SEMINAR ON MYOCARDIAL INFARCTION

INTRODUCTION
A heart attack occurs when the flow of blood to the heart is severely reduced or blocked.
The blockage is usually due to a buildup of fat, cholesterol and other substances in the heart
(coronary) arteries. The fatty, cholesterol-containing deposits are called plaques. The process of
plaque buildup is called atherosclerosis. Sometimes, a plaque can rupture and form a clot that
blocks blood flow. A lack of blood flow can damage or destroy part of the heart muscle. A heart
attack occurs when an artery that sends blood and oxygen to the heart is blocked. Fatty,
cholesterol-containing deposits build up over time, forming plaques in the heart's arteries. If a
plaque ruptures, a blood clot can form. The clot can block arteries, causing a heart attack. During
a heart attack, a lack of blood flow causes the tissue in the heart muscle to die. A heart attack is
also called a myocardial infarction. A blockage of blood flow to the heart muscle. a heart attack
is a medical emergency. A heart attack usually occurs when a blood clot blocks blood flow to the
heart. Without blood, tissue loses oxygen and dies. symptoms include tightness or pain in the
chest, neck, back or arms, as well as fatigue, lightheadedness, abnormal heartbeat and anxiety.
Women are more likely to have atypical symptoms than men. Treatment ranges from lifestyle
changes and cardiac rehabilitation to medication, stents and bypass surgery.
DEFINITION
Myocardial infarction (MI), colloquially known as "heart attack," is caused by decreased
or complete cessation of blood flow to a portion of the myocardium. Myocardial infarction may
be “silent," and go undetected, or it could be a catastrophic event leading to hemodynamic
deterioration and sudden death.

Myocardial Infarction is a diseased condition in which is caused by reduced blood flow in

a coronary artery due to atherosclerosis and an occlusion of an artery by an embolus or
thrombus.

MI or Heart attack is the irreversible damage of the myocardial tissue caused by

prolonged ischemia and hypoxia.

INCIDENCE

The total incidence of myocardial infarction is 15%, with a maximum incidence of eight
cases in the 51-60 year age group, which is consistent with the study, which found 12.7%
incidence of acute myocardial infarction in cerebrovascular accident patients.

Approximately 70% of fatal MI cases are attributed to occlusion caused by

atherosclerotic plaques. As atherosclerosis is the predominant cause of MI, risk-factors for
atherosclerotic disease are often mitigated in disease prevention. Modifiable risk factors account
for 90% of MI cases in men and 94% in women. These modifiable risk factors include cigarette
smoking, physical inactivity, hypertension, obesity, elevated cholesterol levels
(particularly LDL), and high triglyceride levels. In contrast, age, sex, and family history are
nonmodifiable risk factors for atherosclerosis and MI.

The global prevalence of MI in individuals < 60 years was found 3.8%. Also, following
the assessment of 20 eligible investigations with a sample size of 5,071,185 individuals (> 60
years), this value was detected at 9.5%.
TYPES
MI can be divided into several types depending upon the underlying cause:

 Type 1- spontaneous MI in which the symptoms develop spontaneously without any

underlying obstructive coronary artery disease
 Type 2- MI results from ischemia due to an imbalance between oxygen demand and supply.
The imbalance includes coronary artery spasm, coronary artery embolus, endothelial
dysfunction, arrhythmias, anemia, respiratory failure, hypotension, and hypertension.
 Type 3- MI results in sudden death in the non-availability of cardiac biomarkers. It could be
due to the reason that cardiac biomarkers could not be drawn from blood, or they were not
released yet in the blood.
 Type 4a- MI is related to the percutaneous intervention (PCI) in which the blockage in
coronary arteries is evident from imaging along with loss of viable myocardium and wall
motion defects.
 Type 4b- MI related to stent thrombosis
 Type 5- MI related to coronary artery bypass graft (CABG)

Another classification is based on the types of acute coronary syndromes in which there is a
sudden loss of oxygen supply to the cardiac muscle resulting in ischemia or necrosis. These types
include:

 ST-elevation MI (STEMI)- ECG waves, in this case, show ST-segment elevation

 Non-ST elevation MI (NSTEMI)- ECG waves do not show ST-segment elevation

RISK FACTORS

Common risk factors

 Male gender
 Middle age
 Smoking
 Hypercholesteremia
 Family history of cardiac diseases
 Hypertension
 Diabetes
 Obesity
  Stress
 Sedentary lifestyle
 Coronary trauma
 Drugs such as cocaine and amphetamine
 Heavy exertion
 Severe anemia
 Respiratory infections

Non modifiable Risk Factors

 Sex
 Age
 Family history
 Male
Modifiable Risk Factors
 Smoking
 Dyslipidemia
 Diabetes mellitus
 Hypertension
 Obesity
 Sedentary lifestyle
 Poor oral hygiene
 Presence of peripheral vascular disease

 Elevated levels of homocysteine

 Age. Men age 45 and older and women age 55 and older are more likely to have a heart
attack than are younger men and women.
 Tobacco use. This includes smoking and long-term exposure to secondhand smoke. If
you smoke, quit.
 High blood pressure. Over time, high blood pressure can damage arteries that lead to the
heart. High blood pressure that occurs with other conditions, such as obesity, high
cholesterol or diabetes, increases the risk even more.
 High cholesterol or triglycerides. A high level of low-density lipoprotein (LDL)
cholesterol (the "bad" cholesterol) is most likely to narrow arteries. A high level of
certain blood fats called triglycerides also increases heart attack risk. Your heart attack
risk may drop if levels of high-density lipoprotein (HDL) cholesterol — the "good"
cholesterol — are in the standard range.
  Obesity. Obesity is linked with high blood pressure, diabetes, high levels of triglycerides
and bad cholesterol, and low levels of good cholesterol.
 Diabetes. Blood sugar rises when the body doesn't make a hormone called insulin or can't
use it correctly. High blood sugar increases the risk of a heart attack.
 Metabolic syndrome. This is a combination of at least three of the following things:
enlarged waist (central obesity), high blood pressure, low good cholesterol, high
triglycerides and high blood sugar. Having metabolic syndrome makes you twice as
likely to develop heart disease than if you don't have it.
 Family history of heart attacks. If a brother, sister, parent or grandparent had an early
heart attack (by age 55 for males and by age 65 for females), you might be at increased
risk.
 Not enough exercise. A lack of physical activity (sedentary lifestyle) is linked to a
higher risk of heart attacks. Regular exercise improves heart health.
 Unhealthy diet. A diet high in sugars, animal fats, processed foods, trans fats and salt
increases the risk of heart attacks. Eat plenty of fruits, vegetables, fiber and healthy oils.
 Stress. Emotional stress, such as extreme anger, may increase the risk of a heart attack.
 Illegal drug use. Cocaine and amphetamines are stimulants. They can trigger a coronary
artery spasm that can cause a heart attack.
 A history of preeclampsia. This condition causes high blood pressure during pregnancy.
It increases the lifetime risk of heart disease.
 An autoimmune condition. Having a condition such as rheumatoid arthritis or lupus can
increase the risk of a heart attack.

ETIOLOGY
Acute myocardial infarction occurs due to decreased coronary blood flow, leading to
insufficient oxygen supply to the heart and cardiac ischemia. Decreased coronary blood flow is
multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to
acutely decreased blood flow in the coronary. Other etiologies of myocardial ischemia include
coronary artery embolism, which accounts for 2.9% of patients, cocaine-induced ischemia,
coronary dissection, and coronary vasospasm.
 The majority of cases of MI are caused by atherosclerosis. Atherosclerosis is defined as the
thickening of the vessel wall due to the build-up of cholesterol inside the lumen. The build-up
can form plaque that ruptures and obstructs the lumen of the entire vessel. Atherosclerosis can be
caused by various reasons such as high cholesterol levels in the body, high blood pressure, etc.
Nonatherosclerotic causes are the conditions or diseases that involve coronary vessels or cardiac
muscles. These include certain drugs, myocarditis, coronary trauma, etc.

 Imbalance between myocardial oxygen supply and demand due to atherosclerosis.

 Coronary Artery Vasospasm
 Coronary Artery thrombus
 Presence of dysrhythmia
 Coronary embolism
 Cocaine use associated with spasm
 Congenital anomalies of coronary circulation
Other Causes of MI
 Trauma
 Vasculitis
 Drug use (cocaine)
 Coronary artery anomalies
 Coronary artery emboli
 Aortic dissection
 Excess demand on the heart (hyperthyroidism, anemia)

PATHOPHYSIOLOGY

Atherosclerosis Arterial spasm Atherosclerosis + Plaque Split

+ Thrombus

Sudden not
Gradual usually reversible

Obstruction Sudden reversible

Occlusion
obstruction

Ischemia
 Hypoxia

Angina
Reduced oxygen
demand

Thrombolysis
Unstable angina

Permanent thrombus

MYOCARDIAL
Necrosis INFARCTION

The rupture of an atherosclerotic plaque initiates an inflammatory response of monocytes

and macrophages, leading to thrombus formation and platelet aggregation. This
process decreases oxygen delivery through the coronary artery, resulting in
inadequate oxygenation of the myocardium . The subsequent inability to produce ATP in the
mitochondria triggers an ischemic cascade, ultimately leading to apoptosis (cell death) of the
endocardium or myocardial infarction. With some exceptions due to genetic variation, coronary
arteries exhibit unique and diagnostic territorial distributions. For example, the left anterior
descending coronary artery supplies blood flow to the interventricular septum, anterolateral wall,
and ventricular apex. The left circumflex artery supplies blood to the inferolateral wall. The right
coronary artery supplies the right ventricle. The inferior wall is supplied either by the left
circumflex or right coronary artery.

SIGNS AND SYMPTOMS

Following are the signs and symptoms of myocardial infarction:
 Characteristic chest pain lasting for about 30-60 minutes, sharp, continuous, and intense in
character. It radiates to the lower jaw, left arm, shoulder, and back. In some patients, it can
be in the epigastric region mimicking acidity.
 Sweating
 Shortness of breath
 Nausea or vomiting
 Fatigue
 Malaise
 Increased heart rate
 Increased rate of breathing
 Increased blood pressure. In right ventricular MI, blood pressure is decreased
 Coughing, wheezing may also occur

Common heart attack symptoms include:

 Chest pain that may feel like pressure, tightness, pain, squeezing or aching
 Pain or discomfort that spreads to the shoulder, arm, back, neck, jaw, teeth or sometimes the
upper belly
 Cold sweat
 Fatigue
 Heartburn or indigestion
 Lightheadedness or sudden dizziness
 Nausea
 Shortness of breath

DIAGNOSTIC EVALUATION

History collection

The history and physical examination alone may not always diagnose AMI definitively. The
history should focus on the onset, quality, and associated symptoms. Recent studies suggest that
diaphoresis and bilateral arm radiating pain are more commonly associated with MI in
men. Other associated symptoms may include the following:
  Lightheadedness
 Anxiety
 Cough
 Choking sensation
 Diaphoresis
 Wheezing
 Irregular heart rate

Physical Examination
The physical examination should include the patient’s vital signs and appearance, including
diaphoresis, pulmonary evaluation, and cardiac auscultation. Specific vital aspects of the
examination are as follows:

 Heart rate: Tachycardia, atrial fibrillation, or ventricular arrhythmia may be present,

indicating cardiac electrical disturbances.

 Pulses: Unequal pulses may be observed if the patient has an aortic dissection, indicating
a potential arterial problem.

 Blood pressure: Blood pressure is typically high in AMI but may become hypotensive if
the patient is in shock due to compromised cardiac function.

 Respiratory findings: Tachypnea and fever may be present, indicating an inflammatory

response.

 Neck veins: Distended neck veins may be observed, suggesting right ventricular failure
and increased central venous pressure.

 Cardiac findings: The heart may exhibit lateral displacement of the apical impulse, a
soft S1 sound, a palpable S4 sound, and a new mitral regurgitation murmur. A loud
holosystolic murmur radiating to the sternum may indicate ventricular septal rupture.

 Pulmonary findings: Wheezing and rales may be heard if the patient has developed
pulmonary edema, indicating fluid accumulation in the lungs.
  Extremities: Edema or cyanosis may be present in the extremities, with a sensation of
coldness due to compromised circulation.

Laboratory Studies
 Cardiac troponins should be the only marker ordered
 CBC
 Lipid profile
 Renal function
 Metabolic panel

 A cardiac troponin test should be the only cardiac marker test ordered. CDC, lipid
profile, renal function, and metabolic panel are relevant labs.
 Cardiac biomarkers are helpful in the diagnosis of AMI, particularly NSTEMI. Troponin,
creatine kinase-MB (CK-MB), and LDH are cardiac markers observed.
 A troponin test is the most specific lab test for early detection of AMI; levels of the
troponin isoforms I and T are measured. Troponin levels peak at 12 hours and remain
elevated for 7 days. High-sensitivity troponin has been approved for use in the United
States after being heavily studied and utilized in Europe. Although it is more sensitive
than conventional troponin, it is also less specific. Thus, potential challenges include
numerous false-positive interpretations.
 The level of CK-MB, an isoenzyme of creatine kinase usually found in the myocardium,
reaches its peak at 10 hours and normalizes within 2 to 3 days. CK-MB is also not
clinically utilized due to its low specificity, rapid rise, and normalization.
 LDH levels reach their peak after 72 hours and return to normal within 10 to 14 days. In
clinical practice, LDH is not used to diagnose acute MI.
 B-type natriuretic peptide (BNP) should not be ordered as a marker for MI; instead, it is
more valuable for risk stratification, particularly in patients with MI who subsequently
develop heart failure.

ECG
The resting 12 lead ECG is the first-line diagnostic tool for the diagnosis of acute coronary
syndrome (ACS). It should be obtained within 10 minutes of the patient’s arrival in the
emergency department. Acute MI is often associated with dynamic changes in the ECG
waveform. Serial ECG monitoring can provide important clues to the diagnosis if the initial EKG
is non-diagnostic at initial presentation. Serial or continuous ECG recordings may help
determine reperfusion or re-occlusion status. A large and prompt reduction in ST-segment
elevation is usually seen in reperfusion.

ECG findings suggestive of ongoing coronary artery occlusion (in the absence of left ventricular
hypertrophy and bundle branch block):

ST-segment elevation in two contiguous lead (measured at J-point) of

1. Greater than 5 mm in men younger than 40 years, greater than 2 mm in men older than 40
years, or greater than 1.5 mm in women in leads V2-V3 and/or
2. Greater than 1 mm in all other leads

ST-segment depression and T-wave changes

1. New horizontal or down-sloping ST-segment depression greater than 5 mm in 2

contiguous leads and/or T inversion greater than 1 mm in two contiguous leads with
prominent R waves or R/S ratio of greater than 1

The hyperacute T-wave amplitude, with prominent symmetrical T waves in two contiguous
leads, maybe an early sign of acute MI that may precede the ST-segment elevation. Other ECG
findings associated with myocardial ischemia include cardiac arrhythmias, intraventricular
blocks, atrioventricular conduction delays, and loss of precordial R-wave amplitude (less specific
finding).

ECG findings alone are not sufficient to diagnose acute myocardial ischemia or acute MI as
other conditions such as acute pericarditis, left ventricular hypertrophy (LVH), left bundle
branch block (LBBB), Brugada syndrome, Takatsubo syndrome (TTS), and early repolarization
patterns also present with ST deviation.

ECG changes associated with prior MI (in the absence of left ventricular hypertrophy and left
bundle branch block):

1. Any Q wave in lead V2-V3 greater than 0.02 s or QS complex in leads V2-V3
2. Q wave > 03 s and greater than 1 mm deep or QS complex in leads I, II, aVL, aVF or V4-
V6 in any two leads of contiguous lead grouping (I, aVL; V1-V6; II, III, aVF)
  R wave > 0.04 s in V1-V2 and R/S greater than 1 with a concordant positive T wave in
the absence of conduction defect.

Patients that present with myocardial infarction may not have diagnostic ST-elevation ECG
abnormalities. Patients with typical chest pain should be investigated for NSTEMI with subtle
abnormalities on ECG, including ST-depressions and T wave changes. Serial ECGs can be
helpful here as well to look for dynamic changes. ECG without acute changes or any
abnormalities is common in NSTEMI.

There are diagnostic guidelines that can assist the practitioner in determining whether further
testing is useful in identifying patients with NSTEMI. Given the poor sensitivity of ECG for
STEMI, troponins are almost universally used for patients with a suspicious clinical history. The
HEART score has been validated and popularized. It utilizes clinician’s suspicion, patient risk
factors, ECG diagnostics, and troponin level to determine the “risk level” of the patient.

Imaging
Different imaging techniques are used to assess myocardial perfusion, myocardial viability,
myocardial thickness, thickening and motion, and the effect of myocyte loss on the kinetics of
para-magnetic or radio-opaque contrast agents indicating myocardial fibrosis or scars.

Some imaging modalities that can be used are

 Echocardiography
 Radionuclide imaging
 Cardiac Magnetic Resonance Imaging (cardiac MRI).

MANAGEMENT

ACUTE MANAGEMENT

Reperfusion therapy is indicated in all patients with symptoms of ischemia of less than
12-hours duration and persistent ST-segment elevation. Primary percutaneous coronary
intervention (PCI) is preferred to fibrinolysis if the procedure can be performed <120 minutes of
ECG diagnosis. If there is no immediate option of PCI (>120 minutes), fibrinolysis should be
started within 10 minutes of STEMI after ruling out contraindications. If transfer to a PCI center
is possible in 60 to 90 minutes after a bolus of the fibrinolytic agent and patient meets
reperfusion criteria, a routine PCI can be done, or a rescue PCI can be planned. If fibrinolysis is
planned, it should be carried out with fibrin-specific agents such as tenecteplase, alteplase, or
reteplase

Relief of pain, breathlessness, and anxiety:

The chest pain due to myocardial infarction is associated with sympathetic arousal, which
causes vasoconstriction and increased workload for the ischemic heart. Intravenous opioids (e.g.,
morphine) are the analgesics most commonly used for pain relief . he results from CRUSADE
quality improvement initiative have shown that the use of morphine may be associated with a
higher risk of death and adverse clinical outcomes. The study was done from the CIRCUS (Does
Cyclosporine Improve outcome in STEMI patients) database, which showed no significant
adverse events associated with morphine use in a case of anterior ST-segment elevation MI. A
mild anxiolytic (usually a benzodiazepine) may be considered in very anxious
patients .Supplemental oxygen is indicated in patients with hypoxemia (SaO2 <90% or PaO2
<60mm Hg).

Nitrates:

Intravenous nitrates are more effective than sublingual nitrates with regard to symptom
relief and regression of ST depression (NSTEMI). The dose is titrated upward until symptoms
are relieved, blood pressure is normalized in hypertensive patients, or side effects such as
a headache and hypotension are noted.

Beta-blockers: This group of drugs reduces myocardial oxygen consumption by lowering heart
rate, blood pressure, and myocardial contractility. They block beta receptors in the body,
including the heart, and reduce the effects of circulating catecholamines. Beta-blockers should
not be used in suspected coronary vasospasm.

Platelet inhibition: Aspirin is recommended in both STEMI and NSTEMI in an oral loading
dose of 150 to 300 mg (non-enteric coated formulation) and a maintenance dose of 75 to 100 mg
per day long-term regardless of treatment strategy. Aspirin inhibits thromboxane A2 production
throughout the lifespan of the platelet.

Most P2Y12 inhibitors are inactive prodrugs (except for ticagrelor, which is an orally active drug
that does not require activation) that require oxidation by hepatic cytochrome P450 system to
generate an active metabolite which selectively inhibits P2Y12 receptors irreversibly. Inhibition
of P2Y12 receptors leads to inhibition of ATP induced platelet aggregation. The commonly used
P2Y12 inhibitors are clopidogrel, prasugrel, and ticagrelor.

The loading dose for clopidogrel is 300 to 600 mg loading dose followed by 75 mg per day.

Prasugrel, 60 mg loading dose, and 10 mg per day of a maintenance dose have a faster onset
when compared to clopidogrel.

Patients undergoing PCI should be treated with dual antiplatelet therapy (DAPT) with aspirin +
P2Y12 inhibitor and a parenteral anticoagulant. In PCI, the use of prasugrel or ticagrelor is found
to be superior to clopidogrel. Aspirin and clopidogrel are also found to decrease the number of
ischemic events in NSTEMI and UA.

The anticoagulants used during PCI are unfractionated heparin, enoxaparin, and bivalirudin. The
bivalirudin is recommended during primary PCI if the patient has heparin-induced
thrombocytopenia.

LONG-TERM MANAGEMENT

Lipid-lowering treatment: It is recommended to start high-intensity statins that reduce low-

density lipoproteins (LDLs) and stabilize atherosclerotic plaques. High-density lipoproteins are
found to be protective.

Antithrombotic therapy: Aspirin is recommended lifelong, and the addition of another agent
depends on the therapeutic procedure done, such as PCI with stent placement.

ACE inhibitors are recommended in patients with systolic left ventricular dysfunction, or heart
failure, hypertension, or diabetes.

Beta-blockers are recommended in patients with LVEF less than 40% if no other
contraindications are present.
Antihypertensive therapy can maintain a blood pressure goal of less than 140/90 mm Hg.

Mineralocorticoid receptor antagonist therapy is recommended in a patient with left ventricular

dysfunction (LVEF less than 40%).

Glucose lowering therapy in people with diabetes to achieve current blood sugar goals.

Lifestyle Modifications

Smoking cessation is the most cost-effective secondary measure to prevent MI. Smoking has a
pro-thrombotic effect, which has a strong association with atherosclerosis and myocardial
infarction.

Diet, alcohol, and weight control: A diet low in saturated fat with a focus on whole grain
products, vegetables, fruits, and the fish is considered cardioprotective. The target level for
bodyweight is body mass index of 20 to 25 kg/m2 and waist circumference of <94 cm for the
men and <80 cm for the female.

NURSING MANAGEMENT

 Obtain ECG daily

 Always make sure the patient has 2 large-bore IVs
 Monitor cardiac enzymes
 Initiate treatment for acute MI
 Administer morphine for pain
 Start aspirin and nitroglycerin (0.4 mg sublingual)
 Provide oxygen if pulse oximetry is less than 94% at room air
 Ensure patient seen by a cardiologist
 Monitor vitals, daily weight, and urine output
 Administer heparin as ordered for STEMI
 If the patient has cardiac catheterization, check groin for hematoma and feel distal leg
pulses
POST OPERATIVE AND REHABILITATIVE CARE
 Cardiac rehabilitation plays a vital role in the recovery of patients following an AMI.
Research has demonstrated the numerous benefits of cardiac rehabilitation, including
improvements in quality of life, reduction of disability, and a decrease in mortality rates.

The rehabilitation process should be individualized to meet each patient's specific needs,
available resources, established goals, and physical abilities before and after the MI
event. Collaboration among rehabilitation therapists and the rest of the interprofessional care
team is vital for continuity of care.

Cardiac rehabilitation has also been shown to reduce future risk factors for individuals
following an AMI. Annual follow-up results demonstrate that cardiac rehab can reduce
the risk of future cardiovascular events.

PROGNOSIS

Despite many advances in treatment, acute MI still carries a mortality rate of 5-30%; the majority
of deaths occur prior to arrival to the hospital. In addition, within the first year after an MI, there
is an additional mortality rate of 5% to 12%. The overall prognosis depends on the extent of
heart muscle damage and ejection fraction. Patients with preserved left ventricular function tend
to have good outcomes. Factors that worsen prognosis include:

 Diabetes

 Advanced age
 Delayed reperfusion
 Low ejection fraction
 Presence of congestive heart failure
 Elevations in C-reactive protein and B-type natriuretic peptide (BNP) levels
 Depression
COMPLICATION
Type and Manifestation
I: Ischemic
 Reinfarction
 Extension of infarction
 Angina
II: Arrhythmias
 Supraventricular or ventricular arrhythmia
 Sinus bradycardia and atrioventricular block
III: Mechanical
 Myocardial dysfunction
 Cardiac failure
 Cardiogenic shock
 Cardiac rupture (Free wall rupture, ventricular septal rupture, papillary muscle rupture)
IV: Embolic
 Left ventricular mural thrombus,
 Peripheral embolus
V: Inflammatory
 Pericarditis (infarct associated pericarditis, late pericarditis, or post-cardiac injury
pericarditis)
 Pericardial effusion

CONCLUSION
Myocardial Infarction is a life threatening disease caused by many factors, healty
education must be given to the patients with predisposing or risk factors to prevent it. Early
diagnosis also very important far saving the life of the patient.
“PREVENTION IS BETTER THAN CURE”

BIBLIGRAPHY