I'm Tom Lüscher, I'm Professor of Cardiology at the University Hospital in Zurich, Switzerland. We revised the module myocardial infarction. And today we'll talk about the diagnosis and emergency measures of acute coronary syndromes, which is an equivalent of acute myocardial infarction and encompasses all the spectrum of this disease. I would like to start with a prominent patient you hear here, Ike Eisenhower at his state in the union address on TV just before he had a myocardial infarction. Ike's heart attack began while playing golf at Cherry Hills Country Club on September 23, 1955, when he complained of what he thought was indigestion. The president's personal physician, Dr. Howard Snyder, mis-diagnosed the attack as a gastro-intestinal problem and waited 10 hours before sending Eisenhower to the hospital. So, it is important to know the symptoms of acute myocardial infarction, which include: chest pain, which Einsenhower eventually also had, radiation of this pain into the right or left arm, typically in the left arm, sweating, nausea, indigestion as Eisenhower complained of, dizziness, syncope, or even sudden death. Now, what is the differential diagnosis of chest pain in this context? You can have an infarction, as I just indicated. You can have a takotsubo syndrome, a disease where the myocardial no longer contracts, particularly in the apex of the heart, while the coronary arteries are completely open. It's mainly a stress induced disease affecting post-menopausal women. Then aortic dissection, which is a very severe pain, typically between the two shoulders and leading to deaths if untreated by surgery within hours. And eventually also, pulmonary embolism, that can present itself with pain, but typically does so with dyspnea. The diagnosis of acute coronary syndromes relies on symptoms as we just discussed. Then on the ECG pattern either ST-segment elevations or t-inversions, then biomarkers, in particularly troponin, but also prior to creatine kinases that are measured in the blood and the increase as the infarction evolves. And finally, angiography where you visualize subtotal narrowing of an artery or even an occlusion. So the diagnosis goes as follows: You have symptoms and you suspect that this could be chest pain and the basis could be an acute myocardial infarction. To confirm this, you ask the patient how long it has gone, where it radiates, whether he's sweating, whether he feels bad, whether he's pale, whether his blood pressure is low. Maybe the heart rate is high. And then you do an ECG. If there is ST-segment elevation, it's a so-called STEMI myocardial infarction. If there are ST-segment depressions or T-inversions, it's an non-STEMI or non ST-segment elevation myocardial infarction. Biomarkers are measured in all of these conditions, although a STEMI is an urgency as I will show you in a moment and we don't wait for the troponents. But typically, troponents are elevated in all these conditions and in STEMI, also creatinine kinases, are elevated while this is less or not the case in the other two conditions that I will show in a second. So you can make a diagnosis of a ST-segment elevation myocardial infarction and a non ST-segment elevation myocardial infarction or takotsubo. And then you have the following strategy: In a STEMI, the patient has to go to the cath lab for a primary percutaneous coronary intervention as soon as possible. In a non-STEMI, we can wait a bit longer. If the patient has no pain, it should be done within 24 to 48 hours and in talk with tubal patients we only use medications. These are the typical presentations in the ECG. On the left, a non ST-segment elevation myocardial infarction. And on the right, a ST-segment elevation infarction. In the non-STEMI, you see the negative T-waves in the V1, V2 to V4, leitz of the ECG, while on the right hand side, you see a ST-segment elevation myocardial infarctions as was the case in Eisenhower's infarction at the time in 1955. So let's focus on STEMIs, which is a real emergency and leads to death in many patients if untreated. This is how it evolves. This is over decades. A plaque will grow in a coronary artery as you can see here. And the cap is initially solid, but for some reason through an inflammatory burst will rupture and the blood immediately recognizes the underlying plaque and then closes the artery as can be seen here. So, what are the first measures under these conditions? A patient is in pain, he needs first aspirin to inhibit platelets and to provide some relief of the occlusion by the thrombus. He needs heparin to inhibit the coagulation cascade. He needs oxygen to relieve his dyspnea and eventually also morphine to relieve his pain. These are the four pillars that initially should be applied to any patient with an acute coronary syndrome. Now, some patients are losing consciousness. They fall, they don't breath any longer. And what do you do then? This is an absolute emergency and if untreated, the patient usually is dead within 10 minutes. So, with a syncope or a loss of consciousness ask the question: what is it? It usually is pump failure and ventricular fibrillation in the retina that leads to pump failure and suddenly arrests the cardiovascular system. Under these conditions, we need to call for help, an ambulance. We should start cardiopulmonary resuscitation and use an automatic external defibrillator, if available. So, let's see what we do when we have a circulatory arrest: Well, the organ hypoperfusion will particularly be damaging the brain and within 6 to 10 minutes, the brain is no longer functioning and leads to death of the person if untreated. So, we should perform cardiopulmonary resuscitation. And what does that involve? Well, it involves that you push in the middle of the chest, on the sternum heart in the center of the chest as you can see here and try to achieve hundred beats per minute. So, it's quite some exercise, but it saves the life of this patient until the ambulance or defibrillator arrives. This is what ventricular fibrillation looks like, with chaotic electrical excursions on the ECG. And of course as a consequence, a loss of pump function of the heart. Under this condition, the appropriate treatment is defibrillation with an automatic external defibrillator that is part of the equipment of any ambulance arriving. But also in public places, more and more automatic external defibrillators are available and you should look for that or ask a friend to do so. So, what we should do when we have an occlusion of, in this instance, of a right coronary artery, you can see the stump and you can see that, when we actually have performed the balloon angioplasty and placed the stent, how big the artery actually is that was occluded. And this is easy to understand that under these conditions the patient couldn't survive. So, STEMI is an absolute emergency and he should be brought to the cath lab as soon as possible. So, let's now focus on the Non ST-segment elevation myocardial infarction or Non-STEMI with ST-segment depression or T-inversions. In patients with Non-STEMI, the coronary artery is commonly not occluded, contrary to STEMI, but severely narrowed. If the patient is pain-free, primary percutaneous coronary intervention should be performed within 24 to 48 hours. The first measures are the same as in STEMI. And here is an example of a patient. This is a coronary computing tomography with positron emission tomography, where you see actually the red part, which is well perfused and the blue and purple part, which is not. And you can see that the circumflex coronary artery is severely narrowed. This is another example of a right coronary artery in a patient with Non-STEMI that is subtotally occluded and of course caused him pain. But if not occluded, the pain faded away after some treatment with nitroglycerin aspirin, heparin, and possibly morphine. Now, the pathophysiology of this is that the plaque is rupturing, the plaque is growing. It narrows the artery but doesn't occlude it. But the embolie from the thrombus, that are formed at the site of plaque rupture, will eventually occlude small arteries downstream and lead to an increase in troponin. Troponin is a contractor of protein in the myocardium, which is released whenever myocytes are dying. And you can see here on this different curves, holding markers, that we can measure in a patient with suspicion for acute myocardial infarction such as troponin, creatinine, kinases, total and MB isoforms are increasing rapidly during the first hours and days and then really go back to normal. So, in patients with STEMI or biomarkers are activated because of the occlusion of the coronary artery. In patients with Non-STEMI, commonly only troponins are elevated, but not creatinine kinases because there is still some basic flow through the subtlety narrowed artery. Now then, when the patient has a myocardial infarction, he arrives at the hospital in the emergency room, he's brought to the chest pain unit. Then as soon as possible to the catheterization laboratory and eventually to a coronary care unit where he is monitored for 24 to 48 hours depending on his condition. So in summary, in acute coronary syndromes, the first treatments are medications such as aspirin, heparin, then also, if required, morphine and potentially nitroglycerin. But the real treatment is primary percutaneous coronary intervention. The primary problem in acute coronary syndromes is subtotally or totally occluded coronary artery visiskimia, arrhythmia, and pump failure and death as potential consequences. The most effective treatment is reperfusion with balloon angioplasty and stenting of the occluded coronary segment, which is discussed in more detail in another emission of our module on acute coronary syndromes. Thank you very much for your attention.
