1. ‫الرحمن‬ ‫ا‬ ‫بسم‬‫الرحمن‬ ‫ا‬ ‫بسم‬
‫الرحيم‬‫الرحيم‬
{{‫زدني‬ ‫رب‬ ‫وقل‬‫زدني‬ ‫رب‬ ‫وقل‬

2. DR Basem elsaid enany
LECTURER OF CARDIOLOGY
AIN SHAMS UNIVERSITY

3.  Acute myocardial infarction (MI) is defined as death or
necrosis of myocardial cells.
 Myocardial infarction occurs when myocardial
ischemia exceeds a critical threshold and overwhelms
myocardial cellular repair mechanisms that are
designed to maintain normal operating function and
hemostasis.
 Ischemia at this critical threshold level for an
extended time period results in irreversible
myocardial cell damage or death.

4.  From an anatomic or morphologic standpoint, the two
types of MI are
 transmural and
 nontransmural.
 A transmural MI is characterized by ischemic necrosis
of the full thickness of the affected muscle segment(s
 In a nontransmural MI, the area of ischemic necrosis is
limited to either the endocardium or the endocardium and
myocardium.

5.  A more common clinical diagnostic
classification scheme is also based on ECG
findings as a means of distinguishing
between two types of MI—
 one that is marked by ST elevation STEMI
 and one that is not NSTEMI
 The distinction between an ST-elevation MI
and a non-ST-elevation MI also does not
distinguish a transmural from a non-
transmural MI. The presence of Q waves or ST
segment elevation is associated with higher
early mortality and morbidity;

13.  Age
 Gender
 Family history
 Hyperlipidemia
 Smoking
 Hypertension
 Diet
 Diabetes
 Obesity
 High plasma homocysteine levels

14. The most frequent mechanism:
rupture or ulceration of a vulnerable atherosclerotic
Plaque exposes the highly thrombogenic
subendothelium to circulating platelets and
white blood cellsTissue factor activates the extrinsic
coagulation Cascade (Factor VII, and also cleavage of
factor IX, contribute to activation of intrinsic pathway)
activated platelets release powerful promoters of
vasoconstriction and platelet aggregation (thromboxane
A2, serotonin, adenosine diphosphate, and platelet-
activating factor) platelet adhesion and aggregation
 transient thrombosis or subtotal coronary artery
occlusion with dynamic vasoconstriction.

16. If ischemia is neither severe nor prolonged
(usually <20 min) and often recurs at rest, patients
are given a diagnosis of UA. However, if ischemia
lasts longer than 30 minutes (usually 1–2 hr) and
is associated with elevated cardiac markers, a
diagnosis of MI is made.

18. The severity of an MI is dependent on three
factors:
1. The level of the occlusion in the coronary
artery,
2. The length of time of the occlusion
3. The presence or absence of collateral
circulation
 The death of myocardial cells first occurs in
the area of myocardium that most distal to the
arterial blood supply—that is, the
endocardium. As the duration of the occlusion
increases, the area of myocardial cell death
enlarges

20. Ischemia / infarction
chest pain
Diastolic Dysfunction Systolic Dysfunction
cardiac output
catecholamines
MVO2
wall tension
LV diastolic pressurepulmonary
congestion
pO2
(heart rate, BP)

21. Acute infarction,
hours
Acute infarction,
hours to days
Acute
infarction,
days to months

22. HOW TO DIAGNOSE STEMI
1-CLINICAL PICTURE
2-ECG
3-BIOMARKERS

23.  The degree of symptoms ranges from
none at all to sudden cardiac death.
 An asymptomatic MI is not
necessarily less severe than a
symptomatic event; but patients who
experience asymptomatic MI's are
more likely to be diabetic.

24.  Chest pain described as a pressure sensation,
fullness, or squeezing in the midportion of the
thorax or heavy weight or burning or stabbing
 The pain is usually retrosternal in location,
spreading frequently to both sides of the
anterior chest, with predilection for the left
side.
 Radiation of chest pain into the jaw/teeth,
shoulder, arm (sometimes ulnar aspect of the
left arm producing a tingling sensation in the
left wrist, hand, and fingers. ), and/or back
 In some instances, the pain of AMI may begin
in the epigastrium and simulate a variety of
abdominal disorders, a fact that often causes
<MI> to be misdiagnosed as “indigestion

25.  Associated dyspnea or shortness of breath
 Associated epigastric discomfort with or
without nausea and vomiting
 Associated diaphoresis or sweating
 Syncope or near-syncope without other
cause
 Impairment of cognitive function without
other cause

26.  In patients with preexisting angina pectoris,
the pain of infarction usually resembles
that of angina with respect to location.
However, it is generally much more severe,
lasts longer, and is not relieved by rest and
nitroglycerin.
 In some patients, particularly the elderly,
AMI is manifested clinically not by chest
pain but rather by symptoms of <acute>
left ventricular failure and chest tightness
or by marked weakness or frank syncope.

29.  AMI may occur at any time of the day, but
most appear to be clustered around the
early hours of the morning and/or are
associated with demanding physical
activity.
 Approximately 50% of patients have some
warning symptoms (angina pectoris or an
anginal equivalent) prior to the infarct.

30.  20 and 60 percent of nonfatal <MIs> are unrecognized
by the patient and are discovered only on subsequent
routine ECG or postmortem examinations.
 Of these unrecognized infarctions, approximately half
are truly silent.
 The other half of patients with so-called silent
infarction can recall an event characterized by
symptoms compatible with <acute> infarction when
leading questions are posed after the ECG
abnormalities are discovered.
 Unrecognized or silent infarction occurs more
commonly in patients without antecedent angina
pectoris and in patients with diabetes and
hypertension.

31. 31

32.  Pulse rate , may be normal,or bradycardia,
tachycardia, or irregular pulses.
 Up to 60% of patients with AMI present with
diaphoresis.
 Inspiratory rales and an S3 gallop are
associated with left sided failure.

33.  EKG
 12 lead EKG
 ST elevation (>0.05 mV)

34.  Localized change
 Reciprocal changes (v1-v6,I and aVL S-T E ; II,III , aVF S-T
D)
 Progressive changes
<2hr hyperacute T waves
<4hr ST segment elevation
 New elevation at the J point in 2+ contiguous leads
16-24hr ST back to baseline , T wave inversion
Weeks : Q waves usually persist

43.  ST segment elevation V4R highly predictive of
RV infarct
 Higher in-hospital mortality
 Higher incidence of in-hospital complications

47.  Concordant ST segment elevation >1mv
highly suggestive of AMI .
 ST segment depression >1 mV in leads
V1,V2,or V3 highly suggestive of AMI.
 Discordant STsegment elevation >5mm
suggestion of AMI.

50.  Troponin: High sensitivity, high specificity
for myocardial tissue
 CK-MB: less tissue specific, but better
specificity for irreversible injury
 Myoglobin: for rapid diagnosis

53. Protein
Molecular
mass (kD)
First
detection
Duration of
detection
Sensit
ivity
Specif
icity
Myoglobin 16 1.5–2
hours
8–12 hours +++ +
CK-MB 83 2–3
hours
1–2 days +++ +++
Troponin I 33 3–4
hours
7–10 days ++++ ++++
Troponin T 38 3–4
hours
7–14 days ++++ ++++
CK 96 4–6
hours
2–3 days ++ ++

57. ECHOCARDIOGRAPHY
 Unfortunately, the presence of wall motion
abnormalities on the echocardiogram may be due
to an acute MI or previous (old) MI or other
myopathic processes.
 Thus, the usefulness of echocardiography in the
diagnosis of MI is limited.

61. ‫بحمد‬ ‫تم‬‫بحمد‬ ‫تم‬
‫ا‬‫ا‬