Excerpt

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.

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).

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.

Contents

• Guideline development group members
• Acknowledgements
• Acronyms, abbreviations and glossary
• 1. Development of the guideline
  • 1.1. Introduction
  • 1.2. Methodology
  • 1.3. Key messages of the guideline
• 2. Assessment of risk
  • 2.1. Assessing an individual's risk of adverse events
  • 2.2. Balancing the risks and benefits of interventions
• 3. Anti–platelet therapy
  • 3.1. Aspirin
  • 3.2. Clopidogrel
  • 3.3. Glycoprotein IIb/IIIa inhibitors (GPIs)
• 4. Anti–thrombin therapy
  • 4.1. Heparins
  • 4.2. Fondaparinux
  • 4.3. Bivalirudin
• 5. Management Strategies
  • 5.1. Early invasive versus conservative management
  • 5.2. Percutaneous Coronary Intervention (PCI) Versus Coronary Artery Bypass (CABG)
  • 5.3. Intra-aortic balloon counterpulsation
  • 5.4. Testing for ischaemia
  • 5.5. Testing for LV function
  • 5.6. Specialist Care
  • 5.7. Rehabilitation and discharge planning
• References
• Appendix A. Scope
• Appendix B. The analysis of MINAP data for the cost–effectiveness analysis
• Appendix C. A cost-effectiveness model comparing alternative combinations of antiplatelet and antithrombin agents in the treatment of unstable angina and non-ST elevation myocardial infarction (UA/NSTEMI)
• Appendix D. The National Service Framework for Coronary Heart Disease (department of health 2000)
• Appendix E. NICE MI: Secondary prevention clinical guideline cardiac rehabilitation recommendations
• Appendix F. Clinical questions and search strategies
• Evidence tables