by Jamie Lintgen
May 29, 2026
A Myocardial Infarction, MI, or “heart attack” colloquially, is a cardiovascular incident involving the partial or complete obstruction of one of the arteries that carry blood to your heart. The lack of blood supply to the heart causes cells to not receive enough oxygen, and eventually die. This is related very strongly to the amount of time that oxygen is lacking, which is why speed is critical in the treatment of MIs. MIs are most typically caused by the bursting of clumps of fat that build up the coronary arteries. These clumps, called atherosclerotic plaques, are caused by fats in your blood becoming embedded in the inner layer of blood vessels (the “endothelium”), and building up over time. It mostly commonly happens in areas where blood flow is turbulent, like junctions and hard curves. These plaques are made up primarily of fats, particularly LDL cholesterol, as well as other things in the blood flow. The initial creation of the plaque happens when LDL cholesterol infiltrates a damaged part of the inner wall of an artery. These wall cells are particularly susceptible to this infiltration when risk factors like smoking, hyperglycemia, and others are present, since they damage the lining itself. The infiltration is more likely when patients have conditions like high cholesterol (hypercholesterolemia or hyperlipidemia) or high blood pressure (hypertension), since they raise the total fat content of the blood and increase the shear stress on arterial walls respectively. Atherosclerotic plaques grow through time due to further infiltration of LDL cholesterol and others, and eventually reach a point of instability. Eventually, due to inflammation weakening to the top cap of the plaque (the “fibrous cap”), the plaque will burst due to everyday fluctuations in blood pressure caused by exercise, position change, etcetera. When the plaque bursts, the platelets in your blood will be exposed to the area of the tissue behind the surface lining of the artery (the “subendothelial layer”), which will be perceived as a wound to be healed. As such, the platelets will coagulate in an effort to heal the wound. The blood stream (plasma) generally also contains proteins that create blood clots when exposed to tissue, which is generally a mechanism to slow bleeding and help heal damage to blood vessels. However, when these proteins, called clotting factors, are exposed to the inside of the plaque after a rupture, they begin forming a clot (thrombus, in this case), inside the coronary artery. This, combined with platelet aggregation, causes the space that blood can flow to oxygenate cells to be severely limited, and often totally cut off. From a more clinical perspective, MIs classically present with a “squeezing” or “crushing” chest pain, that onsets not necessarily during exercise and lasts for over 30 minutes (often called unstable angina). Asides from angina, MIs also cause elevation of the ST segment on an electrocardiogram (ECG). This is essentially the period of a heart beat after the initial contraction of the ventricles has occurred, but before they relax again. Ischemic parts of the heart often exhibit ST elevation due to a fairly complex mechanism involving the movement of ions that constitutes the electrical activity of the heart, and I may write another article about cardiac electrical activity in the future. The moral of the story though is that acutely ischemic parts of the myocardium appear to have elevated ST segments in the ECG leads measuring that part of the heart. ECGs are measured with 12 leads, (I-III, aVR, aVL, aVF, V1-V6), each measuring a distinct part of the heart's electrical activity. Though it may not appear quite this simple in clinical scenarios, generally ST elevation of II, III, or aVF is due to an inferior infarction, due to occlusion of the right coronary artery (RCA). ST elevation in leads V2-V4 are often highly exaggerated and imply ischemia of the anterior myocardium, caused by occlusion of the left anterior descending (LAD) coronary artery. These are often highly elevated due to the LAD serving a larger amount of the myocardium, leading to larger ischemic areas in the event of occlusion. Elevation of I, aVL, aVF, V5 and V6 often imply a lateral ischemia, due to occlusion of the left circumflex coronary artery (LCX). The final major diagnosis tool for MIs is elevated biomarkers such as the troponin proteins, which are found on a blood test. Cardiac Troponins (cTn) are proteins involved in muscle contraction in the heart, and during myocardial ischemia they are released into the bloodstream. Highly increased cTn in the blood is generally specific to MI, while slightly increased levels may be due alternative cardiac muscle injury. The diagnosis of myocardial infarction generally requires two of the three major indicators (chest pain, ST elevation, elevated cTn levels). Treatment of myocardial infarction is generally a highly time sensitive matter, due to the death of myocardial tissue being directly related to the time of ischemia. When the patient is initially awaiting further analysis and treatment, aspirin is recommended in dosages of 150-300mg. Aspirin is an antithrombolytic, meaning it suppresses the activity of platelets, the primary part of the blood that forms clots. Since occlusion is often caused by a clot forming in the coronary arteries, as discussed previously, aspirin reduces the growth of clots and diminishes existing clots. Opioids such as morphine are often given for pain relief, and have no adverse effects in cases of anterior MI. Beta blockers are also often given to reduce the activity of the ischemic heart to reduce oxygen consumption. During ischemia, the nervous system will often attempt to increase heart rate and blood pressure with sympathetic nerves in the heart. These sympathetic pathways use norepinephrine, binding to beta-adrenergic receptors in the cardiac cells, to increase contractility and heart rate. Beta blocker blocks these receptors, which can result in reduced load on the ischemic heart. To eliminate an MI, two main options exist, including percutaneous cardiac intervention (PCI), or medically induced fibrinolysis, often called thrombolytics. PCI is a procedure that observes the ischemic heart under a radiographic imaging with dye injected into coronary arteries to visualize the blockage. A catheter then may be inserted to attempt to open up the blockage by inflating a balloon or potentially inserting a stent. PCI must be performed by an interventional cardiologist in a catheterization lab, and is the better of the two options. However, it is not as widely available, and if the patient cannot have PCI performed in <120 minutes after the infarctions onset, thrombolytics should be initiated after ruling out contraindications. Thrombolysis is the process of breaking down clots using aggressive medication, which should be started in under 10 minutes if possible. It is extremely important before starting thrombolytics to rule out pericarditis and aortic dissection, which often present with chest pain similar to MI. Acute pericarditis can also present with ST elevations, though notably they are typically present is all leads on ECG rather than one specific area. Pericarditis is the infection of the pericardium, and often, though not always, presents with a “pericardial friction rub” while listening with a stethoscope. This extra sound, often described as a high pitch, scratching rub, is highly specific to pericarditis. However, it is not always present, so further investigation is necessary if other signs of infection are present. Thrombolytics being erroneously started in cases of acute pericarditis can lead to life threatening hemorrhagic pericardial effusion and cardiac tamponade, since the inflamed pericardium is susceptible to bleeding. Aortic dissection is a life threatening condition in which the inner layer of the aorta is ruptured, and blood flows into the space in between the inner and outer layer of the aorta. It is often described as a tearing chest pain, worst at onset, as opposed to the accumulating pain of an MI. It also presents with widened mediastinal range on a chest xray, which is the area between the lungs roughly where the arch of the aorta is vertically. Since aortic dissection is an inherently hemorrhagic event, the dissolving of all clots which have formed is extremely detrimental, and can cause the dissection to spread rapidly and potentially fully rupture. Patients who have had an MI are more likely to have another, so treatment following the initial incident is crucial. Aspirin is recommended lifelong in most cases to reduce formation of further clots. Statin medications, which reduce LDL cholesterol, are also recommended in most cases to stabilize atherosclerotic plaques. If, as a result of ischemia, patients have significant left ventricular failure (ejection fraction <40%), beta-blockers are recommended assuming no contraindications. Antihypertensives should be prescribed as well with a goal of <140/90mmHg. Lifestyle modification are also extremely important, with smoking cessation being the most valuable. Also important are diet, weight, and alcohol control. Bibliography Jebari-Benslaiman S, Galicia-García U, Larrea-Sebal A, et al. Pathophysiology of Atherosclerosis. Int J Mol Sci. 2022;23(6):3346. Published 2022 Mar 20. doi:10.3390/ijms23063346 Ojha N, Dhamoon AS. Myocardial Infarction. [Updated 2023 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537076/ Mair J. The Pathophysiology of Cardiac Troponin Release and the Various Circulating Cardiac Troponin Forms-Potential Clinical Implications. J Clin Med. 2025;14(12):4241. Published 2025 Jun 14. doi:10.3390/jcm14124241