1. Management of ST-Elevation Myocardial Infarction1

2. ST-Elevation Myocardial Infarction (STEMI)
Myocardial infarction (MI): necrosis of the myocardium resulting from ischemia
STEMI: acute MI caused by complete interruption of regional myocardial blood flow
Causes elevation of the ST segment on the electrocardiogram (ECG)
Managed differently than non–ST-elevation MI (partial blood flow blockage) 2

3. Pathophysiology of STEMI
Blood flow to a region of myocardium is stopped (platelet plugging and thrombus formation)
Hydrogen ions accumulate
Local metabolic changes occur
Myocardial injury triggers ventricular remodeling
Degree of residual cardiac impairment depends on amount/location of damage 3

4. Diagnosis of STEMI Chest pain Characteristic ECG changes
Severe substernal, crushing/constricting, down arm and jaw
Characteristic ECG changes
Sweating, weakness, sense of impending doom
20% of patients with STEMI experience no symptoms
Biochemical markers for MI 4

5. Management of STEMI Routine drug therapy Oxygen Aspirin (not NSAIDs)
Morphine
Beta blockers
Nitroglycerin 5

6. Management of STEMI Reperfusion therapy
Primary percutaneous coronary intervention
Fibrinolytic (thrombolytic) therapy
Action: to dissolve clots; converts plasminogen to plasmin 6

7. Management of STEMI Adjuncts to reperfusion therapy Heparin
Antiplatelet drugs 7

8. Management of STEMI Thrombolytic drugs
Alteplase, a tissue plasminogen activator
Reteplase
Streptokinase
Tenecteplase
Urokinase
Percutaneous coronary intervention (PCI) 8

9. Primary Percutaneous Coronary Intervention
Primary refers to the use of angioplasty rather than fibrinolytic therapy
Stents may be placed
Goal: primary PCI within 90 minutes of patient contact
Success rate with PCI somewhat higher than with thrombolytics 9

10. Fibrinolytic (Thrombolytic) Therapy
Dissolves clots
Converts plasminogen to plasmin (proteolytic enzyme)
Alteplase, a tissue plasminogen activator
Reteplase
Streptokinase
Tenecteplase
Urokinase 10

11. Fibrinolytic (Thrombolytic) Therapy
Most effective when patient presents early; not given if pain has been present longer than 12 hours (best if given during first 4–6 hours)
Goal: to improve ventricular function, limit size of infarct, and reduce mortality
Timely administration = Opening of occluded artery in 80% of patients
Guidelines suggest 30-minute target time
Best for patients younger than 75 years 11

12. Adjuncts to Reperfusion Therapy: Management of STEMI
Unfractionated heparin used for treatment lasting less than 48 hours
Low-molecular-weight (LMW) heparin used for treatment lasting longer than 48 hours
Antiplatelet drugs
Clopidogrel (Plavix)
Glycoprotein (GP) IIb/IIIa inhibitors
Low-dose aspirin
May use concurrently with clopidogrel
Should take indefinitely
Higher dose for PCI patients 12

13. Adjuncts to Reperfusion Therapy: Management of STEMI
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs)
Decrease short-term mortality in all patients
Start treatment within 24 hours
ACE inhibitors studied more extensively than ARBs
Calcium channel blockers
Antianginal, vasodilation, and antihypertensive actions 13

14. Complications of STEMI
Ventricular dysrhythmias
Develop frequently and are major cause of death after MI
Prophylactic antidysrhythmics not successful
Cardiogenic shock
Results from tissue perfusion reduction
7%–15% of post-MI patients develop shock in first few days 14

15. Complications of STEMI
Ventricular dysrhythmias
Cardiogenic shock
Heart failure
Cardiac rupture 15

16. Secondary Prevention of STEMI
Discharge 6–10 days after event
5%–5% of patients have another infarct in first year
Outcome improved with risk factor reduction
Cholesterol control, smoking cessation, exercise, blood pressure (BP) control, diabetes control
All post-MI patients should take:
Beta blocker
ACE inhibitor
Antiplatelet drug or anticoagulant 16