Transcript Myocardial infarction

Myocardial Infarction
Background
Myocardial Infarction if the rapid
development of myocardial necrosis by a
critical imbalance between oxygen supply
and demand to the myocardium
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
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 nontransmural MI as determined by pathology
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
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
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
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
Physical
The physical exam can often be
unremarkable
Hypertension
Hypotension
Acute valvular dysfunction may be present
Rales
Neck vein distention
Physical
Third heart sound may be present
A fourth heart sound poor LV compliance
Dysrhythmias
Low grade fever
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
Causes
Cocaine
Arteries
Coronary 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
Risk factors for atherosclerosis
Family History
Sedentary lifestyle
Differentials
Acute coronary syndrome
Anxiety
Aortic stenosis
Asthma
Cholecystitis and biliary colic
Cholethiasis
COPD
Differentials
Aortic Dissection
Endocarditis
Esophagitis
Shock
Myocarditis
Pericarditis
Pulmonary embolism
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
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
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
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
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
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
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
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
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
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
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
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)
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
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
Therapy
The goals of therapy in AMI
are the expedient restoration
of normal coronary flow and
the maximum salvage of
functional myocardium
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
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%.
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
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
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 unfractionated heparin
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
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
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
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
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
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
Thank You!