Myocardial infarction, or heart attack, occurs when blood flow to the heart is blocked, damaging heart muscle. There are two main types - STEMI caused by a complete blockage, and NSTEMI from a partial blockage. Risk factors include age, smoking, high cholesterol, diabetes, and family history. Diagnosis involves history, cardiac biomarkers like troponin that indicate heart damage, ECG showing elevated ST segments, and imaging tests. Treatment focuses on restoring blood flow through medications, angioplasty, or bypass surgery, along with long term preventative medications like aspirin, statins, and beta blockers.

1. Myocardial Infarction
By
Chiranjeevi Pudi
V Pharm D (2013-14)

4. CLASSIFICATION
• Acute coronary syndromes include
ST-elevation MI (STEMI)
Non ST-elevation MI ( NSTEMI)
Unstable Angina

8. 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

9. 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 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

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

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

13. RISK FACTORS FOR
ATHEROSCLEROSIS
• Age
• Smoking
• Hypercholesterolemia and triglyceridemia
• Diabetes Mellitus
• Poorly controlled hypertension
• Family History
• Sedentary lifestyle

17. PATHOPHYSIOLOGY

21. 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

22. 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

23. 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 12-16 hours
Stay elevated for 5-14 days

24. 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

25. CK-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

26. 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 20-36 hours
• Have false positives with skeletal muscle injury
and renal failure

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

28. 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

29. Release of cardiac markers after acute
myocardial infarction (AMI)

30. 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

31. ECG
• An ECG can be used to detect patterns of
ischemia, injury, and infarction
Ischemia
• On the ECG, myocardial ischemia results in T-
wave inversion or ST segment depression in the
leads facing the ischemic area.
• The inverted T wave representative of ischemia is
symmetrical, relatively narrow, and somewhat
pointed.

33. Injury
• the injury process begins in the subendocardial
layer and moves throughout the thickness of the
wall of the heart like a wave.
• If the process is not interrupted, it eventually
results in a transmural MI.
• On ECG, the hallmark of acute myocardial injury
is the presence of ST segment elevations.
• With an acute injury, the ST segments in the
leads facing the injured area are elevated.
• The elevated ST segments also have a downward
concave or coved shape and merge unnoticed
with the T wave

34. (A)ST segment elevation
without T-wave
inversion.
(B) ST segment elevation
with T-wave inversion.
The elevated ST
segments have a
downward concave or
coved shape and merge
unnoticed with the T
wave.

35. INFARCTION When myocardial injury persists, MI is the
result.
• During the earliest stage of MI, known as the hyperacute
phase, the T waves become tall and narrow. This
configuration is referred to as hyperacute or peaked T waves.
• Within a few hours, these hyperacute T waves invert.
• Next, the ST segments elevate, a pattern that usually lasts from
several hours to several days.
• In addition to the ST segment elevations in the leads of the
ECG facing the injured heart, the leads facing away from the
injured area may show ST segment depression.
• This finding is known as reciprocal ST segment changes.
• Reciprocal changes are most likely to be seen at the onset of
infarction, but their presence on the ECG does not last long.
• Reciprocal ST segment depressions may simply be a mirror
image of the ST segment elevations.

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

40. Antiplatelet Agents
• Aspirin at least 160–162 mg on hospital day 1
Followed by 75–162 mg daily starting hospital day 2
and continued indefinitely.
• Interferes with function of cyclooxygenase and
inhibits the formation of thromboxane
• Clopidogrel is also used which acts through a
blockade of ADP receptors on platelets
• 300–600 mg loading dose on hospital day 1
followed by a maintenance dose of 75 mg PO qd
starting on hospital day 2 Administer indefinitely in
patients with an aspirin allergy.

41. Nitrates
• Nitrates promote the release of nitric oxide from the
endothelium, which results in venous and arterial
vasodilation
• Vasodilatation reduces myocardial oxygen demand
and preload and afterload
• 0.4 mg , repeated every 5 min × 3 doses
• 5 to 10 mcg/min by continuous infusion titrated up to
75 to 100 mcg/min until relief of symptoms or
limiting side effects headache or hypotension
• most significant adverse effects - tachycardia,
flushing, headache, and hypotension. Nitrate
• CI - sildenafil and vardenafil within the past 24 hours
and tadalifil within the past 48 hours.

42. 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%.

43. 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
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

44. 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

45. Thrombolytics
• Thrombolytic drugs lyse coronary thrombi by
converting plasminogen to plasmin.
• Thrombolytic therapy provides maximal benefit if
given within the first 3 hours after the onset of
symptoms.
• Significant benefit still occurs if therapy is given up to
12 hours after onset of symptoms.

46. Thrombolytics
• As a class the plasminogen activators have been
shown to restore coronary blood flow in 50-80%
of patients
• Contraindication active intracranial bleeding,
CNS neoplasm, HTN, coagulopathy
• Intracranial bleed risk major drawback

47. 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

48. Revascularization:

49. 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

50. Stenting
•A stent is introduced into a blood vessel on a balloon catheter
and advanced into the blocked area of the artery
• the balloon is then inflated and causes the stent to expand until
it fits the inner wall of the vessel, conforming to contours as
needed
• the balloon is then deflated and drawn back
•The stent stays in place permanently, holding the vessel open
and improving the flow of blood.

51. Angioplasty
• a balloon catheter is passed through the guiding catheter to the area
near the narrowing. A guide wire inside the balloon catheter is then
advanced through the artery until the tip is beyond the narrowing.
• the angioplasty catheter is moved over the guide wire until the balloon
is within the narrowed segment.
• balloon is inflated, compressing the plaque against the artery wall
• once plaque has been compressed and the artery has been sufficiently
opened, the balloon catheter will be deflated and removed.

52. Bypass surgery
 healthy blood vessel is removed from leg, arm or chest
 blood vessel is used to create new blood flow path in your heart
 the “bypass graft” enables blood to reach your heart by flowing
around (bypassing) the blocked portion of the diseased artery. The
increased blood flow reduces angina and the risk of heart attack.

54. 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

55. 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

56. Thank you!!