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normal response of the body, chemical mediators would be released thus
activating thrombosis promoting repair of the ruptured plaque wherein
endothelium would be replaced with fibrotic tissues which contributes to
narrowing of the artery and loss of its elasticity which may eventually
result in another episode of occlusion (figure 3). This transformation of an
atherosclerotic plaque to an unstable lesion follows the different stages in
platelet activation and aggregation. Rupture or ulceration of an
atherosclerotic plaque exposes the subendothelial matrix (primarily
composed of collagen and tissue factor) to circulating blood. This
particular event will result to platelet adhesion through the binding of
platelet glycoprotein (GP) Ib to von Willerbrand factor and GP VI binding
to collagen. Platelet activation ensues leading to a (1) change in shape of
the platelet (from smooth discoid to spiculated form) which increases the
surface area on which thrombin generation can occur, (2) degranulation of
the platelet alpha and dense granules, releasing thromboxane A2,
serotonin and other platelet aggregatory and chemoattractant agents; and
(3) increased expression of GP IIb/IIIa which enhances affinity to
fibrinogen. Lastly platelet aggregation takes place wherein fibrinogen
binds to activated platelet GP IIb/IIIa, creating a growing platelet
aggregate. This process continuously happening which decreases the
arterial lumen in the long run. In line with this, secondary hemostasis
happens wherein plasma coagulation system is activated. Tissue factor
will cause the activation of Factor X changing it to Factor Xa which leads
to formation of thrombin (factor IIa) which play a central role in arterial
thrombosis: (1) thrombin converts fibrinogen to fibrin (2) thrombin
powerfully stimulates platelet aggregation; and (3) it activates factor XIII
leading to cross ± linking and stabilization of fibrin clot. Thrombin
molecules will eventually incorporated to coronary thrombi forming the
nidus of rethrombosis.
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ii. Risk Factors
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Age, Gender, Ethnicity ± the patient was 68 y/o, male and a pacific
islander which according to Braunwald, has an increased risk due
to the degenerative processes of the body.
Elevated serum lipids ± The patient has elevated serum lipids prior
to admission and suffering from ACS NSTEMI as according to the
patient he is taking simvastatin as his maintenance drug.
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is unknown though literatures suggest that exercise increases HDL
levels, enhances fibrinolytic activity thus reducing clot formation.
Pain in the chest which may radiate down the left arm or both arms
and/ or in the jaw is due to lactic acid accumulation in the
myocardium as a by- product of anaerobic respiration as a
compensatory mechanism of the body to the decreased perfusion
of the myocardium. This is often described as:
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× a tightness
× indigestion like pain
× µlike someone sitting on my chest¶.
diminished left ventricular function ± the most affected part during
ischemic attack on the myocardium is the muscles on the left
ventricles as the left ventricles has the greater workload as to
compare with the right ventricle thus needing more oxygen. Due to
damage of the left ventricle, the function of the left ventricle is also
diminished.
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