Definition STEMI is an acronym meaning "ST segment elevation myocardial infarction," which is a type of heart attack.

Heart attacks are divided into two types, according to their severity. A STEMI is the more severe type. In a STEMI, the coronary artery is completely blocked off by the blood clot, and as a result virtually all the heart muscle being supplied by the affected artery starts to die1. This more severe type of heart attack is usually recognized by characteristic changes it produces on the ECG. One of those ECG changes is a characteristic elevation in what is called the "ST segment." The elevated ST segment indicates that a relatively large amount of heart muscle damage is occurring (because the coronary artery is totally occluded), and is what gives this type of heart attack its name. Incidence The incidence of myocardial infarction changed over time. The age and sex-adjusted incidence of myocardial infarction increased from 274 cases per 100,000 person-years in 1999 to a peak of 287 cases per 100,000 person-years in 2000, and then decreased each year thereafter, to 208 cases per 100,000 person-years in 2008 (relative decrease between 1999 and 2008, 24%). There is a difference in the incidence between ST-elevation and non-ST-segment elevation myocardial infarctions. The age and sex-adjusted incidence of ST-segment elevation myocardial infarction decreased each year, from 133 cases per 100,000 persons in 1999 to 50 cases per 100,000 persons in 2008 (relative decrease between 1999 and 2008, 62%; P<0.001 for linear trend), whereas the incidence of non-ST-segment elevation myocardial infarction increased from 155 cases per 100,000 persons in 1999 to 202 cases per 100,000 persons in 2004 before decreasing thereafter2. Causes The common cause of an STEMI is a blood clot (thrombosis) that forms inside a coronary artery, or one of its branches4. This blocks the blood flow to a part of the heart. Blood clots do not

usually form in normal arteries. However, a clot may form if there is some atheroma within the lining of the artery. Atheroma is like fatty patches or plaques that develop within the inside lining of arteries. (This is similar to water pipes that get furred up.) Plaques of atheroma may gradually form over a number of years in one or more places in the coronary arteries. Each plaque has an outer firm shell with a soft inner fatty core. When ruptured, this can trigger the clotting mechanism in the blood to form a blood clot4. Therefore, a build up of atheroma is the root problem that leads to most cases of STEMI. Other causes include the following3: Coronary artery vasospasm Ventricular hypertrophy (eg, left ventricular hypertrophy [LVH], idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease) Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders (Infarcts due to pulmonary disease usually occur when demand on the myocardium dramatically increases relative to the available blood supply.) Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis Cocaine, amphetamines, and ephedrine Coronary anomalies, including aneurysms of the coronary arteries Increased afterload or inotropic effects, which increase the demand on the myocardium Aortic dissection, with retrograde involvement of the coronary arteries Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki disease, Takayasu arteritis, progeria, and cystic medial necrosis (see Myocardial Infarction in Childhood).

Patho Myocardial infarctions with ST-segment elevation are more typically caused by the sudden thrombotic occlusion of a coronary artery that previously was not severely narrowed. When such an occlusion occurs, the abrupt rupture, erosion, or fissuring of a previously minimally obstructive plaque creates a potent stimulus for platelet aggregation and thrombus formation4. If the stimulus for a thrombosis is robust, total arterial occlusion can be resulted. Acute ST segment elevation myocardial infarction usually occurs when thrombus forms on a ruptured atheromatous plaque and occludes an epicardial coronary artery. On occlusion of the infarct-related artery, all the myocardium that is supplied by the artery becomes ischemic, resulting in chest pain and electrocardiographic evidence of transmural (fullthickness) ischemia (ST-segment elevation) in the leads reflective of that region of the heart5. Subsequently, necrosis begins within minutes and progresses during several hours in a wavefront fashion from the endocardial surface to the epicardial surface. If ischemia persists for several hours, transmural infarction results. In contrast, if blood flow is restored during the period of progressive necrosis, the ischemic myocardium is salvaged and the size of the infarct is reduced4. Since morbidity and mortality from a myocardial infarction correlate with the size of the infarct, prompt restoration of blood flow would also be expected to improve left ventricular function and survival.

Histological appearance of a ruptured atheromatous plaque (bottom arrow) and occlusive thrombus (top arrow) resulting in acute myocardial infarction 5

heartdisease.about.com/od/heartattack/g/STEMI.htm

(http://blogs.nejm.org/now/index.php/incidence-of-myocardial-infarction/2010/06/11/) http://emedicine.medscape.com/article/759321-overview Primary PCI for Myocardial Infarction with ST-Segment Elevation

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Ellen C. Keeley, M.D., and L. David Hillis, M.D. N Engl J Med 2007; 356:47-54January 4, 2007)

(BMJ 2003; 326 : 1379 doi: 10.1136/bmj.326.7403.1379 (Published 19 June 2003)

Acute coronary syndrome: ST segment elevation myocardial infarction)