Table Of ContentsSL No. Chapter Page No

1 Infective Endocarditis 1

2 Cardiomyopathy 6

3 Rheumatic Fever and Rheumatic Heart Disease 12

4 Myocarditis 21

5 Pericarditis 23

6 Hemopericardium 24

7 Mitral Valve Prolapse 29

8 Mitral Valve Regurgitation 31

9 Mitral Stenosis 36

10 Cardiac Tumors 45

11 Heart Failure 47

12 Ischemic Heart Disease 67

13 Aortic Stenosis 96

15 Aortic Regurgitation 100

16 Tricuspid Stenosis 107

17 Tricuspid Valve Regurigitation 109

18 Pulmonary Valve Stenosis 110

19 Pulmonary Valve Regurigitation 111

20 Congenital Heart Disease 112

21 Acute Pericarditis 137

1

Infective Endocarditis• Essentially , we have 5 types of Endocarditis

Infective endocarditis ⇒ microbiological inflammation

"Eimaehaseadcendaoisaeoadie"# rheg.mmamticneenmde%aa.fi"

Masantic Endocarditis carcinoid syndrome( Non Bacterial thrombotic . SHT released from carcinoidtumours damages the endocardium

Endocarditis) and values ofthe Rt- Heart.

• Two types of IE basedon

the tempoof the disease

#Eat

• Caused by highly virulent organisms • Caused by organism with low virulenceeg Staphylococcus Aureus / eg-cs.stoaentf.to's?' iooimdmanssai,

• Seen on Heathy heart(as the bacteria is highly virulent) . Predisposing Pathological condition

• stormy onset . Insidious onset

:*'s's:c:÷÷:... .am.. / ::: ::::i÷: ..mn. ..healing and fibrosis

• Leukocytesis• Anemia of Chronic diseases

• Clinical presentation points to cardiac Leucopenia (long term suppression

complications . of marrow by cytokines )

• Non - specific features of systemic• Vegetation are prone to embolizations infection .

leading to abscess formation where they lodge . causative organisms : -" 'Ii: gelation) orenigooocoagianiovmadeasnaheahtehgg / H A C E K 90040

. issocinnaaltganeiisofpie.is".""" t ca.aiotaae.im t t

I::¥÷÷÷÷i¥÷÷q""mom".sn#n!......Eikenenakingena

Embolization( septic)

1

Causes of increased risk of Infective Endocarditis

① vsD - L- R shunt produces lesions onthe Rt- Heast ⑦ Prosthetic valvesendocardium ⇒ lossof anticoagulant property (usually infected by coagulaseof the endocardium (Jetlesions)

Negative s - aureus (cons)↳ formationof microthrombi ⇒ promoteseg s - epideomidis

bindingof bacteria to the endocardium

At flanks of get blood flow , - S-visidansformation of low DoesSuze÷÷÷Ei÷÷÷÷÷÷÷÷÷÷:÷÷÷ ÷÷÷:÷÷:÷:÷÷..

G

tha:%sToth::a%ea:es::.e%:%a÷:as.gg:1?edn+:ithwiEn::i:seby complement system. Carcinoma and ulcerative colitis.

(Streptococcus bovis)② Valvular diseasesL Rheumatic Heart disease

③ mitral valve Prolapse④ Bicuspid aortic valve with lwithout calcification⑤ calcific aortic stenosis

⑥ Tetralogy of Fallot , PDA (CHDs)

Host factors in Infective Endocarditis

① Immunodeficiency syndrome② Therapeutic immunosuppression③ malignancy④ Neutropenia⑤ Diabetes mellitus

⑥ Chronic Alcoholism

⑦ i - v drug abusers (Rt- sideof the heart , m- c cause⇒ s - aureus)

⑧ Indwelling catheters

RING ABSCESS

• Vegetations on the valve dueto Acute Infective endocarditis may involve

::: demi:: ti:":::b.in::':c:::::: omridngthnesieas's.

-- -

- - -,

÷:÷÷::÷::!÷÷i÷÷tne conduction .sum

2

VEGETATIONS OF SUBACUTE INFECTIVE ENDOCARDITIS

µ ✓""naicaimntaiampmnaa;% .ie?so:emnoenuogjepsiisbmpnocyies

- → Dysfunctional valve

⇒o..

. anana,¥;÷ www.men.emi.oo.gan.ms

takes place . I • lesser chances of ring abscess formationAntigens released may

"o less chances of leading to suppurative

leadto formation of antigen -antibody pericarditis .complexes ( chronic antigenemia) • lesser embolization potential

↳may get deposited in microcirculation

• Non - specific features , Nocardiac complications.

••# • Deposition ofthese Ag- Ab complexes maylead to activationa.a Garza of complement system throughthe classical pathwayC' 928252-1 •¥740 cza

#TIY andmay ultimately progress to vasculitis lesions.

Type II NOTE : This usually occurs only in subacute IE dueto

Hypersensitivity longer disease process and indolent nature .reaction

↳ Clinical features

① Deposition ofthese Ag - Ab complex in the sublingual (below nail ) capillariesleads to their damage andultimately long , flame shapedhemorrhages known as splinter Hemorrhages

② Inflammatory , painful , red lesion under fingertips knownas Osler Nodes③ Janeway lesions ⇒ nontender lesions in the palms and soles④ Petechia hemorrhages⑤ Circular, boat shaped lesions in the retina with pale yellow centres :

Roth spots⑥ Diffuse Glomerulonephritis ⇒ Proteinuria, Hematuria

AA fever with changing muomuot splenomegaly ⇒ Infective Endocarditis until

proven otherwise

Investigations : ① Blood culture → Transesophageal ECHO② Echocardiography sensitivity - 951.

↳ Transthoracic ECHO

sensitivity - 6Gt.

3

Other clinical features of Infective Endocarditis.

• fever ⇒ Highgrade - AcuteIE , Low grade - subacuteIE• weight loss ] common in subacute endocarditis• Anemia of Chronic disease• Prostration

• Clinical features pointing tocardiac complications - Acute IE• Pericardial Rub• pleuritic Rub• Polyaothyzilis

Duke 's criteria

← -Te mince

→ Caodiac Abnormalities• Positive Blood culture • some predisposition

④Typical organism in 2. cultures to IE ↳ i.v drug abuse 2

Persistently⑤ Blood cultures• Fever 338°C

( 308 more , 12hours apart ) • Vascular / immunological signsL Roth spots

• Evidence of endocardium involvement Losier nodes↳⑤ ECHO findings (vegetations, abscesses LJaneway lesions

dehiscence of prosthetic valve) L splinter hemorrhagesL petechial hemorrhages( New valvular L GlomerulonephritisLpolyaothzitis

• Blood culture⑤ but not qualifying mayorcriteria

• ⑤ ECHO findings but not qualifying asmayor criteria

Diagnosis2 mayor criteria

ematmAll 5 minor criteria

4

RHD IE

- -hi AteneoHAHA HAHA

• small, warty vegetations (verrucae) • large , sterile , friable

along theline ofclosure vegetation• sterile • 9 inflammatory cells• do not embolize o embolization .•

immune mediated

MARANTIC ENDOCARDITIS(NBTE)I. Non Bacterial thrombotic endocarditis

⇒ . Hypercoagulable statecauses

H1N1 malignancies:::ng;:%: on:3 'k • Boons• Poomyelocylic Leukemia

• initially sterile C Bland thrombi )• X inflammatory reaction• along line ofclosure or atthe cusps

SLE

(Libman -sacks Vegetation s) CARCINOID SYNDROME

- -

eitchoesgsideotmucopolysaccharides

YMHA """"" "" HAMP• may form on either orboth sides . Production of SHT, Kalleiksinin, Histamine

of the valve leaflets by carcinoid tumours in a IT

• sticking⇒ x embolization . usually these metabolites are destroyedin lives unless a secondary develops

• may have LE cells (hematoxylin bodies) in the lives itself.• immune mediated • Rt. Heart is more exposed as some

metabolites are also destroyed inthe lungs preventing exposure ofIt- side

5

Cardiomyopathy• Conditions and theirassociated cardiac dysfunction, that are not involved in (MPs : -

• men• (PMs are group of diseases of the myocardium which include

7÷te " """" " """""" d#" "" the MY"""" '

• Inflammation

cardiomyopathy pathologic patterns→

DilatedCaodiomyopath# Hypertrophic RestrictivelyAsymmetric H - C- M

ۤ""""""9 ""%h%%" /"""" ""

s

- Ji--.* ÷: ÷

(duringsystole ) tcompliance←

• Global impairment in contractility • Hypeskinetic Heart • Failure to relaxationof myocardium . Septal hypertrophy . Diastolic dysfunction

• Hypokinetic heart . Obstruction of LV outflow • Ventricular wall is• Systolic dysfunction tract during systole infiltrated with :-• Ventricles become ballooned (Also known as Hypertrophic ① Amyloid depositsout, pathologically dilated Obstructive cardiomyopathy) ② Hemochromatosis

③ Sarcoid granulomas• Banana shaped ventricular!÷÷÷÷÷÷÷÷÷÷:

SOY.

Familial sporadic• Most common cause of| suddenafhqredpeiag death in young /

6

• Hypertrophic obstructive cardiomyopathy is the most common cause of SCD in

young athletes .9 activity⇒ Vigorous ventricular⇒ Approximation of ⇒ Lv outflow tract

contraction septum with anterior obstruction

!7E%EEsion⇐aa%aeing"s%aoy÷:÷I:!sigi%⇐taTnicpoesthe peripheral circulation in muscles

↳ Conduction defects ⇒ Fatal Arrhythmia

• ✓ 9Of- of allDilated cardiomyopathy cases

[ 9JVP • Also knownas congestivecardiomyopathyat D↳ i

- --. Baflaiyyared Trap|/lpp ↳

pumo.ngyygnedemacit.ventoiculao failures• Dyspnea• Paooxysomal Nocturnal Dyspnea

od failure : tmhopnasay crepitations• HepatomegalyThen#

• Patienthas featuresof pulmonary-CT congestion dueto LV failure andT.LT#kdauenfoesrvofsasiygtgemiccongesiion6↳

in pcap→ Generalized edemaAscites

other clinical features• weak pulse• Haemoptysis• 53 heard during rapid filling of

' '

overfilled"

ventricles• Dilatation of RV , LV leads to dilatation / stretching of fibrous annulus to whichthe bicuspid andtricuspid valve leaflets are attached ⇒ Insufficiency of AV valves (failure toclose)

• Functional mitral valve regurgitation• Functional Tricuspid valve regurgitation• Mural thrombi are common due to stagnant blood ⇒ Thromboembolism• Arrhythmias as conductiontime through > Relative Refractory Period

sing ofmuscle

7

CAUSES OF DILATED CPM(Peripartum DCM)

A B C C C D H P>

Alcohol Bti- Beri cotxg.ggksieoctainecn.gs/geaasseDox!ouoacinXemocnsoni:[is"

• Genetic factors in 30% cases a- dystooglycan• Defects in force generation and force

transmission ⇒ systolic dysfunction ⑧→ 8 - Saxoglycan

cqoossboidg.esCaomst head) \, p - Dystooglycan .

•• # • •

• 6*-0§n•X¥←, ,qq£••}→ Dystrophin

F- • •.heiu÷÷÷.m÷&÷smin#••mmI

• •Titigestpoenmoee • •

① Mutant Dystrophin ⇒ Instability of sarcomere dueto loss of appropriateconnection with basement membrane

• X - linked DCM↳If force generating mechanisms are impaired , d IT , and accordingto Laplace law PAIR , Radius increases dramatically withincrease in F-DV -

→ ft pressure

② Deletions in mitochondrial genes that transcribe enzymes ofoxidative phosphorylation ] ⇒ impaired energy③ Defects in enzymes of p- oxidation ( FA breakdown) production

⑨ Titin CMN) mutations

8

Hypertrophic Cardiomyopathy• In 1/3 cases , intermittentventricular outflow

@ tract obstruction is seen ⇒

Hypertrophic Obstructive CMP

qq.gg#aggqqnz , ,, Dynamic obstruction during systole

was , I - - iBanana shaped cavity

→

n-sygempe.at,oic§↳ • Hypeaoocomnpetonasaiog ,hearthypertrophy

T• 100T cases have a underlying genetic defect ⇒ impaired force generation/ → Sot.

So

Familial sporadic(Autosomal dominant)

qsthad'

mutations hgmjuypeotoophi.ccPM )-##↳muumuu mmmm ① mutation in Heavy chain p-myosin--¥÷÷En÷÷i÷÷÷ me-_↳it •

• Mfs B- myosin Heavy chaintree ot•-mmI ② Mutation of

Titigestpoeinmoee • • (98diac Troponin - T

A#÷meoes⇒goowthaos⇒Hypoph•y- Tropomyosin

• MORPHOLOGY

↳ Myocyte hypertrophy↳ Myofiber disarray⇒ haphazard arrangement of myocytes

↳ Disarray of sarcomere arrangement inindividual myocytes .[

Interstitial fibrosis

9

ameoioomitoaneaaet

. '%5Ya9 mwidaiisgsefseaptheoxh.fm#aokoictnueenah'LIFE .mitral leaflet

ha:*.t.nemse.nae.no#ena.maiEiefigneIsoanni:Ee'nethae.I 6The contact point on the endocardium ofthe

endocardial"

outflow tract also thickens and forms amural plaque endometrial plague .

• Jerky Pulse (Hyperdynamic pulse)• Focal myocardial ischemia due to perfusion : tension mismatch ( Demand > supply)

↳ Anginal pain• Tachyaoohythmia → Sudden cardiac Death. ( in young adults during physical activity)• exertionat dyspnea dueto diastolic failure and accompanying pulmonary congestion .• Risk of Infective Endocarditis

① (No su) . Sound of Hypertrophic• LA HYPE't KYU . . netta!! sound ( last filling phases s"""d'"• sound of Dilated -

S3• Intractable Heart failure Heart

°

µ Duetoventricular tract obstruction, there is abnormally

) ('

high velocity blood flow which leads to"

Harsh systolic Muomuo "¥⑤ .

:*:S:÷÷÷÷÷o÷÷÷÷ie¥⇒F-DV

• It becomes important to distinguish this harsh systolic muomuo fromthat dueto Aortic stenosis

• Fixed obstructionmo

::::÷:::::::::::e::::m..• TED V r fmurmur

Venoconstriction170

to To distinguish between muomuo caused by Aortic stenosis and HCM , Askthe patient to Squat evenOconstriction)

t.toAortic stenosis Venous Return HCM

Muomuo 999Ito

← F-Dvr-Murmur htt

10