Infective

Endocarditis,
Valvular Heart
Disease
Presented by : Boon & Raiha
 SEMINAR OUTLINE
1. Cardiac cycle & valvular functions
2. Aetiology of valvular heart disease (Congenital & Acquired)
3. Types of valvular dysfunctions, clinical manifestations, investigations
& management
4. Complications of valvular heart disease.
5. Definition & Diagnostic criteria of infective endocarditis
6. Classification of infective endocarditis
7. Risk factors & aetiological pathogens
8. Clinical features, investigations & management of infective
endocarditis
9. Complications of endocarditis & Indications for surgery
10. Antibiotic prophylaxis
Cardiac Cycle
Isovolumetric
relaxation
(ventricular
diastole -
early)
Duration : 0.10s
Ventricles start to relax,
pressure falls below that in the
great vessels causing semilunar
valve to close, producing 2nd
heart sound (S2)
No changes in ventricular
volume
 Ventricular
filling
(ventricular
diastole - late)
Ventricular pressure drops further,
causing atrioventricular valve to
open.
Early Rapid Passive Filling
Duration : 0.1s
Ventricular volume increase by about
50 mL Producing 3rd heart sound (S3)
Slow Filling (Diastasis)
Duration : 0.2s
Ventricular volume increase by
another 10 mL
Last Active Filling
Atria contract to push the last 10 mL
of blood into the ventricles.
Atrial contraction
(Atrial systole)
Duration : 0.10s
Occur immediately after atrial
depolarization.
Pressure increases in atria, causes
blood flow into the ventricles.
Produces 4th heart sound.

Atrial relaxation
(Atrial diastole)
Duration : 0.70s
Occur simultaneously with
ventricular systole First 300ms:
only atria fill with blood as
ventricles still in systole
Next 400ms: both atria & ventricles
fill with blood.
Isovolumetric
contraction
Duration : 0.05s
Ventricular pressure
increase, causing closure
of atrioventricular valve.
Produces 1st heart sound
(S1)
No change in ventricular
volume.
 Ventricular
contraction
(ventricular systole)
Once pressure exceeds the mean
pressure in pulmonary artery on the
right & aorta on the left, semilunar
valve will open.

Rapid Ejection
Duration : 0.1s
Ejected about 50mL of blood

Slow Ejection
Duration : > 0.2s
Ventricular pressure begin to drop &
20 mL of blood is ejected but at a
lower rate of flow.
Normal
Anatomy
Valvular
Function

Function to regulate blood flow by

1. maintaining one-way direction of
blood
2. prevent backflow of blood
 Aetiology of
Valvular Heart
Disease
Congenital
Mitral Valve Prolapse
(MVP)
Bicuspid Aortic valve
Mitral valve leaflets are
Aortic valve has only two cusps
Congenital valvular heart abnormally thickened or
instead of the normal three. This
elongated, causing them to bulge
diseases are present at birth increases the risk of aortic
(prolapse) into the left atrium.
and result from stenosis, regurgitation, and aortic
Typically asymptomatic but can
aneurysms over time.
developmental defects lead to mitral regurgitation in
some cases.
during fetal heart formation.
This occurs when valves do
not form correctly. These
conditions are often
geneticaly linked where the
Tricuspid Valve
fetus inherited mutations in
Pulmonary Valve Stenosis Abnormalities
genes that control heart
development This includes tricuspid valve
Narrowing of the pulmonary
stenosis or regurgitation, often
valve, leading to obstruction of
secondary to other congenital
E.g. Mutations in the NOTCH1 blood flow from the right ventricle
conditions like Epstein’s anomaly
to the lungs. This can lead to right
gene, responsible for valve (a malformation of the tricuspid
heart failure if severe.
valve).
development.
 Acquired valvular heart diseases develop later in
life, often as a result of infections, degenerative
changes, or other systemic conditions.
ETIOLOGY
OF Degenerative
ACQUIRED Connective tissue disease

VALVULAR
HEART Inflammatory
Rheumatic fever, etc
DISEASE
Ischaemic etc.
Drugs, Iatrogenic, Carcinoid, Eosinophilia
 Ehlers-Danlos syndrome

DEGENERATIVE : Defects in collagen synthesis, lead

to hyperelastic skin, hypermobile
Connective Tissue joints, and fragile blood vessels.

Disease Common manifestations: mitral

regurgitation and aortic
regurgitation
Affect the fibrous tissues and collagen causing heart valves to
become weakened, deformed, or unable to function properly.
Primarily related to abnormalities in the extracelular matrix
(ECM) and valve leaflet architecture, which ultimately affect the
strength, elasticity, and integrity of the valves.

Marfan Syndrome
Mutations in the fibrillin-1 gene
(FBN1), impairs the structural
integrity of connective tissue
throughout the body, including in the
heart and blood vessels (aorta)
Primary forms: mitral regurgitation
and aortic regurgitation
 Rheumatic Fever
An infection with Group A Streptococcus (commonly caused by strep
throat) triggers an autoimmune response, where the body’s immune
Inflammatory system mistakenly attacks its tissues, including the heart valves. Leads
to rheumatic heart disease

Systemic Lupus Erythematosus (SLE)

Autoimmune response results in the deposition of immune complexes
on the heart valves which trigger inflammation, leading to valvular
thickening, fibrosis, and vegetation formation.

Rheumatoid Arthritis (RA)

Chronic inflammation in RA can lead to rheumatoid valvulitis, where
the heart valves become thickened and fibrotic. The mitral and aortic
valves are most often affected, leading to mitral regurgitation or aortic
regurgitation.
 Iatrogenic Causes
Ischemic and
Prosthetic heart valve dysfunction: Surgical
Others replacement of a native valve with a prosthetic
valve can lead to valve failure, either from
degeneration, infection, or thrombosis.

Ischemic Heart Disease Surgical trauma: Structures such as the annulus,

chordae tendineae, or papilary muscles can be
Ischemic damage to papillary muscles: Mitral valve
and tricuspid valve are directly affected due to
damaged during surgery leading to valvular
infarction of the papilary muscles that help anchor insufficiency or stenosis.
the valve leaflets via the chordae tendineae.

Ischemic dilatation of the heart: Left ventricular Catheter-based interventions: Invasive procedures
dilation can stretch the mitral valve annulus, leading such as baloon valvuloplasty or percutaneous valve
to functional mitral regurgitation. This prevents the
mitral leaflets from closing properly, causing replacement can cause valvular rupture, injury, or
leakage of blood back into the LA during systole. dissection of the valve apparatus
 Other Causes

Drugs Eosinophilia Carcinoid

Fenfluramine and Dexfenfluramine Eosinophilic infiltration leads to fibrosis, Due to the release of serotonin and
(Fen Phen): Can cause pulmonary thickening, and calcification of the other bioactive substances by
hypertension and valvular heart valves, primarily affecting the carcinoid tumors, particularly
regurgitation (especialy of the mitral mitral and aortic valves originating from GIT or lungs. Serotonin
and aortic valves), through Hypereosinophilic syndrome, the and other vasoactive substances cause
mechanisms involving serotonin excessive presence of eosinophils in the fibrosis of the valve leaflets, leading to
receptors on the heart valves. bloodstream causes inflammation in thickening, retraction, and calcium
Dopamine Agonists & Ergot Alkaloids: the heart, resulting in valvular deposition.
Involves 5-HT2B serotonin receptor dysfunction such as regurgitation or Primarily affects the right-sided heart
activation, leading to excessive colagen stenosis valves, leading to tricuspid regurgita
deposition in the valve leaflets. Can cause Eosinophilic valvulitis can tion and pulmonary valve stenosis.
Antibiotics: Long-term use of lead to mitral regurgitation, aortic Left-sided valvular disease is less
penicilamine can lead to fibrosis of the regurgitation, and even heart failure if common but can occur if the tumor
mitral valve and other valves, left untreated. secretes substances that pass through
contributing to valvular regurgitation. a patent foramen ovale (PFO) into the
left heart. In this case, mitral valve and
aortic valve involvement may occur.
Type of valvular
dysfunction,
Clinical
manifestations,
Investigation
 Types of Valvular Dysfunction

Stenotic Lesions Regurgitation Lesions

“Stenotic lesion” refer to a “Regurgitant lesions” indicated
heart valve that is narrowed, inability of heart valve to close
restricting blood to flow properly, causing back flow and
forward through the valve. leaking of blood through the
valve.
 STENOTIC LESION

Aortic Stenosis Mitral Stenosis

Aortic valve become Mitral valve become

narrowed, increasing heart narrowed, blocking the flow
workload to pump out the of blood from left atrium to
blood from left ventricles. left ventricles.
Most common valve lesion Rheumatic fever is the
among adult patients with leading cause of mitral
chronic valvular heart stenosis
disease.
Clinical Manifestation of AS

SYMPTOMS SIGNS

Exertional dyspnoea High volume pulse collapse

Angina pectoris Ejection systole murmur
Exertional syncope Bruit sound
Fatigue and dyspnoea
Reduced effort tolerance
 Clinical Manifestation of MS
SYMPTOMS SIGNS

Dyspnea Low volume pulse collapse

Cough Loud S1 sound
Haemoptysis Taping apex beat
Anemia Presystole with increase in
Pulmonary changes and accentuation
hypertension Mid diastolic murmur
Opening snap + low pitch, rough,
rumbling murmur (Bell)
 Investigations
AORTIC STENOSIS MITRAL STENOSIS
1. ECG
1. ECG Tall and peaked P wave in lead II and
ST Depression upright in lead V1
T Wave inversion Normal QRS complex
2. Echocardiogram Right axis deviation
Thickening RV hypertrophy
Calcification 2. Echocardiogram
Reduced systolic opening of valve Decreased orifice
leaflets Thickened cusps
LV Hypertrophy 3. Chest X ray
3. Chest X-ray Thickening of the upper left boarder or the
Hypertrophy without dilatation cardiac silhouette
Rounding cardiac apex Dilatation of upper lobe pulmonary veins
Dilated proximal ascending aorta Posterior displacement of oesophagus by
Aortic valve calcification enlarged LA
Kerly B lines prominent in lower/ mid lung
Management for Aortic Stenosis
Management for Mitral Stenosis
 Aortic Stenosis
MEDICATION
Medications for hypertension/CAD,
Nitroglycerin relieve
eg. beta blockers & ACE inhibitors,
angina pectoris.
safe for asymptomatic patients.

SURGICAL
Percutaneous Transcatheter Surgical Aortic
Aortic Balloon Aortic Valve Valve Replacement
Valvuloplasty. Implantation (TAVI). (SAVR)
 Mitral Stenosis
MEDICATION SURGICAL
Penicillin prophylaxis of group A Mitral
β-hemolytic streptococcal Commissurotomy.
infections.
Beta blockers.
Non-dihydropyridine calcium
channel blockers e.g.verapamil.
Vitamin K antagonist therapy
(warfarin).
 REGURGITANT LESION
Aortic Regurgitation Mitral Regurgitation

Aortic valve doesn't close Mitral valve doesn't close

properly, causing backflow of properly, causing backflow of
blood from aorta back to the left blood from left ventricle to left
ventricle. atrium
 Clinical Manifestation of AR
SYMPTOMS SIGNS

Pulmonary edema / cadiogenic Low volume pulse collapse

shock in acute severe JVP elevation
Sinus tachycardia during Wide pulse pressure
exertion Early distolic murmur (sitting)
Palpitations Pan/ mid systole murmur
Head pounding
Exertional dyspnea
Diaphoresis
Chest pain
 Clinical Manifestation of MR
SYMPTOMS SIGNS

Fatigue No pulse collapse

Exertional Dyspnoea Slow S1 sound
Orthopnoea Pan/ mid systole murmur
Hepatic congestion Prominent at MV
Ankle edema Best heard when maneuver to left
Pulmonary hypertension (Bell)
Radiation of the pansystolic
murmur of mitral regurgitation in
left axilla
 Investigations
AORTIC REGURGITATION MITRAL REGURGITATION
1.ECG
1.ECG Left atrial enlargement
ST Depression Left Ventricular hypertrophy
T Wave inversion QRS axis deviation
T wave inversion
2.Echocardiogram AF
LV size increase
2. Echocardiogram
Rapid, high frequency diastolic
fluttering of anterior mitral leaflets
3. Chest X RAY
LA massively enlarged and forms the right
3.Chest X RAY border of cardiac silhouette
Apex displaced downward and to the Pulmonary venous congestion
left (frontal) Interstitial oedema
LV displaced posteriorly and Kerley B lines
encroaches on the spine (laterally) Calcification of mitral leaflets
Assymetric pulmonary oedema
Management for Aortic Regurgitation
Management for Mitral Regurgitation
 Aortic Regurgitation
MEDICATION SURGICAL

Intravenous (IV) diuretics . Aortic valve replacement (AVR).

Transcatheter aortic valve implantation
Vasodilators (ACE inhibitors, (TAVI).

[ARBs].

Dihydropyridine calcium channel

blockers, or hydralazine.

Nitroglycerin relieve angina

pectoris,
 Mitral Regurgitation
MEDICATION SURGICAL

Diuretics. Mitral valve

replacement.
Beta blockers.

ACE inhibitor.

Antibiotic prophylaxis

for history of IE.

 Complications of VHD

1. Heart failure
Impaired ability to pump blood effectively.
5. Pulmonary Hypertension
Common in severe aortic stenosis & mitral regurgitation. Increase pressure in LA, strains right side of the heart.

2. Arrhythmias 6. Left ventricular dysfunction

Due to change in structure and electrical conduction. Pressure or volume overload leads to dilation of LV.
Result in decrease cardiac output and heart failure.
3. Infective Endocarditis
Damage valves are prone to bacterial infection. 7. Stroke

4. Embolism 8. sudden cardiac death

Common in mitral stenosis or atrial fibrillation.
 Definition &
Diagnostic criteria
of infective
endocarditis
What is Infective
Endocarditis?

Infection of the endocardium, causing the

inflammation of the inner lining of the heart,
as well as cardiac valves (one or more).

It is primarily a disease caused by virulent

microorganism (usually bacteria) and has a
wide array of manifestations and sequelae.
Diagnostic
Criteria
CLASSIFICATION
OF
INFECTIVE
ENDOCARDITIS
1) Based on type of valve involve and
Clinical course
2) Based on location of valve involve
Etiological
Pathogen
The etiologic agents of infective endocarditis include the
following:
• Streptococci: 60% to 80%
• Viridans streptococci: 30% to 40%
• Enterococci: 5% to 18%
• Other streptococci: 15% to 25%
• Staphylococci: 20% to 35%
• Coagulase-positive organisms: 10% to 27%
• Coagulase-negative organisms: 1% to 3%
• Gram-negative aerobic bacilli: 1% to 13%
• Fungi: 2% to 4%
 IVDU: Commonest S. aureus, Pseudomonas aeruginosa

Prosthetic valves:
Early(<2 months after valve replacement): Staphylococci, 40% to 60%
(Coagulase-negative staphylococci, 30% to 35% and S. aureus, 20% to
25%)

Late(>12 months): more likely to have the organisms most commonly

seen in patients with native valve endocarditis, with one exception:
coagulase-negative staphylococci
more frequently (approximately 10%–12%) in
patients with prosthetic valves
Risk Factors

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 Demographics Non Cardiac Risk Factors

Poor dental status

Male
Dental procedures
Age >60 Non sterile venous injections (IV
drugs use)
Intravascular devices
Surgery
Chronic hemodialysis
Immunocompromised (HIV
infections, DM)
Other bacterial infections
(UTIs,spondylodiscitis, periodontal
Cardiac Conditions
infection)

Acquired valvular disease

Prosthetic heart valves
Congenital heart defects
Previous IE
Cardiac implantable
electronic device (CIED)
 Clinical Features of Infective Endocarditis
SIGN
SYMPTOMS
Heart murmur (68%).
Congestive heart failure. Fever (90%).
New cardiac conduction disturbance. Chills.
Cerebral complications (stroke, Malaise.
meningitis). Dyspnea.
Peripheral emboli and abscesses Poor appetite.
(renal, splenic, vertebral, or peripheral Weight loss.
arterial). Weakness (focal or
Septic pulmonary emboli. generalized).
Fever or sepsis of unclear origin. Back pain.
Splinter hemorrhages.
Roth spots.
Glomerulonephritis.
Clinical
Features
of Infective
Endocarditis
 Investigations of IE
DUKE CRITERIA

Standard diagnostic
tool for infective
endocarditis (IE).
It includes major and
minor criteria, and a
diagnosis is made
based on their
combination
 Investigations of IE
ECHOCARDIOGRAPHY
Key for detecting and following the progress of Mitral valve
vegetations endocarditis
For assessing valve damage
For detecting abscess formation

Transthoracic Echo Transesophageal Echo

Aortic valve
Used in patient with likelihood Detects vegetations in >90% vegetation
of endocarditis (<5%) of cases.
Disadvantages: Optimal for evaluating
Cannot detect vegetations <2 prosthetic valves.
mm in diameter. Detects abscesses, valve
Not adequate for evaluating perforation, and intracardiac Perivalvular
prosthetic valves. fistulae. abscess of aortic
Unable to detect intracardiac valve
complications.
 Investigations of IE
SEROLOGICAL TEST OTHER LABORATORY RESULTS

Anaemia
Helpful in diagnosis of : Leucocytosis
Bartonella Haematuria
Legionella Elevated ESR
C. burnetii Rheumatoid factor level
Circulating immune complex titre
Decrease in serum complement
concentration
 Management of IE
Anti-microbial therapy Surgical treatment
Must be bactericidal and prolonged Should be considered early in course of illness in patients
Most patient fever disappears within 5-7 days with indications
Requires emergency surgery if patient develops:
Blood culture should be repeated until sterile,
Acute aortic regurgitation with preclosure of mitral
rechecked if recrudescent fever occur and valve
rechecked again at 4-6 weeks after therapy Sinus of valsalva abscess rupture into right heart
to confirm cure to IE Should not be delayed when patient develops :
Evaluation of paravalvular or ectracardiac Severe valvular dysfunction with progressive CHF
Uncontrolled or perivalvular infection
abscess should be perform if patient is febrile
Should be delayed for :
for 7 days despite having antibiotic therapy
2-3 weeks when patient had non haemorrhagic
embolic stroke 4 weeks
When patient had haemorrhagic embolic stroke

Ruptured mycotic aneurysm should be and cerebral

edema need to be resolved prior to cardiac surgery
Anti-microbial treatment
 Indication for surgery in IE
Optimal outcome Improve outcome
Moderate to severe CHF due to valve Perivalvular extension of infection
dysfunction Poorly responsive S. aureus endocarditis
Partially dehisced unstable prosthetic involving aortic or mitral valve
valve Large (>10 mm diameter) hypermobile
Persistent bacteremia despite optimal vegetations with increased risk of
antimicrobial therapy embolism
S. aureus PVE with intracardiac Persistent unexplained fever (>10 days)
complication in culture negative NVE
Relapse of PVE after optimal Poorly responsive or relapsed
antimicrobial therapy endocarditis due to highly antibiotic
resistant enterococci or gram-negative
bacilli
 Antibiotic Prophylaxis for Procedures
OralCavity,Respiratory Genitourinary & GIT
Tract,Esophageal High risk patients :
Standard Regiment : -IV Ampicillin + Gentamicin within 30 min of
-PO Amoxicillin before procedure procedure
-Repeat IV Ampicillin/Amoxicillin 6 hours later
Inability to take oral medication :
High risk & penicillin allergic patients :
-IV Ampicillin within 30 min of the procedure
-IV Vancomycin + Gentamicin within 30 min
Penicillin allegry :
before procedure
-PO Clarithromycin/Cephalexin/Cefadroxil 1
Moderate risk patient :
hour before procedure
-PO Amoxicillin 1 hour before procedure
-IV Clindamycin 30 min before procedure
-IV Ampicillin within 30 min before procedure
Penicillin allergy & inability to take oral
Moderate risk & penicillin allergic patients :
medication :
-IV Vancomycin within 30 min of procedure
-IV Cefazolin 30 min before procedure
Thank
You!