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1. CARDIOVASCULAR
SYSTEM…

3. Congenital Heart Disease
• Congenital heart diseases are abnormalities of the heart
or great vessels that are present at birth.
• Most such disorders arise from faulty embryogenesis
during gestational weeks 3 through 8, when major
cardiovascular structures develop.
Pathogenesis:
• Cause is unknown in almost 90% of cases.
• Environmental factors, such as congenital rubella
infection, are causal in many instances.
• Genetic factors are also clearly involved, as evidenced by
familial forms of congenital heart disease and by well-
defined associations with certain chromosomal
abnormalities (e.g., trisomies 13, 15, 18, and 21 and
Turner syndrome).

4. • Congenital heart diseases subdivided into 3 groups:
1. Malformations causing a right-to-left shunt: pulmonary
circulation is bypassed -> poorly oxygenated blood enters
the systemic circulation -> dusky blueness of the skin
(cyanosis) Eg: cyanotic congenital heart diseases -
tetralogy of fallot, transposition of great arteries, tricuspid
atresia, total anomalous pulmonary venous connection,
persistent truncus arteriosus.
2. Malformations causing a left-to-right shunt: increase
pulmonary blood flow, (no cyanosis atleast initially) ->
Increased pressure and volume in pulmonary circulation ->
pulmonary hypertension -> Right ventricular hypertrophy
and shunt reversal -> cyanosis. Eg: VSD, ASD, PDA
3. Malformations causing obstruction: Eg: Coarctation of
aorta, aortic valvular stenosis, pulmonary stenosis.

5. Left-to-right shunts
1. ATRIAL SEPTAL DEFECT
• An abnormal, fixed opening in the atrial septum caused
by incomplete tissue formation that allows
communication of blood between the left and right atria
• ASDs are usually asymptomatic until adulthood
• Three major types of ASDs
• Secundum ASDs (90%) - deficient or fenestrated oval
fossa near the center of the atrial septum.
• Primum anomalies (5%) adjacent to the AV valves.
• Sinus venosus defects (5%) located near the entrance of
the superior vena cava and may be associated with
anomalous pulmonary venous return to the right atrium.

7. 2. VENTRICULAR SEPTAL DEFECT
• Incomplete closure of the ventricular septum, allowing free
communication of blood between the left to right
ventricles, is the most common form of congenital cardiac
anomaly
• Most VSDs are associated with other congenital cardiac
anomalies such as tetralogy of Fallot
• About 90% involve the region of the membranous
interventricular septum (membranous VSD).
• The remainder lie below the pulmonary valve (infundibular
VSD) or within the muscular septum.
• Although most VSDs are single, those in the muscular
septum may be multiple (so-called "Swiss-cheese" septum).

9. 3. Patent Ductus Arteriosus
• PDA results when the ductus arteriosus, an essential fetal
structure that normally spontaneously closes, remains
open after birth and shunts blood from the aorta to
pulmonary artery.
4. Atrioventricular Septal Defect
• AVSD, also called complete atrioventricular canal defect
results from the embryologic failure of the superior and
inferior endocardial cushions of the AV canal to fuse
adequately.
• Incomplete closure of the AV septum and malformation of
the tricuspid and mitral valves.
• Two forms – partial AVSD and complete AVSD.

10. LEFT TO RIGHT SHUNTS

11. Right-to-left shunts
1. Tetralogy of Fallot
• Four cardinal features of TOF are
(1) VSD
(2) obstruction of the right ventricular outflow tract
(subpulmonary stenosis)
(3) an aorta that overrides the VSD
(4) right ventricular hypertrophy
• Results from anterosuperior displacement of the
infundibular septum.
• Heart is often enlarged and may be "boot-shaped" due to
marked right ventricular hypertrophy, particularly of the
apical region.
• The VSD is usually large

12. • An ASD may be present – pentalogy of fallot
• A right aortic arch may be present in ~25% patients.
• If the subpulmonary stenosis is mild, the abnormality
resembles an isolated VSD, and the shunt may be left-to-
right, without cyanosis (so-called pink tetralogy).
• As the obstruction increases in severity, there is greater
resistance to right ventricular outflow -> right-sided
pressures approach or exceed left-sided pressures -> right-
to-left shunt develops -> cyanosis (classic TOF).
• Most infants with TOF are cyanotic from birth or soon
thereafter

13. RIGHT TO LEFT
SHUNTS

16. Myocardial Infarction (MI)
• Death of cardiac muscle due to ischemia.
Leading cause of hospital admissions/ morbidity and
mortality
Risk Factors: old Age, Atherosclerosis , hypertension,
smoking, obesity , Diabetes mellitus , Fatty diet ,
hypercholesterolemia, hyperlipoprotenemia.

17. Pathogenesis.
• Coronary arterial occlusion: Sequences
• Change in Atheromatous plaque…disruption, erosion
hemorrhage, rupture, fissuring.
• Platelet adhesion, aggregation, activation, release of
aggregators- thromboxane, serotonin, platelet factor 3, 4.
• Vasospasm
• Other mediators– bulk of thrombus increase
• Within minutes thrombus evolves to occlude lumen

18. Myocardial Response
Functional, biochemical, morphological changes:
CA occlusion Reduce blood flow to myocardium
(Ischaemia) Myocardial dysfunction Myocyte Death
• Biochemical: anaerobic metabolism – production of
phosphates- accumulation of lactic acid.
• Accumulation of noxious metabolites
• ATP depletion

19. Events in Ischemic cardiac Myocytes
• Feature Time
• ATP depletion Seconds
• Loss of contractility < 2 min
• ATP reduced to 50% of normal 10 min
• ATP reduced to 10% of normal 40 min
• Irreversible cell injury 20-40 min
• Microvascular injury > 1 hr

20. • LAD: ant. wall Lt ventr, ventr septum, apex
• RCA: Rt ventr, Post third ventr septum
• LCX: lat wall left ventr.

21. Gross & Microscopic appearance
• Depend on duration of survival
Duration Gross Micro
½-4 hrs None waviness of fibers
• After 3 hrs: slice of cardiac tissue immersed in triphenyltetrazolium
chloride (TTC)- brick red color in non-infarcted area
• -Infarct area is pale unstained

22. GROSS- INFARCTION

24. 1-2 days

25. 3-7 days

26. Diagnosis
• Clinical Features: Sudden on set of chest pain for more than 30
mins. Rapid weak pulse, sweating, Dyspnoea,
Asymptomatic- 10-15 %
• ECG: ST segment elevation, New Q waves, T wave inversion
• Imaging studies
• Laboratory evaluation of cardiac marker cTnT , cTnI , CK-MB

27. • Laboratory evaluation of Acute MI
Cardiac troponins T & I :
2-4 hrs, peak 48 hrs. 7-10 days remain elevated.
Creatinine kinase. CK-MB : MM, BB
2-4 hrs, peak 24 hrs, normal within 72 hrs.
Lactate dehydrogenase. 12-24 hrs. peak 2-3 days, decrease 5-14
days.
Myoglobin. SGOT
C-reactive protein, ESR, Complete blood count

28. Consequences and complications
• Consequences: Prognosis- good in proper set up.
• Complications: ¾ will have one or more complications.
• Contractile dysfunction. Pump failure
• Arrhythmias
• Myocardial rupture, false aneurysm
• Pericarditis
• Rt ventricular infarct
• Infarct extension: adjacent area
• Infarct expansion: weakening, thinning, stretching,
• Mural thrombus
• Ventricular aneurysm
• Progressive late heart failure.

29. Infective Endocarditis
Infective endocarditis (IE) characterized by colonization or
invasion of the heart valves or mural endocardium by
microbe.
vegetations composed of thrombotic debris and
organisms, often associated with destruction of underlying
cardiac tissues.
Classified into acute and subacute forms.
Acute IE - infection of previously normal heart valve by
highly virulent organism that produces necrotizing,
ulcerative, destructive lesions.
Subacute IE - caused by organisms of lower virulence;
insidious infections of deformed valves that are less
destructive

30. Etiology
Bacterial – most common
1. Staph. aureus – acute IE, IV drug users
2. Strep Viridans – most common etiology of
subacute IE
3. Staph epidermidis – prosthetic valves
4. HACEK group

31. Morphology
The hallmark of IE is presence of friable, bulky, potentially
destructive vegetations containing fibrin, inflammatory
cells, and bacteria on heart valves.
The aortic and mitral valves are the most common sites of
infection, although the valves of the right heart may also be
involved, particularly in intravenous drug abusers
May form emboli -> septic infarct
Microscopically, the vegetations of typical subacute IE often
have granulation tissue indicative of healing at their bases.
With time, fibrosis, calcification, and a chronic
inflammatory infiltrate can develop.

32. B
Infective (bacterial)
endocarditis. A: Endocarditis
of mitral valve (subacute,
caused by Streptococcus
viridans). The large, friable
vegetations are denoted
by arrows.
B: Histologic appearance of
vegetation of endocarditis
with extensive acute
inflammatory cells and fibrin

33. Diagnostic criteria for IE – Duke’s Criteria
I. Pathologic criteria
• Microorganisms, demonstrated by culture or histologic
examination, in a vegetation, embolus from vegetation, or
intracardiac abscess
• Histologic confirmation of active endocarditis in vegetation
or intracardiac abscess
II. Clinical criteria
Major
• Blood culture(s) positive for a characteristic organism or
persistently positive for an unusual organism
• Echocardiographic identification of a valve-related or
implant-related mass or abscess, or partial separation of
artificial valve
• New valvular regurgitaion

34. Minor
• Predisposing heart lesion or intravenous drug use
• Fever
• Vascular lesions, including arterial petechiae,
subungual/splinter hemorrhages, emboli, septic infarcts,
mycotic aneurysm, intracranial hemorrhage, Janeway
lesions
• Immunological phenomena, including glomerulonephritis,
Osler nodes, Roth spots, rheumatoid factor
• Microbiologic evidence, including a single culture positive
for unusual organism
• Echocardiographic findings consistent with but not
diagnostic of endocarditis, including worsening or changing
of a preexistent murmur

35. • Diagnosis by these guidelines, called the Duke
Criteria, requires either pathologic or clinical
criteria; if clinical criteria are used, 2 major, 1
major + 3 minor, or 5 minor criteria are required
for diagnosis.

36. Noninfected vegetations
• Noninfected (sterile) vegetations - caused by
1. Nonbacterial thrombotic endocarditis (NBTE) and
2. Endocarditis of systemic lupus erythematosus (SLE),
called Libman-Sacks endocarditis
• NBTE - characterized by the deposition of small sterile
thrombi on the leaflets of the cardiac valves
• The lesions are 1 mm to 5 mm in size, and occur singly or
multiply along the line of closure of the leaflets or cusps.
• Histologically they are composed of bland thrombi that
are loosely attached to the underlying valve. The
vegetations are not invasive and do not elicit any
inflammatory reaction.
• NBTE is often encountered in debilitated patients, such as
those with cancer or sepsis

37. • Libman-Sacks endocarditis - Mitral and tricuspid
valvulitis with small, sterile vegetations, called Libman-
Sacks endocarditis, is occasionally encountered in SLE.
• The lesions are small (1-4 mm in diameter) single or
multiple, sterile, pink vegetations that often have a
warty (verrucous) appearance
• Histologically the vegetations consist of a finely granular,
fibrinous eosinophilic material that may contain
hematoxylin bodies, homogeneous remnants of nuclei
damaged by anti-nuclear antigen bodies

38. Comparison of the 4 major forms of vegetative endocarditis. RHD is marked by small,
warty vegetations along the lines of closure of the valve leaflets. Infective endocarditis
(IE) is characterized by large, irregular masses on the valve cusps that can extend onto
the chordae. Nonbacterial thrombotic endocarditis (NBTE) typically exhibits small,
bland vegetations, usually attached at the line of closure. One or many may be
present. Libman-Sacks endocarditis (LSE) has small or medium-sized vegetations on
either or both sides of the valve leaflets.

39. Rheumatic Heart Disease (RHD)
Acute Rheumatic Fever (RF)
Def: Acute Post-streptococcal systemic, immune-mediated,
inflammatory disease –affects tendons, joints, muscle, heart,
arteries, brain
Incidence:0.3 to 3 %.
Age: Children and young adults. 5-15 yrs
Sex: Female – more.
Socio-economic status: Poor , overcrowding.

40. • Etiology: Post streptococcal pharyngitis
• Beta Hemolytic streptococci Group A Type
• Mortality and morbidity improved with rapid diagnosis &
treatment

41. Pathophysiology
• Group A streptococcal pharyngitis
• Host immune response to group A streptococcal antigens
that cross-react with host proteins
• Abs , CD4 +T cells directed against M proteins recognise
cardiac Ags
• Complement activation & cytokine production
damage

43. Clinical features
Modified Jones criteria:
The Major diagnostic criteria include –
• Carditis,
• Polyarthritis,
• Chorea- Sydenhams
• Subcutaneous nodules-attached to deeper structures
like tendons, ligaments, fascia or periosteum ; Characteristic
locations are extensor surfaces of the wrists, elbows, ankles ,
knees.
• Erythema marginatum.

44. The Minor diagnostic criteria include
• Fever,
• Arthralgia,
• Previous h/o RF
• Prolonged PR interval on the ECG
• Elevated acute phase reactants (increased
ESR), presence of C-reactive protein, and
leukocytosis.

45. Lab evidence of previous group A streptococcal
pharyngitis is must to diagnose rheumatic fever.
One of the following must be present:
• Positive throat culture or rapid streptococcal
antigen test
• Elevated or rising streptococcal antibody titer
• History of previous rheumatic fever or rheumatic
heart disease
The Jones criteria require the presence of 2 major or 1
major and 2 minor
+ Lab evidence

46. Morphology: Aschoff bodies
• Pathognomonic of RHD
• In interstitial tissue of myocardium , endocardium
• 3-4 weeks to develop.
• Consist T lymphocyte , plasma cells , & macrophages
• Anitschkow cell- cardiac histiocyte/ macrophage
• Cells with abundant cytoplasm , round ovoid nucleus
with slender wavy chromatin condensation(Cater pillar –
longitudinal section)

47. Anitschkow cell
Caterpillar

48. Anitschkow cell
Owl’s eye

49. Aschoff nodule

50. Subcutaneous nodule

51. Pathology
• ARF: diffuse inflammation & Aschoff bodies lead
to Pancarditis
• Early stage- Fibrinoid degeneration
• Intermediate stage- Proliferative
• Late stage- Healing
• Inflammation of Endocardium & Left side valves
lead to Fibrinoid necrosis

52. Fibrinous Pericarditis.

53. • Overlying necrotic foci and along lines of closure
, small vegetations / verrucae form
• Mac Callum plaques
• Mitral V cardinal changes: leaflet thickening ,
commisural fusion & shortening & thickening
fusion of tendinous cords

54. Valvular lesions
• Mitral stenosis: RF – common cause of Mitral
stenosis, 90%
• Pathology: Mitral valve leaflets, along lines of
closure margins. Diffuse thickening. Fibrosis, fish
mouth or button hole configuration.
• Mitral valves. Most affected
• Mitral + Aortic Valves
• Tricuspid , pulmonary V-rare

55. Small verrucous vegetations

56. Mitral stenosis

57. Mitral stenosis - Fish mouth
appearance

59. Diagnosis of RF, RHD
• Clinical
• Electrocardiogram and Imaging studies.
• Laboratory diagnosis:
• Throat swab.
• Culture.
• test for Streptococcal antigen
• ESR, TLC, CRP
• Anti Streptolysin - S and O Rising titer.
• Anti M antibodies.
• Histological findings

60. THANK YOU……