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 may be caused by artery blockages, rupture,
mechanical compression or vasoconstriction, the resulting lesion is
referred to as an infarct (from the Latin infarcts, "stuffed into").
-Infarction occurs as a result of prolonged ischemia, which is the
insufficient supply of oxygen and nutrition to an area of tissue due to a
disruption in blood supply. The blood vessel supplying the affected area
of tissue may be blocked due to an obstruction in the vessel,
compressed by something outside of the vessel causing it to narrow
(1), ruptured by trauma causing a loss of blood pressure downstream of
the rupture, or vasoconstricted
-Hypertension and atherosclerosis are risk factors for both
atherosclerotic plaques and thromboembolism
 -Myocardial infarction: is the partial death of heart tissue
commonly known as a heart attack.

-The phrase "heart attack" is often used non-specifically to refer to a

myocardial infarction and to sudden cardiac death. An MI is different
from "but can cause"cardiac arrest, where the heart is not contracting at
all or so poorly that all vital organs cease to function, thus causing
death. It is also distinct from heart failure, in which the pumping action
of the heart is impaired. However, an MI may lead to heart failure
-Most MIs occur due to coronary artery disease. Risk factors include
high blood pressure, smoking, diabetes, obesity, high blood cholesterol,
poor diet, and excessive alcohol intake, among others. MIs are less
commonly caused by coronary artery spasms, which may be due to
cocaine, significant emotional stress, and extreme cold, among others.
-A number of tests are useful to help with diagnosis, including
electrocardiograms (ECGs), blood tests, and coronary angiography. An
ECG may confirm an ST elevation MI (STEMI) ,Commonly used blood
tests include troponin and less often creatine kinase MB.
 Classification:
-myocardial infarction is classified by etiology. The universal definition
differentiates patients with myocardial infarction due to plaque rupture
(type 1) from those due to myocardial oxygen supply-demand
imbalance (type 2) secondary to other acute illnesses. Patients with
myocardial necrosis, but no symptoms or signs of myocardial ischemia,
are classified as acute or chronic myocardial injury. This classification
has not been widely adopted in practice,
-both myocardial injury and type 2 myocardial infarction are common,
occurring in more than one-third of all hospitalized patients. These
patients have poor short-term and long-term outcomes with two-thirds
dead in 5 years. The classification of patients with myocardial infarction
continues to evolve, and future guidelines are likely to recognize the
importance of identifying coronary artery disease in type 2 myocardial
infarction.
>>Aim of the research:
Is to be able to identify and define the following:
A>Myocardial infarction definition and Etiology
B>Myocardial infarction pathogenesis
C>Morphology >Gross and microscopic
D>Treatment and Control of myocardial infarction
 Chapter 2:

>>this chapter contains:

A>introduction
B>classification
C>Causes of myocardial infarction
d>Mechanism "Pathogenesis"
E> Morphology
F> Treatment and control
G> Epidemiology
Point 1:Introduction: -Myocardial infarction: is the partial death of
heart tissue as a result of prolonged ischemia commonly
known as a heart attack.

-The most common symptom is chest pain or discomfort which may

travel into the shoulder, arm, back, neck, or jaw. Often it occurs in
the center or left side of the chest and lasts for more than a few
minutesThe discomfort feel like heartburn. Other symptoms may
include shortness of breath, nausea, feeling faint, a cold sweat, or
feeling tired. Among those over 75 years old, about 5% have had an
MI with little or no history of symptoms. An MI may cause heart
failure, an irregular heartbeat, cardiogenic shock, or cardiac arrest .

-Treatment of an MI is time critical. Aspirin is an appropriate immediate

treatment for a suspected MI. Nitroglycerin or opioids may be used to
help with chest pain
 Point2>classification:
-The classification distinguishes between type 1 myocardial infarction due
to thrombosis of an atherosclerotic plaque and type 2 myocardial infarction
due to myocardial oxygen supply-demand imbalance in the context of
another acute illness. Myocardial infarctions presenting as sudden death
(type 3), or after percutaneous coronary intervention (type 4) and coronary
artery bypass grafting (type 5) are also defined. Acute myocardial injury is
classified where troponin concentrations are elevated , whereas in chronic
myocardial injury troponin concentrations remain unchanged on serial
testing. This is an important distinction, as the underlying pathological
mechanisms in acute and chronic myocardial injury are likely to differ.

-Patients classified with type 2 myocardial infarction are heterogeneous and

have myocardial ischemia secondary to a variety of acute medical or
surgical conditions. Based on the current criteria, a diagnosis of type 2
myocardial infarction could be applied to patients without coronary artery
disease. At present, there is no guidance on the optimal cardiac
investigation, management or treatment strategy for patients with type 2
myocardial infarction.
 . Point3: Causes of myocardial infarction
A-Atherosclerosis and High levels of blood cholesterol: is a known risk factor,
particularly high low-density lipoprotein, low high-density lipoprotein, and
high triglycerides.Atherosclerosis is a disease in which the inside of
an artery narrows due to the build of plaque. Initially there are generally no
symptoms.
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. The narrowing
of arteries limits the flow of oxygen-rich blood to parts of the body. Diagnosis is
based upon a physical exam, electrocardiogram, and exercise stress test among
others.
Prevention is generally by eating a healthy diet, exercise, not smoking, and
maintaining a normal weight. Treatment of established disease may include
medications to lower cholesterol such as statins, blood pressure medication, or
medications that decrease clotting, such as aspirin. A number of procedures may
also be carried out such as percutaneous coronary intervention, coronary artery
bypass graft, or carotid endarterectomy.
Atherosclerosis generally starts when a person is young and worsens with
age. Almost all people are affected to some degree by the age of 65
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.
Family history of ischemic heart disease or MI, particularly if one has a male first-degree
relative father, brother) who had a myocardial infarction increases a person's risk of MI.

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 regular hard work causes heart
muscles to thicken and grow. This alters the way the heart functions. 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.
Family history of ischemic heart disease or MI, particularly if one has a male first-degree
relative (father, brother) who had a myocardial infarction before age 55 years, or a
female first-degree relative (mother, sister) less than age 65 increases a person's risk
of MI.
4-Other Important Factors causing MI:
old age,diabetes mellitus ,alcohol use, Diet , actively smokingobesity: Smoking
appears to be the cause of about 36% and obesity the cause of 20%
of coronary artery disease .
 Point 4: 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.

A>>The most common mechanism of a myocardial infarction is the rupture

of an atherosclerotic plaque on an artery supplying heart muscle.
Plaques can become unstable, rupture, and additionally promote the
formation of a blood clot that blocks the artery; this can occur in minutes.
Blockage of an artery can lead to tissue death in tissue being supplied
by that artery. Atherosclerotic plaques are often present for decades
before they result in symptoms.
-The gradual buildup of cholesterol and fibrous tissue in plaques in the
wall of the coronary arteries or other arteries,typically over decades,
is termed atherosclerosis. 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:
 Point 6: 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. Treatment depends 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. In addition, the main treatment for
myocardial infarctions with ECG evidence of ST elevation (STEMI)
include thrombolysis or percutaneous coronary intervention, although PCI is
also ideally conducted within 13 days for NSTEMI.The following is used in
treatment and management of:
Pain:The pain associated with myocardial infarction may be treated
with nitroglycerin or morphine.
Coagulation: Anticoagulants like:Aspirin, an antiplatelet anticoagulant, is given
Angiogram:Primary percutaneous coronary intervention (PCI) is the treatment
of choice for STEMI.
 Point 7: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.
 Chapter 3: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, which may be due to cocaine, significant
emotional stress, and extreme cold, among others.> A number of tests are
useful to help with 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 is an appropriate
immediate treatment for a suspected MI.] Nitroglycerin or opioids
may be used . In a STEMI, treatments attempt to restore blood flow
to the heart, and include percutaneous coronary intervention (PCI),
where the arteries are pushed open and may be stented,
or thrombolysis, where the blockage is removed using
medications. 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 ex: Physical
activity can reduce the risk of cardiovascular disease and treatment
of underlying risk diseases like: DM and hypertension.
 Chapter 4 > 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)