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ACUTE CORONARY SYNDROME DR CHEVAAN HENDRICKSE INTERVENTIONAL CARDIOLOGIST Conflicts of interest None ACUTE CORONARY SYNDROMES CHRONIC CORONARY SYNDROMES (2019) CASE STUDY 50 YEAR OLD Risk factors : Hypertension, Smoker Central,

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  1. ACUTE CORONARY SYNDROME DR CHEVAAN HENDRICKSE INTERVENTIONAL CARDIOLOGIST

  2. Conflicts of interest None

  3. ACUTE CORONARY SYNDROMES

  4. CHRONIC CORONARY SYNDROMES (2019)

  5. CASE STUDY • 50 YEAR OLD • Risk factors : Hypertension, Smoker • Central, dull chest pain when playing touch rugby. @ 15 min into the game. Pain occurring more frequently. Other atypical pain syndromes. • Presentation via his GP with unstable angina • Reported to my rooms: Electrocardiogram within 10 min

  6. ELECTROCARDIOGRAM

  7. 1. TROPONIN I < 30 ng/L � repeat at 2 hours < 30 ng/ L 2. Mild dyslipidaemia: t chol 5.8, LDL 3.4, HDL 0.9, TG 0.75 3. Normal echocardiogram 4. Normal CXR

  8. Differential diagnosis

  9. Unstable angina 1. New onset angina over 2 months (central, constricting, radiation) 2. Accelerating tempo (crescendo) of symptoms over 48 hrs 3. Resting angina (pain> 20 min) 4. Nocturnal angina 5. Post-infarct angina 6. Post-intervention

  10. What should we do next? 1. INVASIVE ANGIOGRAPHY ? 2. EXERCISE STRESS TESTING ? 3. STRESS ECHOCARDIOGRAPHY ? 4. CT CORONARY ANGIOGRAPHY ? 5. MYOCARDIAL PERFUSION STUDIES ? 6. CARDIAC MRI ?

  11. TREATMENT FOR HEART FAILURE

  12. Electrocardiogram

  13. Exercise stress test

  14. Invasive coronary angiography and percutaneous coronary intervention

  15. MYOCARDIAL INFARCTION THEORETICAL CONCEPTS

  16. 1. Myocardial infarction Type (Type 1-5) 2. Myocardial infarction vs myocardial injury 3. Troponin 4. hs troponin

  17. Non ST elevation MI (NSTEMI) ST elevation MI (STEMI) PRICIPLES OF MANAGEMENT

  18. The greatest challenge is the integration of clinical presentation with information derived from ECG, troponin assessment and imaging modalities into a standardised management strategy GRACE SCORE: Accurate stratification of risk both on admission and at discharge. (GRACE 2.0 risk calculator) > 120 TIMI risk score CRUSADE SCORE: BLEEDING RISK HASBLED SCORE

  19. RISK STRATIFICATION FOR UAP/NSTEMI TIMI GRACE • AGE</> 65 • AGE • HEART RATE • RISK FACTORS • BLOOD PRESSURE • >0.5 MM ST DEVIATION • SERUM CREAT • CHEST PAIN<24 HRS AGO • KILLIP HF CLASS • POSITIVE BIOMARKER • CARDIAC ARREST • USE OF ASPRIN IN LAST 7 DAYS • INITIAL ENZYMES • ST DEVIATION

  20. IMMEDIATE INTERVENTION

  21. EARLY INTERVENTION WITHIN 24-28 HRS

  22. INTERVENTION WITHIN 72 HOURS

  23. WHAT IS THE ROLE OF THE GENERAL PRACTITIONER ? 1. DIAGNOSIS 2. INITIAL RISK STRATIFICATION 3. STABALIZATION 4. INITIATION OF MEDICAL THERAPY

  24. ANTI-THROMBOTIC THERAPY 1) ANTIPLATELET AGENTS (DUAL ANTIPLATELET THERAPY) ASPRIN + P2Y12 INHBITOR 2) ANTICOAGULATION 3) INTRAVENOUS ANTIPLATELET THERAPY (ANTI-IIb/IIIa)

  25. ANTIPLATELET TRIALS

  26. ANTICOAGULATIO N DO NOT SWITCH ANTICOAGULATION BEFORE PCI Arixtra 2.5 mg SC daily FONDAPARINUX VS CLEXANE OASIS-5 TRIAL

  27. CORONARY ANGIOGRAPHY

  28. PERCUTANEOUS CORONARY INTERVENTION

  29. WHAT ABOUT PATIENTS ON ORAL ANTICOAGULANTS ?

  30. Suggested strategies to reduce bleeding risk related to PCI 1) RADIAL APPROACH 2) ADD A PROTON PUMP INHIBITOR

  31. EVIDENCE-BASEDPERFORMANCE MEASURES

  32. ST ELEVATION MYOCARDIAL INFARCTION 1. ST-segment elevation 2.5mm in men < 40 years, in leads V2– V3 2. 2mm in men > 40 years in leads V2–V3 3. 1.5mm in women in leads V2–V3 4. 1mm in the other leads [in the absence of left ventricular (LV) hypertrophy or left bundle branch block LBBB)].

  33. ER MANAGEMENT (ACLS/ABC)

  34. WHEN ANTICIPATING PRIMARY PCI

  35. IF NO PRIMARY PCI

  36. • Discovered in 1930 • 1945: VTE Rx • 1980’s: AMI • ISIS TRIALS • ASA RR 25% • STREP RR 25%

  37. FIBRINOLYTICS tenecteplase tissue plasminogen activator (TNK-tPA) is equivalent to accelerated tPA in reducing 30 day mortality, but is safer in preventing non-cerebral bleeds and blood transfusion, and is easier to use in the pre-hospital setting

  38. 1. Tenecteplase tissue plasminogen activator (TNK- tPA) is equivalent to accelerated tPA in reducing 30 day mortality, 2. TNK is safer compared to TPA in preventing non- cerebral bleeds and blood transfusion, and is easier to use in the pre-hospital setting

  39. ANTICOAGULANT CO-THERAPIES

  40. CONTRAINDICATIONS

  41. EARLY ANGIOGRAPHY AND PCI AFTER FIBRINOLYSIS 1. PCI RECOMMENDED BETWEEN 2-24 HRS

  42. PERCUTANEOUS INTERVENTION

  43. ANTICIPATE AN ADMISSION FOR 48-72 HRS TO SCREEN FOR COMPLICATIONS 1. MYOCARDIAL DYSFUNCTION AND CARDIAC FAILURE 2. MECHANICAL COMPLICATIONS (FREE WALL RUPTURE, PAPILLARY MUSCLE RUPTURE, VSD) 3. ARRHYTHMIAS (VT, AF, VF) 4. PERICARDITIS

  44. MYOCARDIAL INFARCTION WITH NON- OBSTRUCTED CORONARY ARTERIES

  45. MEDICAL THERAPY Dual Antiplatelet Therapy FOR 12 MONTHS

  46. STRATEGIES OF MEDICAL MANAGEMENT

  47. IN SUMMARY 1. Have an institutional approach to chest pain 2. Exclude other possible fatal causes • ACS and the differential diagnosis as discussed 3. Electrocardiogram within 10m minutes of arrival 4. Biomarkers and repeat at 3 hours to confirm or exclude a rise/fall. 5. If unsure, then pick up the phone and call 6. If suspecting an ACS, commence AspIrin loading and activate the ACS network 7. STEMI: time is muscle. If no PCI � Lysis

  48. References • Uptodate • ESC guidelines • ESC textbook of cardiovascular medicine 2019 • NEJM • JACC • Brawnwald’s Cardiovascular disease: ninth edition • Personal experience (Life) • Google images

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