Vasospastic Angina: Pathogenesis

by Carlo Raj, MD

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    00:01 Welcome to vasospastic angina. A third and final type of angina, we, up until this point have categorized angina as being chest pain, depending as to whether or not there is rest or upon exertion. And I told you at the time that when we were discussing unstable and stable angina, that we would leave vasospastic separately because it doesn't necessarily fall into the same pathogenesis of stable, unstable and then MI. The spectrum that we had walked through there and you want to make sure that you travelled through that pathogenesis so that as you go through it, you are integrating the physio; you are looking at the disease and then how do you want to manage your patient. With stable angina, do you remember that patient? There is chest pain upon exertion, nitroglycerin so that you can relieve some of that pain.

    00:57 And so by doing so, you are decreasing the preload, decreasing the afterload and making it much easier for the heart to then function. Correct? Unstable angina. My goodness now the atherosclerotic plaque, key point, atherosclerosis. The plaque is getting bigger. We went through the pathogenesis of that and then remember the cardiac enzymes were negative, black and white. Keep things simple so that at least you have a definitive answer and you are confident with your response. Now clinically, there is always room for overlapping in that gray area, but at this point let us just keep things very straightforward.

    01:35 So with vasospastic as the name implies, formerly known as Printz medal, maybe you have known it as being variant, but a much more clinically relevant term would be vasospastic. That's exactly what is occurring in your coronary artery. Let us take a look. With focal coronary artery spasm, the operative word here is spasm. What is causing this? Well, we'll get to the risk factors. It is rather, let us say mysterious, could be because you have to have a atherosclerotic plaque. How can you confirm that? Take a look at this. Angiographically there is absence of narrowing of the coronary artery, which means what exactly is causing this chest pain that could mimic angina. ST-segment elevation. What does that even mean? Well let's just make sure that we're clear about the different type of changes that we've seen thus far. Remember in medicine, it is about reinforcement and repetition and we will keep talk about this over and over again until well whenever a question has been post to you, you are able to reflexively answer and you have come up with the right one every single time. An ST elevation, with anginas, remember in stable angina at rest, there is no pain. The EKG looked normal. You were induced perhaps in your clinic, stress either through chemical drugs or a treadmill test. Upon doing so, what did you find on EKG? Find an ST depression.

    03:07 What? Then you had unstable angina. With unstable angina, you might have changes there as well, but it would be non-STEMI. Maybe there is an ST depression and the pain there occurred at rest. Now the point is this, cardiac enzymes were negative with angina because it is not myocardial infarction. The myocardium has not been destroyed. You are not releasing troponin I. Here as well, with vasospastic angina, has nothing to do with atherosclerosis.

    03:35 You usually do not find narrowing. The spasms are taking place. You might find an ST-elevation but you normally will not find cardiac enzymes. Is that clear? Now when you hear about ST elevations, a couple of things that should come to mind and you need to make sure that you confirm your findings before you chose any type of answer. For example, if it is an ST-elevation and there is no cardiac enzyme, highly unlikely that this is myocardial infarction.

    04:01 So what might it be? Was your patient taken up coccaine, smoking? Was there hypertension? Things of that nature and if there was, that ST-elevation would then diagnose your patient most likely with vasospastic angina. Is that clear? I hope so. Now the vasospasms could be superimposed with an atherosclerotic plaque so that you want to be careful of. So here once again you might find an ST-elevation with vasospams. It is important that you go back and take a look at the history. Is your patient obese? Then at that point, you are looking at more of a type of unstable angina perhaps, especially if the pain of the chest is occuring at rest. If your patient has a history of smoking and you find an ST-elevation with your cardiac enzymes being negative. Are you listening what I am saying? Then what is your most likely diagnosis, please? Good. Vasospastic angina. Let us continue.

    05:00 Now the clinical manifestations are the following. Your patients here tend to be younger. That is key, isn't it? Whereas when we were referring to unstable angina and company, then those patients well if it was a male, a little bit youger than a female, but still 45 and above in a male, and if it is a female remember that estrogen is protective, isn't it, for female? And so therefore 55 and above perhaps, for atherosclerosis in a female. Now one of the hyperlipidemias that we referred to was type II hyperlipidemia or hypolipoproteinemia.

    05:34 Do you emember type II? What was the problem there? Good. LDL receptor deficiency. That is where the problem took place. If the LDL receptors aren't working properly specifically in the liver, then how is the LDL ever going to be properly accepted and absorbed. It is not. You are going to start accumulating more and more LDL. Now there could be the familial type and you then call that what, please? Familial hypercholesterolemia, is that clear? Now that patient could be young, granted. All of that is dealing with atherosclerosis. And by younger we mean to say that well, autosomal dominant with type II. In their 40s, that patient would be heterozygous or homozygous? What do you remember from genetics? What type of gene pattern is more dangerous? Homozygous. So that patient might only, oh boy, 18 to 20, whereas if he had heterozygous, then you're looking at a patient maybe perhaps in their 40s. But that is all atherosclerosis, is that clear? Our topic at hand is vasospastic and all I am trying to do here is to make sure that you have differentials in your mind before you confirm. How do you confirm your finding is which you truly asking yourself every single time. It occurs in an atypical pattern, frequently at rest and clustered. So that is quite different.

    07:00 Patients here, the chest pain very much like angina. What does that mean? Substernal chest pain, may be radiating up into the jaw and to the left side and such.

    07:10 Take a look at the risk factors and pay attention to this, please. Smoking, cocaine, and maybe perhaps even diabetes mellitus, but what kind here please? What kind of patient most likely is going to then offer insulin resistance? An obese patient. When those insulin receptors are not properly functioning, a type II type diabetic mellitus.

    07:33 Risk factors are huge here. As you can see, really has nothing to do with atherosclerosis.

    07:39 Vasospastic angina. Let's continue. The ST segments are transiently elevated resolves

    About the Lecture

    The lecture Vasospastic Angina: Pathogenesis by Carlo Raj, MD is from the course Ischemic Heart Disease.

    Included Quiz Questions

    1. It mainly affects the elderly population
    2. It occurs frequently at rest, usually in the evening until early morning
    3. The pain is similar to classic angina
    4. There may be no initiating factors prior to attacks
    5. Risk factors include cocaine use, smoking, and insulin resistance
    1. Focal coronary spasm
    2. Coronary narrowing
    3. Generalized cardiac hypokinesia
    4. Temporary embolization
    5. Arterial stenosis
    1. ST segment elevation
    2. Prolonged PR interval
    3. Peaked T waves
    4. P and QRS complex dissociation
    5. J waves
    1. Obese patients
    2. Elderly patients
    3. Pediatric patients
    4. Male patients
    5. Female patients

    Author of lecture Vasospastic Angina: Pathogenesis

     Carlo Raj, MD

    Carlo Raj, MD

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