Pathology of the Heart By: K.Mozaffari, MD, AP, CP.
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Transcript of Pathology of the Heart By: K.Mozaffari, MD, AP, CP.
Pathology of the Heart
By:
K .Mozaffari, MD, AP, CP
Topics
Congestive heart failure Ischemic heart disease Hypertensive heart disease Cor pulmonale Valvular heart disease Primary myocardial disease Congenital heart disease Pericardial disease Cardiac tumors
CONGESTIVE HEART FAILURE( CHF)
Inadequate output, forward failure Venous congestion, backward failure Left ,right or all chambers involved Adaptive changes: 1-Catecholamines 2-Hypertrophy & dilation ischemic injury 3-2ndary hyperaldosteronism
Consequences
Decompensation Venous congestion Pulmonary edema peripheral edema
MORPHOLOGY
Heart :dilated chambers Lungs :boggy & congested with frothy
fluid
septal widening
pale pink fluid
hemorrhages & heart failure cells
fibrosis, hemosiderin,brown induration
MORPHOLOGY
Edema of soft tissues Fluid in body cavities Liver:nutmeg appearance
centrilobular hemorrhagic necrosis
cirrhosis
Clinical features
Dyspnea Orthopnea,PND Venous congestion,edema Embolism Effusions Cyanosis,acidosis Ventricular arrhythmias
Ischemic heart disease
Angina pectoris Acute MI Sudden cardiac death Chronic IHD with CHF
Epidemiology
Any age, peak (60 in men,70 in women) Factors: HTN, DM, smoking, high LDL,
genetics Regular exercise
Pathogenesis
Critical stenosis:75% Acute plaque change Coronary artery thrombosis Coronary artery vasospasm
Acute plaque change
Fissuring, hemorrhage, rupture Disrupted plaque:
Necrotic core & lipid
Thin fibrous cap
Rich in T cells & macrophages
Coronary artery thrombosis
Plaque rupture Platelet aggregation Thrombus formation Embolization
Coronary artery vasospasm
Tx-A2 Endothelial dysfunction Increased adrenergic activity Smoking
Angina pectoris
Typical (stable): episodic pain to left arm
75% narrowing
Relieved by rest or TNG Unstable : preinfarction
increased frequency of pain Prinzmetal: at rest or sleep
spasm
Myocardial Infarction
1.5 million / yr in the U.S 500.000 deaths Men 4-5 times compared to women Risk factors the same as atherosclerosis
Pathogenesis
Necrosis begins 20-30 min after occlusion Subendocardial area more vulnerable Full size in 3-6 hrs Location of MI: site & anatomy of vessels
involved (LAD,RCA) Size of MI: proximal lesions ,larger infarcts
collateral vessels limit the size
MORPHOLOGY
LAD 40-50%:anteroapical RCA 30-40%:posterior LV wall & septum LCX15-20% :lateral LV wall Transmural MI Subendocardial MI, inner third Isolated RV or atrial infarction,rare
No gross changes before 12 hrs 18-24 hrs:slight pallor ,mottling 12-18 hrs:coagulation necrosis Wavy fiber change at periphery 18-24 hrs:PMNs,peak on 3rd day Contraction band at periphery with
hemorrhage due to reperfusion Myocytolysis,subendocardial cells with
influx of water(vacuolated)
4th-7th day: pale center, hyperemic border Macrophages, fibroblasts,capillaries migrate to
center 10th day: yellow,soft,sunken necrosis
Red-purple periphery
Granulation tissue & phagocytosis continue for weeks
4th wk: resorbed necrosis
less vascularity, more collagen 8th wk: Dense scar
thin,firm gray healed infarct
Recent MI
1 day old MI
Necrosis Wavy fiber PMNs
3-4 day old
Dense PMNs
Necrosis Hemorrhage Contraction band
7-10 days
Complete
phagocytosis
Granulation tissue
Healed MI
Scar tissue
Complications of MI
Papillary muscle dysfunction & rupture External rupture of infarct Rupture of septum Mural thrombi Acute pericarditis Ventricular aneurysms
Papillary muscle dysfunction & rupture
About 3 days after MI
LV failure
External rupture of infarct
Tamponade Between day 4-7
Rupture of septum
Left-to-right shunt
CHF
Mural thrombi
Emboli to brain
Acute pericarditis
Within 2-4 days
May cause effusion
Ventricular aneurysms
Thin-walled,fibrous outpouching
Emboli CHF Papillary muscle
dysfunction arrhythmias
Clinical features Chest pain:neck,jaw,epigastrium,left arm Rapid pulse,Diaphoresis & Dyspnea Pulmonary congestion & edema Cardiogenic shock ,if 40% of LV involved “Silent MI” in DM, HTN, elderly pts ECG:Q waves,ST abnormality,T wave
inversion
Lab markers
1-Total CK : sensitive, but not specific
CK-MB: 2-4 hrs rise, 18 hrs peak
MI excluded if no CK rise in first 2 days 2-cTnI: more specific than CK-MB
Troponin remains elevated for 4-7 days 3-LD: used in the past
Chronic Ischemic Heart Disease
Ischemic cardiomyopathy Progressive heart failure episodes of angina or MI Clinically similar to dilated CMP Severe coronary atherosclerosis Dilated chambers, fibrosis, hypertrophy Wall thickness may be normal Myocytolysis (vacuolated sarcoplasm)
Sudden cardiac death
Death within 24 hrs The most common cause is IHD VF is the most common cause Acute plaque rupture, thrombosis,vasospasm
Causes of sudden cardiac death
Coronary artery diseases Myocardial diseases Valvular diseases Conduction system abnormalities
Hypertensive heart disease
LVH(AS or IHSS must be excluded) Pressure overload Increased metabolic needs Predisposed atherosclerosis IHD,CHF,MI,arrhythmias
Morphology
Concentric hypertrophy Free wall >2cm Heart >450 g Enlarged hyperchromatic rectangular
“box-car” nuclei Fibrosis Infarcts
Cor pulmonale
Pulmonary heart disease
Acute (emboli)
>50% of vascular bed
Chronic
COPD RVH
Valvular heart disease
Rheumatic fever & heart disease Calcific aortic stenosis. Mitral valve prolapse Nonbacterial thrombotic Endocarditis Libman-sacks Endocarditis Infective Endocarditis Prosthetic cardiac valves
Rheumatic fever & heart disease
Clinical features 10 d-6 wk after pharyngitis Genetic susceptibilitiy Peak 5-15 yrs Streptolysin O, DNAse B Streptozyme test Migratory polyarthritis Pericardial effusion, tachycardia, CHF AF in MS Emboli endocarditis
Morphology
Acute rheumatic fever:
synovium,joints,skin,heart Fibrinoid necrosis Mixed inflammation Granuloma Fibrosis
Acute rheumatic carditis
Pancarditis Aschoff bodies Anitschkow cells Diffuse interstitial infiltrates Fibrinous pericarditis Serous or serosanguineous effusion Verrucous endocarditis
Aschoff body
Verrucous endocarditis
Chronic rheumatic heart disease
Mitral valve 95% Aortic & mitral valves 25% Right-sided valvular disease,uncommon Stenosis and/or regurgitation Heart failure Infective endocarditis
Chronic rheumatic mitral valvulitis Fish mouth Fused cords More in Females LA thrombi Passive lung
congestion Regurgitation
less frequent
Chronic aortic valvulitis
More in males Always with mitral
valvulitis AS lesds to
LVH,CHF Fibrosis may cause
AR
Other organs in rheumatic disease
Arthritis: large joints , self-limited Pulmonary: chronic inflammation Subcutaneous nodules (Aschoff body) Erythema marginatum (maculopapular)
Time for a quiz !
1
What is a heart failure cell?
Alveolar macrophage filled with hemosiderin
2
Nutmeg –like appearance is seen on the cut surface of which organ?
Centrilobular hemorrhagic necrosis of hepatocytes in CHF
3
Silent MI is seen in which of the following?
1-diabetes mellitus 2-hypertensive patients 3-elderly patients 4-all of the above
4
Which enzyme is more specific for myocardial injury?
Total CK CK-MB Troponin I LD
5
Anitschkow cells are seen in……….
Acute rheumatic carditis
6
Fish mouth deformity is seen in …….
Mitral stenosis
7
Erythema marginatum is seen in………
It is a maculopapular rash in acute rheumatic fever
8
Which coronary artery is more likely to sustain an infarction?
Left anterior descending coronary artery Right coronary artery Left circumflex coronary artery
9
Which morphological finding appears later in the course of an MI?
Coagulation necrosis Wavy fiber change PMN infiltration Granulation tissue
10
What is your diagnosis?
Cor pulmonale
Have a good day !
Calcific aortic stenosis
Degeneration due to aging
Sclerosis & calcification Angina,syncope,CHF Symptoms occur 10-20
yrs earlier in bicuspid valves
Mitral valve prolapse
The most common cause of isolated MR 3-5% of general population More in females, 20-40 yrs of age Loose ground substance, floppy valve Also in marfan syndrome No symptoms or palpitation, fatigue, atypical
chest pain Valve rupture, endocarditis,sudden death, LA thrombi
Nonbacterial thrombotic Endocarditis (NBTE) Small, sterile, friable
(fibrin & platelets) Aortic > Mitral valve Hypercoagulable state ( DVT) Adenocarcinoma in 50 % Marantic endocarditis Free from inflammation
or fibrosis After healing: lambl
excrescences Emboli to brain or IE
Libman-sacks Endocarditis
Sterile In SLE patients On mitral or tricuspid
valves No predilection for
closure lines
Infective Endocarditis
Vegetations on Valve or mural endocardium Acute: little host response Subacute: abnormal valves
local response
granulation tissue
Vegetations on Valve or mural endocardium Acute: little host response Subacute: abnormal valves
local response
granulation tissue
Etiology & Pathogenesis
Bacteremia:
procedures, urinary or intravascular catheters
Tooth brushing
NBTE
IVDA (right-sided valves)
Prosthetic valves (10-20% of cases)
Cardiac abnormality:
( calcific AS, VSD, RHD , MVP )
Clinical features
High fevers, chills, septicemia Low-grade fever, malaise ,weight loss Changing murmurs Splenomegaly, clubbing of digits Emboli: infarcts, mycotic aneurysms,
petechiae GN (Immune complex mediated )
Microorganisms in IENative valve:
S.Viridans
(50-60%)
S.Aureus
(10-20%)
Enterococci & HACEK (oral commensal)
Prosthetic valve:
Staph
epidermidis
G¯ bacilli Fungi
IVDA: S.aureus G¯ bacilli Fungi & Strep
Acute Endocarditis
Valve destruction Ring abscess Emboli Abscess at sites of
emboli
Organisms Fibrin Blood cells
Subacute Endocarditis
Firmer vegetations Less valve destruction Granulation tissue at base of vegetation Fibrosis,calcification Systemic emboli ,less likely to undergo
suppuration
Prosthetic cardiac valves
Bioprosthetic (porcine,bovine,human) mechanical
complications
Stiffening, calcification, perforation Thrombi Infective endocarditis Paravalvular leaks Hemolysis
Primary myocardial disease
Myocarditis Cardiomyopathies
Myocarditis
Infections Immune-mediated
unknown
Viral,chlamydial,
Rickettsial,
bacterial,
Fungi,protozoal,
helminthic
Postviral,
Rheumatic,
SLE,
Drug-induced,
Transplant rejection
Sarcoidosis
Giant cell
myocarditis
Clinical features
Coxackieviruses,the most common cause
Asymptomatic to severe CHF Sudden death Dilated CMP
Morphology
Flabby,pale myocardium Mottled by hemorrhage Abscess in bacterial cases CMV inclusions Lymphocytic infiltrate & necrosis Later fibrosis is seen
Viral myocarditis
Chagas disease
Microabscess
Cardiomyopathies
Dilated CMP
Hypertrophy, dilation, contractile dysfunction late stage of viral myocarditis Alcohol abuse Cobalt,doxorubicin Peripartum Cytoskeletal proteins mutations (dystrophin gene) Sarcomere protein genes (myosin,troponin)
Clinical features
The most common CMP (90% of cases) The most common Dx in transplant candidates At any age (peak 20-60 yrs) Sporadic or familial More in men EF <25%, progressive CHF In peripartum cases 50% recover
Morphology
Large,flabby heart >900 g Hypertrophy & dilation
in all chambers Fibrosis scant inflammation Fragile mural thrombi Emboli
Hypertrophic CMP
IHSS (LVOT obstruction) Abnormal diastolic filling Systolic anterior motion of mitral leaflet β myosin heavy chain gene mutation Dyspnea, ischemia,angina,sudden death Risk of IE Later fibrosis & CHF
Morphology
Hypertrophy of LV septum
>800 g Haphazard
hypertrophy & branching myocytes
Restrictive CMP Endomyocardial fibrosis:
idiopathic,tropical Eosinophilic endomyocardial fibrosis: (loffler syndrome) Endocardial fibroelastosis: <2 y/o children,valvular abnormality Cardiac amyloidosis Hemochromatosis Radiation injury to heart
Clinical features
Impaired diastolic filling due to inelastic ventricle
Fatigue,dyspnea,chest pain,CHF Mural thrombi in loffler syndrome Conduction system involvement by fibrosis DDx;constrictive pericarditis
Morphology
Thick & opaque fibrotic endocardium Eosinophilic infiltration(loffler syndrome) Endocardial fibroelastosis:
porcelain-like appearance,may be local Amyloidosis:green birefringence,congo red Hemochromatosis:iron stained blue,perl stain
Congenital heart disease
L-R shunts : 1-ASD 2-VSD 3-PDA R-L shunts : 1-Tetralogy of Fallot 2-TGA Coarctation of aorta
Etiology
8/1000 live births Genetic factors(trisomies) Environmental factors(rubella) Idiopathic (multifactorial):90% L-R shunt,no cyanosis until reversal of
flow due to PH R-L shunt,cyanosis from birth
Atrial septal defect (ASD)
Foramen ovale closes at birth Ostium secundum ASD:75% Ostium primum ASD :15% Sinus venosus ASD:10% The most common congenital cardiac
disease first diagnosed in adults
ASD
Ventricular septal defect (VSD)
The most common congenital heart defect at birth
Many close spontaneously in childhood
Risk of IE
VSD
Patent ductus arteriosus(PDA)
Functional closure: 1-2 days after birth Ligamentum
arteriosum: after a few months In RDS :delayed
closure Machinary murmur Risk of IE
Tetralogy of Fallot
The most common cyanotic congenital heart disease
VSD Dextraposed
overriding aorta RVH RVOT obstruction
Morphology
Boot-shaped heart Shunt extent determined by RVOT obstruction Cyanosis PH does not develop Erythrocytosis, clubbing digits IE risk Emboli:brain abscess
Transposition of great arteries
Complete form incompatible with life
Those who survive have ASD,VSD or PDA
RVH cyanosis
Coarctation of aorta
Isolated lesion in 50% Also common in turner syndrome Preductal (infantile type):
CHF, lower limbs cyanosis
weak femoral pulses Postductal (more common):
Hypertension of upper limbs
Weak pulses in legs
Coarctation of aorta
Pericardial disease
Pericarditis Pericardial effusions
Pericarditis
Primary, uncommon: Viral (most cases) Bacteria, fungi, mycobacteria Secondary, more often: Following MI or cardiac surgery Radiation Uremia (the most common systemic disorder) RF & SLE Metastases (bloody)
Course
Immediate hemodynamic complications (significant effusion)
Resolution without sequelae Progression to chronic fibrosing process
Clinical features
Atypical chest pain & friction rub Tamponade in acute forms:
distant heart sounds, distended neck veins reduced cardiac output, shock
Chronic constrictive form:
Fibrotic scar tissue
venous distention & low output
DDx: restrictive CMP
Morphology
Fibrinous exudation Shaggy Bread & butter
Pericardial effusions Serous: CHF, Albumin Serosanguineous: blunt chest trauma, malignancy Chylous: lymphatic obstruction Hemopericardium (pure blood): Aortic or myocardial rupture, penetrating trauma
Cardiac tumors
Metastases: More common than primary tumors Most often involve pericardium Lung, breast, melanoma & hematopoietic
are frequent primaries
Primary tumors (rare): Myxoma Lipoma Papillary elastofibroma Rhabdomyoma Angiosarcoma Rhabdomyosarcoma
Myxoma Most in LA Any age Sessile or pedunculated Stellate cells Mucopolysaccharide-rich stroma Smooth muscle cells Emboli Ball-valve obstruction Syncope & death
Myxoma
Rhabdomyoma
Most common primary cardiac tumors in childhood
Seen with tuberous sclerosis
Mass projecting into lumen
Solitary or multifocal
Rhabdomyoma
Spider cells contain glycogen
Wake up! we have a quiz now
1
A 20 y/o girl with atypical chest pain & fatigue has mitral regurgitation on echocardiography. which statement is false:
1-fish mouth deformity of mitral valve 2-loose edematous valve tissue 3-association with marfan syndrome 4- risk of endocarditis or death
2
A 50 y/o man with advanced gastric cancer has small vegetations on mitral valve.After an embolic episode,leading to brain lesions he died.This lesion is called :
1-libman-sacks endocarditis 2-nonbacterial thrombotic endocarditis 3-subacute infective endocarditis 4- rheumatic endocarditis
3
A young boy fell unconscious & died immediately,while playing basketball.Autopsy showed a large heart with disarray of myocytes.what is your diagnosis?
1-myocarditis 2-hypertrophic cardiomyopathy 3-restrictive cardiomyopathy 4-dilated cardiomyopathy
4
Alcohol is likely to cause…….. 1-dilated CMP 2-ischemic CMP 3-hypertrophic CMP 4-restrictive CMP
5
Amyloidosis & hemochromatosis are examples of……………..
1-dilated CMP 2-ischemic CMP 3-restrictive CMP 4-hypertrophic CMP
6
Loffler syndrome is associated with all of the following ,except….
1-thrombi & emboli 2-hypereosinophilia 3-constrictive pericarditis 4-restrictive cardiomyopathy
7
Which lesion is associated with early cyanosis?
1-ASD 2-VSD 3-PDA 4-tetralogy of fallot
8
What is the most common primary cardiac tumor in adults?
1-lipoma 2-rhabdomyoma 3-angiosarcoma 4-myxoma
9
Stellate cells in a loose stroma with smooth muscle cells are seen in……
1-rhabdomyoma 2-lipoma 3-myxoma 4-angiosarcoma
10
Vegetations of subacute infective endocarditis are distinguished from those of the acute form by……..
1-presence of fibrin & blood cells 2-size of the vegetations 3-location of vegetations 4-granulation tissue formation
11
All lesions cause hemopericardium, except?
1-uremia 2-ruptured aortic aneurysm 3-penetrating trauma to heart 4-ruptured MI
12
What is this type of endocarditis called?
13
What is this lesion called?
14
What do you see in the photographs?
15
A 22 y/o IV drug abuser is likely to present with which of the following?
1- Eosinophilic infiltration of myocardium 2-Tricuspid valve endocarditis 3-constrictive pericarditis 4- Hypertrophic cardiomyopathy
16
A 50 y/o man with a history of malignant melanoma presents with dyspnea & muffled heart sounds.what is your diagnosis?
1-Nonbacterial thrombotic endocarditis 2-Restrictive cardiomyopathy 3-Bloody pericardial effusion 4-Infective endocarditis
17
A 10 y/o child has a cardiac mass ,the cells of which contain glycogen. what is your diagnosis?
1-lipoma 2-myxoma 3-rhabomyoma 4- angiosarcoma
18
A girl with turner syndrome has high blood pressure in her upper limbs & weak pulses in her legs. what is your diagnosis?
1-tetralogy of fallot 2-ASD 3-VSD 4-coarctation of aorta
19
A 55 y/o man with bicuspid aortic valve is likely to have
1-floppy valve 2-calcification 3-fish mouth deformity 4-all of the above
20
Most cases of primary pericarditis are due to….
1-Viruses
2-Bacteria
3-Fungi or mycobacteria
4-MI or cardiac surgery
Good bye & Good luck