cardiovascular pathology

Pathology Cardiovascular Practicals Reviewer of 20

Atrial Septal Defect (ASD) • Incomplete closure of the fossa ovalis allowing inter-arterial communication • Often a mild disease not detected until adult life

o Due to pressure and volume handled by the atria level is lower compared to the systemic level • Pulmonary flow is increased to about twice the systemic output

o Pressure (Left > Right) o blood preferentially goes from Left Right atrium = ↑ Pulmonary blood flow

• RV is dilated and hypertrophied o Adaptation of the right ventricle to the ↑ workload(hypertrophy) dilatation

Complication

o Pulmonay HPN o RV failure (due to dilatation)

death also from CHF (due to arrhythmia) and IHD o Shunt reversal (Late cyanosis)

↑ pressure from right side to left Mixing of unoxygenated blood from right side to the left to systemic circulation

ASD

Types: 1. Fossa or Ostium seccundum (most common) 2. Outlet (Primum SD) 3. Sinus Venosus defect 4. Coronary sinus defect

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Fossa Ovalis 2 flaps of muscles should overlap to close to fossa

Left Atrium Right Atrium


Ventricular Septal Defect (VSD) • Most common cardiac anomaly in children (recognized early) • incomplete closure of ventricular septum left to right interventricular communication

o inadequate growth or absent fusion of embryologic septal components • Increases risk for infective endocarditis • Functional disturbance depends on the size of the defect

o ↑ defect = ↑ disturbance and vice versa o Small defects can sometimes close spontaneously as the heart enlarges o Surgery (1st year) to prevent irreversible obstructive pulmonary vascular disease

• Large VSDs result in overload of both ventricles o Similar to ASD (movement is from L R) o Right ventricle carries the initial burden

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Complications

• Eisenmenger syndrome o Pulmonary HPN o shunt reversal o cyanosis (Late cyanosis)

VSD

Muscle band

Muscle band

Infraventricularis Defect

Supraventricularis Defect


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Patent Ductus Arteriosus (PDA) • 90% occur as isolated anomalies (common in babies whose mothers had rubella) • Rough machine-like murmur (S4) on auscultation • Permanent closure of the DA is usually complete by 8 weeks after birth

o Patency due to failure to contract and become fibrotic in response to ↑ arterial oxygen o Large caliber of the ductus incomplete closure

• should be closed as early in life as feasible Complications

PDA o Pulmonary HPN o Shunt reversal o Cardiac hypertrophy

Adaptation to ↑ workload eventually leads to heart failure

o Dilated pulmonary artery

Pulmonary Artery

Aorta (take note of the 3 branches)

Patent Ductus Arteriosus

Left Pulmonary Artery

Left Pulmonary Artery

Patent Ductus Arteriosus (w/ probe)

Pulmonary Artery (Opened)

Aorta (Opened)


Tetralogy of Fallot • Most common cyanotic congenital anomaly • Four Components:

o Large VSD o Stenosis of pulmonary outflow tract

Narrowing of the lumen due to subpulmonic muscle block o Biventricular origin of the aorta (overrides the right ventricle)

septal defect is below overriding aorta receives blood from the RV and LV EARLY cyanosis

o Right ventricular hypertrophy 0.6-1cm thick (normal – 0.5cm)

• results from anterosuperior & leftward displacement of the infundibular septum Complications Left to Right Shunt Initial L R Shunt No Shunt

Tetralogy of Fallot VSD PDA ASD PTA

Coartaction of the aorta Pulmonary stenosis Aortic stenosis

o Heart failure o Polycythemia o ↑ risk for thrombosis o ↑ risk for infective

endocarditis

Aorta

Stenotic Pulmonary Artery

VSD

RV hypertrophy

VSD

Stenosis

RV hypertrophy

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Pulmonary Hypertension in Congenital HD w/ Left and Right Shunts

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Tunica Adventitia

Grade IV – Plexiform Lesions (Irreversible)

Newly formed Capillaries

Fibrous Tissue

Grade III – Intimal Fibrosis (Irreversible)

Hypertrophied Tunica Media

Fibrous tissue in the Tunica Intima (Occlusion of the lumen)

Grade II – Intimal Hyperplasia (Reversible)


Internal Elastic Membrane

External Elastic Membrane

Intimal Hyperplasia

External Elastic Membrane

Internal Elastic Membrane

Tunica Intima Single layer of Endothelial cells (simple squamous)


Grade I – Medial Hypertrophy (Reversible)


Rheumatic Heart Disease • cardiac involvement in rheumatic fever • Rheumatic Fever: immunologic hypersensitivity rxn to Strep antigens (NO BACTERIA present)

o Ig & complement demonstrable in myocardial fiber membrane o Cross reacting Ab against Strep protein and myocardial sarcolemma in patient’s sera

Ab w/c supposedly should be specific for Strep antigen will also attack the tissue of the heart due to similarity of the heart’s antigen to the strep antigen

• Jone’s Criteria: 2 major or 1 major + 2 minor Major Criteria Minor Criteria

Carditis Polyarthritis Chorea Subcutaneous nodules Erythema marginatum

RHD or previous rheumatic fever Athralgia Fever Elevated esr Postive CrP Leukocytosis Prolonged PR interval on ECG

Acute Lesion Pancarditis (all layers)

Pericarditis – fibrous type Endocarditis – verrucae along lines of closure of valve leaflets Myocarditis – Aschoff bodies in granulomatous stage (histologic hallmark of rheumatic activity)

Pericarditis (Gross)

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Fibrous type (Bread and Butter Pericarditis)

Pericarditis (Microscopic)

Fibrin deposits

Epicardial layer

Myocardial fibers


Rheumatic Heart Disease Endocarditis (Gross)

Mitral Valve (Translucent = Normal)

Verucae (Vesicle like structures)

Thickened Papillary Muscles

Endocarditis (Microscopic)

Fibrin deposits

Neutrophilic infiltrations

Aschoff Bodies in Myocarditis

• special type of interstitial inflammation • a perivascular focus of swollen eosinophilic collagen surrounded by lymphocytes, monocytes and

plasma cells Three Stages

1. Exudative stage 2. Granulomatous stage 3. Healed Stage

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Exudative Stage

Exudate with Neutrophilic infiltrations

Blood Vessel Lumen

Cardiac Muscles

Granulomatous Stage

Granuloma formation (with epithelial histiocytes and macrophages)

Healed Stage

Myocardial layer

Blood Vessels

Fibrosis around the BV

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Rheumatic Heart Disease Chronic Lesion

• commisures fused; cusps thickened and fibrotic; chordae tendinae thickened, shortened and fused • Most commonly involved valve- mitral, alone or in combination with others

Fused Commisures

Fibrotic and smooth mitral valve

Deformed orifice (Fish Mouth Deformity)

Short, thickened and fused together Chordae tendinae

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Infective Endocarditis • Invasion of the heart by microbiologic agent (friable vegetations laden with organisms) • Predisposing factors:

o Rheumatic heart disease (valves become fibrotic), congenital heart disease, calcific stenosis, artificial valves, immunodeficiency/ immunodepression, IV drug abuse

Types:

ACUTE SUBACUTE virulent organisms affects previously normal valve highly destructive bulkier vegetations valve perforation common

low virulence superimposed on damaged valves; less destructive smaller vegetations

Complications:

• Sepsis • Cardiac – valve insufficiency, myocardial abscess • Embolic • Renal – embolic infarction, focal glomerulonephritis, abscesses

Bulky Vegetations

Aortic Valve

Vegetations

Perforation

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Mitral Valve Prolapse (Floppy Valve) • Degenerative change, in 6% of population, young women • Accumulation of mucopolysaccharides in valve leaflet causing ballooning of the valve • Myxomatous degeneration of spongiosa layer, degeneration & attenuation of fibrosa layer

Three Layers of the Valve

1. Auricularis layer (from atrium) 2. Ventricularis layer (from ventricles) 3. Spongiosa layer thickens

Complications • Mitral Insufficiency • Chordal rupture

o Due to stretching • Infective endocarditis

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Abundant amount of tissue (Bulging appearance)

Thin Ventricularis layer

Thin Auricularis layer

Thick Spongiosa layer

Myocardial layer

Bulging Valve

Ruptured Chordae Tendinae

Stretched Chordae Tendinae


Ischemic Heart Disease Syndromes resulting from imbalance between supply and demand of the heart for oxygenation

1. Increased demand (increased heart rate) 2. Diminished oxygen transport (sever anemia, congenital heart disease) 3. Diminished coronary blood flow

Coronary atherosclerosis is the most common cause of diminished blood flow 1. 75% narrowing is significant 2. Stenosis within 2cm of left anterior descending and circumflex artery

Ischemic syndromes 1. Angina pectoris 2. Myocardial infarct 3. Sudden cardiac death

Calcium deposits (make vessel more brittle)

Large deposits of Atheromatous plaques

Narrowed lumen

Blood clot (complete occlusion)

↑ BP injures the surface of the blood vessel coagulation cascade thrombus formation blood clot

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Myocardial Infarct Transmural – necrosis of full thickness of the LV wall, associated with occlusive thrombi in 90% Subendocardial – necrosis limited to inner 1/3, diffuse coronary atherosclerosis, no thrombus

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Infarct (Left Main CA) Full Thickness of the Ventricle (Anterior wall, anterior 2/3 of septum and lateral ventricular wall)

Infarct (Left Main CA and Right CA) (Anterior wall, anterior 2/3 of septum, lateral ventricular wall and posterior wall)


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Pathology Cardiovascular Practicals Reviewer Page 14 of 20

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yocardial Infarct M

Wavy myocardial fibers

½ to 1 hr After Myocardial Infarct

Early Coagulation Necrosis

<12 hr After Myocardial Infarct

Full Blown Coagulation Necrosis (Inflammatory cells to take up the dead myocardial fibers)

3-7 days After Myocardial Infarct

Fibrosis (Disappearance of dead myocardial cells)

7th week After Myocardial Infarct


Myocardial Infarct

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plications • Cardiac arrhythmias • Left ventricular failure with pulmonary edema

o Decreased hydrostatic pressure • Cardiogenic shock

o Failure of the heart as a pump • Myocardial rupture • Thromboembolism

o Relaxation of the muscle wall during an infarct stasis of blood promotes coagulation o Coagulation mural thrombosis (fragile) fragmented and turns into an embolus

Com

Infarct

Rupture of the infarct part of the heart collection of blood in the pericardial sac causing cardiac tamponade


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opathy • Failure of the ventricle to empty in systole

ased ventricular end-systolic and diastolic volumes – biventricular dilatation and failure ic features – irregular hypertrophic and atrophic myocardial fibers with

holism, delayed pregnancy, hypo and hyperthyroidism

Congestive Cardiomy

• Incre• Non-specific histolog

progessive fibrosis • No detectable cause • associated with alco

Normal Carotid Sinus

Normal Aortic Valve

Normal Mitral Valve

Normal Chordae Tendinae

Dilated Ventricle

Everything is normal except the biventricular dilatation

Fibrous tissue (between the fibers)

Fibrous tissue (between the fibers)

Hypertrophy

Hypertrophy


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y le with resistance to diastolic filling

ized myocardial fibers

Hypertrophic Cardiomyopath• Marked hypertrophy of the ventricular musc• 20-30% are familial, autosomal dominant inheritance pattern • Greater thickening of ventricular septum than the LV free wall • Histology: disorgan

Thick Septum

Aorta

Bulge prevents blood flow to Aorta

Left Ventricle

Right Ventricle

Subaortic stenosis due to thick septum

Right Atrium enlargement

Asymmetric Septum

Disorganized myocardial fibers


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Obliterative Cardiomyopathy • Marked subendocardial fibrosis – encroachment of the lumen, decreased ventricular filling and

cardiac failure • Endocardial fibroelastosis – collagen and elastic tissue is laid down beneath the endocardium in

infancy • Endomyocardial fibrosis, common in Africa

Restrictive Cardiomyopathy • Decreased compliance of the ventricular muscle, increased resistance to filling, and cardiac failure • Many cases are due to cardiac amyloidosis

Mitral Valve (translucent = normal)

Overwhelming deposits (Obscured Trabeculae Carnae)

Thrombus

Endocardial Fibrosis (whiteness of the wall)


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t sources) Slides Review (taken from differen Acutely Injured Heart Removal of Dead Myocardial cells

Clearance of Dead Tissues

Granulation Tissue (Trichome)

Healed Infarct (Trichome)

Hypertrophy with Healed Infarct


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ypertrophy with Healed Infarct Purulent PericarditisH

Coronary Atherosclerosis

Purulent Pericarditis

Atrophy

Atrophy

cardiovascular pathology

Documents

patent ductus

left main

lateral ventricular

congenital

pulmonary

incomplete

anterior wall

pulmonary