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ACUTE CORONARY SYNDROME

ACUTE CORONARY SYNDROME. DEFINITION ACS includes myocardial infarction (MI) and the various patterns of unstable angina: new-onset angina, rest angina, or crescendo-pattern angina. ACS includes a variety of clinical presentations (UA, NSTEMI, and STEMI). 1-UNSTABLE ANGINA

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ACUTE CORONARY SYNDROME

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  1. ACUTE CORONARY SYNDROME

  2. DEFINITION ACS includes myocardial infarction (MI) and the various patterns of unstable angina: new-onset angina, rest angina, or crescendo-pattern angina.

  3. ACS includes a variety of clinical presentations (UA, NSTEMI, and STEMI). 1-UNSTABLE ANGINA Three Principal presentations: Rest angina:occurs at rest with prolonged duration, usually >20 minutes.

  4. New-onset angina:occurs with marked limitation of ordinary physical activity. Crescendo angina:Chronic stable angina that has become more frequent, longer in duration, and lower in threshold.

  5. 2-NSTEMI Characterized by typical cardiac pain, increased biomarkers of myocardial injury and normal ECG. 3-STEMI Characterized by typical cardiac pain, increased biomarkers of myocardial injury and ECG changes of MI.

  6. Braunwald classification of UA 1-According to characteristics. A-Exertional angina. B-Acute rest angina. C-Subacute rest angina. 2-According to clinical circumstances. A-Primary UA. B-Secondary UA. C-Post-infarction UA.

  7. CLINICAL PRESENTATION

  8. ACS is characterised by chest pain, ST-segment changes in the ECG and a rise in the serum markers of myocardial injury/infarction. Chest pain is frequently spontaneous in onset, and unrelated to the usual stressors known to precipitate SA.

  9. The pain is more severe or more prolonged. Less frequently, ACS may present with little or no chest pain but rather with atypical pain.It may be accompanied by the features of an acute transient reduction in COP, pulmonary venous congestion, or, rarely, a potentially lethal ventricular tachyarrhythmia.

  10. Pathophysiology of an ACS event

  11. Can be divided into three phases: 1-Phase one: The development of the unstable atheroma that will rupture. 2-Phase two: The acute ischemic event. 3-Phase three: The long term risk of recurrence.

  12. Causes of atheroma unstability and ruputure 1-Atheoma composition. 2-Inflammation and the released mediators. 3-Infection by chlamedia. 4-Mechanical factors like ↑ HR & BP. 5-Anatomical sites and shearing stress.

  13. Processes that may contribute to the development of ACS: 1-Atherom rupture and thrombosis. 2-Dynamic obstruction. 3-Progressive mechanical obstruction. 4-Inflammation and infection. 5-Secondary causes which can increase demand or decrease suplly.

  14. Cascade of events leading to ACS 1-Rupture of unstable atherosclerotic plaque. 2-Disruption of protective endothelial layer. 3-Exposure of subendothelial layer. 4-Platelet adhesion to area of injury (GP 1b + Von Willobrand factor or fibrinogen ). 5-Platelet activation and exposure of Glycoprotein (GP) IIb/IIIa receptors.

  15. 6-Platelet aggregation: Caused by fibrinogen binding to GP IIb/IIIa receptors. 7-Fibrin deposition within the Platelet plugs. 8-Occlusion of coronary artery. 9-STEMI if occlusion is complete and NSTEMI if occlusion is not complete.

  16. RISK STRATIFICATIONS

  17. Risk stratification is essential to enable triage of patients to the optimal level of care and specific therapy. Careful clinical assessment is the cornerstone of this risk stratification.

  18. All patients should be evaluated for systemic factors such as febrile illness, anaemia or hyperthyroidism that might precipitate or aggravate cardiac ischemia. If present, they should be treated aggressively.

  19. Points of stratification 1-Haemodynamic instability = 6. 2-Recurring chest pain or symptoms refractory to treatment, ST depression or transient ST elevation or T wave inversion, or elevation of troponin T/I or other serum markers of cardiac injury, each = 3. 3-Age > 65 years, risk factors for CAD, Use of aspirin within 7 days, Known CAD, Prior CHF, each = 2.

  20. Formula for assigning high/intermediate/low risk: For haemodynamic instability, score = 6. For each event-related risk indicator, score = 3. For each pre-existing risk indicator, score = 2. High risk = total score 6 or more. Intermediate risk = total score 5 or less. Low risk = score zero.

  21. Late risk: 1-Reversible ischaemia on functional testing (ST segment depression in the stress ECG, wall motion abnormality induced in stress echo, reversible defect with myocardial perfusion imaging). 2-Left ventricular dysfunction. 3-Elevated high-sensitivity CRP.

  22. The risk indicators of a poor outcome in ACS: 1-Event-related: Ongoing or recurring chest pain, ST-segment depression/new ischaemia in the ECG, raised serum markers of cardiac injury/infarction, or haemodynamic instability. 2-Pre-existing: Age over 65 years, multiple risk factors for CAD (=/> 3), especially diabetes, aspirin use within 7 days, known CAD, or prior left ventricular dysfunction.

  23. INVESTIGATIONS

  24. 1-Invasive investigations like coronary cathetarization. 2-Non-invasive like: A-Stress ECG. B-Stress Echocardiography. C-Stress thallium. D-Resting ECG. E-Biomarkers like Troponins, CRP, myiloperioxidase, CD40 ligand.

  25. MANAGEMENT OF ACS

  26. GOALS OF TREATMENT 1-MEDICAL THERAPY. 2-REVASCULARIZATION. GOALS OF MEDICAL THERAPY 1-Rapid initiation of antiplatelets and antithrombotic agents. 2-Relief on pain by antiangianal agents like BBs and nitrates.

  27. PRIORITY OF TREATMENT: 1-Aspirin. 2-Antiangianal. 3-Antithrombotics. 4-GP ||a & |||b receptors antagonists.

  28. NITRATES IN ACS Who gets it? All patients with Ischemic chest discomfort. Who does not get it? Initial systolic pressure <90 or Heart rate <50. When to start IV nitrates? When symptoms not relieved with 3 serial NTG spray/tablets, Morphine, Intravenous beta-blocker, or patients not hypotensive.

  29. Use of Morphine in ACS Indication: when symptoms not relieved with 3 serial NTG or recur despite adequate anti-ischemic therapy. Contraindication: hypotension, intolerance, allergy.

  30. Benefits:Analgesic and anxiolytic & venodilation (reduction in systolic BP and heart rate). Side effects:Nausea, vomiting, and respiratory depression. Alternative in patients allergic to morphine:Meperidine hydrochloride

  31. Beta blockers in ACS When to start? As early as possible. Route of administration? IV followed by oral in high risk patients and those with ongoing chest pain and Oral for intermediate and low risk patients. Choice of effective agents: Cardioselective without intrinsic sympathomimetic activity.

  32. Absolute contraindications: Severe CHF, 2nd or 3rd degree AV block, 1st degree with PR >0.24 seconds, severe acute asthma. Effective regimen: Metoprolol 25-50 q6 for 48 hours then 100 mg twice daily, in COPD reduce dose, 12.5mg bid.

  33. ACE Inhibitors in ACS Indications: 1-High risk patients. 2-HTN persists despite NTG and BBs. 3-Evidence of anterior infarct. 4-Histor of previous infarct. 5-Systolic dysfunction. 6-ACS patients with diabetes.

  34. Contraindications: 1-Systolic BP <100 mm Hg. 2-Clinically relevant renal failure. 3-History of bilateral renal artery stenosis. 4-Known history of allergy to ACEI.

  35. Aspirin in ACS 1-Initial dose: 160mg to 325 mg. 2-Chewable aspirin absorbed more quickly in early hours after infarction. 3-If patients cannot tolerate ASA orally due to GI side effects, ASA can be safely given as rectal suppository. 4-Optimal daily dose of aspirin should be 75mg/81mg per day.

  36. Clopidogrel in ACS Indications: UA and NSTEMI Particularly when PCI is not planned. Dose: Initial dose 300mg (chewable), then 75mg daily for 9 months stop 5 days prior to CABG to control bleeding.

  37. Glycoprotein IIb/IIIa inhibitors Mechanism of action: Inhibits critical step in thrombus formation, by preventing binding of thrombin to activated platelets. Indications: 1-Definit benefit for those who undergo Percutaneous Coronary Intervention (PCI).

  38. 2-Modestly benefit for those who are not routinely scheduled, but who may benefit from PCI. 3-Questionable benefit in patients who do not undergo PCI. FDA approved GP IIb/IIIa inhibitors: Abciximab (Reopro), Tirofiban (Aggrastat) and Eptifibatide (Integrilin).

  39. Oral anti-platelet agent: 1-Aspirin: Initially 300 mg p.o, then 75 - 150 mg daily. 2-Clopidogrel (Plavix): Initial loading dose of 300 mg then 75 mg daily. Heparins: 1-Unfractionated heparin: Heparin sodium (Heparin 60 U/kg IV bolus (monitor PTT, keep at 50 - 70 seconds0, to a maximum of 4000 unit, then 12 units/kg/h infusion to a maximum of 1000 units/h. 2-LMWH: Dalteparin (Fragmin) 120 IU/kg SC every 12-hour or Clexane 1 mg/kg SC every 12-hour.

  40. Glycoprotein IIb/IIIa inhibitors 1-Eptifibatide. 180 µg/kg IV over 1 - 2 min, then 2 µg/kg/min infusion over 72 h or until hospital discharge, whichever occurs. 2-Tirofiban. 0.4 µg/kg/min IV over 30 min, then 0.1 µg/kg/min infusion for 48 - 108 h. 3-Abciximab. 0.25 mg/kg IV bolus 10-60 min then 10 µg/min IV infusion for 12 h

  41. Low-molecular-weight heparin Advantages over unfractionated heparin: 1-Better bio-availability. 2-Higher ratio (3:1) of anti-Xa to anti-IIa activity. 3-Longer anti-Xa activity, avoid rebound. 4-Induces less platelet activation. 5-Ease of use (subcutaneous - qd or bid). 6-No need for monitoring.

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