ST elevation myocardial infarction pathophysiology
ST Elevation Myocardial Infarction Microchapters
ST elevation myocardial infarction pathophysiology On the Web
ST elevation myocardial infarction is largely influenced by the role of plaque rupture.
The Role of Plaque Rupture in ST Elevation Myocardial Infarction
Atherosclerosis, or hardening of the arteries, is the gradual buildup of cholesterol and fibrous tissue (collagen and smooth muscle cells) throughout the vascular tree. When there is localized accumulation of lipids and scar tissue, this is called a "plaque". Somewhat paradoxically, it is not the most severe plaque narrowing that leads to ST elevation MI. Pathological studies indicate that it is often mild-to-moderate, lipid-laden, inflamed plaques that are the ones most likely to rupture and cause an ST elevation MI (STEMI) or a non ST elevation MI (NSTEMI).  The role of plaque rupture in STEMI and NSTEMI is supported by studies demonstrating that plaque rupture is present in about 70% and superficial erosion is present in 30% of patients who die suddenly in whom there is documented coronary artery disease.  Exposure of the blood stream to the thrombogenic components of the plaque leads to activation of the coagulation cascade and thrombus formation. In STEMI, the clot completely occludes the epicardial artery, and there is a complete lack of blood flow to the involved territory. This causes transmural injury and ST elevation. In NSTEMI, there is partial obstruction with embolization. This causes ischemia and subendocardial injury that are manifested by ST depression.
Pathophysiology of and Risk Factors for Plaque Rupture
- Macrophage accumulation has been shown to be present to a greater degree in patients with acute coronary syndromes than in those patients with chronic stable angina   These activated macrophages can release enzymes such as metalloproteinases, interstitial collagenase, gelatinase, and stromelysin that degrade collagen, elastin, and proteoglycans.  This enzymatic degradation in turn leads to breakdown of the fibrous cap. The thin shoulders or edges of the fibrous cap appear to be particularly vulnerable to erosion and breakdown.
- Neovascularization of the plaque Moreno et have shown that microvessel density was increased in ruptured plaques when compared with nonruptured plaques (P=0.0001). Furthermore, among lesions with severe macrophage infiltration at the fibrous cap, microvessel density was increased (P=0.0001) was well as at the edges or shoulders of the plaque (P=0.0001). Intraplaque hemorrhage was also associated with an increase in microvessel density (P=0.04) as was the presence of thin-cap fibroatheromas (P=0.038). Microvessel density at the base of the plaque was identified as an independent (P=0.003) correlate of plaque rupture. 
- High oscillatory shear stress
- Spontaneous coronary dissection
Pathophysiology of and Risk Factors for Thrombosis Following Plaque Rupture
There are numerous systemic risk factors associated with thrombus formation following plaque rupture:
- Smoking: Smoking increases platelet aggregation and plasma epinephrine levels 
- Fibrinogen: Elevated levels of fibrinogen have been associated with thrombosis including abnormal levels of fibrinogen 
- Von Willebrand factor antigen 
- Tissue plasminogen activator 
- Anticardiolipin antibodies 
- Cross-linked fibrin-degradation products 
- Polymorphisms of a platelet glycoprotein receptor 
Gross Pathology Findings in Plaque Rupture
Plaque Rupture Histopathological Findings
The Consequence of Plaque Rupture and Vessel Occlusion: The Time Dependent Wavefront of Necrosis
Irreversible injury of ischemic myocytes occurs first in the subendocardial zone. With more extended ischemia, a wavefront of cell death moves through the myocardium to involve progressively more of the transmural thickness of the ischemic zone. The precise location, size, and specific morphologic features of an acute myocardial infarction depend on:
- The location, severity, and rate of development of coronary atherosclerotic obstructions,
- The size of the vascular bed perfused by the obstructed vessels
- The duration of the coronary artery occlusion
- The metabolic / oxygen needs of the myocardium at risk,
- The extent of collateral blood vessels
Decrease of ATP levels in myocytes in reaction to ischemia starts within seconds and causes loss of contractility in first two minutes. If ischemia persists, ATP levels reduced to its half level within 10 minutes and to 1/10 within 40 minutes. Irreversible cell injury occurs between 20-40 minutes and microvascular level injury starts if ischemia lasts more than an hour.
If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction. As a result, the patient's heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias.
Pathophysiology of ST segment elevation on the electrocardiogram
In ST segment myocaridal infarction (STEMI), the ST segments on the ECG are by definition elevated and there is myonecrosis (death of myocytes) as reflected by elevation of biomarkers such as creatine kinase MB fraction (CK-MB) or troponin T or I (tn). The ST segments are elevated due to full thickness injury of the myocardium.
Videos of STEMI pathophysiology
The following are excellent videos demonstrating the underlying pathophysiology.
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