Myocardial infarction

Disscused with head Supervisor:

Dr.yassmeen Ahmed
of Pathology
department:Prof.Dr.Manal El-nemr.
This research contains the following:
-Chapter 1: General overview "introduction" of
myocardial infarction
-Chapter 2: Review of the (causes, types, mechanisms,
Morphology, prevention, control and management
"treatment" and Epidemiology)
Chapter 3: Conclusion of the research -
Chapter 4: References
Chapter 1:
An overview of infarctions and myocardial infarction:

Infarction:
is tissue death (necrosis) due to inadequate blood supply to the
affected area.
It occurs as a result of prolonged ischemia.
Due to >>>>
An obstruction in the vessel,
External compression of the vessel narrowing it (1)
ruptured by trauma
Hypertension and atherosclerosis are risk factors for
atherosclerotic plaques and thromboembolism
 Myocardial infarction: is the partial death of heart tissue commonly
known as a heart attack.

MI can cause cardiac arrest and heart filature.

* cardiac arrest: the heart is not contracting at all or so poorly
that all vital organs cease to function, thus causing death.
* heart failure: the pumping action of the heart is impaired.
Most MIs occur due to coronary artery disease.
Risk factors: high blood pressure, smoking, diabetes, obesity,
high blood cholesterol, poor diet, and excessive alcohol intake.
MIs are less commonly caused by coronary artery spasms,
which may be due to cocaine, significant emotional stress, and
extreme cold.
MIs diagnosis:

Electrocardiograms (ECGs) >>> May confirm ST

elevation MI (STEMI
Blood tests >>> troponin and less often creatine
kinase MB.
Coronary angiography.
 Classification
According to etiology:
Type 1: MI due to plaque rupture
Type 2: MI due to myocardial oxygen supply-demand imbalance.

Myocardial injury (acute / chronic): Patients with myocardial necrosis,

but no symptoms or signs of myocardial ischemia
Myocardial injury and type 2 MI are common, > 1/3 of hospitalized
patients.
They have poor short-term and long-term outcomes with two-thirds dead
in 5 years.
Introduction:
Myocardial infarction: is the partial death of heart tissue as a result of
prolonged ischemia commonly known as a heart attack.

Symptoms
1- chest pain / discomfort which may travel into the shoulder, arm, back,
neck, or jaw. It lasts for more than a few minutes.
2- Others: shortness of breath, nausea, feeling faint, a cold sweat, or
feeling tired.
3- 5% of Patients over 75 years old, had an MI with little / no history of
symptoms.
4- An MI may cause heart failure, an irregular heartbeat, cardiogenic
shock, or cardiac arrest .
Treatment of an MI is time critical.
* Aspirin.
*Nitroglycerin or opioids
 classification:
Type 1: MI due to thrombosis of an atherosclerotic plaque
Type 2: myocardial infarction due to myocardial oxygen supply-demand
imbalance.
Type 3: MI presenting as sudden death.
Type 4: MI after percutaneous coronary intervention
Type 5: coronary artery bypass grafting
Acute myocardial injury : troponin concentrations are elevated
chronic myocardial injury :troponin concentrations remain unchanged on serial
testing.
 Causes of myocardial infarction
A-Atherosclerosis and high levels of blood cholesterol: is a known risk factor.
Atherosclerosis is narrowing of the artery due to the build of plaque. It limits the flow of
oxygen-rich blood to parts of the body
The cause is not known.
Risk factors include high blood pressure, diabetes, smoking, obesity, family history, and an
unhealthy diet.
Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood.
Diagnosis is based upon a physical exam, ECG, and exercise stress test
Prevention is generally by eating a healthy diet, exercise, not smoking, and maintaining a
normal weight.
Treatment medications to lower cholesterol such as statins, blood pressure medication, or
medications that decrease clotting, such as aspirin.
procedures such as percutaneous coronary intervention, coronary artery bypass graft,
or carotid endarterectomy.
B-Genetics: The heritability of coronary artery disease has been estimated between
40% and 60%.Genome-wide association studies have identified around 60 genetic
susceptibility loci for coronary artery disease.

C-hypertension: In general, the heart problems associated with high blood pressure relate
to the hearts arteries and muscles:
1>Arteries : Narrowing of the arteries: The excess strain and resulting damage from high
blood pressure causes the coronary arteries to slowly become narrowed from a
buildup of fat, cholesterol and other substances that together are called plaque.

2>Heart muscle: Thickening and enlargement of the heart

These changes usually happen in the left ventricle. The condition is known as left
ventricular hypertrophy (LVH).
3-Thrombotic or embolic events:
Thrombosis is the formation of a blood clot inside a blood vessel, obstructing
the flow of blood through the circulatory system.
When a blood vessel is injured, the body uses platelets (thrombocytes)
and fibrin to form a blood clot to prevent blood loss.
Even when a blood vessel is not injured, blood clots may form in the body
under certain conditions.
A clot, or a piece of the clot, that breaks free and begins to travel around the
body is known as an embolus.

4-Other Important Factors :

old age, diabetes mellitus ,alcohol use, Diet , actively smoking, obesity:
 pathogenesis: -
The pathogenesis can include:
Occlusive intracoronary thrombus - a thrombus overlying a plaque causes 75% of
myocardial infarctions, with superficial plaque erosion present in the remaining
25%.
Vasospasm - with or without coronary atherosclerosis and possible association
with platelet aggregation.
Emboli - from left sided mural thrombosis, vegetative endocarditis, or paradoxid
emboli from the right side of heart through a patent foramen ovale.

>>> The most common mechanism of MI is the rupture of an atherosclerotic

plaque on an artery supplying heart muscle, promote the formation of a blood
clot that blocks the artery
Atherosclerosis is gradual buildup of cholesterol and fibrous tissue in plaques
in the wall of the arteries.
Atherosclerosis is characterized by progressive inflammation of the walls of
the arteries.
Inflammatory cells, particularly macrophages, move into affected arterial
walls. Over time, they become laden with cholesterol products,
particularly LDL, and become foam cells.
A cholesterol core forms as foam cells die.
In response to growth factors secreted by macrophages, smooth muscle and
other cells move into the plaque and act to stabilize it.
A stable plaque may have a thick fibrous cap with calcification. If there is
ongoing inflammation, the cap may be thin or ulcerate. Exposed to the
pressure associated with blood flow, plaques, especially those with a thin
lining, may rupture and trigger the formation of a blood clot
(thrombus). The cholesterol crystals have been associated with plaque
rupture through mechanical mechanism and inflammation.
 B>Tissue death :
If impaired blood flow to the heart lasts long enough, it triggers a process called
the ischemic cascade; the heart cells in the territory of the blocked coronary artery
die (infarction), chiefly through necrosis, and do not grow back.

A collagen scar forms in their place. When an artery is blocked, cells lack oxygen,
needed to produce ATP in mitochondria. ATP is required for the maintenance of
electrolyte balance >> particularly through the Na/K ATPase. This leads to an
ischemic cascade of intracellular changes, necrosis and apoptosis of affected cells.

Cells in the area with the worst blood supply, just below the inner surface of the heart
(endocardium), are most susceptible to damage. Ischemia first affects this region,
the subendocardial region, and tissue begins to die within 1530 minutes of loss of
blood supply.
Tissue death and myocardial scarring alter the normal conduction pathways of the
heart, and weaken affected areas. The size and location puts a person at risk
of abnormal heart rhythms (arrhythmias) or heart block, aneurysm of the heart
ventricles, inflammation of the heart wall following infarction, and rupture of the
heart wall
C>other causes<mechanisms>A myocardial infarction may result
from a heart with a limited blood supply subject to increased
oxygen demands, such as in fever, a fast heart
rate, hyperthyroidism, too few red blood cells in the
bloodstream, or low blood pressure. Damage or failure of
procedures such as percutaneous coronary
intervention or coronary artery bypass grafts may cause a
myocardial infarction. Spasm of coronary arteries may cause
blockage
Point 5: Morphology:
 Treatment and Control:
>>A myocardial infarction requires immediate medical attention.
Treatment aims to preserve as much heart muscle as possible, and to prevent
further complications depending on whether the myocardial infarction is
a STEMI or NSTEMI.
Treatment in general aims to unblock blood vessels, reduce blot clot
enlargement, reduce ischemia, and modify risk factors with the aim of
preventing future MIs.
The main treatment for MI with ECG evidence of ST elevation (STEMI)
include thrombolysis or percutaneous coronary intervention
Pain: treated with nitroglycerin or morphine.
Coagulation: Anticoagulants like:Aspirin, an antiplatelet anticoagulant
Angiogram:Primary percutaneous coronary intervention (PCI) is the
treatment of choice for STEMI.
 Epidemiology:
The World Health Organization estimated in 2004, that 12.2% of
worldwide deaths were from ischemic heart disease; with it
being the leading cause of death in high- or middle-income
countries and second only to lower respiratory
infections in lower-income countries.

Worldwide, more than 3 million people have STEMIs and 4

million have NSTEMIs a year. STEMIs occur about twice as
often in men as women.
 Conclusion:
>>MI occurs when blood flow decreases or stops to a part of the heart, causing damage to
the heart muscle.
Most MIs occur due to coronary artery disease.
Risk factors include high blood pressure, smoking, diabetes, lack of exercise, obesity, high
blood cholesterol, poor diet, and excessive alcohol intake, among others.
The complete blockage of a coronary artery caused by a rupture of an atherosclerotic
plaque is usually the underlying mechanism of an MI.
MIs are less commonly caused by coronary artery spasms,
Diagnosis, including electrocardiograms (ECGs), blood tests, and coronary angiography. An
ECG, which is a recording of the heart's electrical (4.4)
activity, may confirm an ST elevation MI (STEMI) if ST elevation is present. Commonly used
blood tests include troponin and less often creatine kinase MB
.>> Treatment of an MI is time critical.
Aspirin
Nitroglycerin or opioids.
In a STEMI, treatments attempt to restore blood flow to the heart,
and include percutaneous coronary intervention (PCI),
thrombolysis
People who have a non-ST elevation myocardial infarction (NSTEMI)
are often managed with the blood thinner heparin, with the
additional use of PCI in those at high risk.
>>Prevention is done by changing in life style and treatment of
underlying risk diseases like: DM and hypertension.
 References:

-Robbins Pathologic Basis of Disease (1.2) (1.3) (1.4)

-William boyd: textbook of pathology (2.1)(2.2) (2.3)(2.4)
-Pathology Illustrated by Robin Reid (3.1)(3.2)(3.3)(3.4)
-Rapid Review Pathology by Edward F. Goljan (4.1) (4.2)
-Robbins and Cotran Review of Pathology (4.3) by Edward Klatt
-Muir's textbook of pathology. (4.4)