Acute Coronary Syndrome

1. Acute Coronary Syndrome By: Dr Tengku Abdul Kadir B TengkuZainalAbidin Supervisor: Dr Wan Rohaidah

2. Main reference 

3. Terminology • Acute coronary syndrome is a clinical spectrum of ischemic heart disease ranging from unstable angina, non-ST-elevation myocardial infarction (NSTEMI) to ST-elevation myocardial infarction (STEMI) depending upon the degree and acuteness of coronary occlusion.

4. Acute Coronary Syndromes: Definitions • Acute coronary syndrome: • Constellation of clinical symptoms compatible with • acute myocardial ischemia • ST-segment elevation MI (STEMI) • Non-ST-segment elevation MI (NSTEMI) • Unstable angina • Unstable angina: • Angina at rest (usually > 20 minutes) • New-onset of class III or IV angina • Increasing angina (from class I or II to III or IV)

5. Acute Coronary Syndromes Ischemic Chest Discomfort ECG ST Elevation No ST Elevation – + Cardiac markers Non -ST Elevation MI ST Elevation MI Unstable Angina

6. Pathogenesis of Acute Coronary Syndromes Plaque rupture Platelet adhesion Platelet activation Partially occlusive arterial thrombosis & unstable angina Microembolization & non-ST-segment elevation MI Totally occlusive arterial thrombosis & ST-segment elevation MI

7. Structure of Thrombus Following Plaque Disruption UA/NSTEMI:Partially-occlusive thrombus (primarily platelets) STEMI:Occlusive thrombus (platelets, red blood cells, and fibrin) Intra-plaque thrombus (platelet-dominated) Intra-plaque thrombus (platelet-dominated) Plaque core Plaque core UA = Unstable Angina NSTEMI = Non-ST-segment Elevation Myocardial Infarction STEMI = ST-segment Elevation Myocardial Infarction SUDDEN DEATH

8. Unstable angina: • NSTEMI: Myocardial infarction due to acute sub-total occlusion of the coronary artery • STEMI: Myocardial infarction due to acute total occlusion of the coronary artery .

10. UA/NSTEMI vs. STEMI • STEMI is typically more severe, while UA/NSTEMI is more pervasive • Patient with STEMI have higher rates of • In hospital mortality • Mechanical complications • Cardiogenic shock

11. Clinical diagnosis of STEMI • Clinical history of ischaemic type chest pain • ECG changes • New onset ST-segment elevation of: • ≥ 0.1 mV in 2 contiguous limb leads, or V4 to V6 and/or • ≥ 0.2 mV in 2 contiguous precordial leads V1 to V3 Presumed new left-bundle branch block • Biomarker elevation – Myocardial injury/necrosis

12. Chest pain • typically : • retrosternal, severe, crushing, squeezing or pressing in nature > 30 mins, • a/wprofuse sweating, N & V and SOB. • sometimes described as chest tightness only. • may radiate to the jaw or down the left upper limb. • rest or with activity. • may be burning in nature • may be in the epigastricregion • Atypical: unexplained nausea and vomiting, weakness, dizziness, lightheadedness and syncope.

13. ECG hyperacute changes of a tall peaked T-wave  ST segment elevation  Q-wave,  return of the ST segment to isoelectric and T-wave inversion. • ST segment elevation are ≥ 0.2mV in leads V1, V2, or V3 and ≥ 0.1mV in other leads. • should be present in 2 or more contiguous leads. • The presence of new onset or presumably new left bundle branch block (LBBB) in a patient with typical type chest pain indicates an infarct.

14. Serum cardiac biomarkers • Troponin I • Troponin T • CK – MB • CK • Myoglobin • Fatty acid binding proteins

15. BIOCHEMICAL CARDIAC MARKERS IN PTS WITH SUSPECTED ACS WITHOUT STEMI • CK MB • Rapid, cost efisien, accurate • able to detect early reinfarction Advantages • Troponin • Sensitive and specific • Detection of MI up to 2 weaks • Detection of reperfusion • Useful for selection of therapy • Detection of reperfusion • Myoglobin • High sensitivity • Useful in early detection ofMI • Detection of reperfusion • Most useful in ruling out MI

16. BIOCHEMICAL CARDIAC MARKERS IN PTS WITH SUSPECTED ACS WITHOUT STE Disadvantages • Troponin • Low sensitivity in early phase (<6h) • Limited ability to detect late minor infarct • CK MB • Lack of specificity • Low sensitivity during early MI (<6h) or late (>36h) • Myoglobin • Very low sepecificity w skeletal ms injury/disease • Rapid return to normal

19. Management on STEMI • Early management of STEMI is directed at: • Pain relief • Establishing early reperfusion • Treatment of complications - arrhythmias

20. Once patient in the hospital! • Asses and stabilize patient’s haemodynamics. • Sublingual GTN if chest pain persists (unless systolic blood pressure (SBP) < 90 mmHg). • Continuous ECG monitoring. • Aspirin 300mg • Clopidogrel 300mg • Oxygen by nasal prongs / facemask. • IV line and blood taking : cardiac biomarkers, FBC, RP,RBS,LP • Pain relief – IV morphine 2-5mg every 5-15 minutes • Anti-emetics ( IV maxolon10mg or promethazine 25mg ) • Assessment for reperfusion strategy.

21. ECG Reperfusion therapy! The goals of time to reperfusion therapy should be within: • 30 minutes door to needle time • 90 minutes door to balloon time

22. Fibrinolyticvs PCI • Early presentation (within 3hours) : equally effective except: • fibrinolytic therapy is contraindicated • high-risk patients • PCI time delay [(door-to-balloon time) – (door-to-needle time)] < 60 mins. • Latepresentation(3 – 12hours) Primary PCI is preferred • The door to balloon time : • within 90 min : if the patient presents at a PCI capable facility. • <2H : if transferred • If the time delay to primary PCI is longer fibrinolytic therapy should be given. • Verylatepresentation(> 12 hours) Both primary PCI and fibrinolytic therapy are not routinely recommended in patients who are asymptomatic and haemodynamically stable.

24. High Risk patient These include patients with: • Large infarcts • Anterior infarcts • Cardiogenic shock • Elderly patients • Post revascularization (post CABG and post PCI) • Post infarct angina

25. Fibrinolytic Therapy • Given within 1h from onset of chest pain  reduce 50% of mortality • Door to needle < 30 minutes • Patient presenting with hypotension (SBP < 90mmhg)  Started first with inotrope

26. Contraindications • Absolute contraindications • Risk of Intracranial haemorrhage • Any history of intracranial haemorrhage Ischaemic stroke within 3 months • Known structural cerebral vascular lesion (e.g. arteriovenous malformation) • Known intracranial neoplasm • Risk of bleeding Active bleeding • Significant head trauma within 3 months • Suspected aortic dissection

27. Contraindications • Relative contraindications • Risk of intracranial haemorrhage • Severe uncontrolled hypertension on presentation (BP > 180/110 mm Hg)* • Ischaemic stroke more than 3 months ago • History of chronic, severe uncontrolled hypertension • Risk of Bleeding Current use of anticoagulation in therapeutic doses (INR > 2) • Recent major surgery < 3 weeks • Traumatic or prolonged CPR >10 minutes • Recent internal bleeding (e.g. gastrointestinal or urinary tract haemorrhage) within 4 weeks • Non-compressible vascular puncture • Active peptic ulcer • Others : • Pregnancy • Prior exposure (>5 days and within 12 months of first usage) to streptokinase (if planning to use same agent)

28. Streptokinase • Not fibrin specific and is less efficacious than fibrin selective agents • Lower risk of intracranial haemorrhage • is antigenic and promotes the production of antibodies. • utilization of this agent for re-infarction is less effective if given again 5 days after the first administration • PCI or fibrin specific agents should then be considered. • Regimen: • 1.5 mega units in 100 ml normal saline or 5% dextrose over 1 hour. • 1.5 mega units over 20 minutes, or - 0.75 mega unit bolus and then repeated at the same dose after an interval of 50 minutes if there is no clinical reperfusion.

29. Anteplase • fibrin specific and achieves better reperfusion at 90 min as compared to streptokinase • higher rate of reocclusion. • heparin needs to be given for 48 hours. • Regimen: • For patients > 65 kg : 15 mg bolus; then 50 mg over 30 min and 35 mg over the next 60min • For patients < 65 kg 15 mg bolus; then 0.75 mg/kg over 30 min and 0.5 mg/kg over the next 60min

30. TenecteplasetPA • second generation fibrin specific agents are as efficacious as alteplase • have a slightly lower bleeding risk as compared to alteplase • easier to administer. • given as single or double bolus injections • do not induce antibody production. • Regimen: single i.v. bolus • 30mg if < 60kg • 35mg if 60 to < 70kg • 40mg if 70 to < 80kg • 45mg if 80 to < 90kg • 50mg if >90kg • Heparin needs to be given for 48 hours

32. Successful reperfusion • resolution of chest pain (may be confounded by the use of narcotic analgesics). • ST segment: • return to isoelectric line • Or decrease height by 50% from the highest ST segemen within 60-90mins of initiation of fibrinolytic therapy. • early peaking of CK and CK-MB levels. • restoration and/or maintenance of haemodynamic and/or electrical stability

33. Failed reperfusion • continuing chest pain, • persistent ST segment elevation • hemodynamic instability. rescue PCI

34. Percutaneous Coronary Intervension (PCI) • Primary PCI • FacilitatedPCI • Rescue PCI

35. Rescue PCI • failed fibrinolytic therapy / recurrent chest pain and/or ischaemic complications. • Those who may benefit are patients with: • ongoing chest pains • haemodynamic and electrical instability • cardiogenic shock in patient < 75 years old, • within 36 hours of STEMI and <18 hours of shock whose coronary anatomy is suitable for revascularization • heart failure and onset of chest pain within 12 hours • cardiogenic shock – In these high risk patients, those who are <75 years of age and who present within 36 hours of STEMI and <18 hours of shock may be considered for rescue PCI if their coronary anatomy is suitable for revascularization

36. ICU/CCU management • General measures • 24h bed rest • Analgesic, sedatives • Prevent constipation • Monitoring • Vital signs , spo2, ECG • Concomitant therapy

37. Monitoring • Vital signs • Hypotensive? Tachy/Bradycardia? • Oxygenation • Hypoxic? • ECG , changes? • Hb • Cardiac biomarker

38. Concomitant therapy • O2 therapy • Antiplatelet • Beta blockers • ACEI • Nitrates • Ca channel blockers • Anti thrombotic agents

39. O2 Therapy (2-4 liters/minute) • Up to 70% of ACS patient demonstrate hypoxemia • May limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevation

40. Ventilation? • Mechanical ventilation ensures oxygenation and relieves the heart of the work of breathing. • constant, stable ventilation  avoidance of psychomotor excitement exhaust the patient. • Weaning  hemodynamic stability, absence of myocardial ischemia, and absence or regression of inflammation or infection.

41. Antiplatelet • A) Aspirin • is indicated in all patients at diagnosis and should be continued indefinitely unless contraindicated. • initial dose 100-300mgmaintenance dose,75 - 150mg OD. • B) Clopidogrel • +aspirin and fibrinolytic therapy in STEMI,  reduce occluded infarct related artery, death or reinfarction without risk of bleeding. • loading dose of 300 mg maintenance dose 75 mg OD. • recommended for at least 1 month after fibrinolytic therapy. • Following PCI, (up to 12 months) particularly when drug-eluting stents are used.

42. Beta Blockers • 14% reduction in mortality risk at 7 days at 23% long term mortality reduction in STEMI • Approximate 13% reduction in risk of progression to MI in patients with threatening or evolving MI symptoms • Be aware of contraindications (CHF, Heart block, Hypotension) • Reassess for therapy as contraindications resolve

43. ACEI • Start in patients with anterior MI, pulmonary congestion, LVEF < 40% in absence of contraindication/hypotension • Start in first 24 hours • ARB as substitute for patients unable to use ACE-I

45. STEMI complications • arrhythmias • left ventricular dysfunction and shock • mechanical complications • right ventricular infarction • others e.g. pericarditis

46. Arrythmias • Tachyarrhythmias • Pulseless ventricular tachyarrythmias. • pulseless VT and VF - Defibrillate immediately. • Early VF occurs within the first 48 hours and is due to electrical instability. • Late VF is associated with large infarcts and poor pump function and carries a poor prognosis • Stable VT - arise from ischaemia/myocardial scar. Treatment of ischaemia termination • Ventricular Premature Contractions (VPC) : benign and do not require treatment. • Accelerated Idioventricular Rhythm (AIVR) :No treatment. • AF - commonly elderly , large infarcts and atrial infarcts  poorer prognosis, risk of thromboembolism. • Bradyarrhythmias • Sinus bradycardia. : No treatment unless a/w symptoms and/ or hypotension. • Atrio-ventricular Block

48. LV dysfunction / shock

49. Killip Classification • is frequently used during acute myocardial infarction. • First published in 1967, Class I: No evidence of heart failure (mortality 6%) Class II: Findings of mild to moderate heart failure (S3 gallop, rales < half-way up lung fields or elevated jugular venous pressure (mortality 17%) Class III: Pulmonary edema (mortality 38%) Class IV: Cardiogenic shock defined as systolic blood pressure < 90 and signs of hypoperfusion such as oliguria, cyanosis, and sweating. (mortality 67%)

50. Cardiogenic shock • a systolic BP of < 90 mmHg a/w signs of tissue hypoperfusion, and central filling pressure (PCWP) is >20mmHg or cardiac index is <1.8L/min/m2.