Acute myocardial

Infarction

Frequency
AMI is a leading cause of morbidity and mortality
in all European countries. Approximately 1.3
million cases of nonfatal AMI are reported each
year.
Mortality/Morbidity:
Approximately 500,000-700,000 deaths caused
by ischemic heart disease occur in the United
States alone.
More than one half of deaths occur in the
prehospital setting.
In-hospital fatalities account for 10% of all
deaths. An additional 10% of deaths occur in the
first year postinfarct.

Within six years after a heart

attack:

18 percent of men and 35 percent of women will

have another heart attack.
7 percent of men and 6 percent of women will
experience sudden death.
22 percent of men and 46 percent of women will
be disabled with heart failure.
8 percent of men and 11 percent of women will
have a stroke

Acute myocardial infarction (AMI)

is the rapid development of myocardial

necrosis caused by a critical imbalance
between the oxygen supply and demand
of the myocardium.

Myocardial infarction

usually results from plaque rupture with

thrombus formation in a coronary vessel,
resulting in an acute reduction of blood
supply to a portion of the myocardium.

Conditions that may cause acute

myocardial infarction

Coronary emboli (left atrial or ventricular

thrombi, infective myocarditis, intracardiac
neoplasms, other)
Coronary vasculitis (polyarteritis nodosa,
rheumatism, Takayasus disease, other)
Trombotic coronary artery disease (sickle cell
anemia, thrombotic thrombocytopenic purpura,
leukemia, other)
Congenital coronary anomalies
Other

Transmural infarcts involve the whole thickness of

myocardium from epicardium to endocardium and are
usually characterized by abnormal Q waves on ECG.
Nontransmural (subendocardial or subepicardial)
infarcts do not extend through the ventricular wall and
cause only ST segment and T-wave abnormalities.
Myocardial
Infarction

Transmural
Myocardial
Infarction

Nontransmural
Myocardial
Infarction

Because the transmural depth of necrosis cannot

be precisely determined clinically, infarcts are
better classified by ECG as Q wave and non-Q
wave.
Myocardial
Infarction

Q-wave
Myocardial
Infarction

Non-Q-wave
Myocardial
Infarction

Note!

MI is predominantly a disease of the LV,

but damage may extend into the right
ventricle (RV) or the atria. RV infarction
usually results from occlusion of the right
coronary or a dominant left circumflex
artery and is characterized by high RV
filling pressure, often with severe tricuspid
regurgitation and reduced cardiac output.

Pathogenesis

The life history of an atheroma.

The normal human coronary artery has a typical

trilaminar structure.

In early atherogenesis, recruitment of

inflammatory cells and the accumulation of lipids
lead to formation of a lipid-rich core.

If inflammatory conditions prevail the lipid

core may grow, and proteinases secreted
by the activated leukocytes may degrade
extracellular matrix, whereas
proinflammatory cytokines such as
interferon- can limit the synthesis of new
collagen. These changes can thin the
fibrous cap and render it friable and
susceptible to rupture.

With plaque rupture, elements of the bloodstream are

exposed to the highly thrombogenic lipid-, tissue-factor-,
and collagen-containing plaque core and matrix.
Platelets adhere, become activated, and aggregate;
vasoconstrictive and thrombogenic mediators are
secreted; vasospasm occurs; thrombin is generated and
fibrin formed; and a partially or totally occlusive plateletand fibrin-rich thrombus is generated.

When coronary flow is occluded, STelevation acute MI developed. Partial

occlusion, occlusion in the presence of
adequate collateral circulation, and/or
distal coronary embolization results in
unstable angina or non-ST-elevation MI

Criteria for diagnosis:

Typicall clinical picture
ECG
Cardiac enzyms
Note!!! 2 of 3 criteria are necessary to
determinate the diagnosis.

Symptoms can include:

Discomfort, pressure, heaviness, or pain in the

chest, arm or below the breastbone
Discomfort radiating to the back, jaw, throat or
arm
Fullness, indigestion or choking feeling (may feel
like heartburn)
Sweating, nausea, vomiting or dizziness
Extreme weakness, anxiety or shortness of
breath
Rapid or irregular heartbeats

Clinical types of AMI

Anginous form
Astmatic form
Abdominal form
Painless (silent) form
Cerebrovascular form
Arrythmic form

Anginous form

The caracter of pain varies: the patient may feel

constriction, compression, heaviness, burning.
Pain locates in the centre of sternum (retrosternal pain),
or in the left arm, or in the left shoulder, or in the region
of the heart, or in the all chest
Pain radiates into left shoulder, into left arm, neck
Pain is usually sever and the patient develops fear of
death
Pain persists for long time (longer than 20 minutes)
Pain is not removed by nitroglycerin

Astmatic form
Attack of dyspnea
Or pulmonary oedema
!!! Without chest pain!!!
Occurs mostly in patients with secound
infarction

Abdominal form
Pain in the abdomen (mostly in the
epigastrium region)
Nausea
Vomiting
This form occurs mostly in patients with
infarction of posterior wall of the left
ventricle.

Painless (silent) form

Elderly patients and patients with diabetes

are particularly prone to painless MI

Cerebrovascular form
Headache
Dizzines
Disturbance of vision
Disturbance of consciousness
Acute psychosis

Arrythmic form

new rhythm disorders or conduction

disorders without chest pain (ventricular
fibrillation, ventricular tachycardia, sudden
death, sino-atrial or atrio-ventricular
blocks)

Physical examination
Frequently, physical examination
findings are normal.
Patients with ongoing symptoms usually
will lie quietly in bed and appear pale.
Hypertension.
Hypotension.
Dysrhythmias

Physical examination

Acute valvular dysfunction may be present.

This

dysfunction usually involves the papillary muscle.

New or worsening mitral regurgitant murmur may be
noted.

Congestive heart failure (CHF) may occur.

Neck

vein distention
Third heart sound (S3)
Rales on pulmonary examination

Electrocardiographic
examination

The electrocardiogram
is the most important tool.
It may be normal in the very early
stages of an acute myocardial infarction
and therefore should be repeated after half
an hour.
The earliest sign is the hyperacute T
wave, followed by ST segment elevation,
T wave inversion, and Q waves.

Localization of AMI based on

distribution of ECG abnormalities is as
follows:
Inferior wall - II, III, aVF
Lateral wall - I, aVL, V4-V6
Anteroseptal - V1-V3
Anterolateral - V1-V6

Thus an anterior myocardial infarction

produces ST elevation in leads V2-V4

Inferior myocardial infarction in

leads II, III, aVF

NOTE! New onset left bundle branch block

can also signify an acute myocardial
infarction

Laboratory
examinations

SERUM CARDIAC MARKERS

The increasing sensitivity and specificity of

serum cardiac markers have made them the
"gold standard" for detection of myocardial
necrosis.
Note! However, because there is a delay of from
1 to 12 hours after onset of symptoms before
markers become detectable or diagnostic, the
decision to the treatment strategy must be
based on the clinical history and initial ECG.

SERUM CARDIAC MARKERS

serum cardiac markers of acute MI are

macromolecules (proteins) released from
myocytes undergoing necrosis. Clinically
ideal markers are not present normally in
serum, become rapidly and markedly
elevated during acute MI, and are not
released from other injured tissues.

Creatine kinaseMB (CK-MB)

Levels

begin to rise within 4 hours after injury,

peak at 18-24 hours, and subside over 3-4
days.
Serial sampling over periods of 6-9 hours has
the sensitivity to nearly 90%.

Troponin I and T
For

early detection of myocardial necrosis,

sensitivity of this study is superior to that of
the CK-MB. Troponin I is detectable in serum
3-6 hours after an AMI, and its level remains
elevated for 14 days.
Troponin T has similar release kinetics and
specificity for myocardial necrosis, but it is
slightly less sensitive than troponin I within the
first 6 hours.

OTHER NONSPECIFIC MARKERS

Myoglobin This is a very sensitive early marker of

acute myocardial necrosis, but it is not specific for
myocardial cell necrosis.

LDH, aspartate serum transaminase (AST,

formerly SGOT), and myosin light chain assays
are not recommended because of lower specificity
and sensitivity than cTnI, cTnT, and CK-MB.

Complete blood count

Leukocytosis

may be observed within several

hours after an AMI. It peaks in 2-4 days and
returns levels within the reference range
within 1 week.
CBC may be useful if anemia is suspected as
a precipitant.
Erythrocyte sedimentation rate (ESR) rises
above reference range values within 3 days
and may remain elevated for several weeks.

Treatment

First step

Aspirin should be given to all patients

unless contraindicated (125-375 mg)

Treatment
Treatment is designed to relieve distress,
reverse ischemia and limit infarct size,
reduce cardiac work,
prevent and treat complications

RECANALIZATION THERAPY.
(reverse ischemia, limit infarct size)

Early reperfusion of infarcting myocardium

represents the most important for ST-elevation
acute MI and is the primary therapeutic goal.
Coronary recanalization is accomplished by
using thrombolytic (fibrinolytic) therapy or a
primary PCI with angioplasty and, commonly,
stenting.

Thrombolytic therapy:

Streptokinase 1.5 million U infused in 30 to 60 min may

induce allergic reactions, it has a lower incidence of
complicating intracerebral hemorrhage, does not require
concomitant heparin therapy, and is relatively
inexpensive.
Alteplase is used in dosage of 100 mg IV in 90 min as
follows: 15 mg bolus, then 0.75 mg/kg over the next 30
min (maximum 50 mg), followed by 0.50 mg/kg over 60
min (maximum 35 mg). concomitant IV heparin is
recommended. Alteplase is nonallergenic, has a higher
recanalization rate than the other drugs, and is
expensive.
Anistreplase is administered 30 mg IV in 5 min. It has a
long half-life and is allergenic.
Reteplase is similar to alteplase and is given as a 10-U
2-min bolus repeated after 30 min.

Primary percutaneous transluminal

cardiac angioplasty (PTCA):

Using PTCA as initial treatment is at least as

effective and, may be better than thrombolysis in
reducing infarct size, additional cardiac events,
and mortality in patients with elevated ST
segment MI or bundle branch block.
However, only a few acute MI patients have
access to a skilled cardiac catheterization team.

Concomitant antithrombotic
therapy:

The use and route of heparin therapy depends on the

thrombolytic drug used and the thrombolic-embolic
risk.
IV heparin is given with alteplase therapy as a rapid
injection of 70 U/kg with an initial maintenance dosage of
about 15 U/kg/h adjusted to maintain a PTT 1.5 to 2
times control (50 to 75 sec) for 48 h. IV heparin may be
continued > 48 h for patients at high risk for
thromboembolic events.
IV heparin is not currently recommended for adjuvant
therapy with other thrombolytic drugs

Drugs to reduce cardiac work:

-Blockers reduce the incidence of VF and are

recommended if not contraindicated, especially in highrisk patients.
ACE inhibitors appear to reduce mortality in MI
patients, especially in those with anterior infarction, heart
failure, or tachycardia. ACE inhibitors should be given >
24 h after thrombolysis
Vasodilators may be useful for judicious reduction of
myocardial work in selected patients with acute MI.

Complications

Arrhythmia in some form occurs in > 90% of MI patients.

Conduction disturbances can reflect damage to the sinus node, the
atrioventricular node, or specialized conduction tissues.
Heart failure
Cardiogenic shock
Functional papillary muscle insufficiency occurs in about 35% of
patients.
Myocardial rupture occurs in three forms: rupture of the papillary
muscle, rupture of the interventricular septum, and external rupture.
Ventricular aneurysm
Pericarditis
Post-MI syndrome (Dressler's syndrome)