" Myocardial Infarction "

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. Most myocardial infarctions are due to
underlying coronary artery disease, the leading cause of death in the United States. With
coronary artery occlusion, the myocardium is deprived of oxygen. Prolonged deprivation
of oxygen supply to the myocardium can lead to myocardial cell death and necrosis.
Patients can present with chest discomfort or pressure that can radiate to the neck, jaw,
shoulder, or arm. In addition to the history and physical exam, myocardial ischemia may
be associated with ECG changes and elevated biochemical markers such as cardiac
troponins. This activity describes the pathophysiology, evaluation, and management of
myocardial infarction and highlights the role of the interprofessional team in improving
care for affected patients

risk factors :-

1. Abnormal lipid profile/blood apolipoprotein (raised ApoB/ApoA1)

2. Hypertension
3. Diabetes mellitus
4. Abdominal obesity (waist/hip ratio) (greater than 0.90 for males and greater than 0.85 for
females)
5. Psychosocial factors such as depression, loss of the locus of control, global stress,
financial stress, and life events including marital separation, job loss, and family conflicts
6. Lack of daily consumption of fruits or vegetables
7. Lack of physical activity
8. Alcohol consumption (weaker association, protective)
9. Smoking

Other risk factors include a moderately high level of plasma homocysteine, which is an
independent risk factor of MI. Elevated plasma homocysteine is potentially modifiable
and can be treated with folic acid, vitamin B6, and vitamin B12.

Some non-modifiable risk factors for myocardial infarction include advanced age,
male gender (males tend to have myocardial infarction earlier in life), genetics (there
is an increased risk of MI if a first-degree relative has a history of cardiovascular
events before the age of 50) The role of genetic loci that increase the risk for MI is
under active investigation
 Pathophysiology :-

The acute occlusion of one or multiple large epicardial coronary arteries for more than 20
to 40 minutes can lead to acute myocardial infarction. The occlusion is usually
thrombotic and due to the rupture of a plaque formed in the coronary arteries. The
occlusion leads to a lack of oxygen in the myocardium, which results in sarcolemmal
disruption and myofibril relaxation.These changes are one of the first ultrastructural
changes in the process of MI, which are followed by mitochondrial alterations. The
prolonged ischemia ultimately results in liquefactive necrosis of myocardial tissue. The
necrosis spreads from sub-endocardium to sub-epicardium. The subepicardium is
believed to have increased collateral circulation, which delays its death. Depending on
the territory affected by the infarction, the cardiac function is compromised. Due to the
negligible regeneration capacity of the myocardium, the infarcted area heals by scar
formation, and often, the heart is remodeled characterized by dilation, segmental
hypertrophy of remaining viable tissue, and cardiac dysfunction.
 Complications :-

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
Clinical guidline for the treatment of the myocardial infarction

Treatment for myocardial infarction according to clinical recommendations usually consists of

medication, procedures like stenting or angioplasty, and lifestyle modifications. Aspirin, beta-
blockers, ACE inhibitors, statins, and antiplatelet medications are frequently prescribed. In order
to restore blood flow to the damaged portion of the heart, the guidelines also emphasize the
significance of early reperfusion therapy, which is typically accomplished via percutaneous
coronary intervention (PCI) or thrombolytic therapy. Changes in lifestyle such as giving up
smoking, eating a heart-healthy diet, exercising frequently, and controlling stress are also
necessary for long-term care and the avoidance of future incidents.Apart from medicine and
therapies, it is imperative to regularly monitor patients for consequences such arrhythmias, heart
failure, or cardiogenic shock. Patients are frequently advised to participate in rehabilitation
programs, such as cardiac rehabilitation, in order to aid in their recovery and enhance their
general heart health. In order to lower the risk of more cardiovascular events, long-term care
includes regular monitoring of heart function, making necessary drug adjustments, and
encouraging lifestyle modifications. Patients should also make sure they follow their treatment
plan and see their doctor on a regular basis for follow-ups.
Mechanism of action of the Drugs used :-

Antiplatelet Agents: These drugs, including aspirin and clopidogrel, prevent platelets from
clumping together to form clots. Aspirin inhibits the enzyme cyclooxygenase, which reduces the
production of thromboxane, a molecule that stimulates platelet aggregation. Clopidogrel blocks
the P2Y12 component of ADP receptors on the platelet surface, which inhibits platelet activation
and aggregation.
Anticoagulants: Heparin and enoxaparin are examples of anticoagulants used to prevent the
formation of new clots and the growth of existing clots. Heparin enhances the activity of
antithrombin III, which inhibits thrombin and factor Xa, crucial components in the blood
coagulation cascade. Enoxaparin, a low molecular weight heparin, specifically inhibits factor Xa.
Thrombolytics: Drugs like streptokinase and alteplase dissolve blood clots by activating
plasminogen to plasmin, an enzyme that breaks down fibrin, the structural component of blood
clots. This class of medication is often used in the early stages of an MI to restore blood flow
through blocked arteries.
Beta-Blockers: Medications such as metoprolol and atenolol decrease the heart's workload by
reducing heart rate and blood pressure. They block beta-adrenergic receptors in the heart, which
are normally activated by adrenaline and noradrenaline, thus reducing the effects of these stress
hormones.
ACE Inhibitors: Drugs like lisinopril and enalapril help in dilating blood vessels to improve
blood flow and reduce the heart's workload. They inhibit the angiotensin-converting enzyme
(ACE), which is involved in the production of angiotensin II, a molecule that narrows blood
vessels.
Angiotensin II Receptor Blockers (ARBs): Losartan and valsartan are ARBs that also dilate
blood vessels but work by directly blocking the receptors for angiotensin II on blood vessels,
preventing vasoconstriction.
Statins: These drugs lower cholesterol levels and have anti-inflammatory effects that help
stabilize the plaques in the arteries, reducing the risk of them rupturing and causing a heart
attack. They inhibit HMG-CoA reductase, an enzyme involved in the production of cholesterol
in the liver.
 Diagnostic criteria:-

The diagnosis of acute myocardial infarction (AMI) or heart attack primarily involves clinical
assessment, electrocardiogram (ECG) findings, and biomarker measurements. Here's an
overview of the main diagnostic criteria and tests used for AMI:

1. **Clinical Symptoms**
- Chest pain or discomfort, which may radiate to the arms, neck, jaw, stomach, or back.
- Symptoms such as shortness of breath, nausea, vomiting, sweating, and unusual fatigue.

2. **Electrocardiogram (ECG)**
- The ECG is crucial for diagnosing AMI. It can show patterns indicative of ischemia or
infarction, such as ST-segment elevation (STEMI) or non-ST-segment elevation (NSTEMI).
- Specific changes in the ECG, including Q waves, ST-segment changes, and T wave
abnormalities, help in localizing and determining the extent of the myocardial infarction.

3. **Cardiac Biomarkers**
- **Troponins (T and I)**: These proteins are released into the bloodstream when heart muscle
is damaged. Elevated troponin levels are a key marker of myocardial infarction. Troponin levels
are considered the most sensitive and specific tests for myocardial injury.
- **Creatine kinase-MB (CK-MB)**: This enzyme may also be elevated in AMI, but it is less
specific than troponins since CK-MB can be elevated in conditions affecting muscles other than
the heart.
- Timing of biomarker tests is important, with tests done at the time of presentation and
repeated at 3-6 hours after symptom onset, or later if the initial tests are negative and suspicion
remains high.
4. **Imaging Tests**
- **Echocardiography**: Can identify areas of the heart that are not contracting well due to
damage from a heart attack. Also useful in diagnosing complications of AMI.
- **Coronary angiography**: Not used in all cases but can be performed in the setting of AMI
to identify blocked coronary arteries that might be amenable to reperfusion therapy, such as
angioplasty and stenting.

5. **Risk Factors and History**

- A patient's risk factors for coronary artery disease (such as age, hypertension, diabetes, high
cholesterol, smoking, and family history) and the nature of their symptoms are considered in the
overall clinical assessment.

Diagnostic Criteria
For a diagnosis of AMI, typically:
- There must be evidence of myocardial injury, indicated by abnormal cardiac biomarkers
(troponins).
- There should be signs of myocardial ischemia, evidenced by symptoms, ECG changes, or
imaging findings.

Additional Tests
- **Blood tests**: Complete blood count, lipid profile, kidney function tests, and others to assess
overall health and rule out other causes.
- **Stress testing**: Performed after stabilization to evaluate the heart's response to exercise and
identify areas of reduced blood flow.

The approach to diagnosing AMI can vary based on the clinical presentation and the healthcare
setting. Rapid diagnosis and treatment are critical to improve outcomes in patients with AMI.
Reference

1- https://www.mayoclinic.org/diseases-conditions/heart-attack/symptoms-causes/syc-
20373106

2-https://vsearch.nlm.nih.gov/vivisimo/cgi-bin/query-meta?v
%3Aproject=medlineplus&v%3Asources=medlineplus-
bundle&query=clinical+guidelines+for+the+treatment+of+myocardial+infarction

3- https://pubmed.ncbi.nlm.nih.gov/30580647/
4-Arora S, Matsushita K, Qamar A, Stacey RB, CaugheyMC. Early
versus late percutaneous revascularization in patients hospitalized with
non ST-segment elevation myocardial infarction: The atherosclerosis
risk in communities surveillance study. Catheter CardiovascInterv.
2018 Feb 1. 91 (2):253-259. [QxMD MEDLINE Link].
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