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Acute Coronary Syndrome The Essentials

Acute Coronary Syndrome The Essentials. Percy Pentecost, MD University of New Mexico School of Medicine. Acute Coronary Syndrome Impact. Incidence: 3 million people estimated to have acute ST-elevation MI each year 4 million people estimated to have non-ST-elevation MI.

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Acute Coronary Syndrome The Essentials

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  1. Acute Coronary SyndromeThe Essentials Percy Pentecost, MD University of New Mexico School of Medicine

  2. Acute Coronary SyndromeImpact • Incidence: • 3 million people estimated to have acute ST-elevation MI each year • 4 million people estimated to have non-ST-elevation MI • A Shift in Populations • Myocardial Infarction used to be seen predominantly in developed countries, but… • …it is now becoming increasingly more common in developing countries..

  3. Acute Coronary SyndromeImpact • Why a shift towards developing countries as well? • Progressive urbanization…. • Increasing rates of obesity • Increasing rates of diabetes • Increasing rates of coronary heart disease

  4. Acute Coronary SyndromeImpact • Why is this epidemiology stuff important anyway? • According to the INTERHEART study of over 15,000 patients, 90% of myocardial infarctions were attributable to modifiable risk factors in men, and 94% in women!!!

  5. Acute Coronary SyndromeRisk Factors • ..modifiable risk factors…such as… • Smoking • Dyslipidemia • Hypertension • Abdominal Obesity • Diabetes

  6. Acute Coronary SyndromeDefinitions • Acute Coronary Syndrome describes a spectrum of conditions… • Unstable Angina • Non-ST-elevation Myocardial Infarction • ST-elevation Myocardial Infarction

  7. Acute Coronary SyndromeDefinitions • Acute Coronary Syndrome describes a spectrum of conditions… • Unstable Angina • Non-ST-elevation Myocardial Infarction • ST-elevation Myocardial Infarction

  8. Acute Coronary SyndromeDefinitions • Unstable Angina vs. Non-ST-elevation Myocardial Infarction..is there a difference? • Patients with these two entities often present similarly • Distinction between the two can be made only many hours to days later when the results of the cardiac enzymes are available…

  9. Acute Coronary SyndromeDefinitions • Even though, ST-elevation MI’s sound more exciting..they’re not… • Acute Coronary Syndromes account for 1.57 million hospitalizations each year… • 1.24 million of those are for Unstable Angina and NSTEMI • Only .33 million are for STEMI

  10. Acute Coronary SyndromeDefinitions • Quick Quiz…A 75 y/o man presents to you with new onset exertional chest pain x 1 day…Is this stable or unstable angina?

  11. Acute Coronary SyndromeDefinitions • So what? … • …unstable angina implies that there is an unstable or ruptured plaque…which is bad news..

  12. Acute Coronary SyndromePathogenesis • Disruption of a formed atherosclerotic plaque is central to the initiation of acute coronary syndromes…

  13. Acute Coronary SyndromePathogenesis • Quick Quiz… • Which type of plaques are the most vulnerable to rupture – big plaques or small plaques???

  14. Acute Coronary SyndromePathogenesis • The arterial lesions of patients with unstable angina frequently have complex, eccentric morphologic features on angiography that have been found to represent ruptured plaque with superimposed thrombus…

  15. Acute Coronary SyndromePathogenesis • Mature plaques are made up of (1) a lipid-rich core and (2) a fibrous cap • The presence of large, eccentric lipid pools and infiltration of foam cells are most frequently associated with fissured or ruptured plaques

  16. Acute Coronary SyndromePathogenesis • The majority of these plaques rupture at sites of greatest mechanical stress, notably at the junction of the plaque cap and the adjacent normal intima…or the shoulder regions of the lipid pool…

  17. Acute Coronary SyndromePathogenesis • Local thrombosis occurring after plaque disruption results from complex interactions among lipid core, smooth-muscle cells, macrophages, and collagen.. • The lipid core is the most potent substrate for platelet-rich thrombus formation, and both smooth-muscle and foam cells within the core increase expression of tissue factor.

  18. Acute Coronary SyndromePathogenesis • So, why is this important?? • Unstable angina is the part of a spectrum of conditions that can lead to complete thrombosis and infarction • It is paramount to identify patients at high risk early in order to prevent progression of this condition

  19. Acute Coronary SyndromePathogenesis • And…knowing the pathogenesis will also help you understand the medical therapy for acute coronary syndromes… • Anti-platelet therapy • Anti-thrombin therapy • Anti-ischemic therapy

  20. Acute Coronary Syndrome Risk Stratification and Management

  21. Acute Coronary Syndrome • What do we mean by risk stratification? • The relative instability of a plaque is a huge unknown… • …so risk stratification helps us delineate how likely it is for a given patient to progress to full infarction, or death…

  22. Acute Coronary Syndrome • The TIMI (Thrombosis in Myocardial Infarction) Trials… • The TIMI Risk score accurately predicts the risk of an adverse cardiac event in the setting of a suspected Acute Coronary Syndrome…

  23. Acute Coronary Syndrome • The TIMI Risk Factors… • …one point for each… • Age ≥ 65 years • At least 3 risk factors for CAD • Prior coronary stenosis of ≥50% • ST-segment deviation on ECG presentation • At least 2 anginal events in prior 24 hours • Use of aspirin in prior 7 days • Elevated serum cardiac biomarkers

  24. Acute Coronary Syndrome • The TIMI Risk Score • Composite primary outcome measure = All-cause mortality, recurrent MI, urgent coronary revascularization

  25. The TIMI Risk Factors

  26. Acute Coronary Syndrome • Case 1…A 75 y/o man with a h/o HTN, DM, and smoking presents with a 2 day history of progressively worsening angina. He has had multiple episodes in the past 24 hours. He takes HCTZ, glyburide, and a baby aspirin daily. On exam, vitals stable, ECG normal. Initial troponin elevated at 1.52. • What is his TIMI risk score? And what does this mean? • TIMI Risk Factors(5) • 3 CAD risk factors • Age ≥65 • ≥2 anginal events in 24° • Aspirin in past 7 days • Elevated biomarkers • Composite Primary Outcome ~ 26.2% chance of death, MI, or need for urgent revascularization…

  27. Acute Coronary Syndrome • Case 2…A 50 y/o woman with a history of DM, HTN, and Smoking presents after an episode of angina while walking up a flight of stairs this morning. She has had no further episodes. She takes glyburide. On exam, vitals stable. ECG normal, and cardiac enzymes negative. • What is her TIMI risk score? • TIMI Risk Factors (1) • Risk ~ 4.7%

  28. Acute Coronary Syndrome • So, the TIMI risk assessment tool helps a clinician estimate the risk involved in an ACS presentation… • …it also helps guide the initial evaluation and management of ACS…

  29. Acute Coronary Syndrome Initial Therapies and Management

  30. Classification of Recommendation and Level of Evidence

  31. Classification of Recommendation and Level of Evidence • To summarize, Recommendations… • Class I – if you don’t do this, you’re an idiot.. • Class II – you should probably do this too.. • Class III – you may find a reason not to do this… • Class IV – if you do this you’re an idiot… • And Evidence… • Class A – lots of great evidence • Class B – a little bit of good evidence • Class C – my grandfather taught me this…

  32. Acute Coronary SyndromeTherapies and Management • Remember the problem… • …plaque rupture, platelet aggregation… • Thrombosis… • Occlusion of vessel..decreased oxygen supply to myocardium • Helps with the solution… • Anti-ischemic therapy (reduce demand/ increase supply) • Anti-platelet therapy • Anti-thrombin therapy

  33. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • Bed Rest • Continuous ECG monitoring • Supplemental oxygen • Nitroglycerin • Beta-blockers • IV morphine • IABP for hemodynamic instability • ACE inhibitor for persistent HTN in patients with persistent systolic dysfunction or CHF

  34. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • Bed Rest – Class IC – recommended for all ACS patients on presentation • Supplemental O2 – Class IB – should be given in ACS patients with O2 sat <90%, respiratory distress, or other high risk features of hypoxemia

  35. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • Sublingual Nitroglycerin – class IC – Patients with ACS should receive sublingual NTG (0.4 mg) every 5” for a total of 3 doses after which assessment should be made about the need for IV NTG • Intravenous Nitroglycerin – class IB – is indicated in the first 48 hours after ACS for treatment of persistent ischemia, CHF, or HTN

  36. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • Oral beta blocker therapy – Class IB – should be initiated within the first 24 hours for patients who do not have (1) CHF, (2) low CO, (3) increased risk for cardiogenic shock, (4) evidence of AVB, or (5) reactive airway disease

  37. Acute Coronary SyndromeTherapies and Management • Quick Quiz… • What is the estimated mortality benefit of beta blockers in the setting of acute coronary syndrome? Yusof et al. JAMA 1988;260:2259-63

  38. Acute Coronary SyndromeTherapies and Management • Quick Quiz…Do nitrates improve mortality?

  39. Acute Coronary SyndromeTherapies and Management • More questions…what adaptive response occurs within 24 hours of nitrate therapy?

  40. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • ACE Inhibitor – class IA – Should be given orally within first 24 hours to ACS patients with pulmonary congestion, or LV EF <40% in the absence of hypotension or other contraindications. • ARB – Can be administered to ACS patients intolerant to ACE inhibitors.

  41. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • Calcium Channel Blockers – class IB – In ACS patients with continuing or recurrent ischemia, and in whom beta blockers are contraindicated, non-dihydropyridine CCB (diltiazem, or verapamil) should be given as initial therapy in the absence of clinically significant LV dysfunction.

  42. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • NSAIDS – class IC – because of increased risks of mortality, reinfarction, hypertension, CHF, and myocardial rupture associated with their use, NSAIDs (except ASA) whether selective or non-selective COX inhibitors should be discontinued at the time a patient presents with an ACS.

  43. Acute Coronary SyndromeTherapies and Management • What is the issue? • Just one example… • COX 1 – mediates platelet production of thromboxane A2 (prothrombotic) • COX 2 – mediates endothelial cell synthesis of prostacyclin (antithrombotic) • So selective COX 2 inhibition will result in unopposed thromboxane production by platelets…

  44. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • Oxygen – class IIC – it is reasonable to give supplemental oxygen during the first 6 hours after presentation in ACS • Morphine – class IIB – in the absence of contraindications to its use, it is reasonable to administer morphine sulfate intravenously to ACS patients if there is uncontrolled ischemic chest discomfort despite nitrogylcerin

  45. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • Intra-aortic balloon pump (IABP) – class IIC --counter pulsation is reasonable in ACS patients for severe ischemia that recurs frequently despite intensive medical therapy, for hemodynamic instability in patients before or after angiography, and for mechanical complications of MI.

  46. Acute Coronary SyndromeTherapies and Management • Anti-Ischemic therapy.. • Nitrates should NOT be given in ACS patients with SBP <90, severe bradycardia, tachycardia in the absence of CHF, or RV infarction (class IIIC) • Nitrates should not be given to ACS patients who have received a phosphodiesterase inhibitor for erectile dysfunction within 24 hours of sildenafil and 48 hours of tadalafil use (class IIIC)

  47. Acute Coronary SyndromeTherapies and Management • Anti- Platelet Therapies • Aspirin • Clopidogrel • GP IIBIIIA Inhibitors • Heparin

  48. Acute Coronary SyndromeTherapies and Management • Antiplatelet therapies…

  49. Acute Coronary SyndromeTherapies and Management • Antiplatelet therapies… • Aspirin – class IA – should be given ASAP unless there is known intolerance • Clopidogrel – class IA should be given to ACS patients who are unable to take ASA

  50. Acute Coronary SyndromeTherapies and Management • Antiplatelet therapies… • Glycoprotein IIB/IIIA inhibitors – consistently reduce 30-day relative risk of composite endpoint of death, MI, or need for repeat revascularization (22 to 56%) when given with heparin and aspirin, but not when given alone

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