Myocardial Infarction
Definition: Myocardial Infarction is the rapid development of myocardial
necrosis by a critical imbalance between oxygen supply and demand to the
myocardium.
Classification of MI
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
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
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
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The presence or absence of collateral circulation
Causes of MI
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
Cocaine
Coronary artery anomalies
Aortic dissection
Pediatrics Kawasaki disease, Takayasu arteritis
Increased afterload which increases myocardial demand
Risk factors for atherosclerosis
Age
Male gender
Smoking
Hypercholesterolemia and triglyceridemia
Diabetes Mellitus
Poorly controlled hypertension
Type A personality
Family History
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Sedentary lifestyle
History of MI
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
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
Physical examination
Hypertension
Hypotension
Acute valvular dysfunction may be present
Rales
Neck vein distention
Third heart sound may be present
A fourth heart sound
poor LV compliance
Dysrhythmias
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Low grade fever
Differential diagnosis
Acute coronary syndrome
Anxiety
Aortic stenosis
Asthma
Cholecystitis and biliary colic
Cholethiasis
COPD
Investigations
1. 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
a. 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
b. Creatinine Kinase ( CK-MB)
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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
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
2. 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
3. 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
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Management of MI
The goals of therapy in AMI are the expedient restoration of normal
coronary flow and the maximum salvage of functional myocardium
1. 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.
2. 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%.
3. 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
4. Beta-blockers
Recommended within 12 hours of MI symptoms and continued
indefinitely
Reduces Myocardial mortality by decreasing arrythmogenic death
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Decrease the rate and force of myocardial contraction and decreases
overall oxygen demand
5. 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
6. 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
7. 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
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
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