Unstable angina and NSTEMI the early management of unstable angina and non-ST-segment-elevation myocardial infarction
This guideline addresses a variety of issues relating to the management of NSTEMI and UA, conditions which are collectively termed non-ST elevation acute coronary syndromes (NSTEACS). It does not address the management of those with STEMI.
| Corporate Authors: | , |
|---|---|
| Format: | eBook |
| Language: | English |
| Published: |
London
Royal College of Physicians
2010, 2010
|
| Series: | Clinical guideline
|
| Subjects: | |
| Online Access: | |
| Collection: | National Center for Biotechnology Information - Collection details see MPG.ReNa |
| Summary: | This guideline addresses a variety of issues relating to the management of NSTEMI and UA, conditions which are collectively termed non-ST elevation acute coronary syndromes (NSTEACS). It does not address the management of those with STEMI. If the volume of thrombus is sufficient to occlude the lumen of the artery, and this is persistent, then acute ST-elevation (an abnormality of the electrocardiogram) myocardial infarction or STEMI' ensues, with progressive death (necrosis) of heart muscle tissue. If the volume of thrombus is insufficient to occlude the artery or does so only temporarily then shortage of blood supply to the affected heart muscle (myocardium) is less severe or is intermittent. In these circumstances there is often some myocardial necrosis, as evidenced by a rise in the cardiac specific serum biomarkers such as troponin; this syndrome is described as non-ST elevation myocardial infarction' (NSTEMI). When myocardial ischaemia is present, but without evidence of actual myocardial necrosis (normal serum troponin level), the clinical syndrome is described as unstable angina (UA). The development of cholesterol-rich plaque within the walls of coronary arteries (atherosclerosis) is the pathological process which underlies coronary artery disease'. However, the clinical manifestations of this generic condition are varied. When the atherosclerotic process advances insidiously the lumen of a coronary artery becomes progressively narrowed blood supply to the myocardium is compromised (ischaemia) and the affected individual will often develop predictable exertional chest discomfort, or stable' angina. However, at any stage in the development of atherosclerosis, and often when the coronary artery lumen is narrowed only slightly or not at all, an unstable plaque may develop a tear of its inner lining cell layer (intima), exposing the underlying cholesterol rich atheroma within the vessel wall to the blood flowing in the lumen. This exposure stimulates platelet aggregation and subsequent clot (thrombus) formation. |
|---|---|
| Physical Description: | 1 online resource ill |