Over time, they become laden with cholesterol products, particularly LDL, and become foam cells. A cholesterol core forms as foam cells die. In response to growth factors secreted by macrophages, smooth muscle and other cells move into the plaque and act to stabilize it. A stable plaque may have a thick fibrous cap with calcification. If there is ongoing inflammation, the cap may be thin or ulcerate. Exposed to the pressure associated with blood flow, plaques, especially those with a thin lining, may rupture and trigger the formation of a blood clot (thrombus). The cholesterol crystals have been associated with plaque rupture through mechanical injury and inflammation. Other causes
Atherosclerotic disease is not the only cause of myocardial infarction, but it may exacerbate or contribute to other causes. A myocardial infarction may result from a heart with a limited blood supply subject to increased oxygen demands, such as in fever, a fast heart rate, hyperthyroidism, too few red blood cells in the bloodstream, or low blood pressure. Damage or failure of procedures such as percutaneous coronary intervention or coronary artery bypass grafts may cause a myocardial infarction. Spasm of coronary arteries, such as Prinzmetals angina may cause blockage. Tissue death
If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the blocked coronary artery die (infarction), chiefly through necrosis, and do not grow back. A collagen scar forms in their place.
It is known to decrease mortality associated with acute myocardial infarction by at least 50%. P2Y12 inhibitors such as clopidogrel, prasugrel and ticagrelor are given concurrently, also as a loading dose, with the dose depending on whether further surgical management or fibrinolysis is planned. Prasugrel and ticagrelor are recommended in European and American guidelines, as they are active more quickly and consistently than clopidogrel. P2Y12 inhibitors are recommended in both NSTEMI and STEMI, including in PCI, with evidence also to suggest improved mortality. Heparins, particularly in the unfractionated form, act at several points in the clotting cascade, help to prevent the enlargement of a clot, and are also given in myocardial infarction, owing to evidence suggesting improved mortality rates. In very high-risk scenarios, inhibitors of the platelet glycoprotein αIIbβ3a receptor such as eptifibatide or tirofiban may be used.There is varying evidence on the mortality benefits in NSTEMI. A 2014 review of P2Y12 inhibitors such as clopidogrel found they do not change the risk of death when given to people with a suspected NSTEMI prior to PCI, nor do heparins change the risk of death. They do decrease the risk of having a further myocardial infarction. Angiogram
Primary percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner, ideally within 90–120 minutes of contact with a medical provider. Some recommend it is also done in NSTEMI within 1–3 days, particularly when considered high-risk.