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;
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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 cellsTissue 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.
15.
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.
17.
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
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.
27.
28.
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.
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.
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
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43. ST segment elevation V4R highly predictive of
RV infarct
Higher in-hospital mortality
Higher incidence of in-hospital complications
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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.
48.
49.
50. Troponin: High sensitivity, high specificity
for myocardial tissue
CK-MB: less tissue specific, but better
specificity for irreversible injury
Myoglobin: for rapid diagnosis
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.
The following ECG criteria (in the absence of QRS confounders [i.e., bundle branch block, left ventricular hypertrophy, Wolff-Parkinson-White syndrome]) have emerged as robust determinants for the diagnosis of myocardial ischemia (Table 3). Such ischemic changes may be associated with evolving MI…The ECG criteria in Table 3 reflect myocardial ischemia and are not sufficient by themselves to define MI. The final diagnosis of myocardial necrosis depends on the detection of elevated levels of cardiac biomarkers in the blood
Contiguous in the frontal plane is: aVL, I, aVR, II, aVF, III
New or presumed new ST segment depression or T wave abnormalities, or both, should be observed in two or more contiguous leads on two consecutive ECGs at least several hours apart.
These biomarkers reflect myocardial damage but do not indicate its mechanism. (e.g. myocarditis…)
Biomarkers are more sensitive, more specific and less costly than imaging techniques for the diagnosis of myocardial necrosis. Injury involving &gt;20% of myocardial wall thickness is required before a segmental wall motion abnormality can be detected by echocardiography. In general, &gt;10 g of myocardial tissue must be injured before a radionuclide perfusion defect can be resolved. Neither technique can distinguish ischemia from infarction.
. For patients in need of an early diagnosis, a rapidly appearing biomarker (such as CK-MB isoforms or myoglobin), plus a biomarker that rises later (e.g., cardiac troponin), is recommended for confirmation of the diagnosis
that there is a continuous relation between minimal myocardial damage, characterized by elevation of cardiac troponin without elevation of other cardiac biomarkers (e.g., CK-MB) and large infarcts, characterized by complications such as heart failure or shock
the magnitude of troponin elevations has correlated consistently with the risk of death and the composite risk of death or non-fatal MI, irrespective of whether the patients had ST elevation or non-ST elevation acute coronary syndromes.3 w16–19