MYOCARDIAL INFARCTION

INTRODUCTION-
The heart requires a balance between oxygen supply and oxygen demand in order to function
properly .The integrity of coronary arteries is an important determinant of oxygen supply to
the heart muscle .Any disorder that reduces the lumen of one of the coronary arteries may
cause a decrease in blood flow and oxygen delivery to the area of the myocardial supplied by
that vessel and lead to acute coronary syndrome of angina , acute myocardial
infarction(AMI) and sudden death.

DEFINITION
MYOCARDIAL INFARCTION is the rapid development of myocardial necrosis caused by a
critical imbalance between oxygen supply and demand of the myocardium. This 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.

INCIDENCE
 Every 29 seconds an American suffers a coronary event and every 1 minute someone dies
of a coronary event.

 Sixty-two per cent of the men and88% of the women had clinically silent CHD in INDIA
 About 250,000 people a year dies of a coronary event without reaching a hospital
 Studies indicate that half of all AMI victims wait more than before getting help
 On the basis of data from the Framingham study , about 45% of all AMIs occur in people
younger than age 65 years and 5% occur in those younger than age 40 .
 85%of people ,who die of AMI are 65 years of age or older.

ETIOLOGY :

The most common cause of Myocardial Infarction is complete or nearly complete occlusion
of a coronary artery , usually precipitated by rupture of a vulnerable atherosclerotic plaque
and subsequent thrombus

formation. Plaque rupture can be precipitated by

 EXTERNAL FACTORS
 INTERNAL FACTORS
1. EXTERNAL FACTORS :

 Strenuous physical activity

 Severe emotional stress
 Sympathetic activity
 Exposure to cold and during morning time.
 Acute sever infection like pneumonia

2.INTERNAL FACTORS:

 Consistency of the lipid core around plaque

 Thickness of the fibrous cap around plaque
 Increased coagulation status of blood
 Degree of arterial vasoconstriction.

Risk factors of myocardial infarction

 MODIFIABLE RISK FACTORS

 NON-MODIFIABLE RISK FACTORS

 MODIFIABLE RISK FACTORS

 Tobacco Smoking , Hypercholesterolemia (more accurately

hyperlipoproteinemia, especially high low density lipoprotein and low high
density lipoprotein)
 Low HDL
 High Triglycerides
 High blood pressure
 Hyper homocysteinemia (high homocysteine, a toxic blood amino acid that
is elevated when intakes of vitamins B2, B6, B12 and folic acid are insufficient)
 Stress (occupations with high stress index are known to have susceptibility
for atherosclerosis)
 Alcohol Studies show that prolonged exposure to high quantities of alcohol
can increase the risk of heart attack
 Obesity] (defined by a body mass index of more than 30 kg/m², or
alternatively by waist circumference or waist-hip ratio).
 Diabetes (with or without insulin resistance) - the single most important risk factor for
ischaemic heart disease (IHD) Use of Combined Oral Contraceptive
 Stress is also a leading cause of MI
 Type A personality
 Sedentary life style

 NON MODIFIABLE RISK FAVTORS

 HEREDITY : Family history of ischaemic heart disease (IHD)
 SEX:
Men acquire an independent risk factor at age 45,

Women acquire an independent risk factor at age 55;

In addition individuals acquire another independent risk factor if they have a first-degree
male relative (brother, father) who suffered a coronary vascular event at or before age 55.
Another independent risk factor is acquired if one has a first-degree female relative
(mother, sister) who suffered a coronary vascular event at age 65 or younger.
Males are more at risk than females

 AGE

Increasing age is a leading risk factor of myocardial infarction

 INDEPENDENT RISK FACTOR

Socioeconomic factorseg lower income and ignorance.

Presence of C-reactive protein.(CRP).
Baldness, hair graying, a diagonal earlobe crease (Frank's sign) .

TYPES OF MYOCARDIAL INFARCTION

1.TRANSMURAL 2.SUBENDOCARDIAL

 Transmural: associated with atherosclerosis involving major coronary artery.

It can be subclassified into a) anterior b) posterior, c) inferior.

Transmural infarcts extend through the whole thickness of the heart muscle and
are usually a result of complete occlusion of the area's blood supply.

 Subendocardial: involving a small area in the subendocardial wall of the left ventricle,
ventricular septum, or papillary muscles. Subendocardial infarcts are thought to be a result of
locally decreased blood supply, possibly from a narrowing of the coronary arteries.

The subendocardial area is farthest from the heart's blood supply and is more susceptible to
this type of pathology.

CLASSIFICATION ACCORDING TO ECG CHANGES:

A) ST elevation MI (STEMI)
B) non-ST elevation MI (non-STEMI)

A 2007 consensus document classifies myocardial infarction into five main types:
 Type 1 - Spontaneous myocardial infarction related to ischaemia due to a primary
coronary event such as plaque erosion and/or rupture, fissuring, or dissection
 Type 2 - Myocardial infarction secondary to ischaemia due to either increased oxygen
demand or decreased supply, e.g.

a)coronary artery spasm, d) arrhythmia

b) coronary embolism, e) hypertension

c) anaemia, f)hypotension

 Type 3 - Sudden unexpected cardiac death, including cardiac arrest, often with symptoms
suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new
LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy,
but death occurring before blood samples could be obtained, or at a time before the
appearance of cardiac biomarkers in the blood
 Type 4 - Associated with coronary angioplasty or stents:
o Type 4a - Myocardial infarction associated with PCI
o Type 4b - Myocardial infarction associated with stent thrombosis as documented
by angiography or at autopsy
 Type 5 - Myocardial infarction associated with CABG
CLINICAL MANIFESTATION
The clinical manifestations associated with AMI result from ischemia of the heart muscle and
the decrease in function and acidosis associated with it.

 Chest pain – The pain may radiate to the neck , jaw , shoulder , back , or left arm.
Atypical chest , stomach , back or abdominal pain.
 described as a sensation of tightness, pressure, or squeezing.
 Levine's sign, in which the patient localizes the chest pain by clenching their fist over the
sternum, has classically been thought to be predictive of cardiac chest pain, although a
prospective observational study showed that it had a poor positive predictive value.
 Nausea or dizziness
 Shortness of breath and difficulty breathing , pulmonary edema
 Unexplained anxiety , weakness or fatigue
 Palpitation , cold sweat or paleness induced by a surge of catecholamine
 Anxiety may accompany the pain.
Women experiencing AMI frequently present with one or more of the less common clinical
manifestation.
 Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and
 Sudden death (frequently due to the development of ventricular fibrillation
Approximately one fourth of all myocardial infarctions are silent, without chest pain or
other symptoms.
These cases can be discovered later on electrocardiograms, using blood enzyme tests or at
autopsy without a prior history of related complaints.
A silent course is more common in the elderly, in patients with diabetes mellitus and after
heart transplantation, probably because the donor heart is not connected to nerves of the host.
In diabetics, differences in pain threshold, autonomic neuropathy, andandpsychological
factors have been cited as possible explanations for the lack of symptoms.

DIAGNOSIS EVALUATION
It is recommended that all clients with a suspected AMI (ischemia – type chest discomfort )
ingest aspirin and obtain baseline cardiac serum markers and a 12 –lead ECG within 10
minutes of arrival in the emergency department

 Electrocardiography
 Laboratory Tests
 Imaging Studies
a) ELECTROCARDIOGRAPY
When blood flow to the heart is decreased , ischemia and necrosis of the heart muscle occur .
These conditions are reflected in altered Q wave , ST segment and T wave on the 12 lead
ECG

Tweleve- lead ECG examines the heart from 12 views , with the view provided from 12
view provided from the V5 lead being the most sensitive in detecting abnormalities .
The Q wave change is significant ; normally the Q wave is small or absent.
Ischemic tissue produces an elevation in the ST segment and a peaked T wave , and
finally the Q wave.
As the myocardium heals , the ST segment and T waves return to normal , but the Q
wave changes persist.
However , an ECG can be completely normal in a client with AMI , especially in the early
hours following infarct.

HOLTER MONITORING(AMBULATORY ECHOCARDIOGRAPHY) :

It is used to detect the dysrhytmias in contiuous basis that may not be detected on a routine
ECG .
LABORATORY DIAGNOSIS
CK-MB : Serum level of CK-MB increases 3 to 6 hours after the onset of chest pain ,
peak in 12 to 18 hours , and return to normal level in 3 to 4 days.
Myoglobin :Myoglobin is a heme protein found in striated muscle fibers.it is rapidly
released when myocardial muscle tissue is damaged . So it can be detected within 2 hours
after AMI.
TROPONIN : The cardiac troponin complex is a basic component of the myocardium
that is involved in the contraction of the myocardial muscle . Cardiac troponin T and I are
more sensitive to cardiac muscle damage than cardiac troponin C.
 Cardiac troponin level increases within to 6 hours after pain has started .Level remain
increased for 14 to 21 days.
 Cardiac troponin I level increases 7 to 14 hours after AMI . Elevation persists for 5 to 7
days
LACTIC DEHYDROGENASE :The LDH is plentiful in heart muscle . Serum level of
LDH elevate 14 to 24 hours after the onset of myocardial damage , peak within 48 to 72
hours , and slowly return to normal over the next 7 to 14 days.
AST : Serum level of AST increases within several hours after the onset of chest pain ,
peak within 12 to 18 hours , and return to normal within to 4 days.
LEUKOCYTOSIS : Leukocytosis ( 10,000 to 20,000 mm3) appears on the second day
after AMI disappears in 1 week .

IMAGING STUDIES
1.Radionuclide imaging studies provide information on the presence of coronary artery
disease as well as the location of ischemic and infracted tissue.

 COLD SPOTS : It is done when client have sudden chest pain .Imaging is done with
radionuclide agents such as thallium , sestamibi , and teboroxime , which helps to identify
infracted tissue.
 HOT SPOTS : This imaging method is useful for those clients who presents to hospital
with the history of chest pain several days after an AMI. Technetium 99 – tagged
pyrophosphate binds with calcium in areas of myocardial necrosis.
2. POSITRON EMISSION TOMOGRAPHY.:It is used to evaluate cardiac metabolism
and to asses tissue perfusion.
3. MAGNETIC RESONANCE IMAGING :It helps to identify the site and extent of an
MI , assess the effects of reperfusion therapy , and differentiate reversible and irreversible
tissue injury.
4. ECHOCARDIOGRAPHY : It is used in assessing the ability of the heart walls to
contract and relax. The transducer is placed on the chest and images are relayed to a monitor
screen.
5. TRANSESOPHAGEAL ECHOCARDIOGRAPHY : It is an imaging technique in
which the transducer is placed against the wall of the esophagus. This technique is used for
viewing the posterior wall of esophagus.

MEDICAL MANAGEMENT
Major goals of care for clients with AMI include the following

 INITIATING PROMPT CARE

 REDUCING PAIN
 DELIVERING SUCCESSFUL TREATMENT FOR THE ACUTE PAIN AND
REPERFUSION OF THE MYOCARDIUM
 PREVENTING COMPLICATIONS
 PREVENTING REMODELING AND HEART FAILURE
 REHABILITATING AND EDUCATING THE CLIENT AND SIGNIFICANT
OTHERS.
 TREAT THE ACUTE ATTACK IMMEDIATELY
The goal for treatment of AMI is ‘’door to needle’’
 Ie. in less than 30 minutes.
 Or specifically from onset of pain till Thrombolytic Therapy within 30 minutes
 Percutaneous angioplasty within 1 hour.
It is recommended that , if conscious , a client can chew an aspirin with the onset of
manifestations, alone, because mortality may reduced with this action alone.
 The client is given oxygen , an intravenous line is inserted and client is connected to
monitor.
 12 lead ECG monitoring is done within 10 minutes of admission.
 Serum cardiac markers are drawn.
 If client is unconscious then defibrillation or cardiopulmonary resuscitation is started.
 REDUCE PAIN
Pain control is priority , and pain is controlled mainly by giving IV Morphine. Continued
pain is a manifestation of myocardial ischemia.

Pain also stimulates the autonomic nervous system and increases preload, which in turn
increases Myocardial Oxygen demand.

 MONITOR HEART RHYTHM

Because Dysrhythmia is common ,so ECG monitoring is essential and antidysrhythmic
medication should be at hand.

 IMPROVE PERFUSION
The general principal of improving perfusion is :

Pharmacologic
therapy

Non surgical
treatment

Surgical treatment.
 PHARMACOLOGIC THERAPY
a. ANTIPLATELET AGENTS:
 The use of aspirin has been shown to reduce mortality from MI.
 Aspirin in a dose of 325 mg should be administered immediately on recognition of MI
signs and symptoms.
 Aspirin irreversibly interferes with function of cyclooxygenase and inhibits the
formation of thromboxane A2.
 Within minutes, aspirin prevents additional platelet activation and interferes with platelet
adhesion and cohesion.

This effect benefits all patients with acute coronary syndromes, including those with
amyocardial infarction.

 Aspirin alone has one of the greatest impacts on the reduction of MI mortality.
 Its beneficial effect is observed early in therapy and persists for years with continued
use. The long-term benefit is sustained, even at doses as low as 75 mg/day.

CLOPIDOGREL is also used as an antiplatelet agent .But the researches shows that if
clopidogrel is used along with aspirin then it