ST-Elevation Myocardial Infarction (STEMI)

1. ST-Elevation Myocardial Infarction (STEMI) Greg Johnsen, MD, FACC, FSCAI

2. Epidemiology of Acute Myocardial Infarction • Coronary Heart Disease • Leading cause of death in high or middle income countries • Leading cause of death in the USA • Rates of death from CHD have declined in most high income countries • Rates of death from CHD have increased in the developing world • In 2004, CHD became the leading cause of death in India

3. It is estimated that 1.25 million Americans have an acute MI each year. ST-Elevation MI accounts for 30 – 40% In the early 1960’s, prior to the era of cardiovascular intensive care units, in-hospital mortality was greater than 30%. Today, in-hospital mortality is 6.5 – 7.5%

6. In the USA • All of the Following Risk Factors • Are Decreasing Except? • Hypertension • Smoking • Hypercholesterolemia • Diabetes

8. Metabolic Syndrome • NCEP ATP III Definition (3 or more) • Abdominal Obesity • WC ≥102 cm in men (40 in), ≥88 cm (35 in) women • Serum TG ≥150mg/dL or drug TX • Serum HDL • Men ≤40 mg/dl, Women ≤50 mg/dl • BP ≥130/85 mmHg or drug Tx • Fasting glucose ≥100 mg/dL or drug Tx

9. Points to Remember • CV deaths have decline markedly since the 1960s • It continues to drop in men but not women • CVD is the leading cause of death but shifting from CAD to HF • Prevalence of risk factors decreasing in US except diabetes

10. Vascular Injury and Atherosclerosis • Atherosclerosis • Chronic inflammatory process that develops in “response-to-injury” • metabolic environmental • genetic • physical infectious

12. Summary • Chronic inflammatory process that develops in “response-to-injury” • Lipoprotein accumulation and oxidation • Monocyte and T-lymphocyte recruitment • Leads to plaque progression • Leads to endothelial dysfunction

13. Acute Myocardial Infarction (MI) • Reduction in myocardial perfusion which is sufficient to cause cell necrosis • Most Common Mechanism of Myocardial Infarction • Thrombus formation in the coronary artery at the site of a ruptured, eroded, or fissured atherosclerotic plaque • Ruptured plaque exposes the thrombogenic lipids in the plaque to the blood which leads to activation of platelets and clotting factors • Coronary plaques most prone to rupture have a rich lipid core and a thin fibrous plaque

14. Other Rare Causes of • Acute Myocardial Infarction • Coronary artery embolism from a valvular vegetation or intracardiac thrombus • Cocaine use • Coronary artery dissection • Anemia • Hypotension • Coronary Spasm

15. Acute Coronary Syndrome Unstable Angina Non-ST-Elevation MI (NSTEMI) ST-Elevation MI (STEMI)

16. The Spectrum of Acute Coronary Syndromes

20. Characteristics of Plaques Prone to Rupture • Thin fibrous caps • Lipid, macrophage-rich • Smooth muscle poor

24. What accounts for the disparity between degree of coronary artery stenosis and producing the acute coronary syndromes? The functional state of the atheroma, not merely its size or the degree of luminal encroachment, determines the propensity for development of acute coronary syndromes

25. Triggers of Plaque Rupture • Emotional Stress • Physical Activity • Increased Sympathetic Tone

26. Triggers of Plaque Rupture • Heart Rate & Blood Pressure • Vasoconstriction • High Shear Stress • Physical and Emotional Stress • Infection • Inflammation

27. In half of patients with STEMI, a precipitating factor or prodromal symptoms can be identified Unusually heavy exercise in habitually inactive patients and emotional stress can precipitate STEMI Accelerating angina and rest angina may culiminate in STEMI Respiratory infections, hypoxemia, cocaine use and non-cardiac surgical procedures can predispose to STEMI

28. Risk Factors for ST-Elevation Myocardial Infarction & Cardiovascular Disease Non-Modifiable Factors Age Male Gender Family History of Cardiovascular Disease

29. Risk Factors for ST-Elevation Myocardial Infarction & Cardiovascular Disease Modifiable Factors Cigarette Smoking Hyperlipidemia Hypertension Diabetes Obesity Physical Inactivity Diet hsCRP

30. Controversial Risk Factors for MI • Baldness • Gray Hair • Diagonal Earlobe Crease • (Frank’s Sign)

31. Symptoms of Acute Myocardial Infarction • Substernal chest pressure, usually described as heavy, squeezing, tightness, crushing and sometimes stabbing or burning pain (Levine’s sign). • In STEMI, sudden onset of chest pain often associated with shortness of breath, diaphoresis, weakness, nausea and vomiting. • The pain sometimes radiates to the C7 – T4 dermatomes (left arm, shoulders, jaw, neck, back and epigastrium). Radiation to both arms is a strong predictor of acute MI. • In 20% of patients (diabetics, elderly, postoperative or female) chest pain may be absent.

37. Inferior Leads = II, III, aVF Right Coronary Artery or Left Circumflex Coronary Artery Anterior Leads = V1 – V6 Left Anterior Descending Coronary Artery Anterior Infarct = leads V2 – V5 Anteroseptal Infarct = leads V1 – V4 Anterolateral Infarct = leads V3 – V6, I + aVL Lateral Leads = I + aVL, V5 – V6 Diagonal Branch Coronary Artery Obtuse Marginal Branch Coronary Artery Intermediate Ramus Branch High Lateral Leads = I + aVL Low Lateral Leads = V5 – V6

38. Left Main Occulsion • ST elevation in aVR >1mm • ST elevation in aVR > V1 • Widespread ST depression in multiple leads most prominent in leads I, II, and V4 – V6 • ST elevation in aVR may also be seen with proximal LAD occlusion and severe triple-vessel disease.

42. Reperfusion Goals in ST-Elevation MI (PCI = Percutaneous Coronary Intervention) Primary PCI: Door to Balloon Time less than 90 minutes Primary PCI: First medical contact to device time less than 90 minutes Primary PCI: When transferred from a different hospital: First medical contact to device time less than 120 minutes Fibrinolytic therapy: Door to needle time less than 30 minutes

43. Guidelines for Primary PCI in STEMI • Class I • Primary PCI should be performed within 12 hours of onset of STEMI • Primary PCI should be performed within 90 minutes of first medical contact as a systems goal when presenting to a hospital with PCI capability • Primary PCI should be performed within 120 minutes of first medical contact as a systems goal when presenting to a hospital without PCI capability • Primary PCI should be performed in patients with STEMI who develop severe heart failure or cardiogenic shock and are suitable for revascularization as soon as possible

44. Guidelines for Primary PCI in STEMI • Class IIa • Primary PCI is reasonable in STEMI if there is clinical or ECG evidence of ongoing ischemia between 12 and 24 hours after symptom onset • PCI is reasonable in patients with STEMI and clinical evidence for fibrinolytic failure or infarct artery reocclusion

45. Time Is Muscle

48. In 2006, the American College of Cardiology launched the D2B Alliance, a campaign to reduce systems delay in the care of STEMI. As a result, median door to balloon times were reduced 32 minutes from 96 minutes to 64 minutes between 2005 and 2010.

49. Pre-hospital ECG Transmission to STEMI Receiving Hospital • Reduces Door-to-Balloon Time • Chart review of STEMI patients between January 1st, 2010 to November 25, 2010. • Mean door-to-balloon time with a pre-hospital ECG was 53 minutes. • Mean door-to-balloon time without a pre-hospital ECG was 77 minutes. (p = .0003) • Catheterization and Cardiovascular Interventions 2011; 77:S1

50. Acute Treatment of ST-Elevation MI • 4 Aspirin 81mg chewed • Plavix 600mg • Heparin 5,000 units IV • Morphine IV as needed for pain control • Nitrates (NTG – sublingual and IV) – Contraindicated in RV Infarct, • Hypotension and severe bradycardia (HR less than 50) • Metoprolol IV – Contraindicated in CHF, Hypotension bradycardia, 1st • degree AV Block, evidence of low-output, asthma, and increased risk of • cardiogenic shock