Transcription
We have now arrived at the heart, and we will talk about coronary heart disease and one of its manifestations.
First of all, what is coronary heart disease? It is an imbalance between oxygen demand and the ability of the coronary arteries to supply this oxygen demand to the heart. We have already discussed many of these concepts in the eskeemia section. If there is a problem with the oxygen supply, eskeemia develops in the tissue. If this persists for a longer period, the result is myocardial infarction. Remember that eskeemia is reversible, but infarction is not. This is one of the key points to keep in mind.
The most common cause of coronary heart disease is atherosclerosis of the coronary arteries. However, in some cases, it can also be caused by embolism of the coronary arteries. Most often in this context, we are talking about trombbo, which can occur for example due to atrial fibrillation. It can also result from conditions like infective endocarditis. For example, bacterial endocarditis leading to embolis formation. Then another possible cause is vasculitis or inflammation of blood vessels. There can also be vasospasm, which is a sudden narrowing of the vessel reducing blood flow, and this can cause pain and even tissue damage. Additionally, stenosis of the valves can play a role. Since the coronary arteries originate from the aorta, if insufficient blood is ejected into the aorta, coronary perfusion will be reduced. Myocardial hypertrophy can also contribute because a larger heart muscle requires more blood supply. Still, the most common cause by far remains atherosclerosis of the coronary arteries.
Angina pectoris is episodic chest pain in the region of the heart caused by lack of oxygen in the heart muscle. Here you can see the classification of angina. First, we will discuss those forms of angina that are not immediately life-threatening, and then we will move on to three types that are grouped under the concept of acute coronary syndrome. I will add right away that this classification is more focused from a pathophysiological perspective. In clinical practice, infarctions are definitely classified differently. For example, into first type, second type, infarction, and so on. Here I am primarily classifying angina and secondly doing so from a pathophysiological point of view. So now we will go through the different types of angina and clarify what distinguishes them from one another.
Let's start with stable angina. It is also called sometimes stable exertional angina. This occurs when one of the coronary arteries is at least 75% narrowed or blocked. The typical symptoms are deep chest pain, usually felt behind the sternum. It is often poorly localized and described as pressure-like, squeezing, or constricting pain. The pain can radiate to the arm, lower jaw, or neck. These are classical symptoms. Now, there may also be accompanying symptoms, although they do not occur all at once, of course, and these accompanying symptoms may be shortness of breath, nausea, vomiting, excessive sweating, fatigue, and dizziness. It is important to remember that not all of these symptoms have to be present at the same time. And the reason why this type of angina is called exertional angina is because the pain typically is triggered by physical activity. But it can also occur during emotional stress. It usually resolves at rest or taking sublingual nitroglycerin, typically within 5 minutes. So, why physical activity? We already clarified that it refers to symptoms occurring during so physical load or stress. The word stable in this context refers to the state of the atherosclerotic plaque. Sometimes the artery can be almost completely blocked, as mentioned, typically at least 75% narrowed, yet an infarction still does not occur. This is because atherosclerotic plaques develop very slowly. As a result, the blood vessel has time to develop collateral circulation, which bypasses the blocked area. Therefore, the myocardium continues to receive adequate blood supply, and infarction does not occur.
Looking at the electrocardiogram, so ECG, in stable angina, at the ECG, usually looks normal at rest. However, during physical activity, it may become abnormal. With that, a stress test is performed under controlled clinical conditions and evaluates how the heart responds to increased demand. This test can also be performed using medications which mimic the effects of physical exercise, meaning these are typically vasodilators. In both cases, vasodilation occurs, but not in the vessels beyond the blockage because those vessels are already maximally dilated. As a result, during stress or pharmacologically induced vasodilation, eskeemia becomes apparent on the ECG as an ST segment depression. Here it is also important to note that cardiac biomarkers such as troponin remain normal. Troponin is one of the most important and commonly used markers of cardiac injury. In this case, it remains normal because there is no infarction, and this is definitely a key point to remember.
Next, we have vasospastic angina. This type usually occurs at rest and is caused by sudden strong constriction or spasm of a blood vessel. You may also read or hear somewhere the term variant angina, which is also known as Princeps angina. Often, this variant or Princeps angina is grouped together with vasospastic angina, and the terms are used as synonyms. However, an international group studying coronary vasomotor disorders has pointed out that Princeps angina is actually a specific form of vasospastic angina. So, we won't go deeper into that distinction here. That is more the field of cardiology. But we will focus on the general concept of vasospastic angina. In this case, there are no cholesterol plaques involved. Instead, what we see are strong vasoconstrictive spasms, which are responsible for the reduced blood supply. The main cause of these episodes is the effect of vasoconstrictive stimuli acting on hypersensitive blood vessels. And here, endothelial dysfunction may also play a role. So, there will be certain triggers, and these triggers include everything that's fun. Okay, I'm joking. Not everything here is fun, despite what I said, but they include smoking, cocaine, alcohol, and triptans. Now, triptans are medication for migraine. So, if a patient with migraine experiences angina symptoms at rest, it may be related to these medications if they contain triptans. Cardiac biomarkers such as troponin remain again normal because again there is no infarction in this situation.
And with that, these are two relatively milder types of angina. Now we move on to the more serious ones, but before that, I will first explain acute coronary syndrome because, as I mentioned in the beginning of the classification, the next three types of angina fall under this category. So, first, let's understand what they all have in common and why this is called acute coronary syndrome. It is called acute because it usually presents a sudden onset angina, which was not present before, or if angina was already present, there is a worsening condition. This worsening may include an increase in frequency of pain episodes, increase in intensity, or attacks during less physical exertion than before, or even occurring at rest. This indicates that the atherosclerotic plaque is no longer stable. In addition to the typical angina symptoms, there may be also atypical symptoms, which are more common in elderly patients, women, and individuals with diabetes, especially when more than one of these factors is present. These atypical symptoms include shortness of breath, fatigue, dizziness, and even cases where chest pain is absent altogether. So, it is possible that classic angina symptoms are not present at all.
Now, let's go through these three types. If we had stable angina, then of course, we also have unstable angina. In this case, the obstruction, or we can also call it an occlusion, is very significant but not complete. As you can see in the image, the cholesterol plaque is no longer stable, and the thrombus has already formed. Another characteristic feature is seen on the ECG. We observe an ST segment depression and also a T-wave inversion, meaning the wave is reversed. It goes downward instead of upward. And still, the cardiac biomarkers, including troponin, remain within normal limits because there is still no necrosis of myocardium. So, this is unstable angina, and still yet no infarction. Logically, the remaining two types will already involve myocardial infarction.
First, we have myocardial infarction without ST elevation. This refers, of course, to the ECG, and the abbreviation is also widely used for that. So, you can safely remember it. Here, finally, as I mentioned earlier, we do have an infarction, and by finally, I mean that the previous types I kept saying there was no infarction, not that infarction is something good. This means that tissue necrosis is present, but it affects only the inner layer of the heart, so the inner layer of myocardium, the subendocardium. The damage does not involve the full thickness of the heart wall. This happens because the subendocardial region is the farthest from the blood supply and at the same time the most sensitive to oxygen deprivation. That's why it is the part of the heart that is affected first during eskeemia. Since we now have infarction, cardiac biomarkers such as troponin are elevated, and on the ECG, we see findings similar to those in unstable angina. But importantly, there is no ST segment elevation, and it is exactly this feature on the ECG that distinguishes this type from the next one.
And the last one is logically myocardial infarction with ST elevation also. Then you can use the abbreviation STEMI. I want to emphasize this here, this sentence, because ST elevation on the ECG strongly indicates this diagnosis. This is a very classic and very important finding that you should definitely remember. So, elevation of the ST segment. In this case, the vessel is completely occluded, and the infarction is acute and transmural. This means that the infarction affects the entire thickness of the myocardial wall. And of course, since this is an infarction, troponin is elevated. And that basically concludes the classification of angina.
But before I finish this part of the lecture, I will say a few words about cardiovascular biomarkers, including troponin, which I have already mentioned a few times. So, troponin, I have been mentioning all the time, but there is another classical biomarker that is also commonly used: the creatine kinase MB fraction, or CK-MB. It is called this because it consists of a combination of the M and B isoenzymes of creatine kinase, and together with troponin I and troponin T, it forms the group of main cardiac biomarkers.
Speaking about troponin, you probably know that it is a protein involved in muscle contraction where calcium binds to it. However, it actually is a bit more complex. The troponin molecule consists of three subunits: I, T, and C. And the C subunit is the one that binds to calcium because C calcium. The T unit is associated with tropomyosin and helps change its conformation, and the I subunit is the inhibitory part, preventing actin and myosin from interacting when calcium is not bound. Now, when irreversible damage to the cardiac cells occurs, the cell membranes are damaged, and intercellular proteins such as troponins and enzymes like CK-MB are released from the cells into the bloodstream. This is why they can be used as ideal biomarkers. Troponin I and T levels in the blood begin to rise within 2 to 4 hours after infarction and reach their peak around 48 hours, and after that, remain elevated for about 7 to 10 days. CK-MB also rises within 2 to 4 hours but reaches its peak earlier, 24 hours, and returns to normal already after 48 hours. Because CK-MB normalizes faster than troponins, it can be useful for diagnosing a reinfarction, that is, a second infarction occurring after about 48 hours, while troponin levels are still elevated from the first event. However, it is also important to note that unlike troponins, this creatine kinase MB fraction is not completely specific to cardiac damage. Its levels can also increase in skeletal muscle injury. For example, after trauma, intense physical exercise, or in conditions such as myopathies. In contrast, troponins are highly specific for cardiomyocyte damage. And that is all about these markers.