properly? A systole dysfunction, stop there. If I can pump my blood forward into the aorta, where is all my blood? In the left ventricle. It is stuck in the left ventricle.

    11:36 How are you going to measure this? On the left side, a central venous pressure or you are going to use a PCWP, a pulmonary capillary wedge pressure. You are correctly telling me PCWP, pulmonary capillary wedge pressure. Where is my blood? In the left ventricle. Why? It is not moving forward. Are you seeing this? Close your eyes and conceptualize, the only way that you get all the questions right. There is my blood lying in my left ventricle, increased preload and your PCWP is increased, correct? Yes. Now the mitral valve wants to open, the blood wants to rush into the left ventricle. But the problem is there is blood still remaining there residually from the previous systolic dysfunction. So could that systolic dysfunction then give rise to a diastolic dysfunction? Yes, it can. What does that mean to you? Pay attention here. What kind of heart sounds are you going to find here? If it is a systolic dysfunction, what does that mean? The blood is not moving forward. So, therefore, my left ventricle could be rather large and it could result in what kind of heart sound? An S3. We talked about that earlier, an S3 gallop, what is happening? It is the fact that because of the systolic dysfunction, you have a large left ventricle, as soon as a mitral valve opens, it create an S3, stop there. Well what if the blood starts accumulating in your left ventricle? Right. So now that's a diastolic dysfunction because you cannot properly fill up the left ventricle and that blood now that is rushing from your left atrium, are you seeing this? That blood that is rushing from the left atrium through the mitral valve, into the left ventrical, hitting the blood in your left ventricle, is going to create a what? A fourth heart sound. What does a fourth heart sound mean to you? You have heard of this as being hitting a stiff left ventricle. But with all that blood in there, it might as well be stiff. If you haven’t understood that, please make sure that you go back and review what I just told you with that particular statement. Do you understand how much clinical relevance there is with each one of these statements? Some more than others, especially when it comes to pathology. Continue. Insufficient or significant damage myocardium, it cannot do what? It cannot maintain the proper heart function.

    About the Lecture

    The lecture Management of Angina and Myocardial Infarction by Carlo Raj, MD is from the course Ischemic Heart Disease. It contains the following chapters:

    • Management of Angina and MI
    • NSTEMI / STEMI: Treatment
    • Contraindications to Thrombolytics
    • After (N)STEMI: Treatment & Complications

    Included Quiz Questions

    1. Pain reduction leads to a reduction in adrenergic drive which lowers the oxygen demand of the heart.
    2. The only purpose of morphine is to provide pain control for the patient to improve their comfort.
    3. Morphine works as a direct vasodilator in addition to pain control.
    4. Morphine induces clot breakdown by an unknown mechanism.
    5. Pain control is needed to ensure patient compliance.
    1. Inhibition of ADP-mediated activation of glycoprotein IIb/IIIa thereby irreversibly inhibiting platelet aggregation.
    2. Inhibition of ADP-mediated activation of glycoprotein IIb/IIIa thereby reversibly inhibiting platelet aggregation.
    3. Irreversible inactivation of COX enzyme, thereby suppressing production of thromboxanes and prostaglandins.
    4. Inactivation of thrombin and factor Xa by binding to anti-thrombin III
    5. Inhibiting the synthesis of vitamin K-dependent clotting factors.
    1. Inactivation of thrombin and factor Xa by binding to anti-thrombin III
    2. Inhibiting the synthesis of vitamin K-dependent clotting factors.
    3. Irreversible inactivation of COX enzyme, thereby suppressing production of thromboxanes and prostaglandins.
    4. Inhibition of ADP-mediated activation of glycoprotein IIb/IIIa thereby irreversibly inhibiting platelet aggregation.
    5. Reversible inhibition of COX enzyme, thereby suppressing production of thromboxanes and prostaglandins.
    1. Tissue plasminogen activator
    2. Heparin
    3. Aspirin
    4. Beta blocker
    5. Warfarin
    1. History of hemorrhagic stroke 2 years ago.
    2. History of head trauma - 1 year ago.
    3. Uncontrolled coagulation defects.
    4. History of gastrointestinal bleeding 8 months ago.
    5. History of non-hemorrhagic stroke 1 year ago.
    1. Immediate pericardiocentesis.
    2. Immediate fluid resuscitation.
    3. Sublingual nitroglycerin.
    4. Bed rest with leg elevation.
    5. Intravenous administration of diuretics.
    1. Ventricular septal defect murmur due to ventricular septal rupture .
    2. Mitral valve regurgitation murmur due to papillary muscle rupture.
    3. Atrial septal defect murmur due to left ventricular systolic dysfunction.
    4. Mitral valve stenosis murmur due to progressive atherosclerosis.
    5. Aortic valve regurgitation murmur due to thickened left ventricle.

    Author of lecture Management of Angina and Myocardial Infarction

     Carlo Raj, MD

    Carlo Raj, MD

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    Significant Gaps in Management
    By Hamed S. on 18. February 2017 for Management of Angina and Myocardial Infarction

    The lecture on management was extremely superficial and not suitable for board exams. No mention of: Newer agents such as ticagrelor/prasugrel When you would choose PCI vs thrombolysis risk stratification of NSTEMI patients with the TIMI score and subsequent angio When you would use CABG first line This talk I feel is more step 1 then step 2. Step 2 needs to focus more on decision making rather than lengthy talk on the basic pathophys I had to go back to references to Toronoto Notes to fill this gap