This document defines myocardial infarction and provides classifications. It discusses the epidemiology, risk factors, pathophysiology, diagnostic approach, and treatment strategies for myocardial infarction. Key points are that MI is sudden myocardial necrosis caused by ischemia. Classification includes STEMI and NSTEMI. Risk factors include age, smoking, diabetes, hypertension, and hyperlipidemia. Diagnosis involves ECG and biomarkers. Treatment focuses on dissolving thrombus with aspirin and anticoagulants, reducing atheroma with statins, and selecting an invasive or non-invasive strategy based on risk.

1. MYOCARDIAL INFARCTION
RAMACHANDRA

2. OBJECTIVES
•Define
•Classification
•Diagnosis
•Treatment

3. DEFINITION
Sudden myocardial necrosis caused by an ischemia

4. CLASSIFICATION
• STEMI :FULLTHICKNESS =TRANSMURAL
• NSTEMI :SUBENDOCARDIAL =DYING NEAR POND

5. CONTINUED …..
• I:Atherothrombosis
• II:Supply demand mismatch but not atherogenic
• III:No ECG or biomarker evidence
• IVA :MI during PCI
• IVB:MI due to stent thrombosis
• V:CABG graft occlusion

6. THREE BUT NON SAVES

7. ON THE SPOT

9. EPIDEMIOLOGY
• 80% of deaths from cardiovascular disease worldwide
• The survival rate for those hospitalized due to MI has
reached approximately 95%

10. RISK FACTORS
NOT MODIFIABLE
• Age
• Gender
• Family history
MODIFIABLE
• Smoking:X2-6 TIMES
• Diabetes Control
• Hypertension
• Hyperlipidemia
• Obesity
• Physical Inactivity

11. PATHOBIOLOGY

12. • Ischemia can develop within 10 seconds and if it lasts
longer than 20 minutes, irreversible cell and tissue death
occurs
• As vessel occlusion continues cell death spreads to the
myocardium and eventually to the epicardium.
• Severity of the MI depends on three factors.
• Level of occlusion,length of time of occlusion and presence or
absence of collateral circulation

13. PATHOPHYSIOLOGY
• As vessel occlusion continues cell death spreads to the
myocardium and eventually to the epicardium.
• Severity of the MI depends on three factors.
• Level of occlusion
• Length of time of occlusion
• Presence or absence of collateral circulation

15. DIAGNOSTIC TRIAGE
• History
• ECG
• Biomarkers (Serial measurement)

16. SERUM CARDIAC MARKERS

17. CHEST PAIN
• PQRST assessment for chest pain
• P- Precipitating events
• Q- Quality of pain
• R- Radiation of pain
• S- Severity of pain
• T- Timing

18. RISK MODELS
• Thrombolysis in Myocardial Infarction (TIMI)
•
Global Registry of Acute Coronary Events (GRACE) models

19. GENERAL CARE
• LIMIT ACTIVITY
• ASPIRIN
• NITRO-GLYCERINE:0.3 to .4mg S/L every 5mintes
• STATIN
• OXYGEN :SPO2 <90%
• BETA-BLOCKER/CCB
• MORPHINE:1-6 mg IV every ½ hrs

20. DISSOLVING THROMBUS
• Aspirin :162 to 325 mg; then 81 to 325 mg daily life
long+another antiplatelet
• Anticoagulant therapy:Administer an intravenous
anticoagulant agent to all patients, regardless of treatment
strategy

21. REDUCING ATHEROMA SIZE
• Atorvastatin :40 to 80 mg /Day or
• Rosuvastatin 20 to 40 mg
• Ramipril /Lisinopril/ARB

22. STRATEGY
• INVASIVE
• NON-INVASIVE
(ISCHEMIA-GUIDED)
INITIAL STRATEGY
• THE CHOICE OF EARLY
INVASIVE
MANAGEMENT IS
BASED ON RISK AND
PATIENT’S
PREFERENCES

23. ASPIRIN +2ND
ANTIPLATELET
• THROMBOTIC RISK
• TIMING OF INVASIVE STRATEGY
• , LIKELIHOOD OF NEED FOR SURGICAL
REVASCULARIZATION
• RISK OF BLEEDING

24. ANTICOAGULANT AGENT
• unfractionated heparin
• low-molecular weight
heparin
• fondaparinux
• bivalirudin
• According to the initial
management strategy
(invasive or noninvasive)
• Risk of bleeding

25. TAKE HOME