Heart Attack (Acute Myocardial Infarction):
According to the world health organization, cardiovascular disorder is the leading cause of death worldwide, as well as in the US. Of those, a large proportion is caused by heart attacks, also known as acute myocardial infarctions, or just myocardial infarctions, seldom just called MI. The word infarction means that some area of tissue has died due to a lack of blood flow, and therefore a lack of oxygen. I refer to the muscle, and cardiac refers to the heart tissue.
Causes, Symptoms, Types, & Pathology:
So by a heart attack or MI, you have the death of heart muscle cells because of a lack of blood flow, a process called necrosis. Now the heart’s main job is to pump blood to your body’s tissues right? Well, the heart also needs blood, and then it also pumps blood to itself, using the coronary circulation. The coronary circulation is this system of small arteries and veins that help keep the heart cells supplied with fresh oxygen. Heart attacks happen when these small arteries become blocked and stop supplying blood to the heart tissue, and if this happens for long enough, heart tissue dies. Almost all heart attacks are ultimately a result of endothelial cell dysfunction, which relates to anything that irritates or inflames the smooth inner lining of the artery the tunica intima. One classic irritant is the toxins found in tobacco which float through the blood and damage these cells. That damage then becomes a site for atherosclerosis, a type of coronary artery disease where deposits from fat, cholesterol, proteins, calcium, and white blood cells build up and start to block blood flow to the heart tissue. This mound of stuff should be two parts to it, the soft cheesy-textured interior and the hard outer shell which is called that fibrous cap. Collectively this whole thing’s ominously called plaque. Usually, though, it takes years to the plaque to build up, and this slow blockage only partially blocks the coronary arteries, and so even though less blood makes it to heart tissue, there is still blood. Heart attacks happen when there is a sudden complete blockage or occlusion of a coronary artery so let’s see how that can happen. Since these plaques sit right in the lumen of the blood vessel, they are constantly being stressed by mechanical forces from blood flow, and interestingly it’s often the smaller plaques with softer caps rather than, the larger ones with harder caps that are especially prone to break or get ripped off. Once that happens the cheesy inner filling which remembers is that mix of fat, cholesterol, proteins, calcium, including white blood cells, is thrombogenic, and that means that it tends to form clots very quickly. So platelets, or blood-clotting components in the blood, flow by and get excited; and they adhere to the exposed cheesy material. In addition to piling up, the platelets also release chemicals that enhance the clotting process. Now this happens super fast, think about how quickly a small cut stops bleeding, that’s a very similar process it happens in a matter of minutes, right? And now that coronary artery is fully occluded. So promptly let’s change views a bit, If we take a slice of this heart like this, this side doing posterior, or back, and this being anterior, or front, by that left and right ventricles here, and then produce the three most commonly blocked arteries that left anterior descending, or LAD which supplies blood to this anterior wall and septum of the left ventricle which accounts for 40-50% of cases, the right coronary artery, or RCA which covers the posterior wall, septum and papillary muscles of the left ventricle accounts for about 30-40%of cases, and the left circumflex artery, or LCX which supplies on the lateral wall from the left ventricle about 15-20% of cases. Notice that the majority of those areas supply the left ventricle maximum heart attacks, therefore, involve the left ventricle, where the right ventricle and both atria the upper chamber aren’t as often affected. Each of these areas is called the artery zone of perfusion. If we take a closer look at one of these zones, we’ll see that basically you have got the endocardium, which is the smooth membrane on the inside of the heart, and then the myocardium, all the heart muscle, and the epicardium, the outer surface of the heart, which is where the coronary arteries live. Let’s say the LAD gets blocked, the area of perfusion is now at serious risk, and within about a minute, the muscle cells in this zone don’t see enough oxygen and become ischemic, and the muscle layers ability to contract is severely reduced. This initial stage is extremely sensitive since the ischemic damage to cells in the perfusion zone is potentially reversible. After about 20-40 minutes, though, damage starts to become irreversible, and the cells start to die, and this zone changes to a zone of necrosis, or dead tissue. Once lost, these cells will never return or regrow that’s why quickly identifying and treating an MI quickly is super important. The first area affected is the inner third of the myocardium, since it’s farthest from the coronary artery and the last area to receive blood, and it’s subject to higher pressures from inside the heart. If the blockage suddenly lyses or breaks down and blood flow returns, sometimes patient’s damage will be limited to the inner third, and this would be called subendocardial infarct. An ECG, or electrocardiogram, done at this point typically shows an ST-segment depression, or in other words, it doesn’t show ST-segment elevation, so sometimes we call this an NSTEMI which stands for non-ST elevation myocardial infarction. Other causes of this sort of subendocardial infarcts would be severe atherosclerosis, and hypotension anything that ultimately leads to poor perfusion of the heart tissue. After about 3 to 6 hours, though, the zone of necrosis extends through the entire wall thickness, called a transmural infarct, which this time shows up as ST-segment elevation on ECG, which is why they are sometimes called STEMIs, or ST-elevation myocardial infarctions. So the difference between NSTEMIs and STEMIs is that NSTEMIs don’t have ST-segment elevation, and these are caused by partial infarct of the wall, whereas STEMIs have ST-segment elevation and involve the whole wall thickness. Patients that have an MI will most commonly have severe and crushing chest pain or pressure, that might radiate up to the left arm or jaw, they might have diaphoresis or sweating, nausea, fatigue, and dyspnea. All of these are either a direct result of an end-organ like the heart or the brain not getting enough perfusion so think chest pain and dizziness. Or from the sympathetic response from the body to help the heart work harder and preserve blood pressure so think sweating and clammy skin. Many people also have referred pain where the nerves in the heart are irritated, but that pain can be felt in the jaw, shoulder, arm, or back instead. In addition to an ECG, labs can be very useful in diagnosing an MI. When there is irreversible damage to heart cells, their membranes become damaged and the proteins and enzymes inside escape, and can enter the bloodstream. Three key ones are troponin I, Troponin T, and CK-MB, which is a combination of creatine kinase enzymes M and B. d both troponin I and T levels can be elevated in the blood within 2-4 hours after infarction, and usually peak around 48 hours, but stay elevated for 7-10 days. CK-MB starts to rise 2-4 hours after infarction, peaks around 24 hours, and returns to normal after 48 hours. Since CK-MB returns to normal more quickly, it can be useful to diagnose reinfarction, a second infarction that happens after 48 hours but before trooping I have gone back to normal. A second heart attack happens following 10% of MIs. A major complication with MIs are arrhythmias, or abnormal heart rhythms, with the highest risk being immediately following an MI, since the damage or injury can disrupt how the cells conduct electrical signals. Kind of along the same lines, depending on how much contractile muscle tissue is affected, patients hearts might not be able to pump enough blood to the body, resulting in carcinogenic shock. In the days following an infraction, the tissue around the infracted area becomes inflamed and is invaded by neutrophils, which can lead to pericarditis, inflammation of the pericardium. In the next couple weeks, macrophages invade the tissue, and the healing process begins with the formation of granulation tissue, which is new connective tissue that’s yellow and soft. At this phase, the tissues most at risk of myocardial rupture. After two weeks to several months, the damaged cardiac tissue scarring process finishes, and the resulting tissue becomes grayish-white in color. Since the scar tissue doesn’t help pump blood, over time the remaining heart muscle can grow or change shape to try to compensate for these lost cells and pump harder, but they ultimately continued to fail, which can lead to heart failure. Now a potentially life-saving treatment that can be performed immediately following an MI is fibrinolytic therapy, uses medications to break down fibrin in blood clots. An angioplasty might also be done, which is surgical removal of the blockage. And finally, a percutaneous coronary intervention might also be performed, where a tiny catheter is used to place a stent in the coronary artery to physically open up a blood vessel. Each of these focuses on-establishing blood flow to the dying heart cells since time is tissue. If early enough following blockage, some of these cells that haven’t entered into the irreversible stage can be salvaged and saved, while the others will be destroyed and removed. This can improve both short and long-term function as well as prevent further damage and reduce the overall zone of necrosis. Now an important complication of re-establishing perfusion, or reperfusion therapy, is reperfusion injury, where returning blood flow damages tissue. This is thought to happen because of a couple of mechanisms. First, blood flowing back to cells brings this influx of calcium, and since calcium leads to muscle contraction, the irreversibly damaged cells contract, and since they have been irreversibly damaged, they get stuck like that and can’t relax. This shows up on histology as this characteristic contraction band necrosis. Also though, blood brings along oxygen, right? Yeah it does. Well that oxygen, paradoxically, can actually lead to more cellular damage. The conditions in an ischemic heart seem to cause an increased conversion of the returning oxygen to reactive oxygen species, which go on to damage more heart cells. In addition to reestablishing blood flow through, there are a number of medications that may be given in the acute setting including antiplatelet meds like aspirin, anticoagulants such as heparin, nitrates which relax the coronary arteries and help lower preload, beta blockers that slow down the heart rate and thereby cardiac demand, pain medication to help relieve the discomfort, and statins which help improve a patients lipid profile. Now there are many individual factors to consider when it comes to acute management of myocardial infarction, and of course, many long-term issues to consider as well the most important of which is to address the underlying risk factors like an improved diet and quitting smoking.