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myocardial infarction and p. 309
antiarrhythmics after p. 326
β -blockers for p. 245
complications of p. 314
diabetes mellitus p. 350
diagnosis of p. 313
on ECG p. 310, 313
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heart failure caused by p. 316
heparin for p. 440
homocystinuria p. 81
hypertensive emergency and p. 304
shock caused by p. 319
thrombolytics for p. 442
According to the world health organization, cardiovascular disease is the leading cause of death worldwide, as well as in the US. Of those, a large proportion are caused by heart attacks, also known as acute myocardial infarctions, or just myocardial infarctions, sometimes 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. “Myo” refers to the muscle, and “cardial” refers to the heart tissue. So with a heart attack, or MI, you have death of heart muscle cells because of a lack in 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 so 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 slippery inner lining of the artery—the tunica intima. One classic irritant are the toxins found in tobacco which float around in the blood and damage these cells. That damage then becomes a site for atherosclerosis, a type of coronary artery disease where deposits of fat, cholesterol, proteins, calcium, and white blood cells build up and start to block blood flow to the heart tissue. This mound of stuff has two parts to it, the soft cheesy-textured interior and the hard outer shell which is called the fibrous cap. Collectively this whole thing’s ominously called plaque. Usually, though, it takes years for 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’s still blood. Heart attacks happen when there’s 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’re 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 inner cheesy filling which remember is this mix of fat, cholesterol, proteins, calcium, and white blood cells, is thrombogenic, and this 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.
Myocardial infarction (MI), also known as a heart attack, occurs when the blood supply to part of the heart muscle is blocked. This is usually caused by a buildup of fatty deposits in the lining of an artery that supplies blood to the heart, a process called atherosclerosis. Symptoms of MI include crushing chest pain or pressure that might radiate up to the left arm or jaw, sweating, nausea, and dyspnea. Treatment of MI includes re-establishing blood flow using medications, angioplasty, or percutaneous coronary intervention.
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