Preferred Label : Acute Myocardial Infarction Pathway;
NCIt related terms : Acute Myocardial Infarction;
Alternative definition : BIOCARTA: Myocardial infraction (MI) is the condition of irreversible necrosis of
the heart muscle that results from prolonged ischemia. Nearly 1.5 million people in
US sustain an MI each year, and this event proves fatal in approximately one third
of patients. Approximately 90% of MI results from formation of an acute thrombus that
obstructs an atherosclerotic coronary artery. The thrombus transforms a region of
plaque narrowing to one of complete vessel occlusion. The responsible thrombus appears
to be generated by interactions between the atherosclerotic plaque, the coronary endothelium,
circulating platelets, and dynamic vasomotor tone of the vessel wall, all of which
overwhelm natural protective mechanisms. The endogenous protective mechanisms against
thrombosis include: 1) Inactivation of thrombin by antithrombin III (ATIII), the effectiveness
of which is enhanced by binding of ATIII to heparin sulfate. The antithrombin binding
region of commercial heparin consists of sulfated disaccharide units; 2) Inactivation
of clotting factors Va and VIIIa by activated protein C (protein C*), an action that
is enhanced by protein S. Protein C is activated by the thrombomodulin (TM)-thrombin
complex; 3) Inactivation of factor VII/tissue factor complex by tissue factor pathway
inhibitor (TFPI). Coumarin drugs (Warfarin) blocks the g-carboxylation of Glu residues
in prothrombin and factors VII, IX and X which results in incomplete molecules that
are biologically inactive in coagulation (left panel); 4) Lysis of fibrin clots by
tissue plasminogen activator (tPA); 5) Inhibition of platelet activation by prostacyclin
and EDRF-NO. Platelets adhere to exposed collagen and are activated at the site of
endothelial damage in the blood vessel. Activated platelets release adenosine diphosphate
(ADP), serotonin (5-HT), and thromboxane A2 (TXA2), which activate additional platelets.
Binding of thrombin further activates the platelets. Three adjoining platelets are
shown in the process of viscous metamorphosis (top right). Increased cellular Ca2
facilitates binding of fibrinogen. If the intraluminal thrombus at the site of plaque
disruption totally occludes the vessel, blood flow beyond the obstruction will cease,
prolonged ischemia will occur and MI (usually Q-wave MI) will likely result. (This
definition may be outdated - see the DesignNote.);
NCIt note : The BIOCARTA Definition (ALT_DEFINITION) for this pathway concept was provided by
BioCarta. This property was not created by, nor is it maintained by the NCI Thesaurus
staff. Additionally, BioCarta is no longer updating its pathway data; thus, the BIOCARTA
Definition might be outdated or inaccurate. Please see the Terms and Conditions for
Use at http://www.biocarta.com/.;
Biocarta ID : h_amiPathway;
Origin ID : C38985;
UMLS CUI : C1521999;
Automatic exact mappings (from CISMeF team)
- Semantic type(s)
- has_gene_product_element
- pathway_has_gene_element
