1. Myocardial Infarction
Khaled Dajani, MD, MBA
Division of Cardiology

2. Background
Myocardial Infarction if the rapid development of myocardial necrosis by a critical imbalance between oxygen supply and demand to the myocardium

3. Classification Acute coronary syndromes include
ST-elevation MI (STEMI)
Non ST-elevation MI ( NSTEMI)
Unstable Angina
Cardiac markers in circulation indicates myocardial infarction and help categorize MI and is a useful adjunct to diagnosis

4. Classification Anatomic or morphologic Transmural= Full thickness
Non-transmural= Partial thickness
ECG
Q wave MI
Non Q wave MI
Does not distinguish transmural from a non-transmural MI as determined by pathology

5. Prevalence
In the US, 1.3 million cases of nonfatal MI were reported in 2006
Incidence of 600 per 100,000 people
Increase in the proportion of NSTEMI compared to STEMI
Approximately 500,000 to 700,000 deaths are caused by heart disease annually in the United States

6. History
The history is critical in making the diagnosis of MI and sometimes provide only the only clues that lead to the diagnosis in the initial phase of presentation

7. History Chest Pain- anterior precordium tightness
Pain may radiate to jaw, neck and epigastrium
Dyspnea- angina equivalent, poor LV function
Nausea/abdominal pain with posterior MI
Anxiety

8. History Nausea with and without vomiting Diaphoresis or sweating
Syncope or near syncope
Elderly present with MS changes, fatigue, syncope or weakness
As many as half of MI are clinically silent

9. Physical The physical exam can often be unremarkable Hypertension
Hypotension
Acute valvular dysfunction may be present
Rales
Neck vein distention

10. Physical Third heart sound may be present
A fourth heart sound poor LV compliance
Dysrhythmias
Low grade fever

11. Causes
Most frequent cause is rupture of an atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation
Coronary artery vasospasm
Ventricular hypertrophy
Hypoxia
Coronary artery emboli

12. Causes Cocaine Arteries Coronary anomalies Aortic dissection
Pediatrics Kawasaki disease, Takayasu arteritis
Increased afterload which increases myocardial demand

13. Risk factors for atherosclerosis
Age
Male gender
Smoking
Hypercholesterolemia and triglyceridemia
Diabetes Mellitus
Poorly controlled hypertension
Type A personality

14. Risk factors for atherosclerosis
Family History
Sedentary lifestyle

15. Differentials Acute coronary syndrome Anxiety Aortic stenosis Asthma
Cholecystitis and biliary colic
Cholethiasis
COPD

16. Differentials Aortic Dissection Endocarditis Esophagitis Shock
Myocarditis
Pericarditis
Pulmonary embolism

17. Mechanisms of Myocardial damage
The severity of an MI is dependent of three factors
The level of the occlusion in the coronary
The length of time of the occlusion
The presence or absence of collateral circulation

18. Cardiac Biomarkers
Cardiac biomarkers are protein molecules released into the blood stream from damaged heart muscle
Since ECG can be inconclusive , biomarkers are frequently used to evaluate for myocardial injury
These biomarkers have a characteristic rise and fall pattern

19. Troponin T and I These isoforms are very specific for cardiac injury
Preferred markers for detecting myocardial cell injury
Rise 2-6 hours after injury
Peak in hours
Stay elevated for 5-14 days

20. Creatinine Kinase ( CK-MB)
Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB)
Increased in over 90% of myocardial infraction
However, it can be increased in muscle trauma, physical exertion, post-op, convulsions, and other conditions

21. Creatine Kinase (MB) Time sequence after myocardial infarction
Begins to rise 4-6 hours
Peaks 24 hours
returns to normal in 2 days
MB2 released from heart muscle and converted to MB1.
A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injury

22. Myoglobin
Damage to skeletal or cardiac muscle release myoglobin into circulation
Time sequence after infarction
Rises fast 2hours
Peaks at 6-8 hours
Returns to normal in hours
Have false positives with skeletal muscle injury and renal failure

23. Renal Failure and Renal Transplantation
Diagnostic accuracy of serum markers of cardiac injury are altered in patients with renal failure
Cardiac troponins decreased diagnostic sensitivity and specificity in patients receiving renal replacement therapy
Current data show levels of troponin I are unaltered while levels of troponin T may be elevated

24. CBC CBC is indicated if anemia is suspected as precipitant
Leukocytosis may be observed within several hours after myocardial injury and returns returns to levels within the reference range within one week

25. Chemistry Profile
Potassium and magnesium levels should be monitored and corrected
Creatinine levels must be considered before using contrast dye for coronary angiography and percutanous revascularization

26. C-reactive Protein (CRP)
C- reactive protein is a marker of acute inflammation
Patients without evidence of myocardial necrosis but with elevated CRP are at increased risk of an event

27. Chest X-Ray
Chest radiography may provide clues to an alternative diagnosis ( aortic dissection or pneumothorax)
Chest radiography also reveals complications of myocardial infarction such as heart failure

28. Echocardiography
Use 2-dimentional and M mode echocardiography when evaluating overall ventricular function and wall motion abnormalities
Echocardiography can also identify complications of MI ( eg. Valvular or pericardial effusion, VSD)

29. Electrocardiogram A normal ECG does not exclude ACS
High probability include ST segment elevation in two contiguous leads or presence of q waves
Intermediate probability ST depression
T wave inversions are less specific

30. Localization of MI ST elevation only Inferior wall- II, III, aVF
Lateral wall_ I, aVL, V4-V6
Anteroseptal- V1-V3
Anterolateral- V1-V6
Right ventricular- RV4, RV5
Posterior- R/S ratio >1 in V1 and T wave inversion

31. Therapy
The goals of therapy in AMI are the expedient restoration of normal coronary flow and the maximum salvage of functional myocardium

32. Antiplatelet Agents Aspirin at lease 160mg immediately
Interferes with function of cyclooxygenase and inhibits the formation of thromboxane
ASA alone has one of the greatest impact on the reduction of MI mortality.
Clopidogrel, ticlopidine, have not been shown in any large scal trail to be superior to Aspirin in acute MI

33. Supplemental Oxygen
Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and other tissues may be diminished
Supplemental oxygen should be administered to patient with symptoms and or signs of pulmonary edema or pulse oximetry readings less than 90%.

34. Nitrates
IV nitrates to all patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI
Primary benefit vasodilator effect
Metabolized to nitric oxide in the vascular endothelium, relaxes endothelium
Vasodilatation reduces myocardial oxygen demand and preload and afterload

35. Beta-blockers
Recommended within 12 hours of MI symptoms and continued indefinitely
Reduces Myocardial mortality by decreasing arrythmogenic death
Decrease the rate and force of myocardial contraction and decreases overall oxygen demand

36. Unfractionated heparin
Forms a chemical complex with antithrombin III inactivates both free thrombin and factor Xa
Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with alteplase

37. Low-molecular weight heparin
Direct activity against factors Xa and IIa
Proven to be effective in treating ACS that are characterized by unstable angina or non ST- elevation MI
Their fixed doses are easy to administer and laboratory testing to measure their therapeutic effect is not necessary makes them attractive alternative of un-fractionated heparin

38. Thrombolytics
Indicated with MI and ST segment elevation greater than 0.1mV in 2 contiguous ECG leads, or new onset LBBB, who present less than 12 hours but not more than 24 hours after symptom onset
The most critical variable in achieving successful fibrinolysis is time form symptom onset to drug administration

39. Thrombolytics
As a class the plasminogen activators have been shown to restore coronary blood flow in 50-80% of patients
Contraindication active intracranial bleeding, CVA 2months, CNS neoplasm, HTN, coagulopathy
Retaplase slightly higher angiographic patency but did not translate into survival benefit
Intracranial bleed risk major drawback

40. Glycoprotein IIb/IIIa Antagonists
Potent inhibitors of platelet aggregation
Use during PCI and in patients with high risk features ACS have been shown to reduce the composite end points of death, reinfraction and the need for target lesion

41. Percutanous Coronary Intervention
Alternative if performed by skilled operator in an experienced center
Standard is a “ door to balloon” time of 90 minutes
PCI can successfully restore coronary blood flow in 90 to 95% of MI patients
PCI definitive survival advantage over fibrinolytics for MI patients who are in cardiogenic shock

42. Surgical Revascularization
Emergent or surgical revascularization in setting of failed PTCA in patients with hemodynamic instability and coronary anatomy amendable to surgical grafting
Also indicated of mechanical complications of MI including VSD, free wall rupture, or acute MR
Carries a higher risk of perioperative mortality than elective CABG

43. Lipid Management
All post MI patients should be on AMA step II diet ( < 7% of calories from saturated fats)
Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try to lower levels to <100 mg/dl
Recent data indicate that all MI patients should be on statin therapy, regardless of lipid levels or diet

44. Long term Medications
Most oral medications instituted in the hospital at the time of MI are continued long term
Aspirin, beta blockers and statin are continued indefinitely
ACEI indefinitely in patients with CHF, ejection fraction <.40, hypertension, or diabetes

45. Thank You!