ACUTE

MYOCARDIAL
INFARCTION
DEFINITION

Acute myocardial infarction (AMI),

commonly known as a heart attack, is the
irreversible necrosis of heart muscle
secondary to prolonged ischemia.
▪ This results from an imbalance in oxygen
supply and demand, caused by plaque rupture
with thrombus formation in a coronary vessel,
resulting in an acute reduction of blood supply
to a portion of the myocardium.
 HISTORY IN DETECTING THE MYCORDIAL
INFARCTION
The Egyptian mummies had evidence of cardiovascular disease especially atherosclerosis.

In 1578-1657, William Harvey i-e physician to king Charles, discovered the blood circulation in the body by heart.

In 1660-1742, Friedrich Hoffmann i-e chief professor of medicine at the university of Halle, discovered the disease as reduced
passage of blood within the coronary arteries.

In 1768, the William Heberden discovered the disease as something to do with blood circulating in the coronary arteries.

In 1849-1919, William Osler i-e physician in chief and professor of clinical medicine at Johns Hopkins Hospital, worked on
angina and was first to indicate it as syndrome rather than disease itself. The 1900s marks a period of increased interest, study
and understanding of heart disease.

In 1915, a group of physicians and social workers formed an association in new York.

James B. Herrick emphasized total bed rest as the treatment for this condition and by 1919 had used electrocardiography to
diagnose it . These approaches were the standard of care for patients with myocardial infarction until the mid-20th century.
CONTRIBUTION OF SCIENTISTS
 EPIDEMIOLOGY
▪ The most common form of CHD is the myocardial infarction (MI). MI occurs when a
coronary artery is occluded or almost occluded, which creates a severe reduction in the blood
flow, causing some of the heart muscle being supplied by that artery to become infarcted.
▪ Prior to 1900, infectious diseases and malnutrition were by far the most common causes of
death. However, with an unprecedented transformation in disease profiles throughout the
20th century, chronic diseases, such as CVD and cancer, now dominate mortality figures.
▪ One study of global trends states that in 1990 CVD was responsible for 28.4% of deaths in
the developing world, whereas by 2020 this is estimated to be 36.3%.
▪ Acute myocardial infarction incidence, mortality, and case-fatality increased exponentially
with age. Myocardial infarction is responsible for over 15% of mortality each year, among
the vast majority of people. The prevalence of myocardial infarction (MI) is higher in men in
all age-specific groups than women.
▪  Although the incidence of MI is decreased in the industrialized nations partly because
of improved health systems and implementation of effective public health strategies,
nevertheless the rates are surging in the developing countries such as South Asia, parts
of Latin America, and Eastern Europe.
▪ Risk factors such as dyslipidemia, smoking, psychosocial stressors, diabetes mellitus,
hypertension, obesity, alcohol consumption, physical inactivity, and a diet low in fruits
and vegetables were strongly associated with acute MI.
▪ History of patient:
The patient history is critical in diagnosing myocardial infarction. Patients with acute
MI present with chest pain and may have symptoms of fatigue, chest discomfort.
 WHAT CAUSES AMI?
 Causes: Usually coronary artery disease
 A heart attack occurs when one or more coronary
arteries becomes blocked. Over time, a buildup of fatty
deposits, including cholesterol, form substances called
plaques, which can narrow the arteries
(atherosclerosis). This condition, called coronary
artery disease, causes most heart attacks.
 The most common cause 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.
FACTORS LEADING TO BLOCKAGE OF
CORONARY ARTERIES
 Bad cholesterol:
• also called low-density lipoprotein (LDL)
• leading cause of a blockage in arteries

 Saturated fats:
• buildup plaque in coronary arteries

 Trans fat:
• known as hydrogenated fat, it also contributes to clog arteries
• usually produced artificially
 RISK
FACTORS
MODIFIABLE RISK FACTORS:

➦ High blood pressure/

hypertension: We are at
greater risk for heart
attack if we have high ➦ High cholesterol levels:
blood pressure. High Having high levels of cholesterol
in our blood puts us at risk for ➦ High triglyceride levels:
blood pressure that
acute myocardial infarction. We A high level of triglycerides,
occurs with other a type of blood fat related
conditions Such as may be able to lower our
cholesterol by making changes to to our diet, also increases
obesity, high cholesterol our risk of a heart attack.
our diet or by taking certain
or diabetes, increases our
medications called statins.
risk even more
MODIFIABLE RISK FACTORS:

➦ Diabetes:  High
blood sugar levels ➦Smoking:
can damage blood Smoking tobacco products
vessels and increases our risk
eventually lead
to coronary artery
disease. ➦ Obesity: Chances of
having a heart attack are
for heart attack.  It
higher if we’re very may also lead to other
overweight cardiovascular conditions
MODIFIABLE RISK FACTORS

➦ Alcohol: Acute and

➦Stress: We might
➦ Physical inactivity: respond to stress in
Being inactive contributes ways that can
prolonged intake increase our risk of a
to high blood high of heart attack.
cholesterol levels and
obesity. People who
exercise regularly have quantities of alcoholic
better heart health,
NON-MODIFIABLE RISK FACTORS

➦ Family history: If our

siblings, parents or
grandparents have had ➦ Gender:  Even
early heart attacks by after menopause,
➦ Age: The risk of
age 55 for males and by when women’s death
having a heart attack
age 65 for females), we rate from heart
increases with age.
might be at increased
risk.
disease
increases, it’s not as
 PATHO-
PHYSIOLOGY
▪ Blood vessels in the heart are surrounded by cardiac tissues,
Cardiomycocytes. The blood flowing in the arteries caries
oxygen which is taken up by cardiomycocytes.
▪ When a plaque is accumulated in one of these arteries or the
blood volume is low or there are cardiac intoxicity the flow of
blood decreases, thus decreases the level of O2 in arteries and
the cardiomycocytes are left oxygen depleted.
▪ These cardiomycocytes then send pain signals to the Heart
indicating heart attack.
FORMATION OF THROMBUS:
To compete the level of oxygen the heart pumps faster and the blood cells
and platelets accumulate along with the plaque forming a thrombus
PRODUCTION OF ADRENALINE:
 The nerves from the oxygen hungry cardiomycocytes carries the message to
the heart and as a result Adrenaline is produces.
 Adrenaline causes the heart to race, beat faster, which instead of improving
the condition worsen it and the artery becomes completely blocked.
 The cardiomycocytes present along that area becomes weak, causing that part
of the heart to beat slowly until it stops.
 The dying cardiomycocytes starts disintegrating and release Troponins in the
blood arteries.
 As the blood gets accumulated in the heart and is not transported to the Lungs
and Brain a person might feel shortness of breath and dizziness during the
onset of heart attack.
CLASSIFICATION
OF ACUTE
MYOCARDIAL
INFARCTION
CATEGORIES
Mayocardial INFARCTION can be classified into two categories,
based on pathology:
1. Transmural Infarction or STEMI
2. Subendocradial (nontransmural) Infarction or NSTEMI
TRANSMURAL INFARCTION OR
STEMI
Definition:

“Transmural infarction is myocardial necrosis which

includes the whole thickness of the heart muscle from
endocardium to epicardium”

 Transmural infarction mainly results due to occlusion of

the major artery of heart that supplies nutrient rich blood
and oxygen to heart muscle.
Transmural infarction or STEMI (ST
elevated myocardial infarction) shows
 Elevated ST segment in ECG

It causes enough damage to be considered as

major heart attack.
SUBENDOCARDIAL (NON
TRANSMURAL) INFARCTION OR
NSTEMI
Definition:

“Subendocardial or nontransmural infarction is a typical

chest pain which involves blockage of small area in
subendocardial wall of the left ventricle , ventricular
septum or papillary muscles”

▪ In STEMI, there is partial blockage of coronary artery.

ECG of NSTEMI ( Non ST elevation myocardial
infarction) shows
 Depressed ST wave

Inversion of T wave

NSTEMI is less damaging to heart as compared to

STEMI
 SIGNS
AND
SYMPTOMS
Chest Pain:
▪ Characteristics: Severe, immobilizing chest pain.

▪ Usually described as sensation of tightness,

heaviness, pressure and burning.
▪ Location: Just below the sternum, behind the
breastbone or in the area of upper abdomen.
▪ Radiation: Pain radiates to the left arm, lower jaw,
neck, right arm and back.
▪ Duration: Lasts for 20 minutes or more.

▪ Palpitations
▪ Nausea and vomiting:
Vomiting results as a reflex from severe pain.
Vasovagal reflexes initiated from area of ischemia.

▪ Shortness of breath (Dyspnea):

Failure of left ventricle causes the pulmonary edema.
Difficulty in breathing.

▪ Diaphoresis:
Excessive sweating

▪ Light-headedness or sudden dizziness

▪ Loss of consciousness:
Inadequate blood flow to the brain and causes unconsciousness.
▪ Elevation in blood pressure:
Blood pressure is increases due to peripheral arterial vasoconstriction.
▪ Oliguria:
Decreased urinary output may indicate cardiogenic shock.
▪ Respiratory rate:
Respiratory rate also increased due to anxiety.
▪ Other symptoms:
Some other symptoms like coughing, wheezing, fever, fullness, gas, cold
sweats, pale appearance on skin and sudden death.
DIAGOSIS
PHYSICAL EXAMINATION
The general appearance of patients may vary according to the following experienced
symptoms:
▪ Increased respiratory rate
▪ Irregular pulse
▪ Elevated or decreased blood pressure
▪ Vasoconstriction causes cool and pale skin
▪ May have low grade fever (38–39 °c)
▪ Swelling of legs due to peripheral edema
ECG CHANGES
▪ ST segment elevation, followed by T wave inversion and Q waves, are
associated with Transmural Infarction.

▪ ST segment depression and T wave inversion are associated with

Subendocardial Infarction.
SERUM CARDIAC BIOMARKERS
The combination of CPK MB and Troponin testing is used for the purpose of
diagnosis myocardial infarction:
 The CPK-MB test: It measures the
blood level of CK-MB (creatine
kinase myocardial band), the bound
combination of two variants
(isoenzymes CKM and CKB)
 Troponin Testing: High sensitivity i.e.
Rise and/or fall of troponin
MANAGEMEN
T OF ACUTE
MYOCARDIAL
INFARCTION
How to manage acute myocardial infarction?

When it comes to the management of the disease it involves two different

type of approaches which are:
▪ Non-pharmacological management: In this type of management we look for
methods that are helpful in the management of disease without the use of
medicines/drugs. Mostly these methods are helpful in long term as its effect are
long lasting.
▪ Pharmacological management: in this type of management doctors or experts
prescribes medicines to the patient to recover from the disease. It is mostly used
in case of emergency as the response which it provides is quick. It also reduces
the frequency and intensity of pain.
NON-PHARMACOLOGICAL MANAGEMENT

▪ Experts raise awareness among patients by educating them about proper

management of disease.
▪ Proper counselling of patient is done.
▪ Alcohol consumption and smoking is prohibited.
▪ Healthy lifestyle is adopted like doing exercise for 30 minutes daily.
▪ Patient is asked to follow a proper and healthy diet to combat with disease.
▪ Patients are advised to restrict the salt consumption.
PHARMACOLOGICAL MANAGEMENT
Medication that is used in proper management of disease involves:
▪ Thrombolytic agents
▪ Anti-coagulants
▪ Anti-platelet agents
▪ Anti-hypertensive agents
▪ Lipid lowering drugs
▪ Vasodilators
▪ Other medications like: analgesics, anti-ulcer drugs and anti-
depressants.
PREVENTIVE MEASURES MANAGEMENT
Hypertension should be managed and Patients with CAD should have their blood
pressure maintained at less than 130/80 mm Hg. This may be achieved by:
▪ Healthy Lifestyle
▪ Quit Smoking and alcohol consumption
▪ Medication
▪ Physical activity and exercise: This helps control blood cholesterol, diabetes and
obesity, as well as help lower blood pressure which can lower your heart disease
risk.
▪ Diet modification: Diets rich in soluble fiber, vegetables, fruits, and whole grains,
and low in saturated fat/trans fat and cholesterol should be encouraged.
 TREATMENT
AND
MEDICATIONS
TREATMENTS
Immediate treatment is required for treating heart related issues there are two ways for
treating the problem it involves surgical treatment and medicinal treatment.
Surgical Treatment:
▪ Angioplasty: in this procedure arteries are unblocked to supply blood to the heart.
During the surgery a catheter is inserted which is a long and a thin tube to reach the
blockage. Catheter is inflated to remove blockage by opening up the arteries, a mesh
tube stent is placed at the site pf blockage to prevent the closing of arteries again.
▪ Coronary artery bypass graft: in this case surgeon change the route of blood flow in
artery and vein so that blood flows around the blockage it is mostly done after heart
attack.
MEDICATIONS
Medications that are used to treat acute myocardial infarction are:
▪ Blood thinning tablets like aspirins that will help out in breaking blood clots and eventually it will
improve the blood flow.
▪ Thrombolytics are very beneficial in dissolving clots.
▪ Nitroglycerin tablets are given to heart patients for opening up blood vessels for improved blood
flow.
▪ Anti-platelet drugs are given to the patient for preventing formation of new clots and it also prevents
previously existing clots from growing.
▪ Beta-blockers are used for lowering blood pressure and helps to relax heart muscles
▪ ACE-inhibitors helps out in lowering blood pressure and ultimately also controls stress.
▪ Pain killers are also medicated to relieve pain and reduce discomfort.
THANK
YOU