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Acute Myocardial Infarction/ Stroke - Article Example

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The American Heart Association has named these plaques as developed human fibrolipid plaques. Such plaques form as a result of low density lipoproteins being oxidized and…
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Acute Myocardial Infarction/ Stroke
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Acute Myocardial Infarction (AMI) Pathophysiology Figure Summary of the pathological processes involved in AMI Plaque Formation V Plaque Rupture
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V
Thrombosis
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V
Myocardial Ischemia
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V
Myocardial Infarction
The start of the pathophysiology of acute coronary syndromes like AMI lies in the formation of plaque. The American Heart Association has named these plaques as developed human fibrolipid plaques. Such plaques form as a result of low density lipoproteins being oxidized and consumed by macrophages. In this process the macrophages are transformed into foam cells, which accumulate within the smooth muscle cell layer of coronary arteries to form plaque. Calcification of the surrounding tissue of the smooth muscle follows. The ensuing consequence of this plaque formation is thrombosis, in which there is reduced oxygen supply. This starving of the heart muscles of oxygen leads to myocardial ischemia and on to death of the heart muscle or myocardial infarction. Acute myocardial infarction is the acute coronary syndrome that results from myocardial infarction (Galvagno, 2003).
Patients presenting themselves with the following symptoms are at risk for Acute Coronary Syndrome (ACS) or AMI.
Chest Pain
History or evidence of ischemic heart disease
Age, gender and comorbidities (atypical presentation in female, elderly and diabetic)
Presence of cardiac risk factors.
A key element is the type of chest pain which is to be identified from typical angina, atypical angina or non-anginal chest pain. Recognizing AMI and its severity cannot be done without an electro-cardiogram (ECG). This means an ECG needs to be done immediately on a patient presenting with chest pain.
In patients with new or typical chest pain ST elevation of more than 1mm in two or more contiguous limb leads, or equal to 2mm or more precordial leads these findings show that they need to be considered as having AMI. Patients that show new or presumably new left bundle branch block (LBBB); the treatment mode is the same as that which is given to patients with ST-segment elevation. This is despite the fact that some of the patients presenting with LBBB may not prove to have AMI. The reason for this is that thrombolytic therapy of patients with LBBB is found to reduce patient mortality.
Treatment
Early treatment involves the use of aspirin, heparin, enoxaparin, nitrates, beta-blockers and clopidogrel. Aspirin reduces the possibility of mortality, reinfarction and stroke. Combining heparin/enoxaparin in conjunction with aspirin and reperfusion therapy is not universally accepted, but it appears to enhance patency.
All patients with AMI should be given chewable aspirin as soon as it is possible and continued indefinitely. For patients unable to take aspirin, clopidrogel is the alternative. When the probability of urgent coronary artery bypass graft is low early use of clopidrogel should be considered. Evidence supports the use of enoxaparin as an alternative to intravenous heparin. In high risk patients early use of subcutaneous low-molecular-weight heparin (enoxaparin 1mg/kg subcutaneous every 12 hours) or intravenous unfractionated heparin (70units/kg load then 12 to 15 units/kg/hr to achieve partial thromboplastin time levels 1.5 to 2.5 the control) with aspirin and/or clopidrogel is known to decrease the incidence of AMI and ischemia. Enoxaparin has demonstrated a moderate benefit over intravenous access heparin in reducing the mortality rate, myocardial infarction and recurrent ischemia. However, enoxaparin needs to be used with caution in patients with renal insufficiency (Diagnosis and Treatment of Chest Pain and AcuteCoronary Syndrome (ACS).
Literary References
Diagnosis and Treatment of Chest Pain and AcuteCoronary Syndrome (ACS). 2008. Retrieved October 12, 2009, from ICSI Web Site: http://www.icsi.org/acs_acute_coronary_syndrome/acute_coronary_syndrome_and_chest_pain__diagnosis_and_treatment_of_2.html
Galvagno, S. M. (2003). Emergency Pathophysiology: Clinical Applications for Prehospital Care, Jackson: Teton NewMedia. Read More
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