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Acute Coronary Syndrome

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Acute Coronary Syndromes
Acute Coronary Syndromes
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Acute Coronary Syndrome

  1. 1. Acute Coronary Syndrome (ACS) 3 Aug 2011 Khanittha L,M.D Naresuan University Hospital
  2. 2. Coronary Artery
  3. 3. Hospital Hx PE EKG Ventricular systolic dysfunction (LV/RV) Recurrent ischemia/infarct • Inhospital admission • After discharged ACS Mechanical complication •Myocardial rupture •MR •VSD Electrical instability •VT/VF •Heart Block •Atrial arrhythmia
  4. 4. หัวใจล้มเหลว ล้ามเนื้อหัวใจขาดเลือดซ๊ำ๊า n-hospital admission fter discharged ACS หัวใจเต้นผิด จังหวะ •VT/VF •Heart Block •Atrial arrhythmia ภาวะแทรกซ๊้อนทาง mechanical •Myocardial rupture •MR •VSD
  5. 5. Coronary Artery Disease (CAD) *Acute coronary syndrome *Unstable angina *Acute non ST-elevation myocardial infarction *Acute ST-elevation myocardial infarction *Chronic coronary artery disease : chronic stable angina
  6. 6. Spectrum of CAD/ACS No ST elevation Stable angina Unstable angina ST elevation NSTEMI ACUTE CORONARY SYNDROMES CAD = coronary artery disease; NSTEMI = non-ST-segment elevation myocardial infarction; STEMI = ST-segment elevation myocardial infarction. Source (Photos): Davies MJ. Heart. 2000;83:361-366. STEMI
  7. 7. Pathophysiology of ACS Subtotal artery occlusion Non ST elevation ACS (UA/NSTEMI) Complete total occlusion ST elevation ACS (STEMI)
  8. 8. Structure of thrombus following plaque disruption UA/NSTEMI Non-occlusive thrombus (platelets, some fibrins) STEMI Occlusive thrombus (platelets, fibrins, red cell) Plaque core Intra-plaque thrombus (platelet dominated)
  9. 9. Understanding Myocardial Ischemia Imbalance
  10. 10. Understanding Myocardial Ischemia Decrease O2 Supply Increase Demand Mechanical Obstruction Dec. Oxygenated Blood Flow Increase cardiac output……….. (Thyrotoxicosis) Atheroma Anemia Myocardial Hypertrophy Thrombosis Carboxyhemoglobinemia Spasm Hypotension CAUSING DEC CORONARY PERFUSION PRESSURE Embolus Coronary arteritis Coronary trauma (AS,HTN)
  11. 11. Plaque Fissure or Rupture Platelet Adhesion Platelet Activation Platelet Aggregation Thrombotic Occlusion
  12. 12. Consequence of Acute Coronary Occlusion
  14. 14. Clinical Presentation Of ACS
  15. 15. Focused History • Aid in diagnosis and rule out other causes – Palliative/Provocative factors – Quality of discomfort – Radiation – Symptoms associated with discomfort – Cardiac risk factors – Past medical history -especially cardiac • Reperfusion questions – Timing of presentation – ECG c/w STEMI – Contraindication to fibrinolysis – Degree of STEMI risk
  16. 16. Symptom * Acute chest pain * Nausea/ vomiting * Sweating * Dyspnea * Palpitation * Syncope * Pulmonary edema * Epigastric pain * Post-op hypotension * Oliguria * Acute confusional state * Stroke * Diabetic hyperglycemia state
  17. 17. ACS Clinical Presentation * Substernal chest pain or pressure (>20-30 min) * Localization or radiation to arms, back, throat, jaw * Accompanying features * Dyspnea * Nausea/vomiting * Diaphoresis * Weakness * Atypical: syncope
  18. 18. Risk Factor for Acute Coronary Syndrome *Non-modifiable *Modifiable
  19. 19. Risk Factor *Age Incidence increase with age. *Male gender * Men > premenupausal women * After menupause , incidence is almost same *Family History of IHD
  20. 20. Modifiable Risk Factors •Smoking •Hyperlipidemia •Hypertension •Diabetes mellitus •Lack of exercise •Blood coagulation factors •Personality •Obesity
  21. 21. Targeted Physical Examination *Vital signs *Cardiovascular system *Respiratory system *Abdomen *Neurological status *Recognize factors that increase risk *Hypotension *Tachycardia *Pulmonary rales, JVP, pulmonary edema, *New murmurs/heart sounds *Diminished peripheral pulses *Signs of stroke
  22. 22. Acute coronary syndromes Aortic dissection Esophageal reflux Pneumothorax Chest pain Myocarditis Costochronditis Acute pulmonary embolism Acute pericarditis Psychosomatic
  23. 23. Acute Coronary Syndromes ST-elevation MI Cardiac marker +ve Non-ST elevation ACS Cardiac marker +ve Unstable angina Cardiac marker - ve
  24. 24. *Normal *ST-depression *T-wave inversion *ST-elevation or *LBBB *Repeat EKG when patient is in pain *Continuous ST – segment monitoring
  25. 25. Cardiac Markers
  26. 26. Timing of Release of Various Biomarkers After Acute Myocardial Infarction Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157 Copyright ©2007 American College of Cardiology Foundation. Restrictions may apply.
  27. 27. Cardiac Markers Troponin ( T, I) CK-MB isoenzyme *Very specific and more sensitive *Rises 4-6 hours after injury and than CK *Rises 4-8 hours after injury *May remain elevated for up to two weeks *Can provide prognostic information *Troponin T may be elevated with renal dz, poly/dermatomyositis peaks at 24 hours *Remains elevated 36-48 hours *Positive if CK/MB > 5% of total CK and 2 times normal *Elevation can be predictive of mortality *False positives with exercise, trauma, muscle dz,
  28. 28. Chest pain Non Cardiac Diagnosis – – – – Assess 12 lead ECG Initial assesment Hx PE EKG and EKG monitoring CXR Possible Chronic ACS Stable Angina Goal = 10 min Definite ACS
  29. 29. Chest Pain Suggestive of Ischemia Immediate assessment within 10 Minutes Initial labs and tests *12 lead ECG *Obtain initial cardiac enzymes *Electrolytes, CBC, lipids, BUN/Cr, glucose, Coags *CXR Emergent care  IV access  Cardiac monitoring  Oxygen  Aspirin  Nitrates History & Physical     Establish diagnosis Read ECG Identify complications Assess for reperfusion
  30. 30. แนวทางการรักษาคนไข้ ACS *Prevent plaque rupture : Statins *Decrease O2 need *Decrease platelet activation and aggregation *Open blocked vessel
  31. 31. Acute ST Elevation Myocardial Infarction
  32. 32. Assessments and treatments to consider for patients who present with ACS Initial general treatment (“M O N A C”) *Morphine 2-4 mg q 5-10 min *Oxygen 4 L/min *NTG sublingual or spray, followed by infusion for persistent chest pain *Aspirin 160 -325 mg chew and swallow or/and *Clopidogrel 300mg oral
  33. 33. Specific Treatment : Reperfusion Therapy Fibrinolysis vs primary PCI “Time is muscle”
  34. 34. Treatment of ASTEMI  Open coronary artery within 12 hr  Reperfusion  Fibrinolytic  Primary Therapy agents : Streptokinase, tPA PTCA
  35. 35. Reperfusion Therapy จุดมุ่งหมาย : ให้การวินิจฉัยและรักษาผู้ปวย STEMI ่ อย่างรวดเร็ว * Door to needle time ( หรือ First medical contact-to-needle time) ระยะเวลาที่เริ่มให้ fibrinolytic therapy ควรอยู่ภายใน 30 นาที * Door to balloon time ( หรือ First medical contact-to-balloon time )
  36. 36. Contraindications and Cautions for Fibrinolysis in STEMI • Any prior intracranial hemorrhage • Known structural cerebral vascular lesion Absolute (e.g., arteriovenous malformation) Contraindications • Known malignant intracranial neoplasm (primary or metastatic) • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours • Suspected aortic dissection • Active bleeding or bleeding diathesis (excluding menses) • Significant closed-head or facial trauma within 3 months ACC/AHA Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction 2004
  37. 37. Contraindications and Cautions for Fibrinolysis in STEMI • History of chronic, severe, poorly controlled Relative hypertension Contraindications • Severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg) • History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications • Traumatic or prolonged (> 10 minutes) CPR or major surgery (< 3 weeks) ACC/AHA Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction 2004
  38. 38. การรัก ษาผู้ป ่ว ย ST-Elevation MI หรืelevation หรือ new LBBB อ New LBBB ST > 12 hour < 12 hour Eligible for reperfusion Rx Thrombolytic is contra-indicated 1° PCI Thrombolytic Rx : Streptokinase : rt-PA Not candidate for reperfusion Rx Other medical treatment B-blocker ACEI / ARB Nitrate Statin Persistent symptom No Yes Consider reperfusion Rx
  40. 40. Door to Needle Time and Mortality In hospital mortality (%) 20 18 16 14 12 10 8 6 4 2 0 18.1 14.14 10.3 6.3 4.3 0-30 16 31-60 Door to Balloon Time and Mortality 61-90 >90 no thrombolysis 14.1 14 12 10 10 8 6 9.1 7 5.6 4 2 0 <60 61-90 91-120 120-180 >180 Thai ACS registry
  41. 41. Comparison of Approved Fibrinolytic Drugs Feature SK t-PA Fibrin-specific - ++ Half-life (minutes) 20 5 Antigencity Y N 90 minutes patency 60 84 Rate of ICH 0.34 0.69 Requires concomitant heparin +/- Y Weight adjusted dosing N Y Dose 1.5 mL units IV over 60 minutes 15 mg IV /1-2min 0.75 mg/kg IV/30 min (max 50 mg) 0.5 mg/kg IV/60 min (max 35 mg) SK Bolus administration N N Cost per dose (Baht) 9,606 49,857 50
  42. 42. ACS : Unstable angina or NSTEMI
  43. 43. การแบ่งผู้ป่วยทีมาด้วย chest pain ตามปัจจัยเสี่ยงถึงความน่าจะ ่ เป็นโรคหัวใจโคโรนารี (CAD)ตามลักษณะทางคลินิก และ EKG แรกรับ
  44. 44. ปัจจัยเสี่ยงต่อการตาย และ nonfatal MI ในผู้ป่วยทีมี chest pain ่ สงสัย ischemia
  45. 45. ACS : NSTEMI or UA
  46. 46. ACS : NSTEM or UA Fibrinolytic Antithrombin UFH, LMWH Stabilized Severe stenosis Antiplatelets Subtotal occlusion ASA, clopidogrel, G2b3a inhibitors
  47. 47. Assessments and treatments to consider for patients who present with ACS Initial general treatment (“ M O N A C ”) *M orphine 2-4 mg q 5-10 min *O xygen 4 L/min *N TG sublingual or spray, followed by infusion for persistent chest pain *A spirin 160 -325 mg chew and swallow or/and *C lopidogrel 300mg oral
  48. 48. ACS : NSTEACS or UA PCI ยา
  49. 49. Initial Conservative Strategy : Early Hospital Care *ASA; clopidogrel if intolerant (I, A) *Anticoagulant therapy should be added to antiplatelet therapy as soon as possible after presentation (I, A) *Enoxaparin or UFH (I, A) *Fondaparinux (I, B) *Enoxaparin or fondaparinux preferable (IIa, B) *Initiate clopidogrel, loading dose + maintenance dose (I, A) ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction
  50. 50. Adjunctive Therapies * Beta-blocker *ถ้าไม่มีข้อห้าม * IV nitroglycerine *สำาหรับ recurrent ischemia, large anterior MI, heart failure, antihypertensive effects * ACE inhibitor *โดยเฉพาะ large anterior wall MI, heart failure ควรให้ หลัง 24 ชม.
  51. 51. Secondary Prevention and Long Term Management Goals Smoking Goal: Complete Cessation Recommendations • Assess tobacco use. • Strongly encourage patient and family to stop smoking and to avoid secondhand smoke. • Provide counseling, pharmacological therapy (including nicotine replacement and bupropion), and formal smoking cessation programs as appropriate. 61
  52. 52. Secondary Prevention and Long Term Management Goals Blood pressure control: Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes Recommendations If blood pressure is 120/80 mm Hg or greater: • Initiate lifestyle modification (weight control, physical activity, alcohol moderation, moderate sodium restriction, and emphasis on fruits, vegetables, and low-fat dairy products) in all patients. If blood pressure is 140/90 mm Hg or greater or 130/80 mm Hg or greater for individuals with chronic kidney disease or diabetes: • Add blood pressure-reducing medications, emphasizing the use of beta-blockers and inhibitors of the renin-angiotensinaldosterone system. 62
  53. 53. Secondary Prevention and Long Term Management Goals Physical activity: Minimum goal: 30 minutes 3 to 4 days per week; Optimal daily Recommendations • Assess risk, preferably with exercise test, to guide prescription. • Encourage minimum of 30 to 60 minutes of activity, preferably daily but at least 3 or 4 times weekly (walking, jogging, cycling, or other aerobic activity) supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, household work). • Cardiac rehabilitation programs are recommended for patients with STEMI. 63
  54. 54. Secondary Prevention and Long Term Management Goals Lipid management: (TG less than 200 mg/dL) Primary goal: LDL-C << than 100 mg/dL Recommendations • Start dietary therapy in all patients (< 7% of total calories as saturated fat and < 200 mg/d cholesterol). Promote physical activity and weight management. Encourage increased consumption of omega-3 fatty acids. • Assess fasting lipid profile in all patients, preferably within 24 hours of STEMI. Add drug therapy according to the following guide: LDL-C < 100 mg/dL (baseline or on treatment): Statins should be used to lower LDL-C. LDL-C ≥ 100 mg/dL (baseline or on treatment): Intensify LDL-C–lowering therapy with drug treatment, giving preference to statins. 64
  55. 55. Secondary Prevention and Long Term Management Goals Lipid management: (TG 200 mg/dL or greater) Primary goal: Non–HDL-C << 130 mg/dL Recommendations If TGs are ≥ 150 mg/dL or HDL-C is < 40 mg/dL: Emphasize weight management and physical activity. Advise smoking cessation. If TG is 200 to 499 mg/dL: After LDL-C–lowering therapy, consider adding fibrate or niacin. If TG is ≥ 500 mg/dL: Consider fibrate or niacin before LDL-C–lowering therapy. Consider omega-3 fatty acids as adjunct for high TG. 65
  56. 56. Secondary Prevention and Long Term Management Goals Weight management: Goal: BMI 18.5 to 24.9 kg/m2 Waist circumference: Women: < 35 in. Men: < 40 in. Recommendations Calculate BMI and measure waist circumference as part of evaluation. Monitor response of BMI and waist circumference to therapy. Start weight management and physical activity as appropriate. Desirable BMI range is 18.5 to 24.9 kg/m2. If waist circumference is ≥ 35 inches in women or ≥ 40 inches in men, initiate lifestyle changes and treatment strategies for metabolic syndrome. 66
  57. 57. Secondary Prevention and Long Term Management Goals Diabetes management: Goal: HbA1c < 7% Recommendations Appropriate hypoglycemic therapy to achieve near-normal fasting plasma glucose, as indicated by HbA1c. Treatment of other risk factors (e.g., physical activity, weight management, blood pressure, and cholesterol management). 67
  58. 58. Management Strategies in Acute Coronary syndrome(ACS) Symptoms of Acute Coronary Syndrome ST elevation (STEMI) EKG Reperfusion approach All patients 1. ASA 1. Anti-ischemic medications 2. Heparin(UFH or LMWH) Beta-blocker 3. Clopidogrel Nitrated 4. Choose reperfusion method+/-Ca++ channel blocker a. Fibrinolytic drug 2. General measures b. Primary PCI Oxygen Pain control (morphine) 3. Additional therapies ACE inhibitor Statin No ST elevation (UA/NSTEMI) Antithrombotic approach 1. ASA 2. Heparin(UFH or LMWH) 3. Clopidogrel 4. For high risk patients GP IIb/IIIa inhibitor Proceed to cathlab
  59. 59. “ABCDE” A- antiplatelets, ACE-I B- beta-blocker, blood pressure control C- cholesterol lowering, cigarette smoking cessation D- diet, diabetes management E- exercise

Editor's Notes

  • Note: Plavix® (clopidogrel bisulfate) is not indicated for all the conditions listed on this slide.
    Vascular disease is the common underlying disease process for MI, ischemia and vascular death.
    Acute coronary syndrome (ACS) is a classic example of the progression of vascular disease to an ischemic event.
    ACS (in common with ischemic stroke and critical leg ischemia) is typically caused by rupture or erosion of an atherosclerotic plaque followed by formation of a platelet-rich thrombus.
    Atherosclerosis is an ongoing process affecting mainly large and medium-sized arteries, which can begin in childhood and progress throughout a person’s lifetime.
    Stable atherosclerotic plaques may encroach on the lumen of the artery and cause chronic ischemia, resulting in (stable) angina pectoris or intermittent claudication, depending on the vascular bed affected.
    Unstable atherosclerotic plaques may rupture, leading to the formation of a platelet-rich thrombus that partially or completely occludes the artery and causes acute ischemic symptoms.
  • Platelets are recognized to play an integral role in acute coronary syndromes and arterial thrombosis. After plaque fissure or rupture, there is platelet adhesion and activation. This leads to platelet aggregation within the coronary artery, and ultimately partial or complete occlusion of the coronary artery.