Acute Myocardial

Infarction

DR.LIU LIXIN
DEFINITION
 Acute myocardial infarction (MI) is
defined as death or necrosis of
myocardial cells.
 It is a diagnosis at the end of the
spectrum of myocardial ischemia or
acute coronary syndromes.
 From an anatomic or morphologic
standpoint, the two types of MI are
 transmural : STEMI
 nontransmural:NSTEMI
ACS Types
Pathophysiology

Mechanisms of Occlusion:
 Most MIs are caused by a disruption in

the vascular endothelium associated

with an unstable atherosclerotic plaque
that stimulates the formation of an
intracoronary thrombus, which results in
coronary artery blood flow occlusion. If
such an occlusion persists long enough
(20 to 40 min), irreversible myocardial
cell damage and cell death will occur.
Vulnerable Plaque
Pathogenesis OF AMI
Clinical Manifestation

 Premonitory Pain: a recent onset

of angina, a worsening angina, or a
worsening angina pectoris poorly
responsive well to a nitrate.
 Pain Of Infarction:more severe,
long lasting, and relieved little by
rest or nitroglycerin.
Clinical Manifestation
 Associated Symptom: Nausea
and vomiting ,abdominal
bloating,cold sweat,SOB
 Painless infarction: 20% silent or
atypical
 Sudden death & early
arrhythmias:ventricular
fibrillation
Clinical Manifestation
 Arrhythmias : 75~95% of patients
develop cardiac arrhythmias . Any type
of arrhythmias may be found
 Cardiac failure :Heart failure occurs in
about 32-48% of hospitalized patients
with acute MI
 Cardiogenic shock :A loss of
myocardium greater than 40% generally
leads to cardiogenic shock
Clinical Manifestation
 Signs:HR is usually increased (but
inferior MI commonly leads to
bradycardia). S1 is low, S4 (atrial
gallop) is noted and an S3
(Ventricular gallop) is present
when develop LV failure
Laboratory
findings
ECG for AMI
• Q wave duration of more than
0.04 seconds
• Q wave depth of more than 25%
of ensuing r wave
• ST elevation in leads facing
infarct (or depression in opposite
leads)
• Deep T wave inversion overlying
and adjacent to infarct
• Cardiac arrhythmias
 Sequence of changes in
evolving AMI
R
R
ST
T R
ST
P P
P
T
QS
Q
Q

1 minute after onset 1 hour or so after onset A few hours after onset

ST R
P P ST
T
P
T
T
Q Q
Q
A day or so after onset Later changes A few months after AMI
 Anterior infarction
Anterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left
coronary
artery
 Inferior infarction
Inferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right
coronary
artery
 Lateral infarction
Lateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left
circumflex
coronary
artery
 Echocardiography :to estimate
ventricular wall motion
abnormalities and left ventricular
function.
 Radioisotope studies:
Technetium 99m
 Hemodynamic Measurement:
Diagnosis and
Differential Diagnosis
Complications
 Dysfunction or rupture of
papillary muscle
 Rupture of the heart
 Embolism
 Ventricular aneurysm
 Postmyocardial infarction
syndrome
 Shoulder-hand syndrome
Treatment

 Monitoring: coronary care unit

(CCU)
 Rest and bedside care
 Oxygen
 Relief of pain :give morphine
sulfate, 3~5mg IV slowly.
nitroglycerin can be given
sublingually
Drugs
 Nitroglycerin
 Beta block
 Calcium channel blockers
 Angiotensin converting enzyme
inhibitor (ACEI)
 Anti-platelet agents
Aspirin 300mg qd
Clopidogrel 75mg qd
Drugs
 Anti-coagulation agents
LMWH (Low-molecular-weight
Heparins )
Enoxaparin 1 mg/kg SC q12h
Fraxiparine 5000u SC q12h
Lipid-lowering drugs:Statin
agents
Atorvastatin 20mg qn
Thrombolytic therapy
 Thrombolytic therapy is indicated for MI
and ST segment elevation greater than
0.1 mV in 2 contiguous EKG leads, or
new onset of a bundle branch block,
who present less than 12 hours but not
more than 24 hours after symptom
onset.
 Intravenous streptokinase and
recombinant tissue-type plasminogen
activator (rt-PA)
 the "door-to-needle" time is 30 minutes
or less
Percutaneous Coronary
Intervention(PCI)
 Emergency PCI is recommended
for patients present within 6h of
onset of pain
 "door-to-balloon" time: 90 minutes
 PCI provides a definite survival
advantage over fibrinolysis for MI
patients who are in cardiogenic
shock
PCI-6
TIMI grading system:

 Grade 0 = complete occlusion of the

infarct-related artery.
 Grade 1 = some penetration of the
contrast material beyond the point of
obstruction but without perfusion of the
distal coronary bed.
 Grade 2 = perfusion of the entire infarct
vessel into the distal bed but with
delayed flow compared with a normal
artery.
coronary artery bypass
graft
CABG
Myocardial Bridging
 secondary prevention
A Aspirin
Anti － anginals
B Betaloe
Blood pressure －－
C Cholesterol
Cigarette
D Diet
Diabetes
E Education
Exercise