What is the main pathology of myocardial infarction?
The major cause of acute myocardial infarction (MI) is coronary atherosclerosis with superimposed luminal thrombus, which accounts for more than 80% of all infarcts. MIs resulting from nonatherosclerotic diseases of the coronary arteries are rare.
What labs are elevated after MI?
Troponin (I or T)—this is the most commonly ordered and most specific of the cardiac markers. It is elevated (positive) within a few hours of heart damage and remains elevated for up to two weeks. Rising levels in a series of troponin tests performed over several hours can help diagnose a heart attack.
What is the pathogenesis of an acute MI?
Myocardial infarction usually results from sudden occlusion of the coronary artery when a ‘high-risk’, thrombosis-prone plaque becomes eroded or ruptures. In the vast majority of cases, myocardial infarction results from coronary atherosclerosis with a superimposed luminal thrombus.
What happens after a myocardial infarction?
After myocardial infarction (MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction.
What are the biochemical events that lead to MI?
Myocardial infarction (MI) usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in an epicardial coronary artery, resulting in an acute reduction of blood supply to a portion of the myocardium.
What describes the basic pathophysiology of myocardial infarction?
Myocardial infarction (“heart attack”) is the irreversible damage of myocardial tissue caused by prolonged ischemia and hypoxia. This most commonly occurs when a coronary artery becomes occluded following the rupture of an atherosclerotic plaque, which then leads to the formation of a blood clot (coronary thrombosis).
What is the most common complication of myocardial infarction?
Ventricular free wall rupture. VFWR is the most serious complication of AMI. VFWR is usually associated with large transmural infarctions and antecedent infarct expansion. It is the most common cause of death, second only to LV failure, and it accounts for 15-30% of the deaths associated with AMI.
How is stemi diagnosed?
Classically, STEMI is diagnosed if there is >1-2mm of ST elevation in two contiguous leads on the ECG or new LBBB with a clinical picture consistent with ischemic chest pain. Classically the ST elevations are described as “tombstone” and concave or “upwards” in appearance.
What is the most common complication following an MI?
What is post MI?
post-MI pericarditis (back to contents) Also known as Dressler’s Syndrome, or post-cardiac injury syndrome (although these terms include other causes such as post-CABG pericarditis).
How to diagnose myocardial infarction ( MI ) clinically?
Usually diagnosed clinically – with blood work (troponin, CK-MB) or EKG. MI may be precipitated by cocaine use… and further exacerbated by treatment with a beta-blocker.
What does mi stand for in medical terms?
Myocardial infarction. Contraction band necrosis – a finding of MI. Myocardial infarction, abbreviated MI, is death of cardiac muscle due to a compromised blood supply. In the context of pathology, they are occasionally seen at autopsy . The lay term for MI is heart attack .
What happens to the myocardium after a mi?
Gross inspection – at 12–24 hours post-MI, the myocardium may exhibit dark mottling. 7 By 1–3 days post-MI, the myocardium usually appears mottled with a yellow-tan centre ( Figure 1 ).
Is there a good understanding of the consequences of a mi?
A good understanding of the consequences of an MI is based on a detailed understanding of the morphological features of coronary arteries and myocardium post-MI. For this, it is essential to appreciate the findings in a heart post-MI.
