3- Heart pathology and diseases of the heart

Heart diseases

1. Cardiovascular
Diseases
Part-2
Heart Pathology
Dr. Hassan Otifi
Associate professor of Pathology
1
st
Sem. 1445-2023

2. LEARNING OBJECTIVES:
•To classify the diseases of heart
•To list the causes, explain pathogenesis,
describe morphology, clinical features &
investigations of important diseases.
2

3. CLASSIFICATION of HDs:
1.Congenital Heart Diseases(CHD)
2.Ischemic (Coronary) Heart Disease (IHD)
3.Inflammatory Diseases of Heart (Rheumatic HD, Infective
endocarditisIE, Myocarditis,Pericarditis)
4.Congestive Heart Failure (CHF)

4. Congenital Heart Disease
•ACYANOTIC (Initial Lt to Rt Shunt) - VSD,ASD,PDA,
Ventricular septaldefect(VSD); Patentductusarteriosus
(PDA); Atrial septaldefect(ASD).
•CYANOTIC (Rt to Lt Shunt) - Tetralogy of Fallot
▪ CYANOSE TARDIVE - Eisenmenger syndrome
• NO SHUNT - Transposition of great vessels
(cyanotic),Coarctation of aorta, aortic stenosis(AS),
pulmonic stenosis (PS)

5. Prof. Adiga; cvs-2; Path335;kku.
ETIOLOGY
Multifactorial –
1% incidence in 1
st
pregnancy, increase to 2-15% for 2nd pregnancy
Environmental –
Rubella, diabetes, alcohol, lithium,oestrogen,amphetamine, radiation
Single gene syndrome - <5%
Trisomy 21,18,15,13, Turner syn,DiGeorge syn.

6. ATRIAL SEPTAL DEFECT VENTRICULAR SEPTAL DEFECT
•Most common defect in adults
•Ostium secundum (90%)- near
- septum secundum doesforamen ovale
not enlarge
•Ostium primum- associated with
mitral/tricuspid valve defect, - septum primum
fails to fuse with endocardial cushion
•Complication- Pulmonary hypertension, CHF, IE
a; cvs-2; Path335;kku.
Most common cardiac anomaly at birth Most close
spontaneously in childhood Membranous -90%
Complication- pulmonary hypertension,CHF,
shunt reversal, IE

7. TETRALOGY OF FALLOT
•Pulmonary stenosis
•Right ventricular hypertrophy
•Ventricular septal defect
•Overriding of aorta
•Most common cyanotic CHD
•Severity depend on degree of PS
•Cyanosis, clubbing, polycythemia, IE
•paradoxical emboli, brain abscess.
•Boot shaped heart

8. -
TRANSPOSITION OF GREAT VESSELS
-Failure of spiralrotation
-Incompatible withlife
-Associated PDA, ASD,VSD offer temporary compensation

9. COARCTATION OF AORTA
•Infantile/preductal type-aortic arch hypoplasia with
PDA, cyanosis, RVH
•Adult/postductal type (common)-
Aortic arch dilated,LVH,notching of ribs.
•Common in male
•May be associated with Turners Syndrome, Berry
aneurysm,VSD ASD, bicuspid aortic valve
(mostcommon)

10. ISCHEMIC HEART DISEASE
•DEFINITION
•TYPES
•ETIOLOGY
•PATHOGENESIS
•CLINICAL FEATURES
•MORPHOLOGY
•DIAGNOSIS
•COMPLICATIONS

11. DEFINITION of IHD
•Group of closely related syndromes all due to Myocardial
Ischemia; imbalance between myocardial supply & demand of
oxygenated blood.
ETIOLOGY
•> 90% cases- (Atherosclerotic) Coronary Artery Disease (CAD)
•<10% - Vasospasm,Cocaine, CO,Anemia- LVH, emboli,
vasculitis, BP

12. CLINICAL TYPES
1.Angina Pectoris: Less severe /No Muscle death.
- Stable, Unstable, Prinzmetal types
2.Myocardial Infarction: Most important form
-Causes Muscle Death.
3.Chronic IHD with Heart Failure
Suddencardiacdeath
• Acute Coronary syndrome:
- Due to acute plaque change.
-Myocardial Infarction
-Unstable Angina
-Sudden CardiacDeath

13. Pathogenesis
a; cvs-2; Path335;kku.
Fixed stenosis(>70%)-critical
-stable angina
Fixed stenosis(>90%)-unstable angina
Plaque disruption(acute plaque
change)-
Non-occlusive thrombus/emboli- unstable
angina / subendocardial MI
/ sudden death
Occlusive thrombus- transmural MI /
sudden death
Vasospasm in plaque –
- platelet/inflamatory cells/ endothelium/
circulating adrenergic agonist.

14. IHD – CLINICAL FEATURES
1.. ANGINA PECTORIS
•Paroxysmal Sub sternal Chest pain caused by
transient, reversible myocardial ischemia
•Constricting, chocking, Squeezing, Knifelike
feeling,crushing pain, with referred pain to left
arm/jaw; lasting upto 15 min.
STABLE ANGINA UNSTABLE ANGINA PRINZMETAL angina
Most common Dangerous
Fixed stenosis>70% Plaque disruption/ Fixed
stenosis>90%
Vasospasm+/- plaque
Pain on exertion Pain at rest/mild exertion At rest
Relieved by rest/
vasodilator
No dilator response. May
progress to MI.
Responds to vasodilator

15. 2. MYOCARDIAL INFARCTION
▪Necrosis of the cardiac muscle due to sudden ischemia
▪Main cause is disruption of plaque - fissure/ulcer
▪Severe sudden chestpain radiating to left arm/neck (lasting>20min.),not
relieved by rest/ vasodilator; associated with sweating, nausea, dyspnoea.
▪Silent MI(<15%)-In diabetic/old patients
▪ECG changes & elevated serum cardiac markers

16. 3.CHRONIC ISCHEMIC HEART DISEASE
▪Progressive CHF as a result of long-term ischemic injury, either
previous infarcts or slow myocyte degeneration.
▪MORPHOLOGY - Moderate to severe coronary Atherosclerosis; LV
dilation& hypertrophy with healed infarcts
•MICRO- Myocyte hypertrophy; Interstitial fibrosis;Subendocardial myocyte
vacuolization

17. 4. SUDDEN CARDIAC DEATH
Unexpected death from cardiac causeswithin ONE hour of symptoms,
mostly due to ventricular fibrillation
Etiology:-
80 to 90%: Complication ofIHD(severe atherosclerosis withoutplaque
change), without evidence of myocardial necrosis. But healed MI in 40%
10 to 20%:Non-Atheroscleroticcauses
-Aortic valve stenosis; LVH
-Mitral valve Prolapse
-Myocarditis
-Cardiomyopathy
-Pulmonary Hypertension
-Abnormal conduction defects(channelopathy)
-congenital coronary artery abnormality

18. ACUTEMYOCARDIAL INFARCTION
TYPES:-
1. TRANSMURAL(90%)-STEMI&SUBENDOCARDIAL (10%)-inner 1/3
rd
thickness.
CIRCUMFERENTIAL(10%)
(subendocardial infarct, usually with hypotension)
(ANTERIOR / POSTERIOR /
LATERAL wall)
3. RECENT & OLD
4. LV82%,LV+RV15%,RV3%
2. REGIONAL&
LAD(50%) - ant,apex,2/3septal
LCA(20%) – lateral wall-LV
RCA(30%)post,basal,1/3septal

20. MORPHOLOGY - MI
TIME GROSS MICRO E/M
<30min --- --- Mitochondrial swelling, glycogen
loss
30min-4
hr.
--- Waviness of fibres at
border
Mitochondrial amorphous density
4 – 24hrsDark mottling Coagulation necrosis
1-3 daysYellow centre Dense neutrophils
3-7 daysHyperemic border with
central yellow soft.
Phagocytic
macrophages
7-10 daysMax. yellow & soft with
depressed red margin
Early granulation
tissue at margin
2-8wks grey white scar, from
border to centre
Increased collagen
deposit

21. DIAGNOSIS OF AMI
▪Typical Symptoms + Biochemical Investigations + ECG Pattern
1.Ischemic chest pain
2.ECG – ST elevation
3.ECG – ST depression,T inversion, Q wave
4.Typical Rise of Troponin- I (most specific & sensitive) / More Rapid Rise of
CK-MB
5.B type Natriuretic peptide(BNP)- marker of CHF
6.MPO –Plaque vulnerability
7.Morphologic findings

22. MI- COMPLICATIONS
•Death- Out of hospital(1/3 STEMI); In hospital- 10%
•Arrhythmia -MC cause of sudden death is ventricular fibrillation;
conduction blocks common with post.wall MI.
•LVF(pul.edema); Cardiogenic shock(10%pts with >40% LV damage)
•Mitral regurgitation(papillary muscle dysfunction)
•RVF leading to venous congestion & hypotension
•Myocardial rupture(MC-3 to 7days)–cardiac tamponade(ant.wall), VSD
•Pericarditis(fibrinohemorrhagic)
•Chamber dilation, mural thrombosis, thromboembolism
•Late complications - Ventricular aneurysm & chronic IHD

23. VALVULARHEARTDISEASE
•MS: RHD
•MR: Scarring; IE;
-MV prolapse (myxomatous
degeneration);Papillary muscle
dysfunction, LV dilation; Mitral ring
calcification
Clinical feature : Murmurs
Complications:- CHF,IE,Arrythmia,
thromboembolism.
•AS: Calcific AS(mc); RHD
•AR: Scarring; IE;syphilis,
-Ankylosing spondylitis,RA
(MC-mitral valve)
ETIOLOGY: CONGENITAL - (Bicuspid aortic valve-mc;Valve atresia)
ACQUIRED:-

24. •Learning objectives:
1.To define Rheumatic Fever
2.To explain the etio-pathogenesis of RF.
3.To describe morphology of Rheumatic Carditis & its sequelae(Chronic RHD).
4.To discuss non-rheumaticcauses of endocarditis
5.To compare 4 types of vegetations.
RHEUMATIC HEART DISEASE

25. DEFINITION:-
Acute, Immune Mediated Multisystem Inflammatory Disease.
Occurs a few weeks following an Episode of Group A β- Hemolytic Streptococcal
Pharyngitis.
➢Occurs in 3% of Patients with Strep. Pharyngitis
➢Common sites: joint,heart,skin,brain
➢Age : 5- 15 years
Rheumatic Fever

26. PATHOGENESIS:- Antibodies against M protein of the Bacteria cross react with the
Glycoprotein antigens of heart, Joints & Other tissues (molecular mimicry -autoimmune).
Abs activate C(inflammation).
•Late sequelae due to fibrosis,which takes many years to decades(chronic RHD)
Rheumatic Fever

27. MORPHOLOGY OF HEART
Endocarditis:
•Valves - Mitral(most common) & aortic; Diffuse inflammatory edema.
•Rheumatic vegetation- Small (1-3mm), multiple, line of contact, firm,
adherent,sterile.
•Fate: Fibrosis leads to leaflet Thickening, Commissural Fusion,Thickened and fused
chordae Tendinae, leaflet shortening.
•Stenosis- Fish mouth/button hole/ funnel shape &Incompetence.
PERICARDITIS:
•Acute serofibrinous inflammation(Bread and butter appearance).
•Fate: Fibrosis- Adherent(constrictive) pericarditis.

28. MYOCARDITIS:
•Aschoff bodies, 1-2mm.-pathognomonic.
- most common in myocardium of LV&LA
•Fibrinoid degeneration, lymphocytes, plasma cells, macrophages,
Aschoff giant cells, Anitschow cells.
Fate: Fibrosis.
Complications:-
1.Valvular stenosis (mitral stenosis 60%,mitral and aortic stenosis 25%)/
MR/AR
2.Arrythmia and atrial fibrillation.
3.Subacute bacterial endocarditis.
4.Congestive heart failure.
5.Thromboembolism
6.Pulmonary CVC, Pul. hypertension.

29. Major Criteria:-
1.Rheumatic arthritis, (fleeting, large joints).
2.Chorea (involuntary purposeless movements) encephalitis.
3.Subcutaneous nodules.
4.Erythema marginatum (skin rash).
5.Carditis
3.Raised ESR/CRP
4.Prolonged PR interval
5.Prior h/o rheumatic fever
Diagnostic criteria
:
Serologic evidence of
previous streptococcal
infection (ASO/DNAase)
with 2 or more of major
criteria
Minorcriteria:-
1.Fever /Arthalgia
2.Leucocytosis.

30. INFECTIVEENDOCARDITIS
1Acute infective endocarditis:
Acute suppurative destructive infection of cardiac valves/endocardium leading to
vegetations.
2Subacute bacterial endocarditis:
Subacute/ insidious infection of unhealthy (damaged) valves/endocardium.
PATHOGENESIS: Immunosuppressed, I.V. drug abusers
•Bacteraemia- Tooth extraction, tonsillectomy,dental sepsis.
•Damaged Valves-Rheumatic Heart disease,Congenital Heart Disease, Artificial
valves,Degenerative calcific valvular stenosis.
SBE AIE
ONSET SLOW, low grade fever SUDDEN, high grade fever
Etiology Strep.viridans(mc); Stap.aureus(IV drug abusers)
Pathogenesis Oral commensals(dental sepsis)Septic focus(pneumonia,osteomyelitis)
Heart conditionDamaged valves Healthy
Damage/prognosisLess severe, good Severe, ulcer cusp,myo.abscess

31. 1- Cardiac lesions:
- Mitral and aortic valves(mainly); in drug abusers- tricuspid common.
•Vegetations- valves and chorde tendinae, bulky, large (1-2cm), polypoid,
friable, fibrin, bacteria and polymorphs.
•Valves -ulceration, perforation, abscess (myocarditis),suppurative
pericarditis, specially in acute type.
•Vegetations are slightly smaller &less destructive in subacute type with
granulation tissue/ fibrosis at base..
2- Extra-cardiac lesions:
Septic emboli, pyaemia, infarcts,pyaemic abscesses
•Acute type is fatal in1-3 weeks if not treated.
MORPHOLOGY:

32. Clinical features /complications:
•Fever(low grade in subacute), malaise, anemia,
•Petechiae, splinter hemorrhages under nails, retinal hemorrhage
(Roth spots); painful fingertip nodules(Osler nodes) – due to microemboli.
•Enlarged spleen/autosplenectomy.
•Heart failure, murmurs
•Embolic lesions-infarctions/abscess(spleen, kidney, brain, retina).
•Mycotic aneurysms (cerebral, mesenteric).
•Hemolytic anemia(jaundice)
•Glomerulonephritis (immune- complex mediated)
Investigations:- Positive blood culture & echocardiogram

33. Types of Endocarditis (Vegetations)
Non Bacterial Thrombotic(marantic)Endocarditis:
CAUSES:-Hypercoagulable state - DIC,Mucin producing
Adenocarcinoma of PANCREAS Acute PROMYELOCYTIC
Leukaemia, Hyperestrogenism
Morphology:-
No inflammation/valve damage
Friable vegetations
LIBMAN- SACKS ENDOCARDITIS:
Seen in SLE
Mitral & Tricuspid valvulitis
Small sterile pink granular vegetations
on undersurface of AV valves.

34. MYOCARDITIS
Infections:-
-Viruses: Coxsackie(most common cause), HIV, CMV
-Bacteria: Diphtheria
-Fungi: Candida
-Protozoa: Trypanosoma (chagas disease),Toxoplasmosis
Immune mediated:-
-Rh Fever, SLE, Transplant rejection, Drughypersensitivity
-Sarcoidosis
COMPLICATIONS:- Arrhythmia, CHF
Dilated, flabby heart with
haemorrhage
ETIOLOGY:-
Viral myocarditis with
lymphocytic infiltrate

35. PERICARDITIS
Primary (Infectious)
•viruses (most common)
•pyogenic bacteria
•mycobacteria
•Fungi
MORPHOLOGY: -
-Fibrinous (“bread & butter”)- most common type
•Uremia, MI, SLE,
•acute rheumatic fever
•viral (some cases)
•Purulent
•Bacterial, fungal
-Caeseous:
•Tuberculosis
•Haemorrhagic:
•surgery,TB, metastatic neoplasms
•-Serous: RF,SLE,viral
Secondary:
○myocardial
infarction
○cardiac surgery
○Radiation
○Systemic disorders
uremia
acute rheumatic fever
SLE
metastatic
malignancies
CAUSES

36. Pericardial Effusions
1.Transudate – CHF, hypoalbuminemia
2.Serosanguineous - blunt chest trauma
3.Haemorrhagic –Malignancy, TB
4.Chylous - mediastinal lymphatic obstruction
▪CARDIAC TAMPONADE:
Rapid accumulation of 200ml.fluid or blood. (Shock, CO, distended neck vein,
faint heart sounds)
▪HEMOPERICARDIUM: -
•CAUSES- Ruptured aortic aneurysms
•Ruptured myocardial infarcts
•Penetrating traumatic injury

37. HEART FAILURE
OBJECTIVES:
•To list the causesand types of heart failure
•To recognise the clinical features of left sided & right sided heart
failure
•To describe the morphology of different organs in heart failure

38. TYPES of HF
•Right sided(RVF)andLeft sided(LVF) heart failure
•Forward(reduced C.O.) andBackward failure(increased
venous congestion)
•High output cardiac failure(increased demand as in anemia/
thyrotoxicosis)
•Systolic dysfunction and Diastolic dysfunction
•Acute H. failure andChronic H. failure

39. CAUSESof HF
•Hypertension(most common)
•IHD
•Myocarditis/cardiomyopathy
•Valvular disease
Mitral/Aortic
RVF
•LVF(most common)
•Corpulmonale
•Pulmonary hypertension/
embolism
•Valvular disease
Pulmonary/Tricuspid/MS
CORPULMONALE: -
RVF seconadry to pulmonary disease
ACUTE- massive pulmonary embolus
CHRONIC- Chronic obstructive lung disease, Pulmonary hypertension
LVF

40. •SYSTOLICFAILURE
-MI
-Dilated cardiomyopathy
-AS
-Hypertension
•DIASTOLICFAILURE
-Hypertrophic CMP
-Restrictive CMP
-Constrictive pericarditis
-Cardiac tamponade
CAUSESof HF

41. Clinicalfeatures
1. Hypertrophy and dilatation of LV &LA.
2. Pulmonary edema
(dyspnoea,cough),Pleural effusion.
3. Pulmonary hypertension & RHF.
4. Decreased forward cardiac
output(fatigue,giddiness
2.Distended neck veins( JVP)
3.Chronic V. congestion of liver, spleen,
kidney.
4.Pedal edema(marked), Ascites .
RVF:
1. Hypertrophy and dilatation ofRV&RA.
LVF:

42. CARDIOMYOPATH Y
Dilated CM-
systolic dysfuntn
DEFINITION:- Heart disease due to Primary abnormality in the
myocardium
TYPES & CAUSES:- Dilated- Genetic,viral myocarditis,
alcoholism, peripartal Hypertrophic - AD
Restrictive- endomyocardial fibrosis, Loefflers endocarditis,
amyloidosis

43. HYPERTROPHIC-CM
Clinical Features:-
Common cause of sudden death in young athletes
Dyspnoea ,angina, syncope
Morphology:-
Asymmetric septal hypertrophy
Banana shaped LV cavity LV outflow
obstruction Myocyte disarray

44. CARDIAC TUMOURS
METASTATIC(SECONDARY):
-more common than primary
-Usually present as pericardial effusion
-Commonly from lung,breast,melanoma,lymphoma
PRIMARY:
BENIGN:
Myxomas (mostcommoncardiac tumor in Adults)
Lipomas
Papillary elastofibromas
Rhabdomyomas (most common cardiac tumor in Childhood)
MALIGNANT:
Angiosarcomas
Rhabdomyosarcomas (least common)

45. MYXOMA:
•Most often in left atrium
•Sessile or pedunculated
•Micro- stellate cells in myxoid stroma
•Complications- embolization & obstruction to AV valves

46. THE END