Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Ami Selayang Hospital

3,091 views

Published on

Published in: Health & Medicine
  • Be the first to comment

Ami Selayang Hospital

  1. 1. ACUTE CORONARY SYNDROME Dr. Rashidi Ahmad Med USM, MMed USM (Emergency) Consultant Emergency Physician IJN
  2. 2. Objectives <ul><li>Facts & figures </li></ul><ul><li>Classification of acute coronary syndromes </li></ul><ul><li>Pathophysiology of ACS </li></ul><ul><li>Risk stratification </li></ul><ul><li>Management of ACS </li></ul><ul><ul><ul><li>Anti-ischemic agents </li></ul></ul></ul><ul><ul><ul><li>Antithrombotic agents </li></ul></ul></ul><ul><ul><ul><li>Reperfusion therapy </li></ul></ul></ul><ul><li>Adjunctive therapies for AMI </li></ul>
  3. 3. ACS mortality <ul><li>Pre hospital – 52% </li></ul><ul><li>24H in hospital – 8% </li></ul><ul><li>48H in hospital – 19% </li></ul><ul><li>30 days – 21% </li></ul>AHA statistical data + GUSTO trial data. Circulation, 1994; 90: 2658-65
  4. 4. Causes of death <ul><li>Arrythmias </li></ul><ul><li>Cardiogenic shock </li></ul><ul><li>LV rupture </li></ul><ul><li>Delay in treatment </li></ul>
  5. 5. Incidence of VF <ul><li>Out-of-hospital </li></ul><ul><li>- Br. Med J, 1983; 286: 1405-08: 4% </li></ul><ul><li>- Br. Heart J, 981; 46: 351-7: 18% </li></ul><ul><li>In-hospital </li></ul><ul><li>- Circulation, 1994; 89: 998-1003: 5% </li></ul><ul><li>GISSI </li></ul><ul><li>- Early VF: 3.6% </li></ul><ul><li>- Late VF: 0.69% </li></ul><ul><li>Risky time: VF occurs within 4H after Sx onset </li></ul>
  6. 6. Incidence of cardiac shock & rupture <ul><li>Leading cause of early & late mortality after AMI is LV dysfunction with CCF </li></ul><ul><li>Incidence of cardiac rupture: 10% </li></ul>AHA statistical data + GUSTO trial data. Circulation, 1994; 90: 2658-65
  7. 7. Delay to treatment *Progressive increase in death of 1.6/1000 per hour of delay Am J Cardiol 1998;82:259
  8. 8. In-hospital delay <ul><li>Three time intervals of hospital delay </li></ul><ul><ul><li>1. Door to data (ECG) </li></ul></ul><ul><ul><ul><li>21 min : Goal <10 min </li></ul></ul></ul><ul><ul><li>2. Data to decision </li></ul></ul><ul><ul><ul><li>41 min : Goal <10 min </li></ul></ul></ul><ul><ul><li>3. Decision to drug </li></ul></ul><ul><ul><ul><li>9 min : Goal <10 min </li></ul></ul></ul>Cannon CP, et al. J Thromb Thrombolysis. 1994;1:27-34 In-hospital evaluation constitutes 25 – 33% of delay (Am Heart J. 1999;138:1046-57; Circulation 2000;102:173-8)
  9. 9. Time to treatment remains poor <ul><li>GUSTO I 1990-93 n=41021 2.8h </li></ul><ul><li>GUSTO II 1993-95 n=3053 2.9h </li></ul><ul><li>GUSTO III 1995-97 n=15059 2.7h </li></ul><ul><li>GUSTO V 1999-01 n=16588 2.7h </li></ul><ul><li>InTIME II 1997-99 n=15060 2.9h </li></ul><ul><li>ASSENT II 1997-98 n=16,949 2.8h </li></ul><ul><li>ASSENT III 2000-01 n=6095 2.7h </li></ul>Large Scale Trials (n:113825; mean: 2.8H)
  10. 10. Predictors of Door-to-Balloon Delay in Primary Angioplasty Angeja BG, et al. Am J Cardiol 2002;89:1156-1161
  11. 11. Door to balloon time & mortality JAMA 2000;283:2941-7 Increased mortality if door to balloon > 2 H
  12. 13. Basis of ACS
  13. 14. Plaque features that predispose to rupture
  14. 15. Pathophysiology of ACS After rupture of vulnerable plaque, its content is exposed to the passing blood stream. Vulnerable plaques are laden with lipid & collagen & tissue factor (TF), resulting in activation of the coagulation cascade resulting in deposition of fibrin Thrombin that is generated from activation of coagulation cascade is a PIVOTAL molecule – formation of fibrins & activation of platelets .
  15. 17. Pathophysiology of ACS
  16. 19. Micro-embolization promotes occlusion / spasm in the microvasculature Elevated Trop T/I
  17. 20. Spectrum of Clinical syndromes of CAD
  18. 21. Early outcomes in NSTEMI vs STEMI
  19. 22. Early & late outcome in NSTEMI vs STEMI
  20. 23. Risk stratification <ul><li>Directed therapy </li></ul><ul><li>Avoid unnecessary therapy </li></ul><ul><li>Avoid the potential adverse consequences in pts at low risk </li></ul>
  21. 24. Risk stratification
  22. 26. Risk of death
  23. 27. Directed therapy
  24. 28. Mortality related to cardiac troponin I The risk of subsequent death or MI is ~ 3x higher in patients with +ve troponin result than in those with a -ve result.
  25. 29. New criteria for AMI
  26. 30. Primary goals for patients with ACS <ul><li>Rapid defibrillation when VF occurs </li></ul><ul><li>Prevention of major adverse cardiac events (death, non-fatal MI, & need for urgent revascularization) </li></ul><ul><li>Reduction of myocardial necrosis in patients with ongoing infarction </li></ul>
  27. 31. PURSUIT trial The greatest mortality & morbidity in those with ACS occurs in the first several days. Rapid, efficient, & effective care during this time frame.
  28. 32. 30 min 90 min <ul><li>Consider PCI capable hospital </li></ul><ul><li>CI to thrombolysis </li></ul><ul><li>PCI can be initiated promptly </li></ul><ul><li>High risk patients </li></ul>
  29. 33. Ideally…
  30. 34. Improving Time to Reperfusion Cannon CP, et al. J Thromb Thrombolysis. 1994;1:27-34 . Patient Transport Inhospital Drug Perfusion Current Target A B C D Methods of Speeding Time to Reperfusion A B C D Media campaign 999 Expansion MI protocol Bolus fibrinolytics Patient education Prehosp. Rx Prehosp. ECG Hours from Onset of Pain Door Reperfusion Onset of MI Patient Response Data Decision Drug Started 0 1 2 3 4
  31. 35. 2005 AHA Guidelines for ACS
  32. 36. MX of AMI
  33. 37. Therapeutic approach for ACS
  34. 39. Patient evaluation in ACS
  35. 40. Management of AMI <ul><ul><ul><li>Anti-ischemic agents </li></ul></ul></ul><ul><ul><ul><li>Antithrombotic agents </li></ul></ul></ul><ul><ul><ul><li>- antiplatelets & anticoagulants </li></ul></ul></ul><ul><ul><ul><li>Reperfusion therapy </li></ul></ul></ul><ul><ul><ul><li>Adjunctive therapies for AMI </li></ul></ul></ul>Improves SUPPLY and Reduces DEMAND
  36. 41. Oxygen <ul><li>Advantages: may limit ischemic myocardial injury & may reduce ST segment elevation </li></ul><ul><li>Indications: overt pulmonary congestion OR arterial O2 saturation < 90% </li></ul><ul><li>Reasonable: all pts with ACS for first 6 H of therapy </li></ul><ul><li>Little justification for continuing its routine use beyond 6 H </li></ul><ul><li>Disadvantages: Excess O2 may lead to systemic vasoconstriction. High flow rates may be harmful for COAD pts. </li></ul>
  37. 42. Nitrates <ul><li>↓ preload & afterload </li></ul><ul><li>Relaxation of epicardial coronary arteries </li></ul><ul><li>Recurrent ischemia, nitrates are indicated in first 24-48 H </li></ul><ul><li>IV GTN infusion at 5-20mcg/min </li></ul><ul><li>Increase rate till SX are relieved, MAP  by 10% of its baseline in normotensive pts & 30% for HPT pts </li></ul><ul><li>Nitrates should not be used if hypotension limits administration of B-blockers, which improves survival. </li></ul>
  38. 43. Nitrates <ul><li>Pts with ongoing ischemic discomfort - sublingual nitroglycerin(0.4mg) every 5 min for total of 3 doses, then an assessment should be made about the need for IV nitroglycerin </li></ul><ul><li>IV nitroglycerin is indicated in ongoing ischemic chest discomfort, control of HPT, STEMI a/w LV failure </li></ul><ul><li>Nitrates should not be administered to pts </li></ul><ul><li>- SBP < 90 mmHg or ≥30 mmHg below baseline </li></ul><ul><li>- HR < 50 or >100 OR suspected RV infarction </li></ul><ul><li>- received a phosphodiesterase inhibitor within the last 24 hours </li></ul>
  39. 44. Analgesia <ul><li>AMI and pain contribute to ↑ sympathetic activity. </li></ul><ul><li>Surges of catecholamines may contribute plaques fissuring & thrombus propogation & ↓ threshold for VF. </li></ul><ul><li>Titrating Morphine is analgesic of choice for continuing pain unresponsive to nitrates. </li></ul><ul><li>Cardiac pain is controlled with a combination of nitrates, morphine, O2 & B-blockers. </li></ul>
  40. 45. Morphine <ul><li>↓ restlessness & activity of the sympathetic nervous system - ↓ heart’s metabolic demands. </li></ul><ul><li>In pts with pulmonary oedema complicating MI, morphine : </li></ul><ul><ul><ul><li>promotes peripheral arterial & venous dilatation, </li></ul></ul></ul><ul><ul><ul><li>promotes slowing of HR </li></ul></ul></ul>
  41. 46. Antiplatelet therapy
  42. 47. Aspirin <ul><li>ASA reduce both mortality & the reinfarction rate in the acute phase of MI. </li></ul><ul><li>ASA also prevents reinfarction, stroke & death in patients with previous MI . </li></ul><ul><li>ASA reduce the risk for progression to infarction in patients with UA . </li></ul>
  43. 48. Aspirin <ul><li>ASA produces rapid clinical antithrombotic effect by immediate & near total inhibition of thromboxane A2 production </li></ul><ul><li>Unlike fibrinolytic therapy, there is little evidence of time-dependent effect of ASA on early mortality </li></ul><ul><li>ASA is the first choice of antiplatelet </li></ul><ul><li>Dose: 162-325mg & continued at daily dose 75-162mg </li></ul><ul><li>Chewable ASA is absorbed quicker than swallowed </li></ul><ul><li>Aspirin suppositories (300mg) are safe & can be considered for pts with severe nausea, vomiting or disorders of upper GI tract. </li></ul>
  44. 50. Clopidogrel <ul><li>I nhibits ADP-induced platelet aggregation </li></ul><ul><li>Dose: 300mg loading dose </li></ul><ul><li>Indications: </li></ul><ul><li>- NSTEMI (elevated cardiac markers or new ECG changes consistent with ischemia) </li></ul><ul><li>- suspected of ACS (without ECG or cardiac marker changes) who is unable to take aspirin because of hypersensitivity or major GI intolerance </li></ul><ul><li>- STEMI (up to 75years of age who receive ASA, heparin & fibrinolysis. </li></ul>
  45. 51. ACS algorithm 2005 guidelines
  46. 52. Ticlopidine <ul><li>ADP Inhibitor </li></ul><ul><li>Delay to achieve full effect (benefit only after 2/52 of RX) </li></ul><ul><li>Initial Rx with heparin & probably GP IIb/IIIa inhibitor is required in UA/NSTEMI </li></ul><ul><li>Adverse effects: Neutropenia (2.4%, severe in 0.8%) & rarely TTP </li></ul><ul><li>FBC (with differentials) monitoring every 2 weeks for 1 st 3 months. </li></ul><ul><li>Clopidogrel is preferred to ticlopidine but more rapidly inhibits platelets & more favorably safety profile. </li></ul>
  47. 53. Reperfusion therapy <ul><li>All STEMI patients should undergo rapid evaluation for reperfusion therapy </li></ul><ul><li>Prompt & complete restoration of flow in the infarct artery can be achieved by pharmacological means (fibrinolysis) or PCI (balloon angioplasty +/- stent, with support of pharmacological measures to prevent thrombosis). </li></ul><ul><li>Expeditious restoration of flow in the obstructed infarct artery after onset of symptoms of STEMI is KEY DETERMIINANT of outcome , regardless of whether reperfusion is accomplished with PCI or fibrinolysis. </li></ul>
  48. 54. Fibrinolytic therapy <ul><li>The greatest benefit is when therapy is started within the first 3 hours </li></ul><ul><li>Indications: </li></ul><ul><li>- STEMI pts with onset of Sx ≤ 12 hours & ECG findings of STEMI (ST elevation >0.1mV in 2 or more contiguous precordial adjacent limb leads, new or presumably LBBB) </li></ul><ul><li>- Reasonable to administer fibrinolytics to pts with onset of Sx <12 hours & ECG findings of true posterior MI </li></ul>
  49. 55. LBBB <ul><li>Direct PCI may be preferable to fibrinolytic therapy </li></ul><ul><li>Pts with new or presumably new LBBB coupled with a typical ischemic history should be approached with a plan to rule in MI using 1 of 3 ECG criteria that provide independent diagnostic value (Sgarbossa criteria) </li></ul>LBBB
  50. 56. Sgarbossa criteria <ul><li>ST Elevation ≥ 1 mm & concordant with QRS complex </li></ul><ul><li>ST Depression ≥ 1 mm in V1, V2, V3 </li></ul><ul><li>ST Elevation ≥ 5 mm and discordant with QRS complex </li></ul>
  51. 57. True posterior MI <ul><li>tall R waves in Right precordial leads & ST depression in V1-V4, especially when T waves are upright. </li></ul><ul><li>Repeat ECG with incorporation of additional leads (V7-V9) are more specific for the detection of post infarct. </li></ul>
  52. 58. Fibrinolysis is Not recommended <ul><li>Nor recommended: Pts presenting > 12 hours after onset of symptoms, although it may be considered if continuing ischemic pain is present with ST elevation >1mm in 2 or more contiguous precordial or adjacent limb leads </li></ul><ul><li>Should not be given to asymptomatic pts who presents > 24 hours after onset of Sx </li></ul><ul><li>Should not be given to pts who show ST-segment depression, unless true posterior MI suspecteD </li></ul>
  53. 59. Fibrinolytic agents
  54. 60. Source Gp C streptococci Recombinant human Recombinant Recombinant
  55. 61. Risk of life-threatening bleed
  56. 62. Mortality for fibrinolytic therapy vs control
  57. 65. Limitation of fibrinolytic therapy <ul><li>Despite adequate restoration of flow in the epicardial infarct artery, perfusion of the infarct zone may still be compromised by a combination of microvascular damage & reperfusion injury. </li></ul><ul><li>Microvascular perfusion may be impaired despite achievemnt of TIMI 3 flow & < 50% coronary narrowing. Abnormal microperfusion has negative prognostic implications . </li></ul>
  58. 66. Assessment of reperfusion <ul><li>Relief of symptoms </li></ul><ul><li>Maintenance or restoration of hemodynamic & electrical stability </li></ul><ul><li>Reduction of at least 50% of the initial ST-segment elevation on follow up ECG at 60-90 min after initiation of therapy – good indicator of myocardial perfusion. </li></ul>
  59. 68. <ul><li>In experienced centers, PCI has been shown to be superior to fibrinolysis </li></ul><ul><li>*Individuals who perform > 75 PCI procedures a year, in a lab that performs >200 PCI procedures per year, of which at least 36 are primary PCI for STEMI, and has cardiac surgical capability. </li></ul>PCI in STEMI
  60. 69. PCI versus fibrinolysis ** PCI is preferred in high risk patients
  61. 71. Percutaneous coronary intervention for AMI
  62. 72. <ul><li>Fibrinolytic-ineligible pts within 12 H of symptom onset </li></ul><ul><li>Cardiogenic shock, heart failure (Killip class 3), persistent angina </li></ul><ul><li>In hosp without PCI facilities, rapid administration for fibrinolytic agent & transfer the pt to a PCI facility centre if low-output syndrome or ischemia continues. </li></ul><ul><li>Preferable for RV infarction & LBBB. </li></ul><ul><li>Should not be performed in asymptomatic pts > 12 H after onset of STEMI if they are hemodynamically & electrically stable </li></ul>Recommendation for PCI in STEMI
  63. 74. Heparin in STEMI <ul><li>UFH is recommended for pts ≥ 75yo as ancillary therapy to fibrinolysis (Class IIa) & for any STEMI pts undergoing revascularization. </li></ul>When UFH is used as adjunctive therapy with fibrin-specific fibrinolytics (alteplase/reteplase/tenecteplase) in STEMI, an IV bolus dose of 60U/kg is given followed by infusion at rate of 12U/kg/hr (max bolus 4000U & infusion 1000U/hr for pts >70kg).
  64. 75. Heparin in STEMI <ul><li>IV UFH should be given to pts treated with nonselective </li></ul><ul><li>fibrinolytic agents (streptokinase) who are at high risk for </li></ul><ul><li>systemic emboli (large or anterior MI, AF, previous embolus, known LV embolus). </li></ul><ul><li>It may be reasonable to give IV UFH to pts undergoing reperfusion therapy with streptokinase. </li></ul><ul><li>Aim aPTT of 50-70sec (1.5-2x control value). </li></ul>
  65. 76. Antithrombotic therapy in UA/ NSTEMI
  66. 77. LMWH <ul><li>Indication: UA/NSTEMI </li></ul><ul><li>Enoxaparin is preferred to UFH in UA/NSTEMI , unless CABG is planned within 24 hrs. </li></ul><ul><li>LMWH (enoxaparin) is acceptable alternative to UFH in the ED as ancillary therapy for pts < 75yo who are receiving fibrinolytic therapy (tenecteplase), provided that significant renal dysfunction (serum creatinine >2.5mg/dL in men & 2mg/dL in women) is not present and in pts with STEMI who are not receiving fibrinolysis or revascularization , LMWH in the ED setting </li></ul>
  67. 79. LMWH vs UFH in UA
  68. 80. Direct antithrombins <ul><li>Direct thrombin inhibitors very specifically block thrombin effects without the need of a cofactor such as ATIII. </li></ul><ul><li>Hirudin (Lepirudin - prototype direct thrombin inhibitor, a naturally occuring anticoagulant from medicinal leech) </li></ul><ul><ul><li>is presently indicated only for anticoagulations in pts with heparin-induced thrombocytopenia & for prophylaxis of DVT after hip replacement surgery. </li></ul></ul><ul><ul><li>Superior to UFH in the reduction of death & MI in UA/MSTEMI . </li></ul></ul><ul><li>Bivalirudin (synthetic analogue of hirudin, binds reversibly to thrombin) – could be considered as an alternative to heparin in pts with STEMI who is treated with streptokinase & who has heparin-induced thrombocytopenia (class IIa, LOE B). </li></ul>
  69. 81. Adjunctive therapy for AMI <ul><li>GP IIb/IIIa inhibitors </li></ul><ul><li>B-adrenergic receptor blockers </li></ul><ul><li>ACE inhibitor </li></ul><ul><li>Statin therapy / CCB / Insulin </li></ul>
  70. 82. Summary
  71. 83. Thank you

×