Diseases of Myocardium, Pericardium & Tumours Flashcards
(23 cards)
What is Myocarditis?
Inflammation of myocardium associated with myocyte necrosis and
degeneration.
* MC seen in children (1-10 years old)
Microbial pathogens:
* Coxsackievirus B (MCC)
* Trypanosoma cruzi (Chagas disease)
* Trichinella spiralis (Biopsy: Eosinophils & giant cells)
* Borrelia burgdorferi (Lyme Disease)
* Corynebacterium diphtheria (Biopsy: Fatty change with foci of necrosis)
- Endocardial biopsy done if infection is suspected
- Focal myocyte necrosis
- A lymphocytic infiltrate is highly predictive of Coxsackievirus
Clinical findings:
* Myocarditis can be asymptomatic.
* Can cause acute heart failure or evolve into dilated cardiomyopathy
* Labs:
* Increased troponins & CK-MB.
The interstitial shown here within the myocardium are characteristic for a viral myocarditis, which is
probably the most common type of myocarditis. Many of these cases are probably subclinical. Viral myocarditis can be a
cause for sudden death in young persons. There is often minimal myocardial fiber necrosis. The most common viral agent
is Coxsackie B virus
What is Dilated Cardiomyopathy?
- Dilation of all four chambers of
the heart - Most common form of
cardiomyopathy - massive stretching of the heart impairs contraction and systole
- stretching of the heart and valves makes them regurgitate
- stretching the heart also adds stretch to the conduction system where we see arrythmias
Most commonly idiopathic; other causes
include
* Genetic mutation
* Myocarditis (we see Coxackie virus and lymphatic infiltrate) (a late complication of Myocarditis can be dilated cardiomyopathy)
* Alcohol abuse
* Drugs (e.g., doxorubicin)
* Pregnancy
- Treatment is Heart Transplant
What is Hypertrophic Cardiomyopathy?
- Massive hypertrophy of the left
ventricle - Usually due to genetic mutations
in sarcomere proteins; most
common form is autosomal
dominant - Decreased cardiac output
- Sudden death due to ventricular arrhythmias; common cause of
sudden death in young athletes. - Syncope with exercise: due to assymetrical Interventricular septum thickening causing a black of the aortic valve
** Myofiber hypertrophy with disarray is seen: myocytes should be nicely in order and here there is DISORDER.
** MUTATION IN B-MYOSIN HEAVY CHAIN (MC), MYBPC3 AND TROPONIN
Why is there Diastolic Dysfunction is Hypertrophic Cardiomyopathy but not Systolic dysfunction?
✅ In Hypertrophic Cardiomyopathy (HCM):
There is diastolic dysfunction, not systolic (or “ancestolic”) dysfunction.
Here’s why:
🧱 1. Thick, stiff heart muscle
* In HCM, especially the left ventricle, the wall is abnormally thickened.
* This makes the heart stiff and less compliant.
🩸 2. Problem = poor filling
* During diastole, the heart is supposed to relax and fill with blood.
* But in HCM, the thick muscle doesn’t relax well → diastolic dysfunction.
* Less blood fills the ventricle → less gets pumped out (low stroke volume).
💪 3. Systolic function is usually normal or hyperdynamic
* The heart contracts just fine — it’s not a weak pump.
* In fact, ejection fraction may look high, because it’s squeezing a smaller amount of blood very strongly.
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❌ Not “ancestolic” dysfunction
* You probably meant “systolic dysfunction”.
* But HCM does not have classic systolic dysfunction like in dilated cardiomyopathy.
* The problem in HCM is diastolic filling, not contraction.
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🧠 Simple takeaway:
In HCM, the heart is strong but stiff.
It has diastolic dysfunction because it can’t relax and fill properly.
Systolic function is preserved or even too strong.
💥 Hypertrophic Cardiomyopathy (HCM) — Dual Problem:
1️⃣ Primary Problem: Diastolic Dysfunction
* The main, underlying issue in HCM is a stiff, hypertrophied left ventricle.
* The thickened ventricular walls don’t relax properly → impaired filling during diastole.
* This is why HCM is classified as a diastolic heart failure problem.
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2️⃣ Secondary Problem: Dynamic Outflow Obstruction (Functional Aortic Stenosis)
* In some patients (especially with septal hypertrophy), the thickened septum can:
* Bulge into the left ventricular outflow tract (LVOT) during systole.
* Cause the anterior mitral valve leaflet to get sucked toward the septum (systolic anterior motion, SAM) → this worsens the blockage.
* So now, blood can’t leave the heart properly during systole.
* This creates a dynamic obstruction that mimics aortic stenosis → it’s worse when preload is low or afterload drops (like during standing or exercise).
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⚡ So, Why Is This Important?
* The root of the disease: 👉 Diastolic dysfunction.
* The famous complication: 👉 Systolic outflow obstruction.
* Both happen.
✔️ The heart fills poorly → diastolic problem.
✔️ The heart empties poorly when the LVOT is blocked → systolic problem.
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💡 Think of HCM as:
✔️ Always a diastolic problem.
✔️ Sometimes a functional systolic problem if there’s LVOT obstruction.
Why is there Functional Aortic Stenosis in Hypertrophic Cardiomyopathy?
💡 Why is it called functional aortic stenosis in hypertrophic cardiomyopathy (HCM)?
Because it mimics the effects of real aortic stenosis — but the valve itself is normal.
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🎯 What’s happening in HCM?
In hypertrophic obstructive cardiomyopathy (HOCM), part of the interventricular septum is abnormally thickened — especially near the left ventricular outflow tract (LVOT).
What does that cause?
1. During systole (contraction), the thick septum bulges into the outflow tract.
2. The anterior mitral valve leaflet also gets pulled toward the septum (called SAM – systolic anterior motion).
3. These two things narrow the path that blood takes from the LV → aorta.
➡️ This creates a dynamic obstruction, meaning it changes with things like heart rate, preload, and afterload.
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🤔 So why “functional aortic stenosis”?
Because:
* The outflow obstruction behaves like aortic stenosis — causing a systolic murmur, pressure overload, and LV hypertrophy.
* BUT — the aortic valve is normal!
* The problem is not the valve, but the muscle obstructing the exit from the ventricle.
So it’s called “functional” because the function of blood exiting the LV is impaired, even though the valve itself is structurally fine.
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🧠 Simple takeaway:
In HCM, the thick septum blocks blood flow out of the LV, making it look and sound like aortic stenosis, but the valve is normal — so we call it functional aortic stenosis.
What is Restrictive Cardiomyopathy?
- Decreased compliance of the
ventricular endomyocardium - Restricts filling during diastole
Causes
* Amyloidosis
* Sarcoidosis
* Hemochromatosis
* Endocardial Fibroelastosis
(children)
* Loefller syndrome
Presents as congestive heart failure
* Classic finding is low-voltage ECG
* Diminished QRS amplitudes
What is difference in how Systolic and Diastolic Blood Pressures change?
✅ Not enough blood reaching the aorta vs.
🚫 Blood escaping from the aorta (like in aortic regurg)
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💡 Let’s use a simple analogy first:
Imagine the aorta is a water balloon (the arteries), and the heart is the faucet that fills it.
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🔁 1. In aortic regurgitation:
* The balloon gets filled (during systole).
* But then… the water leaks back out through a hole (the faulty valve) during diastole.
* So the balloon rapidly deflates between beats → low diastolic pressure.
✅ Diastolic pressure falls a lot because the blood is literally leaking out of the aorta during diastole.
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🧊 2. In aortic stenosis or weak ventricles (DCM, HCM):
* The faucet (heart) is weak or blocked, so it doesn’t push in much water to begin with.
* But! There’s no leak in the balloon.
* So even though it fills less, what’s inside stays inside during diastole.
➡️ Diastolic pressure might be normal or only mildly low, because no blood is escaping.
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🔬 Let’s say it in heart terms:
🔴 Aortic regurgitation:
* Blood actively flows backward from the aorta into the LV during diastole.
* This rapid emptying of the aorta lowers diastolic pressure sharply.
* The aorta can’t “hold” its pressure between beats.
🟡 Aortic stenosis, DCM, HCM:
* These problems reduce the stroke volume, meaning less blood is pumped into the aorta.
* So systolic pressure is low (because there’s less force and volume).
* But because the aorta holds onto whatever blood it gets, diastolic pressure doesn’t fall as sharply.
* There’s no backflow to suck pressure out of the aorta.
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🧠 Super-simple takeaway:
Aortic regurg = pressure is lost because blood leaks out.
Weak pump or tight valve = pressure is low because less blood goes in, but what’s in there stays put.
Does Restrictive Cardiomyopathy have Hypertrophy?
🧱 What is restrictive cardiomyopathy (RCM)?
* The heart muscle becomes stiff, not thick.
* This stiffness makes it hard for the ventricles to fill during diastole.
* But the walls of the heart are not hypertrophied (not thickened).
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🧠 So why no hypertrophy in RCM?
Because the problem isn’t pressure overload — it’s infiltration or fibrosis making the myocardium noncompliant (stiff and resistant to stretch), not overworked.
Compare this to hypertrophy:
* Hypertrophy (like in HCM or aortic stenosis) happens when the heart is working against high pressure over time.
* In RCM, the issue is not “working harder,” it’s a mechanical problem: the wall can’t relax and expand.
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🎯 Causes of RCM often involve:
* Infiltrative diseases like amyloidosis or sarcoidosis
* Fibrosis from radiation or endomyocardial fibrosis
* Iron overload (hemochromatosis)
These conditions make the myocardium stiff, not thick.
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🧠 Simple answer:
In restrictive cardiomyopathy, there’s no hypertrophy because the heart isn’t overworking — it’s just stiffened by disease, so it can’t fill, but it doesn’t need to grow thicker.
If there is diminished QRS amplitude in Restrictive Cardiomyopathy, does that mean Systole is impacted?
🟨 First: What does a low QRS amplitude mean?
* The QRS complex on an ECG represents ventricular depolarization — the electrical signal that causes the ventricles to contract.
* Low voltage QRS means the electrical signal is dampened — it’s not getting transmitted strongly to the ECG leads.
So it’s about signal strength, not necessarily muscle strength.
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🟦 In restrictive cardiomyopathy (RCM):
* The myocardium is stiff, often from infiltrative disease (like amyloidosis).
* These infiltrative materials (like amyloid protein) physically block or insulate the transmission of electrical signals.
➡️ That’s why the QRS amplitude is low — not because the heart can’t beat, but because the electrical signal is weakened or muffled.
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💥 So does low QRS mean systole is impaired?
❌ Not directly.
* You can have low QRS amplitude but preserved systolic contraction — especially early in restrictive cardiomyopathy.
* Diastolic dysfunction (trouble filling) is the main problem, not systolic dysfunction.
* But in late-stage or severe cases, systolic function may eventually decline too.
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🧠 Simple takeaway:
Low QRS amplitude in restrictive cardiomyopathy reflects electrical signal dampening (often due to amyloid or fibrosis),
but systolic function can still be normal, especially early on.
The main problem is stiffness and poor filling, not weak contraction
What is Acute Pericarditis?
🔥 What is acute pericarditis?
It’s inflammation of the pericardium, the sac that surrounds the heart.
* Normally, there’s a thin layer of fluid between the two pericardial layers to prevent friction.
* When inflamed, the pericardium becomes irritated, often producing extra fluid → this is called a pericardial effusion.
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💧 Why is it associated with pericardial effusion?
* Inflammation causes capillaries in the pericardium to leak → this leads to fluid accumulating in the pericardial space.
* This is the body’s way of responding to inflammation — like swelling in other tissues.
* If too much fluid builds up quickly, it can lead to cardiac tamponade, a medical emergency.
So:
Pericarditis causes fluid accumulation (effusion) because inflammation leads to leakage into the pericardial space.
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📍 Why does pericarditis happen after an MI, rheumatic fever, or Coxsackie virus infection?
Because all of these conditions can cause inflammation of the heart or nearby structures, and that inflammation can spread to the pericardium.
- 🩺 After an MI (heart attack):
- Necrotic (dead) heart muscle releases inflammatory signals.
- This can irritate the pericardium → acute pericarditis.
- Can happen:
- Early (1–3 days) = local inflammation from necrosis.
- Or late (weeks later) = Dressler syndrome (autoimmune pericarditis from immune response to heart tissue).
- 💉 Acute rheumatic fever:
- It’s an autoimmune reaction to strep infection.
- Your immune system attacks not just the joints and heart valves, but also the pericardium.
- So pericarditis is one of the “pancarditis” components (endo-, myo-, and pericarditis).
- 🦠 Coxsackie virus (and other viruses):
- These viruses cause viral myocarditis, but the infection often spreads to the pericardium, or the immune system attacks both layers.
- So you get pericarditis + effusion as part of the response.
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🧠 Super simple takeaway:
Acute pericarditis is inflammation of the sac around the heart,
and it’s associated with effusion because inflammation leaks fluid.
It often follows things that damage or inflame the heart, like MI, rheumatic fever, or viral infection.
What are the different types of Pericarditis?
- Depending on nature of fluid accumulated
acute pericarditis can be classified into: - Fibrinous pericarditis (MC type):
- MI, Acute RF, & uremia
- Serous pericarditis:
- SLE & viral infection
- Purulent pericarditis:
- Bacterial infections
- Hemorrhagic pericarditis:
- Tumors (MCC), TB, & cardiac surgery
- Caseous pericarditis:
- TB
What are characteristics of Fibrinous Pericarditis?
🧶 What is fibrinous pericarditis?
It’s a type of acute pericarditis where the pericardium becomes:
* Inflamed
* Covered in fibrin, a sticky protein involved in clotting
* Dry and rough, not fluid-filled like serous pericarditis
It’s often called “bread-and-butter” pericarditis because under the microscope (or even grossly), the rough pericardial surfaces look like buttered bread pulled apart — shaggy, granular, and sticky.
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📈 Clinical features:
* Sharp chest pain, often worse with inspiration and better when leaning forward
* Pericardial friction rub on auscultation — sounds like leather rubbing together
* May or may not have significant effusion
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⏱️ When does fibrinous pericarditis happen?
It’s classically associated with inflammatory or necrotic conditions, especially:
🩸 1. Post–myocardial infarction
* Early: within 1–3 days after a transmural infarct
* Due to local inflammation of the pericardium
* (Later: autoimmune form = Dressler’s syndrome = more serofibrinous or hemorrhagic)
🔥 2. Rheumatic fever
* As part of pancarditis, inflammation can involve the pericardium and deposit fibrin.
🦠 3. Uremia
* Seen in patients with advanced kidney failure
* Very common cause of fibrinous pericarditis
🧬 4. Radiation to the chest
🦠 5. Viral infections (e.g., Coxsackievirus)
* Viral pericarditis can sometimes have a fibrinous component, though it may also be serous
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🧠 Simple takeaway:
Fibrinous pericarditis = dry, rough, fibrin-coated pericardium.
Happens in MI (early), rheumatic fever, uremia, radiation, and infections.
Classically causes a friction rub and sharp chest pain relieved by sitting up.
Can Fibrinous Pericarditis lead to Constrictive Pericarditis?
Yes — fibrinous pericarditis can lead to constrictive pericarditis, especially if the inflammation is recurrent or unresolved. Let’s walk through how that happens in a simple, logical way:
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🧱 Step-by-step: From fibrinous to constrictive pericarditis
- 🔥 Fibrinous inflammation begins
- Fibrin is laid down on the inflamed pericardial surfaces.
- The pericardial layers become rough, sticky, and irritated.
- 🧶 Fibrin is not cleared properly
- Normally, fibrin should be removed as inflammation resolves.
- But if inflammation is chronic, persistent, or severe, the fibrin stays and becomes organized.
- 🧬 Healing by fibrosis (not regeneration)
- The body starts replacing fibrin with collagen and scar tissue.
- This leads to fibrosis, thickening, and even calcification of the pericardium over time.
- 🔒 Constriction develops
- The pericardium becomes stiff and non-compliant.
- It starts to restrict the normal filling of the heart during diastole.
- That’s called constrictive pericarditis.
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🧠 Simple definition:
Constrictive pericarditis = a rigid, scarred pericardium that prevents the heart from expanding normally during diastole.
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🚩 Conditions that increase the risk of this progression:
* Tuberculosis (most common cause worldwide)
* Repeated pericarditis episodes
* Uremic pericarditis if not treated
* Post-radiation or post-surgical pericarditis
* Dressler syndrome (rarely)
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📌 So, in short:
Fibrinous pericarditis can → constrictive pericarditis
if the inflammation becomes chronic, leading to fibrous scarring and thickening of the pericardium.
What are symtpoms of acute pericarditis?
🫀 First, what’s normally supposed to happen during inspiration?
* When you inhale, the pressure in your chest (intrathoracic pressure) drops.
* This allows more blood to return to the right atrium from the veins → JVP should go down.
🟢 Normal: Inspiration → more venous return → neck veins collapse a little → JVP decreases
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❌ What goes wrong in cardiac tamponade / large pericardial effusion?
* The heart is compressed by fluid around it.
* The ventricles can’t expand to take in more blood — they’re being squeezed.
* So when venous blood returns during inspiration, the right atrium and ventricle can’t fill properly.
* Blood backs up into the veins — especially the jugular veins.
🔴 Result: Neck veins distend during inspiration instead of collapsing.
This is called:
Kussmaul’s sign = JVP rises during inspiration (abnormal)
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🎯 And why is JVP raised overall?
Because in tamponade, blood can’t enter the heart easily at all — even at rest. It builds up in the venous system, especially the jugular veins → chronically raised JVP.
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🧠 Summary (super simple):
* Raised JVP = blood can’t get into heart → backs up into veins
* Kussmaul’s sign = during inspiration, veins should collapse → but they distend instead because the heart is too compressed to accept the extra blood
Does Acute Pericarditis cause Cardiac Tamponade?
🩸 What is cardiac tamponade?
* It’s when fluid builds up so much or so fast in the pericardial sac that it compresses the heart, especially during diastole.
* This prevents the chambers from filling → decreased cardiac output, hypotension, shock.
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🔥 What is acute pericarditis?
* It’s inflammation of the pericardium.
* This inflammation often causes a pericardial effusion (fluid leaking into the sac).
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So, does acute pericarditis always cause tamponade?
❌ No — most cases of acute pericarditis cause only a small/moderate effusion, and:
* The fluid accumulates gradually.
* The pericardium can stretch to accommodate it.
* So, no tamponade in most cases.
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✅ But: Tamponade can occur if:
* The effusion accumulates rapidly (even a small amount can be dangerous if it’s fast).
* Or the effusion gets very large over time.
* Or if the pericardium is already stiff and can’t expand (like in cancer, TB, or radiation pericarditis).
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🧠 Easy rule:
Acute pericarditis can cause pericardial effusion.
Tamponade happens only if that fluid builds up fast or in large amounts.
What is Constrictive Pericarditis?
🧱 What is constrictive pericarditis?
A chronic condition where the pericardium becomes thickened, fibrotic, stiff, and sometimes calcified, so it restricts the heart’s ability to fill during diastole.
So even though the heart muscle itself is normal, the sac around it (the pericardium) becomes like a tight, inelastic shell, squeezing the heart and preventing normal blood filling.
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🧪 Why does this happen?
It’s usually the end result of long-term or repeated inflammation of the pericardium.
🩺 What happens in the body?
Because the heart can’t fill properly during diastole, you get signs of:
* Right-sided heart failure: raised JVP, ascites, leg swelling
* Kussmaul’s sign: JVP rises with inspiration
* Pericardial knock: early diastolic sound due to sudden stop in ventricular filling
** TB is MCC worldwide in developing countries
** In US, most cases idiopathic
How can acute pericarditis lead to constrictive pericarditis?
🔥 Step 1: Acute pericarditis begins
* There’s inflammation of the pericardial layers.
* This can be due to infection (like viral), autoimmune disease, MI, or uremia.
* Inflammation may cause a fibrinous or serous effusion.
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🧶 Step 2: Fibrin and inflammation stick the pericardial layers together
* The two layers of the pericardium — visceral and parietal — become sticky and start to adhere.
* Normally they’re smooth and glide easily, but now they’re rough and inflamed.
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🧬 Step 3: Healing by fibrosis (not regeneration)
* The body tries to “heal” this damage.
* But it replaces the damaged tissue with fibrous scar tissue (not the original smooth tissue).
* This scar tissue makes the pericardium thicker, stiffer, and less elastic.
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🧱 Step 4: Pericardium becomes fixed and rigid → constriction
* Over time (weeks to months), that fibrous pericardium may:
* Become calcified
* Become tight like a shell around the heart
* It prevents the heart from filling normally during diastole.
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⏱️ When does this happen?
* Usually not right away.
* It can take weeks to months after acute pericarditis, especially if:
* The inflammation is recurrent (keeps coming back)
* The cause is severe (e.g., TB, radiation)
* The patient doesn’t respond to treatment
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🧠 Summary (super simple):
Acute pericarditis → inflammation → fibrin + adhesions → scarring → stiff pericardium → constrictive pericarditis
Acute pericarditis (inflammation) → leads to fibrinous pericarditis (fibrin deposits make pericardial layers sticky and rough) → if healing is abnormal, the fibrin and inflammation get replaced by scar tissue → resulting in fibrous thickening of the pericardium → this stiff, fibrotic pericardium can cause constrictive pericarditis (the heart gets squeezed and can’t fill properly).
So yes, fibrinous (or fibrous) pericarditis is an intermediate step on the way to constrictive pericarditis if the inflammation isn’t resolved cleanly.
What are clinical outcomes of Constrictive Pericarditis?
- Incomplete filling of cardiac chambers:
The thick, fibrotic, stiff parietal pericardium restricts diastolic expansion of the ventricles → so the heart can’t fill fully → leads to decreased cardiac output (CO).- Pericardial knock:
This is an abnormal early diastolic sound you hear on auscultation.
It happens when the ventricles expand quickly at the start of diastole but then suddenly hit the stiff, thickened pericardium, causing a “knock” sound.
- Pericardial knock:
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So in short:
Thickened pericardium → restricted heart filling → low CO + pericardial knock sound during diastole
What is a Myxoma?
What is a myxoma?
* It’s a non-cancerous (benign) tumor that grows inside the heart.
* Made of soft, jelly-like tissue (that’s why it looks gelatinous).
* It’s like a little blob of soft stuff inside the heart, often attached inside the left atrium (the chamber that receives blood from the lungs).
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Why does it matter?
* This blob can block the blood flow through the mitral valve (the door between the left atrium and left ventricle).
* When it blocks this valve, blood can’t flow smoothly, so you might feel dizzy or faint (syncope).
* It can also cause symptoms like shortness of breath or irregular heartbeat.
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Quick facts:
* Most common primary heart tumor in adults (meaning it starts in the heart, not spread from somewhere else).
* Looks like jelly because of lots of gooey material inside.
* It’s not cancer, but because it blocks blood flow, it’s dangerous and often needs surgery.
What is Cardiac Rhabdomyoma
💗 What is a rhabdomyoma?
* A benign tumor made of heart muscle cells (that’s why it’s called a “rhabdo”myoma — rhabdo = muscle).
* It’s actually a hamartoma, which means it’s not a real tumor growing out of control, but rather a disorganized overgrowth of normal heart tissue.
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👶 Who gets it?
* Most common primary heart tumor in children.
* Strongly associated with tuberous sclerosis — a genetic disorder that causes benign tumors in many organs (brain, skin, heart, etc.).
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📍 Where is it found?
* Usually grows inside the ventricles.
* It may be multiple and intramyocardial (growing within the muscle of the heart).
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🧪 What are spider cells?
* On histology, rhabdomyomas show “spider cells” — these are:
* Large heart muscle cells with lots of clear cytoplasm.
* The nucleus sits in the center, and strands of cytoplasm stretch out like spider legs. (EISONOPHILIC)
* These spider cells are a classic microscopic clue for diagnosing rhabdomyoma.
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🚨 Why is it important?
* Even though it’s benign, it can cause problems if:
* It blocks blood flow inside the heart.
* It disturbs the electrical system, causing arrhythmias.
What are Metastatic heart tumours?
metastatic tumors to the heart, which are actually more common than primary heart tumors!
Here’s a super clear breakdown:
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🧬 What are metastatic cardiac tumors?
* These are cancers from other parts of the body that spread to the heart.
* They’re not originally from the heart, but travel there through the blood or lymph.
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💥 More common than primary tumors?
Yes! Tumors that start somewhere else and spread to the heart are much more common than tumors that begin in the heart like myxoma or rhabdomyoma.
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🧪 Common cancers that spread to the heart:
* Breast cancer
* Lung cancer
* Melanoma (skin cancer that spreads widely)
* Lymphoma
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📍 Where do they go in the heart?
* Most commonly involve the pericardium (the sac around the heart).
* This can cause a pericardial effusion — buildup of fluid around the heart.
* If severe, this can lead to cardiac tamponade (where the heart gets compressed and can’t pump properly).
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🔑 Key points to remember:
* Metastatic > primary cardiac tumors in frequency.
* Pericardial involvement is most common → causes effusion.
* Can lead to chest pain, muffled heart sounds, dyspnea, or tamponade.
Is Dilated Cardiomyopathy congestive?
🫀 Why does alcohol cause dilated cardiomyopathy?
Because chronic alcohol use is toxic to heart muscle cells.
1. Direct toxicity:
Alcohol (especially in large amounts over years) damages the mitochondria inside heart cells → less energy → weaker contractions.
2. Thiamine (Vitamin B1) deficiency:
Alcoholism often causes poor nutrition. A lack of thiamine can lead to wet beriberi, which also weakens the heart.
3. Leads to dilation:
The heart muscle gets weak → can’t pump well → blood builds up inside the heart → chambers stretch and dilate.
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💧 Why is it called congestive cardiomyopathy?
Because the weak, dilated heart can’t pump blood forward properly, so blood backs up (gets “congested”) in the lungs and body.
This causes:
* Pulmonary congestion → shortness of breath
* Systemic congestion → leg swelling, jugular venous distension, ascites
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🧠 In short:
* Alcohol → toxic to heart → weak pump → heart dilates
* “Congestive” = blood backs up in lungs and body because heart can’t push it forward
Aren’t the other CM congestive too?
🤔 Is only dilated cardiomyopathy called congestive cardiomyopathy?
Yes — technically, the term “congestive cardiomyopathy” is usually used to describe dilated cardiomyopathy because it’s the one most strongly associated with overt heart failure and congestion (fluid buildup).
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🫀 What makes dilated cardiomyopathy “congestive”?
* The heart is flabby and weak, so it can’t pump blood forward.
* Blood backs up into the lungs (→ pulmonary edema) and body (→ swelling).
* That’s classic congestive heart failure: low output + fluid overload.
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💡 Why aren’t hypertrophic or restrictive cardiomyopathies usually called “congestive”?
* They can eventually cause heart failure, but:
* In hypertrophic cardiomyopathy, the heart is too thick and stiff — the problem is diastolic filling, not pumping.
* In restrictive cardiomyopathy, the heart muscle is rigid, not weak — again, it’s a filling problem.
➡️ They can lead to symptoms of congestion, but they’re not the classic picture of “congestive cardiomyopathy.”
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✅ Summary:
* “Congestive cardiomyopathy” = Dilated cardiomyopathy (weak, dilated pump + fluid overload).
* Other types (hypertrophic, restrictive, arrhythmogenic, etc.) can cause heart failure, but we don’t usually call them “congestive.”
