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❤️ HEART PATHOLOGY — MUHS EXAM NOTES

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1. ATHEROSCLEROSIS

Definition (1 liner for exam)

Atherosclerosis is a progressive disease of the intima of large and medium-sized arteries, characterized by formation of atheromatous plaques (lipid-rich lesions).

Risk Factors (Very important — frequently asked)

LDL vs HDL — Easy Trick

• LDL = "Bad" cholesterol → delivers cholesterol to tissues → increases risk
• HDL = "Good" cholesterol → removes cholesterol from tissues via bile → decreases risk
• Normal cholesterol: 140–240 mg/dL

Pathogenesis — Response to Injury Hypothesis (Steps)

1. Endothelial injury/dysfunction (due to HTN, smoking, high LDL, etc.)
2. Monocytes adhere to damaged endothelium and migrate into intima
3. Monocytes → transform into macrophages → engulf oxidized LDL → become foam cells
4. Smooth muscle cells migrate from media into intima (triggered by PDGF, FGF)
5. Smooth muscle cells proliferate and produce ECM (collagen + proteoglycans)
6. Lipid accumulates both inside cells and outside → plaque grows

Stages of Atheromatous Plaque (remember: 1 to 6)

1. Type 1 – Fatty dot (isolated foam cells; NOT visible to naked eye)
2. Type 2 – Fatty streak (earliest visible lesion)
3. Type 3 – Intermediate lesion
4. Type 4 – Atheroma
5. Type 5 – Mature atherosclerosis (fibroatheroma)
6. Type 6 – Complicated lesion

🔑 Exam trick: "Fatty dot = earliest lesion; Fatty streak = earliest visible lesion"

Microscopy of Fatty Streak

• Foam cells (lipid-filled macrophages) under the endothelium
• Lipid-containing smooth muscle cells
• Few lymphocytes; small lipid droplets, collagen, proteoglycans

Sites of Atherosclerosis (most to least affected)

• Abdominal aorta > coronary arteries > popliteal > carotid

Complicated Plaques — Complications

• Calcification (vessel cracks like egg-shell)
• Ulceration
• Thrombosis
• Hemorrhage
• Aneurysmal dilatation

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2. MYOCARDIAL INFARCTION (MI)

Definition

MI = Coagulative necrosis of cardiac muscle due to prolonged severe ischemia (most commonly due to atherosclerosis of coronary arteries).

Risk Factors — Same as Atherosclerosis

Sequence of Events (Pathogenesis — step by step)

1. Acute Plaque Change → sudden rupture/fissuring of atheromatous plaque → exposes thrombogenic material
2. Microthrombi formation → platelets adhere, activate, aggregate → partial/complete occlusion
3. Vasospasm → activated platelets + inflammatory cells release mediators → artery narrows further
4. Coagulation pathway activated → tissue factor released → thrombus grows bigger
5. Complete vessel occlusion → within minutes
6. Myocardial necrosis → coagulative necrosis of the area supplied by that coronary artery

Which artery → which area affected

• LAD (Left Anterior Descending) → anterior wall of left ventricle (most common, ~40–50%)
• RCA (Right Coronary Artery) → posterior/inferior wall
• LCX (Left Circumflex) → lateral wall

Morphology (Gross & Microscopic changes with time — very commonly asked)

Complications of MI

• Arrhythmias (most common cause of death in first few hours)
• Left ventricular failure → pulmonary edema
• Cardiogenic shock
• Ventricular aneurysm
• Mural thrombus (clot in heart chamber) → embolism
• Pericarditis (Dressler's syndrome)
• Rupture of heart wall, papillary muscle, or septum

Lab Markers (important)

• Troponin I & T → most specific and sensitive (rise in 3–4 hrs, peak 24 hrs)
• CK-MB → cardiac-specific, rises in 4–8 hrs
• LDH → late marker (peaks 3–6 days)

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3. INFECTIVE ENDOCARDITIS (IE)

Definition

IE = Infection of heart valve endocardium by microorganisms, forming vegetations (masses of fibrin, platelets, and microorganisms) on valve leaflets.

Two Types

Pathogenesis (Steps)

1. Underlying valve damage → turbulent blood flow
2. Non-bacterial thrombotic endocarditis (NBTE) forms — sterile platelet-fibrin thrombus
3. Bacteremia → bacteria attach to thrombus on valve
4. More fibrin + platelets deposited → bacteria buried (protected from immune system)
5. Bacteria proliferate → form colonies in vegetation
6. Vegetation detaches → infective emboli → spread to organs/brain

Morphology

• Vegetations: irregular, warty, friable masses on valve leaflets
• Most common valve: Mitral valve → then Aortic
• In IV drug users: Tricuspid valve

Complications of IE

• Ring abscess (erodes into myocardium)
• Perforation/rupture of valve
• Valvular stenosis or insufficiency
• Suppurative pericarditis

• Emboli (septic emboli from left side → brain, kidney, spleen; right side → lungs)
• Janeway lesions — small, non-tender hemorrhagic lesions on palms/soles
• Osler nodes — tender subcutaneous nodules on finger pulp
• Roth spots — retinal hemorrhages with white centre
• Focal segmental glomerulonephritis — "flea-bitten" kidney appearance (antigen-antibody deposition)

Duke Criteria for Diagnosis

• Major: Positive blood cultures + echocardiography evidence
• Minor: Predisposing heart disease, fever, vascular phenomena (Janeway, emboli), immunological (Osler, Roth spots)
• Gold standard: Culture of organism from valve

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4. RHEUMATIC FEVER & RHEUMATIC HEART DISEASE (RHD)

Definition

Rheumatic fever = Acute, post-streptococcal, immune-mediated, multisystem inflammatory disease occurring after Group A Streptococcal pharyngitis (throat infection).

Organs Affected: Heart, Joints, CNS, Skin, Subcutaneous tissues

Pathogenesis — Molecular Mimicry

• Streptococcal M protein antibodies cross-react with cardiac tissue (molecular mimicry)
• Leads to inflammation of all layers of heart = Pancarditis

Aschoff Body — KEY FEATURE (exam favourite!)

• Pathognomonic (diagnostic) feature of rheumatic carditis
• Found in myocardium
• Contains: Aschoff giant cells + Anitschkow cells (caterpillar cells/owl-eye cells) + lymphocytes + fibrinoid necrosis
• Anitschkow cells: large macrophages with caterpillar/owl-eye nucleus

Acute Rheumatic Carditis

• Pericarditis: "bread and butter" pattern (fibrinous pericarditis)
• Myocarditis: Aschoff nodules in myocardium
• Endocarditis: small warty vegetations (1–2 mm) on the line of closure of mitral valve

Chronic RHD — Valve Changes (most important)

• Mitral valve (most commonly affected)
  • Fish-mouth / Buttonhole appearance — fixed narrow opening (stenosis)
  • Thickening and fusion of chordae tendineae
  • Thickening of valve leaflets (fibrosis)
• Aortic valve — second most common; fibrous thickening + fusion of commissures → stenosis
• Tricuspid — affected in recurrent RF (always with mitral + aortic)
• Pulmonary valve — rarely affected

Order of valve involvement: Mitral > Aortic > Tricuspid > Pulmonary

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5. CARDIOMYOPATHY

Definition

Cardiomyopathy = Primary disease of the heart muscle (myocardium) not caused by coronary artery disease, hypertension, or valve disease.

Three Types — Easy Comparison Table

Key Exam Points for HCM

• Mutation in beta-myosin heavy chain (most common gene)
• IHSS = Idiopathic Hypertrophic Subaortic Stenosis
• Obstruction of LVOT (Left Ventricular Outflow Tract) due to bulging septum
• SAM (Systolic Anterior Motion of mitral valve) — causes mitral regurgitation
• Most common cause of sudden cardiac death in young athletes
• Micro: myofiber disarray + interstitial fibrosis

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🔑 QUICK EXAM RECALL — One-Liners

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