Introduction
Myocardial Infarction (MI), commonly known as a heart attack, occurs when the blood and oxygen supply to a part of the heart muscle is suddenly reduced or completely blocked. This blockage usually happens due to a sudden obstruction in the coronary arteries, which supply oxygen-rich blood to the heart.
When a coronary artery gets blocked, the heart muscle becomes starved of oxygen, leading to chest pain and pressure. If blood flow is not restored within 20 to 40 minutes, the heart muscle begins to die. After about 6 to 8 hours, the damage becomes complete, and the dead muscle is replaced by scar tissue.
Definition
Myocardial Infarction is defined as irreversible damage or death of heart muscle caused by prolonged shortage of oxygen (ischemia) and reduced blood flow due to atherosclerosis, thrombus, or embolus in a coronary artery.
Etiology (Causes & Risk Factors)
Common causes and risk factors include:
- Tobacco smoking
- Hypertension (high blood pressure)
- Drug abuse such as cocaine or methamphetamine
- Obesity
- Stress
- Alcohol misuse
- Older age
- Male gender
- Diabetes mellitus
- High cholesterol or hyperlipoproteinemia
- Family history of heart disease
- High levels of homocysteine
- Chronic kidney disease
MI most commonly occurs when an atherosclerotic plaque ruptures and a blood clot forms, suddenly reducing blood flow in a coronary artery. It is the leading cause of death in many countries, and almost half of MI-related deaths occur before reaching the hospital.
Pathophysiology
1. Myocardial Ischemia
Ischemia develops due to:
- Reduced coronary blood flow (e.g., coronary artery disease, shock)
- Increased oxygen demand (e.g., exercise, emotional stress)
- Heart muscle hypertrophy without increased blood supply (e.g., hypertension)
2. Role of Platelets
When an atherosclerotic plaque ruptures, the inner collagen fibers are exposed. Platelets stick to this area, become activated, and form a large platelet mass. This may cause further thrombosis or emboli.
3. Acute Plaque Rupture
Acute MI often results from sudden complications in atherosclerotic plaques:
- Coronary Thrombosis: A blood clot completely or partially blocks the artery.
- Intramural Hemorrhage: Bleeding inside the plaque worsens blockage.
4. Non-Atherosclerotic Causes
About 10% of MI cases occur due to other causes such as coronary artery spasms, arteritis, embolism, trauma or external compression.
5. Location of MI
The location depends on which coronary artery is blocked:
- Left Anterior Descending (LAD): Anterior and apical left ventricle, interventricular septum
- Right Coronary Artery (RCA): Posterior and basal left ventricle
The exact infarction pattern varies based on coronary circulation anatomy.
Signs & Symptoms
Symptoms may develop days or weeks before the heart attack and include fatigue, chest discomfort, and general uneasiness.
Characteristics of MI Chest Pain
- Severe and continuous for 30–60 minutes
- Located under the sternum
- Radiates to the jaw, neck, left arm or shoulder
- Feels like squeezing, pressure, burning or tightness
- Sometimes mistaken for indigestion or abdominal discomfort
Other Symptoms
- Feeling anxious or a sense of impending doom
- Pain spreading to back, stomach, neck or jaw
- Light-headedness or fainting
- Cough
- Nausea or vomiting
- Profuse sweating
- Shortness of breath
- Wheezing
- Rapid or irregular heartbeat
- Indigestion or choking sensation
Diagnosis
1. Clinical Features
- Chest pain
- Indigestion
- Anxiety or restlessness
- Shock
- Low-grade fever
2. Serum Cardiac Markers
- Creatine kinase (CK)
- Lactate dehydrogenase (LDH)
- Cardiac troponins (cTn) – gold standard
3. ECG Changes
- ST-segment elevation
- T-wave inversion
- Deep and wide Q waves
4. Magnetic Resonance Imaging (MRI)
5. Coronary Angiography
6. PET Scan
7. Chest X-ray
These tests help confirm the diagnosis and determine the severity of myocardial damage.
Detailed Notes:
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