Ischemic Heart Disease Flashcards
(32 cards)
What is Ischemic Heart Disease?
When oxygen delivery to the myocardium drops below its demand, the heart muscle becomes ischemic, leading to:
* Angina (chest pain)
* Shortness of breath (Dyspnea)
* Autonomic symptoms (sweating called diaphoresis, anxiety)
⚠️ Pathophysiology
* Imbalance:
O₂ Supply «_space;O₂ Demand → Myocardial ischemia
* Causes:
* Atherosclerotic plaque rupture
* Thrombus formation
* Vasospasm or embolism
🚨 ACS Spectrum (From Least to Most Severe)
1. Stable Angina (triggered by exertion, relieved by rest)
2. Unstable Angina (new/worsening chest pain, at rest)
3. NSTEMI (Non-ST Elevation MI)
4. STEMI (ST-Elevation MI)
Both NSTEMI and STEMI show elevated cardiac biomarkers (e.g., troponin), while unstable angina does not.
What are thee Risk factors and Causes of Ischemic Heart Disease?
- it is usually due to Atherosclerosis of coronary arteries
“BAD HEART”
B= BMI
A= age over 65
D= diabetes mellitus
H= Hypertension
E= Ethanol
A= an increase in LDL and decrease HDL
R= relatives with CAD
T= tobacco use
What are the different groups of Ischemic Heart Disease?
🫀 Ischemic Heart Disease (IHD)
A group of conditions caused by reduced blood flow to the heart muscle, usually due to atherosclerosis of the coronary arteries.
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🔥 Major Types of IHD
- Angina (Chest Pain without Myocardial Necrosis)
a) Stable Angina- Triggered by exertion/stress
- Relieved by rest or nitroglycerin
- Fixed atherosclerotic plaques
b) Unstable Angina
- Occurs at rest or with minimal exertion
- Caused by plaque rupture and thrombosis
- Precursor to myocardial infarction
c) Vasospastic (Prinzmetal) Angina
- Transient coronary vasospasm
- Occurs at rest, often at night
- ST elevation during attacks, resolves with nitroglycerin or CCBs
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- Myocardial Infarction (Heart Attack with myocardial necrosis)
a) NSTEMI (Non-ST Elevation MI)- Subendocardial infarction
- Troponins elevated
- No ST elevation on ECG
b) STEMI (ST Elevation MI) - Full-thickness (transmural) infarction
- Troponins elevated
- ST elevation on ECG + Q waves later
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- Sudden Cardiac Death
- Often due to lethal arrhythmias (e.g., ventricular fibrillation)
- Seen in severe CAD or MI
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- Chronic Ischemic Heart Disease
- Slowly progressive heart failure from long-standing ischemia
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- Coronary Steal Syndrome
- Blood is diverted (“stolen”) from stenotic areas when vasodilators are used
- Can worsen ischemia
What is Stable Angina?
- Chest pain that arises WITH exertion or emotional stress
- due to atherosclerosis of coronary arteries
( must have **greater than 70% stenosis to get angina symptoms, otherwise no symptoms present) - there is a stable atherosclerotic plaque with no plaque ulcerations and no thrombus formation
- Reversible injury to myocytes
- O2 demand is not met during exertion
Why is stable angina not part of Acute Coronary Syndrome?
🩺 Definition of Acute Coronary Syndrome (ACS)
ACS refers to sudden, reduced blood flow to the heart due to an acute plaque rupture and thrombus formation, which can rapidly worsen and cause myocardial infarction.
ACS includes:
1. Unstable Angina
2. NSTEMI
3. STEMI
🔬 Summary:
Stable angina is caused by a fixed narrowing of the coronary arteries, which limits blood flow only during increased demand (like exercise). It is predictable and reversible ischemia. There’s no acute change in the plaque, no thrombus formation, and no myocardial injury — so it’s chronic and not “acute.”
In contrast, ACS involves acute plaque instability, thrombus formation, and potentially irreversible myocardial damage.
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What are symptoms of Stable Angina?
- chest pain that lasts less than 20 minutes (longer than this would cause ireeversible injury and cell death)
- ECG shows ST-segment depression
(** SUB-ENDOCAEDIAL ISCHEMIA) - the coronary arteries begin at the epicardium and divide down to the myocardium and endocardium, therefor, underneath the endocardium (furthest from coronary) is most susceptible to damage
- Relieved by rest of nitroglycerine
How does Nitroglycerine work?
- it vasodilates arteries and most importantly veins, this reduces venous return which in turn reduces preload and the stress placed on the heart
What is the hallmark of ST-Depression?
- subendocardial ischemia
What is Unstable Angina?
- chest pain that occurs AT REST
- there is plaque rupture that leads to thrombus formation
- there is incomplete (subtotal occlusion of a coronary artery) that allow small amount of blood to pass through
- presents reversible injury to myocytes
- ECG shows ST-segment depression of T-wave inversion
- reliebed by Nitroglycerine
- high risl of progression to MI because the thrombus can completely occlude the blood vessel
- we see subendothelial ischemia (ST-segment depression)
What is Vasospastic (Prinzmetal) Angina?
- due to coronary artery vasospasm and NOT ATHEROSCLEROSIS
- leads to episodic chest pain unrelated to exertion (spontaneous)
- Represents reversible injury to myocytes (transient)
- ECG shows ST – segment elevation due to transmural ischemia
- Relieved by Nitroglycerine or Calcium channel blockers (CCB)
What is Myocardial Infarction?
- Necrosis of cardiac myocytes (pain longer than 20 mins)
- Due to rupture of atherosclerotic
plaque with thrombosis - Complete occlusion of coronary artery
- Other causes – coronary artery
vasospasm, emboli, and vasculitis
Symptoms include:
* Severe, crushing chest pain ( more than 20 minutes), elephant sitting on chest
* Diaphoresis (sweating)
* Dyspnea (shortness of breath)
* Symptoms NOT relieved by NG
What are most common coronary arteries affectef in an MI?
🫀 Commonly Occluded Coronary Arteries (Descending Order)
1. LAD (Left Anterior Descending artery) — most common = Anterior wall of LV and anterior septum
2. RCA (Right Coronary Artery) = Inferior wall (posterior LV), posterior septum, RV
3. LCx (Left Circumflex artery) = Lateral wall of LV
Each occlusion leads to ischemia → infarction in the corresponding area, which explains the ECG lead changes used in diagnosing STEMIs (ST-segment Elevation MIs).
Picture or coronary arteries impacted in an MI:
What is Subendocardial Infarct? (NSTEMI)
🔴 Subendocardial Infarct (NSTEMI)
Definition:
* Necrosis (cell death) limited to the inner third (subendocardium) of the heart wall. This layer is the most distal portion from the coronary arteries found in Epicardium layer. (less than 50% of myocardial thickness necrosed)
* Partial thickness infarct — does not extend through the full wall.
Cause:
* Usually due to partial occlusion of a coronary artery.
* Common in NSTEMI (Non-ST Elevation Myocardial Infarction).
ECG Findings:
* ST-segment depression, T-wave inversion
* No ST-elevation
* No Q waves
Biomarkers:
* Troponins ↑ (positive troponin indicates myocardial necrosis)
What is a Transmural Infarct? (STEMI)
🔵 Transmural Infarct (STEMI)
Definition:
* Necrosis involves full thickness of the ventricular wall (endocardium → epicardium).
Cause:
* Due to complete occlusion of a coronary artery.
* Classic in STEMI (ST-Elevation Myocardial Infarction)
ECG Findings:
* ST-segment elevation in leads corresponding to area of infarct
* May develop pathologic Q waves (later)
Biomarkers:
* Troponins ↑ (higher elevation than NSTEMI typically)
Differences between the Anginas:
Stable Angina:
* Cause: Fixed atherosclerotic plaque that narrows coronary arteries.
* Trigger: Physical exertion or emotional stress → ↑ O₂ demand.
* Relief: Rest or nitroglycerin (↓ preload and O₂ demand).
* Duration: Short (<20 minutes).
* ECG during pain: ST depression (subendocardial ischemia).
* Plaque status: Intact fibrous cap, no rupture.
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Unstable Angina:
* Cause: Rupture of an atherosclerotic plaque with incomplete thrombus formation.
* Trigger: Can occur at rest or with minimal exertion.
* Relief: Poor or partial response to nitroglycerin.
* Duration: More prolonged or more frequent episodes.
* ECG: ST depression or T-wave inversion, but no troponin elevation.
* Risk: High risk of progression to MI.
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Prinzmetal (Vasospastic) Angina:
* Cause: Transient coronary artery spasm (not due to plaque).
* Trigger: Often occurs at rest, especially at night or early morning.
* Relief: Responds well to nitroglycerin or calcium channel blockers.
* ECG: Transient ST elevation during chest pain.
* Typical patient: Younger, may be associated with smoking, migraines, Raynaud’s.
What is the most sensitive and specific marker for MI?
- Troponin I
Rises 2 – 4 hours after infarction - Peaks at 24 hours
- Returns to normal by 7 – 10 days
What is the hallmark for irreversible injury?
- Membrane Damage
- with membrane damage, the enzymes inside the cardiac myocytes will leak out into bood (after injury)
What is most useful for detecing reinfarction days after an MI?
- CK-MB
Rises 4-6 hours after infarction - Peaks at 24 hours
- Returns to normal by 48 hours
** troponin I is not a good marker to prove a 2nd MI because it stays elevated 7-10 days after infarction, but CK-MB is BEST because it goes down by day 2 and can prove second MI at day 3,4,5, etc…
What is myocardia reperfusion?
💥 What Is Reperfusion?
Reperfusion means restoring blood flow to the heart muscle (myocardium) that’s been blocked — usually by a clot in a coronary artery.
🧠 Why It Matters:
When a coronary artery is blocked, the heart muscle gets no oxygen, and cells start dying (necrosis) within 20–30 minutes.
If you restore blood flow early, you can:
* ✅ Save some cells that are injured but not yet dead
* ✅ Improve heart function
* ✅ Reduce complications and death
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🔓 How Do We Achieve Reperfusion?
There are 2 main ways:
- Thrombolytic Therapy (aka Fibrinolysis)
- Uses drugs that dissolve clots (this is what “fibrinolysis” means).
- Examples:
- Tissue plasminogen activator (tPA)
- Streptokinase
- Mechanism:
- They activate plasminogen → turns into plasmin → plasmin breaks down fibrin, the main protein in blood clots.
- Used when: No immediate access to catheterization lab for angioplasty.
- Angioplasty (Percutaneous Coronary Intervention - PCI)
- A catheter-based procedure to open the blocked artery.
- Often done with a stent to keep the artery open.
- Preferred method if available quickly (within 90 mins of first medical contact).
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✅ Early Reperfusion Benefits:
* 🛡️ Saves ischemic myocardium before it becomes necrotic
* 💪 Preserves heart function
* 📉 Reduces mortality (both short and long term)
* ⏳ Best when done early — within the first 2–3 hours is ideal
What are damages and changes that can occur due to Reperfusion?
contraction band necrosis and wavy fibers, both of which are microscopic changes seen in myocardial infarction, especially in the context of reperfusion. Let’s break it down clearly:
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💀 Contraction Band Necrosis (CBN)
🔍 What is it?
A type of irreversible myocardial injury seen after reperfusion of previously ischemic tissue.
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🧬 Key Features:
* 🔴 Eosinophilic transverse bands (pink-staining stripes under the microscope)
* 💪 Made of hypercontracted sarcomeres
* 📌 Occurs in dead or dying myocytes
* ⚡ Caused by massive calcium influx during reperfusion
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⚙️ Pathophysiology:
1. Ischemia → ATP levels drop → Ca²⁺ accumulates slowly
2. Reperfusion suddenly floods the cell with oxygen and Ca²⁺
3. Dead cells can’t regulate Ca²⁺ → uncontrolled contraction
4. Sarcomeres hypercontract, forming dense contraction bands
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🧨 Why is it a problem?
* Contributes to reperfusion injury
* Causes more cell damage, arrhythmias, and inflammatory response
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🌊 Wavy Fibers
🔍 What is it?
* Early histologic change in viable but ischemic myocardium
* Seen at borders of infarcted area
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🧬 Key Features:
* Thin, elongated, and wavy-looking myocardial fibers
* Result of mechanical stretching of weakened (ischemic) myocytes by surrounding contracting healthy tissue
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⚙️ Pathophysiology:
* Happens within the first few hours of MI
* Indicates early, reversible ischemic injury
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🔄 Reperfusion Injury
When blood supply is restored to ischemic tissue, it can paradoxically worsen cell injury due to ROS, calcium overload
What are features of Contractile Bands?
Contraction bands
* Zebra-like lines
* Irreversibly injured
myocytes
* Loss of nuclei
* Seen within first 4-24
hours
How does a reperfusion injury happen?
- returning O2 can cause generation of free radicals that can further the myocardium
- this happens because elevated levels of cardiac ezymes in patients, so once you open up blocked vessels, the cardiac enzymes continue to rise = reperfusion injury!
- giving back blood gives back O2 which results in the formation of free radicals which then further damage the myocardium leading to increased cardiac enzymes
📈 Link to Cardiac Enzymes
* Troponin and CK-MB are released from necrotic myocytes.
* When you reperfuse:
* 💥 More myocytes die due to reperfusion injury.
* 🧪 So more enzymes are released into blood, causing a continued or second rise in cardiac enzymes.
* This explains why enzyme levels stay elevated or rise again after reperfusion — not necessarily ongoing infarction, but reperfusion damage.
What are the 3 phases of morphological changes in myocardial infarction?
- coagulative necrosis
- inflammation
- healing
** remember less than 4 hours nothing happens
