Table of Contents
Introduction to Angina and MI
Like any other organ, heart requires a constant supply of oxygen rich blood to function properly when the supply is reduced or blocked by any reason it can leads to Angina and Myocardial Infarction.
Angina is a condition characterised by chest pain or discomfort caused by reduced blood supply to the heart muscles.
Myocardial Infarction(MI) occurs when the complete blockage in one or more coronary arteries, leading to tissue damage or death due to lack of oxygen. It is a medical emergency requiring immediate intervention.
Manifestation of Ischemic Heart Disease (IHD)
Ischemic Heart Disease (IHD), also known as Coronary Artery Disease (CAD), occurs due to reduced blood supply to the heart muscle. Its main manifestations include:
Angina Pectoris – Chest pain or discomfort due to temporary reduced blood flow to the heart. It can be:
Stable Angina – Occurs during physical exertion or stress and is relieved by rest or medication.
Unstable Angina – Occurs even at rest and is more severe, indicating a higher risk of a heart attack.
Myocardial Infarction (Heart Attack) – A complete blockage of a coronary artery leading to permanent damage to the heart muscle. Symptoms include severe chest pain, sweating, shortness of breath, and nausea.
what is Angina?
Stable Angina (Effort Angina):
Stable angina is the most common type of angina. It occurs when the heart needs more oxygen, such as during physical activity or emotional stress. The pain or discomfort usually follows a predictable pattern and lasts for a few minutes. It goes away with rest or after taking prescribed medications like nitroglycerin. Since stable angina follows a pattern, you can often manage it by avoiding triggers and making lifestyle changes.- Most common type of angina.
- Occurs during physical activity or stress.
- Pain goes away with rest or medication (like nitroglycerin).
- Predictable pattern of occurrence.
Unstable Angina:
Unstable angina is more serious than stable angina and does not follow a predictable pattern. It can occur suddenly, even when a person is at rest, and the pain tends to be more intense and long-lasting. Unlike stable angina, this type does not go away easily with rest or medications. Unstable angina is considered a medical emergency, as it increases the risk of a heart attack. If someone experiences sudden and severe chest pain that does not improve, they should seek immediate medical attention.- More severe and unpredictable than stable angina.
- Can occur even at rest.
- Pain lasts longer and is not relieved easily.
- A warning sign of a possible heart attack.
- Variant Angina (Prinz metal’s Angina):
This type of angina is rare and occurs due to a temporary spasm in the coronary arteries, which reduces blood flow to the heart. It often happens at rest, usually during night time or early morning. Unlike other types, variant angina is not directly linked to physical activity or stress. The pain may be severe but can be relieved by calcium channel blockers and nitrates, which help relax the blood vessels. Smoking and drug use (such as cocaine) are known to trigger this type of angina.
- Rare type of angina caused by a spasm in the coronary arteries.
- Can occur at rest, often during night time or early morning.
- Usually relieved by medication like calcium channel blockers.
Microvascular Angina:
Microvascular angina occurs when there is a problem with the small blood vessels (microvasculature) of the heart rather than the larger coronary arteries. It is more common in women and can cause long-lasting chest pain that may not always respond to traditional angina medications. The pain can be triggered by stress or daily activities. Since it involves tiny blood vessels, diagnosis can be challenging, and doctors may need special tests like coronary flow reserve measurement to identify it.- Caused by problems in the small blood vessels of the heart.
- More common in women.
- Chest pain lasts longer than other types and may not be relieved by nitroglycerin.
What is Myocardial Infarction?
Myocardial infarction (MI), commonly known as a heart attack, occurs when there is a complete blockage in one or more coronary arteries, cutting off blood supply to a part of the heart muscle. This causes damage or death of heart tissue, leading to serious complications and even death if not treated quickly. Unlike angina, the pain in a heart attack does not go away with rest or medication.
Types of Myocardial Infarction
ST-Elevation Myocardial Infarction (STEMI)
This is the most severe type of heart attack. It occurs when a major coronary artery is completely blocked, stopping blood flow to a large portion of the heart. It causes extensive damage to the heart muscle. STEMI is a medical emergency that requires immediate treatment, such as clot-busting drugs or emergency angioplasty.- Most severe type of heart attack.
- Occurs due to complete blockage of a major coronary artery.
- Causes extensive damage to the heart muscle.
- Requires immediate treatment (angioplasty, clot-busting drugs).
Non-ST-Elevation Myocardial Infarction (NSTEMI)
In NSTEMI, the coronary artery is partially blocked, leading to reduced blood flow but not a complete stoppage. The damage to the heart is less severe than STEMI, but it still requires urgent medical attention. Doctors diagnose NSTEMI through blood tests and ECG findings, and treatment often includes medications or angioplasty to restore blood flow.- Caused by a partial blockage of a coronary artery.
- Less severe than STEMI but still requires urgent treatment.
- Diagnosed using ECG and blood tests (Troponin levels).
- Treatment includes medications, angioplasty, or bypass surgery.
Silent Myocardial Infarction (SMI)
As the name suggests, a silent heart attack occurs without obvious symptoms. The person may not feel chest pain but may experience mild discomfort, fatigue, or shortness of breath. SMI is more common in older adults and diabetics and is usually diagnosed later through ECG or imaging tests. Despite the lack of symptoms, it can cause significant heart damage over time.- No obvious symptoms (chest pain may be absent).
- More common in diabetics and older adults.
- Often diagnosed accidentally through ECG or imaging.
- Still causes heart muscle damage and increases future heart risks.
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Etiopathogenesis of Angina and Myocardial Infarction
Etiopathogenesis of Angina
The development of angina is primarily due to an imbalance between oxygen supply and demand in the heart muscle, leading to transient ischemia (temporary lack of blood flow). The major causes include:
- Atherosclerosis of Coronary Arteries
- The most common cause of angina.
- Plaque buildup in coronary arteries leads to narrowing (stenosis) and reduced blood flow.
- When the oxygen demand increases (during exercise, stress, or heavy meals), blood supply becomes insufficient, triggering chest pain.
- Coronary Artery Spasm (Vasospasm)
- Temporary narrowing of the coronary artery due to abnormal contraction of smooth muscles.
- Can occur even in normal arteries (Prinzmetal’s angina).
- Often triggered by cold, stress, smoking, or drug use (e.g., cocaine).
- Endothelial Dysfunction
- Damage to the inner lining of blood vessels (endothelium) reduces their ability to dilate properly.
- Leads to decreased nitric oxide (NO) production, causing impaired blood flow regulation.
- Microvascular Dysfunction
- Small coronary arteries may not dilate properly even if large arteries are clear.
- Seen in microvascular angina (common in women).
- Increased Oxygen Demand
- Conditions like hypertension, anemia, hyperthyroidism, or tachycardia can increase the heart’s oxygen demand beyond the available supply, leading to angina symptoms.
Etiopathogenesis of Myocardial Infarction (MI)
Myocardial infarction (heart attack) occurs due to sudden and complete blockage of a coronary artery, leading to irreversible heart muscle damage. The major steps involved in its development are:
- Atherosclerotic Plaque Formation
- Long-term cholesterol and fat accumulation in arteries form plaques.
- High cholesterol, diabetes, smoking, and high blood pressure increases its risk factors.
- Plaque Rupture and Thrombus Formation
- The fibrous cap covering the plaque can rupture due to stress or inflammation.
- Platelets aggregate at the site, forming a blood clot (thrombus) that completely blocks the artery.
- Coronary Artery Occlusion and Ischemia
- The blockage stops oxygen supply to the heart muscle.
- Within minutes, the affected heart tissue starts dying (necrosis).
- Myocardial Cell Death (Necrosis)
- If blood flow is not restored within 20-40 minutes, heart muscle cells undergo irreversible damage.
- Necrotic tissue leads to loss of heart function, increasing the risk of heart failure or arrhythmias.
- Inflammation and Healing
- The damaged area triggers an inflammatory response.
- Over time, the dead tissue is replaced by fibrous scar tissue, but it cannot contract, leading to weakened heart function.
Differences Between Angina and Myocardial Infarction
| Feature | Angina | Myocardial Infarction |
|---|---|---|
Cause |
Partial narrowing of arteries |
Complete blockage of an artery |
Ischemia |
Temporary |
Permanent |
Tissue Damage |
No cell death (reversible) |
Necrosis (irreversible damage) |
Pain Duration |
Short, relieved by rest |
Long-lasting, not relieved by rest |
ECG Changes |
ST depression (except in Prinzmetal’s angina) |
ST elevation (STEMI) or non-ST changes (NSTEMI) |
Management of Angina and MI
Non Pharmacological Management
Stable Angina : The aim of the management to increase blood flow to the ischemic region of the heart and reduce the oxygen requirement of the myocardium.
- Daily Exercise
- Avoid alcohol
- Stop smoking
- Low fat diet
- Low cholesterol food
- Avoid Heavy Exercise.
Unstable Angina and Myocardial Infarction : The aim of the management is to early restoration of blood flow to the ischemic region, prevent of death, relief of ischemic pain, etc.
- Complete bed rest
- Coronary angiography
- Revascularization therapy.
Pharmacological Management of Angina and MI
Pharmacological Management of Stable Angina
Stable angina occurs due to reduced blood flow to the heart, mainly caused by narrowed coronary arteries. The goal of treatment is to reduce chest pain (angina), improve blood flow, and prevent complications like heart attacks.
- Antiplatelet Drug
Example: Aspirin, Clopidogrel- These drugs prevent platelets from clumping together, reducing the risk of blood clot formation (thrombosis) in the narrowed arteries.
- Aspirin is commonly used as a daily low-dose therapy to lower the risk of heart attack.
- Clopidogrel is an alternative for patients who cannot tolerate aspirin.
- Organic Nitrates
Example: Nitroglycerin, Isosorbide Mononitrate- These drugs relax and dilate (widen) blood vessels, reducing the heart’s oxygen demand and improving blood flow.
- Nitroglycerin (sublingual tablet or spray) is used for immediate relief during angina episodes.
- Isosorbide mononitrate is used for long-term angina prevention.
- Beta-Blockers (β-Blockers)
Example: Metoprolol, Atenolol- These drugs reduce heart rate and blood pressure, lowering the heart’s oxygen demand.
- Metoprolol is a commonly used selective beta-blocker, making the heart work more efficiently.
- Beta-blockers are first-line therapy in stable angina.
- Calcium Channel Blockers (CCBs)
Example: Amlodipine, Diltiazem- Amlodipine relaxes the arteries, increasing blood supply to the heart and lowering blood pressure.
- Diltiazem slows the heart rate and reduces workload, helpful for angina patients who cannot take beta-blockers.
- Potassium Channel Opener
Example: Nicorandil- It opens potassium channels, leading to blood vessel relaxation and dilation.
- Nicorandil improves oxygen delivery to the heart and has both nitrate-like and vasodilator effects.
- It is particularly useful for patients who do not respond well to nitrates or beta-blockers.
- Antihyperlipidemic Drugs (Statins)
Example: Atorvastatin, Rosuvastatin- These drugs lower cholesterol levels, reducing plaque formation in arteries.
- Atorvastatin reduces LDL cholesterol and prevents further narrowing of coronary arteries.
- Long-term use reduces the risk of heart attacks and stroke.
- ACE Inhibitors (Angiotensin-Converting Enzyme
Inhibitors)
Example: Ramipril, Enalapril- These drugs lower blood pressure and reduce strain on the heart by relaxing blood vessels.
- Ramipril improves heart function, especially in patients with hypertension or diabetes.
- ACE inhibitors also have a protective effect in preventing future heart attacks.
Pharmacological Management of Unstable Angina and MI
Unstable angina (UA) and myocardial infarction (MI) are acute coronary syndromes (ACS) requiring prompt medical intervention to restore blood flow, alleviate symptoms, and prevent further cardiac events. The pharmacological approach includes several classes of medications, each with specific dosages and administration guidelines. Below is an overview based on current clinical guidelines:
Antiplatelet Agents
- Aspirin
- Loading Dose: 160–325 mg orally, administered immediately upon suspicion of ACS.
- Maintenance Dose: 75–162 mg daily, continued indefinitely to reduce the risk of recurrent events.
- P2Y12 Inhibitors
- Clopidogrel
- Loading Dose: 300–600 mg orally.
- Maintenance Dose: 75 mg once daily.
- Ticagrelor
- Loading Dose: 180 mg orally.
- Maintenance Dose: 90 mg twice daily.
- Prasugrel (for patients undergoing percutaneous coronary intervention [PCI])
- Loading Dose: 60 mg orally.
- Maintenance Dose: 10 mg once daily.
- Clopidogrel
- Aspirin
Anticoagulants
- Unfractionated Heparin (UFH)
- Initial Dose: 60 units/kg intravenous (IV) bolus (maximum 4,000 units).
- Infusion: 12 units/kg/hour (maximum 1,000 units/hour), adjusted based on activated partial thromboplastin time (aPTT).
- Low Molecular Weight Heparin (LMWH) (e.g., Enoxaparin)
- Dose: 1 mg/kg subcutaneously every 12 hours.
- Duration: Typically continued for the duration of hospitalization or until revascularization.
- Fondaparinux
- Dose: 2.5 mg subcutaneously once daily.
- Note: Particularly used in patients at high risk of bleeding.
Nitroglycerin
Sublingual Tablet or Spray: 0.3–0.6 mg every 5 minutes as needed for chest pain, up to three doses.
Intravenous (IV) Infusion: Initiate at 5 mcg/min, titrate by 5 mcg/min every 3–5 minutes as needed, up to 20 mcg/min; further titration may be done by 10–20 mcg/min increments.
Contraindications: Avoid in patients with hypotension or those who have used phosphodiesterase inhibitors within the past 24–48 hours.
Beta-Blockers
Oral Administration: Metoprolol 25–50 mg every 6–12 hours, titrated as tolerated.
Intravenous Administration (if oral not feasible): Metoprolol 5 mg IV every 5 minutes, up to three doses, followed by oral dosing.
Note: Initiate within 24 hours unless contraindicated by factors such as heart failure, bradycardia, or hypotension.
Statins
High-Intensity Therapy: Atorvastatin 80 mg orally once daily.
Note: Initiate as early as possible, regardless of baseline LDL cholesterol levels, to reduce the risk of recurrent events.
Angiotensin-Converting Enzyme (ACE) Inhibitors
Initial Dose: Lisinopril 2.5–5 mg orally once daily.
Target Dose: Titrate up to 10–20 mg daily as tolerated.
Note: Particularly beneficial in patients with left ventricular dysfunction, hypertension, or diabetes.
Analgesia
Dose: 2–4 mg IV every 5–15 minutes as needed for pain relief.
Note: It is given to patients who still have chest pain even after using other treatments for heart-related issues.
Additional Considerations
Oxygen Therapy: Administer if oxygen saturation is below 90% or if the patient is in respiratory distress.
Glycoprotein IIb/IIIa Inhibitors: Consider in high-risk patients undergoing PCI(Percutaneous Coronary Intervention).
Proton Pump Inhibitors (PPIs): Use in patients at increased risk of gastrointestinal bleeding, especially those on dual antiplatelet therapy.