Angina Pectoris Case Analysis

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Angina pectoris is a term used to describe the syndrome of chest pain resulting from myocardial ischemia (Griffin et al., 2008). Normal non-ischemic myocardial tissues differ from the cardiac tissue of an individual with myocardial ischemia because the normal tissue has adequate blood supply whereas the tissue in angina has inadequate blood supply from blocked coronary arteries. Unstable angina is diagnosed when ischemia is neither severe nor prolongs for more than 20 minutes and regularly occurs at rest (Sami & Willerson, 2010). Patients who have unstable angina are at a high risk for a new infarction and its sequelae such as cardiac death until the endothelial injury is repaired. The purpose of this paper is to present a case analysis of…show more content…
The clinical diagnosis can be determined by performing a careful physical examination and an assessment with an electrocardiogram (Wilensky, 2012). A full clinical testing as well as blood tests can be done to diagnose unstable angina. Blood tests include testing for myocardial necrosis with troponin I, troponin T and myoglobin (Marshall, 2011). The presence of these biochemical markers are indicative of a myocardial infarction and not unstable angina. Additional testing includes an echocardiogram to assess cardiac wall abnormalities and left ventricular function (Marshall, 2011) as well as stress testing for ischemia testing (U. S. Department of Health and Human Services,…show more content…
It can be caused by a reduction in coronary artery luminal diameter. According to Wilensky (2012), the artery luminal narrowing can stem from progressive atherosclerotic intrusion into the lumen or by sudden acute vasoconstriction or thrombus. In normal development, the individual does not develop angina because the lumen of the coronary arteries are patent without occlusion from atherosclerotic plaques, vasoconstriction or thrombus. The onset of symptoms is sudden when thrombus formation is the direct cause of unstable angina. Following the onset of symptoms, unstable angina progresses rapidly and ends in severe symptoms at rest. The rupture of a vulnerable plague with thrombus formation influences the fast change from a stable to unstable lesion (Wilensky, 2012).
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