This document defines and describes infective endocarditis. Key points include: - Infective endocarditis involves infection of the heart valves or structures, most commonly the valves. This can lead to valvular dysfunction, sepsis, or embolism. - The infection involves bacterial, viral, or fungal invasion of the endocardium and formation of vegetations on the valves or endocardium. - Risk factors include underlying heart conditions, IV drug use, dental procedures, and indwelling catheters. The aortic and mitral valves are most commonly involved. - Symptoms may include fever, heart murmur, embolic phenomena, and heart failure. Diagnosis

1. Infective Endocarditis

2. Definition
• Conditions in which structures of the heart, most
frequently the valves, harbor an infective process.
• This might lead to:
– Valvar dysfunction
– Localized or generalized sepsis
– Sites for embolism
• The term “Infective Endocarditis” includes:
– Acute, subacute, and chronic
– Bacterial, viral, rickettsial, or fungal
– Native or prosthetic

3. Definition
• Endocarditis:
– Exudative and proliferative inflammatory
alterations of the endocardium
– Characterized by vegetations on the endocardial
surface or within the endocardium
– May occur as the primary disorder (infective
endocarditis) or as a secondary complication of
another disease (SLE, Rheumatic Heart Disease)

4. Definition
• Infective Endocarditis:
– Invasion and multiplication of micro-organisms on
the endocardial surface, within the endocardium,
within the myocardium, or on prosthetic materials
within and around cardiac structures
– Most frequently involves the valvar structures and
it may lead to destruction of these structures,
localized or genertalized sepsis, or sites of
embolism

5. Pathogenesis
• The most common site of involvement is on the
line of closure of the valves
– Atrial side of the atrio-ventricular valves
– Ventricular side of the semilunar valves
• Maturation of the vegetation:
– Bacterial attachment
– Bacterial proliferation + fibrin deposition
• The bacteria remain below the surface of the
vegetation and this protects them from:
– Phagocytes
– High antibiotic concentrations

6. Pathogenesis
• Altered Endocardial Surface to allow deposition of
bacteria and fibrin:
– Rheumatic Valvulitis
– Annular or Valvar Calcification
– Catheter Trauma
• Haemodynamic Factors:
– Jet effect of blood flow through
• PDA
• Restrictive VSD
• Mitral Valve Prolapse
• BAV
• Bacteraemia : 60-80% of normal individuals

7. Pathogenesis
• Compromised or Altered Immune System
– Histopathologic analysis of kidney tissue of the
patients with IE:
• Diffuse proliferative glumerolonephritis
• Evidence of deposition of IgG and IgM
• Circulating immune complexes (CICs) may be found in the:
– Glomerular basement membrane
– Retina
– Peripheral lesions (Janeway lesions and Roth Spots)
• CIC Levels correlate with the duration of the illness
• Drop in CIC levels correlate with the success of the
treatment
– Various manifestations of complement activation

8. Pathogenesis
• 25% of IE happen in normal valves
– Organisms involved are those with increased adhesions
molecules:
• Staphylococcus
• Streptococcus Viridans
• Enterococcus
– Common Risk Factors:
• Overwhelming Sepsis
• Resuscitation from Shock
• Use of Long-Term IDCs
• IVDU
• Fungemia associated with prolonged ABx use
• Only 5% of patients with IDC sepsis have endocarditis and it
is usually due to Staphylococcal Organisms.

9. Pathogenesis
• Iathrogenic IE:
– Those undergoing chronic hemodialysis
– Frequent Staphylococcal bacteremia
– Sclerotic Aortic/Mitral Valves

10. Rodbard Hypothesis for Pathogenesis
PART III Acquired Valvar 674 Heart Disease
Orifice Sink
Vena contracta
Source
Figure 15-1 Flow through a permeable tube. High-pressure source
drives fluid through an orifice into a low-pressure sink. Curved
arrows leaving the stream entering wall in upstream segment rep-resent
normal perfusion of lining layer. Velocity is maximal and
perfusing pressure is low immediately beyond orifice, where
momentum of stream converges stream lines to form a vena con-tracta.
Low pressure in this segment results in reduced perfusion
and may cause retrograde flow from deeper layers of vessel into the
flowing stream. It is at the vena contracta that bacteria and other
formed elements in blood accumulate. (From Rodbard.R4)
• High velocity jets of blood from a high-pressure source
form at an orifice and enter a low-pressure sink
• Venturi currents deposit bacteria immediately beyond
the orifice to form vena contracta and result in
mechanical erosion and deposition of platelets and
thrombin

11. Pathogenesis
• The same mechanism
exists
– Against the stenotic valves
– Opposite to a PDA in
pulmonary artery
– Left atrial side of the
regurgitant mitral valve.
• Most IE lesions of aortic
valve happen on the
ventricular side which
suggest the a role for
valvar regurgitation and
also the venturi effect

12. Morphology
• Vegetations and eorsive cavities are on the:
– Ventricular aspect of the aortic valve cusps
– Base of the atrial side of the mitral valve leaflets
• Often causing separation or discontinuity at the
– Ventriculoarterial junction
– Atrioventricular junction
– Drop Lesions from the aortic valve vegetations occur
on the anterior leaflet of the mitral valve and the
tensor apparatus.
– Discrete perforations also occur by isolated
vegetations.

13. Aortic valve with
vegetation on non-coronary
cusp and
partial destruction
of left coronary
cusp.

14. Aortic valve with
vegetation
between non-coronary
and right
coronary cusps
extending as an
anular abscess

15. Leaflet vegetation
and ring abscess of
posterior medial
aspect of mitral
valve

16. Mitral valve with
drop lesion of
anterior leaflet

17. Morphology
• NVE:
– Non-IV-Drug-Related:
• Left Sided
– IV-Drug-Related:
• Tricuspid Valve 50%
• Aortic and Mitral 50%
• Perianular Abscess (Pseudoaneurysm):
– More common with aortic valve endocarditis than it is with mitral
– It is present in 1/3 of cases studied with TOE
– Predominant organism is : S. aureus
– Clinical features:
• Presence of pericarditis
• Rapid progression of the disease
• High degree of AV Block

18. Morphology
• PVE:
– All or most of the vegetations are on the ventricular
aspect
– Only a small area of sewing ring detachment might be
apparent and it might appear sterile
– A thorough search at operation must be made
beneath the valve to identify the bulk of the
pathologic process
– There may be important detachment without
vegetation. This might be in the absence of an abscess
or even positive blood culture.

19. Loci of Infective Endocarditis Lesions

20. Clinical Features
• IE is present when
– Positive blood cultures associated with:
• New or changing murmurs
• Embolic phenomena
– New or changing murmurs in a patient with congenital
cardiac anomaly or prior valve damage associated
with:
• Embolic phenomena
• Sustained fever, anemia, and splenomegaly
– Some authorities also accept the presence of
progressive heart failure in the presence of positive
blood cultures.

21. Duke’s Criteria - Major
• Positive blood culture
– Typical MOs for IE from 2 separate blood cultures in
the absence of a primary focus:
• Strep Viridans, Strep Bovis, HACEK (Haemophilus,
Actinobacillus, Cardiobacterium, Eikenella, and Kingella),
Community-acquired staph aureus, or Enterococci
– Persistently positive blood cultures, defined as
recovery of a microorganism consistent with IE from:
• Blood cultures drawn more than 12 hours apart
• All of three or majority of 4 or more separate blood
cultures with first and last drawn at least 1 hour apart

22. Duke’s Criteria - Major
• Evidence of Endocardial Involvement:
– Positive echocardiogram for infective endocarditis:
• Oscillating intra-cardiac mass in absence of an alternative
anatomic explanation:
– On valve or supporting structures
– In path of regurgitant jets
– On implanted material
• Abscess
• New partial dehiscence of prosthetic valve
• New valvar regurgitation (increase or change in preexisting
murmur not sufficient for diagnosis)

23. Duke’s Criteria - Minor
• Predisposition:
– Predisposing heart
condition or IV drug use
– Fever ≥38°C
• Vascular Phenomena:
– Major arterial emboli
– Septic pulmonary infarcts
– Mycotic aneurysm
– Intracranial hemorrhage
– Conjunctival
hemorrhages
– Janeway lesions

24. Duke’s Criteria - Minor
• Immunologic
Phenomena:
– Glomerulonephritis
– Osler nodes
– Roth spots
– Rheumatoid factor

25. Duke’s Criteria - Minor
• Microbiological Evidence:
– Positive blood cultures but not meeting the major
criterion
– Serologic evidence of active infection with a MO
consistent with IE
• Echocardiogram:
– Consistent with infective endocarditis but not
meeting major criterion

26. Clinical Feature
• Fever:
– The most common clinical manifestation
– 95-100% present
– Low-grade
– Spiking
– Following the peak of bacteremia by 2 hours
– Those at risk of IE who develop fever for more than 48 hours should have 2 or
more sets of blood cultures drawn from different sites
• Positive blood cultures:
– 95% of cases even when those with right-sided IE, fungal IE, IE in addicts, IE
caused by fastidious organisms are included.
• Culture negative IE: 10%
– Mostly in those with PVE
– Intracellular or fastidious organisms
– Previous antibiotic therapy
– A history of AB therapy and serologic evidence of mycoplasma, or chlamydia
– Other causes:
• Aspergillus, Q-fever, Bartonella

27. Clinical Feature
• Heart Murmur:
– 85-95%
– 10% lack murmur
– Aortic root and valve:
• Short Diastolic Murmur
• Early systolic or midsystolic murmurs also can be present
– Mitral valve:
• Like other MR, systolic murmurs and in the case of anterior leaflet drop lesions there is a
distinct radiation to the back.
• Diastolic murmurs like MS: obstruction with large vegetation.
• Anemia
– Multifactorial causes: Marrow suppression as a result of the chronic disease
• Arthralgia / Arthritis : rarely seen today as a result of earlier diagnosis of
the condition
• Myalgia: common
– Associated with bacteremia
– Occasionally may result from myocardial microabscesses which generally
happen in staph bacteremia

28. Clinical Feature
• Embolic Phenomenon:
– 10-15% presenting manifestation
– 50% of patients with IE have embolic phenomenon:
• Diagnosed on either clinical examination or by an imaging modality
• Evenly distributed between cerebral and peripheral sites
• Classic ones are now rarely seen in surgical practice:
– Osler Nodes
– Janeway Lesions : Staph almost always is the organism
– Roth Spots
– Petechiae
– Clubbing
• Neurologic Abnormalities: 25-30% of patients at initial
presentation:
– TIA/Stroke/Loss of Vision/Seizures/Headache/Backache/Acute
Mononeuropathy

29. Causative Organisms
• Strep and Staph : 80% of cases
– S. aureus:
• The most common cause of IE amongst hospital-acquired and drug-related
• Mitral > Aortic
• Higher occurrence of embolism comparing to the other oranisms
– Strep:
• 30% of IE cases
• Viridans is the most common
• Enterococci:
– The third common
– 10% of cases
– Elderly male
– Multiple comorbidities
– Less common embolic events
– More avidity to Aortic Valve
• Gram-negative bacilli:
– 5% of cases

30. Causative Organisms
• PVE:
– 2 months post-op: Staph. Epidermidis
– Late onset: as NVE
– Enterococcal:
• E. Faecalis/ E. Faecium
• Associated with manipulation of GI or GU tract
• GI or GU tract malignancy

31. Complications
• Heart Failure
• Renal
• Embolic Events
• Neurologic Manifestations

32. Heart Failure
• The most common
• Valvular regurgitation is the cause
• NVE occasionally results is MS and/or TS and infrequently AS
• Perianular Extension
– Major causes of heart failure in PVE.
– 50% of cases with PVE
– 10-40% of NVE
– More commonly involves the aortic valve
– Can lead to:
• Abscess formation / pseudoaneurysm/aortocavitary fistula
• Myocardial abscess:
– S. aureus
– PVE / Aortic Valve / BAV
– Development of conduction abnormalities should prompt further TOE
examination
– Untreated: fistula formation and intracardiac shunting from myocardial
perforation

33. Renal
• At least in 4 forms:
– Pre-renal due to low cardiac output
– Microabscess formation secondary to septic
emboli
– Golmerular dysfunction as a result of CIC
– Renal failure as a result of ABx

34. Embolic Events
• Common:
– NVE : 43%
– IV Drug-Associated : 67%
– PVE: 25%

35. Embolic Events
• Metastatic infection of viscera is typically caused by Staph.
• Multiple Coronary emboli:
– MI
– Ventricular Dysfunction
– Most common causative organisms:
• S. Aureus
• Candida
• HACEK (Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
• Neurologic Manifestations:
– 50% of embolic complications are associated with neurologic manifestations
– 1/4 – 1/3 of patients with NVE or PVE at some time have neurologic
complications of which 90% are related to emboli in the territory of MCA
– S. aureus increases the risk
– Stroke is the most common neurologic event

36. Embolic Neurologic Events
• Cerebral embolism generally happens before the start of antibiotic therapy and
the risk dramatically falls following the commencement of an effective therapy.
– The risk falls from ~ 12% to 4%
• The absolute size of vegetation and failure of decrease in size of the vegetation
following ABx is a risk for embolization.
• HACEK Group and fungi create the large vegetation.

37. Intracerebral Hemorrhage
• The most devastating complication
• 5% of IE
• 50% mortality
• Pathophysiology:
– Septic arteritis with erosion of the vessel wall
during uncontrolled infection
– Hemorrhage following infarction
– Rupture of mycotic aneurysm

38. Treatment
• Antibiotics:
– > 50% of cases can be managed solely with antibiotics
– Once antibiotics started blood cultures should be taken every 1-
2 days and the length of the treatment should be calculated
based on the date the blood cultures have become negative
• Surgery:
– It is necessary in 40-45% of patients
– Goals:
• Remove infected tissues and drain abscesses
• Restore or reconstruct atrioventricular or ventriculo-arterial continuity
• Reverse the haemodynamic abnormality
• Closing the acquired defect / in children: repair of congenital
malformation

39. Indications for Surgery
• NVE:
– Healed: those hemodynamic indications present for
those without IE and similar valvular lesions
– Active:
• Congestive Heart Failure
• Perianular Extension
• Systemic Embolism
• Cerebrovascular Complications
• Persistent Sepsis
• Difficult Organisms
• PVE

40. Indications for Surgery
• Congestive Heart Failure:
– Caused by severe aortic or mitral regurgitation,
more rarely by valve obstruction caused by
vegetations.
– Severe acute aortic or mitral regurgitation with
echocardiographic signs of elevated left
ventricular end-diastolic pressure or significant
pulmonary hypertension.
– As a result of prosthetic dehiscence or
obstruction.

41. Indications for Surgery
• Perianular Extension
• Systemic Embolism
– Recurrent emboli despite appropriate antibiotic
therapy.
– Large vegetations (>10 mm) after one or more clinical
or silent embolic events after initiation of antibiotic
therapy
– Large vegetations and other predictors of a
complicated course
– Very large vegetations (>15 mm) without embolic
complications, especially if valve-sparing surgery is
likely (remains controversial)

42. Indications for Surgery
• Cerebrovascular Complications
– Silent neurologic complication or TIA and other
surgical indications
– Ischemic stroke and other surgical indications
(hemorrhage should have been excluded and the
neurologic complications are not severe and there
is a chance for recovery)

43. Indications for Surgery
• Persistent Sepsis:
– Fever or positive blood cultures persisting > 5-7
days despite appropriate antibiotic regimen,
assuming that vegetations or other cardiac lesions
requiring surgery persist and extracardiac sources
of sepsis have all been excluded
– Relapsing infective endocarditis, esp. when caused
by organisms other than sensitive strep or in
patients with prosthetic valves

44. Indications for Surgery
• Difficult Organisms:
– S. aureus involving a prosthetic valve and most cases
involving a native valve
– IE caused by other aggressive organisms:
• Brucella
• Stpahylococcus Lugdunensis
– IE caused by MRO:
• MRSA
• VRE
– P. aeruginosa IE
– Fungal IE
– Q Fever IE at the presence of other indications for
intervention

45. Indications for Surgery
• Prosthetic valve endocarditis:
– All cases of early PVE
– All cases of PVE and S. aureus
– Late PVE
• With heart failure caused by:
– Prosthetic dehiscence
– Prosthetic obstruction
– Other indications of surgery
• With perianular extension (abscess or fistulous tract)
• With persistent bacteremia, recurrent emboli, or
relapsing infection while on appropriate antibiotics

46. Timing of Surgery
• Emergency (within 24 h):
– Native (mitral or aortic) or prosthetic valve
endocarditis and severe CHF or Cardiogenic Shock:
• Acute valvular regurgitation
• Severe prosthetic dysfunction (dehiscence or
obstruction)
• Fistula into a cardiac chamber or the pericardial space

47. Timing of Surgery
• Urgent (within days):
– NVE or PVE with:
• Persisting CHF
• Signs of poor hemodynamic tolerance
• Abscess
– PVE caused by:
• Staph
• Gram-negative organisms
– Large vegetation (> 10 mm) with:
• An embolic event
• Other predictors of a complicated course
– Very large vegetations (> 15 mm)
– Large abscess and/or perianular involvement with uncontrolled
infection

48. Timing of Surgery
• Early Elective Surgery (During In-Hospital Stay):
– Severe AR or MR with CHF and good response to
antibiotic therapy
– PVE with valvular dehiscence or CHF and good
response to medical therapy
– Presence of abscess or perianular extension
– Persisting infection when extracardiac focus has been
excluded
– Fungal or other infections resistant to medical therapy

49. Surgical Approach
• Considerations:
– Aortic valve IE:
• Anterior leaflet of mitral valve and its chordae should
be examined for drop lesions
• There might be a need for the left atrium to be entered
to examine the posterior leaflet apparatus
– Mitral valve IE:
• Aortic valve involvement is unlikely if:
– Absence of thrill or murmur
– Competent aortic valve
– No echo evidence of vegetations

50. Surgical Approach
• Mitral Valve IE:
– Posteroinferior portion of the mitral annulus
should be inspected to look for myocardial ring
abscess
• Aortic Root Abscess:
– Posterior to the membranous portion of IVS
– Posterior portion of the septum anterior to the
LMCA

51. Surgical Approach
• Mitral Valve Endocarditis
– Repair:
• Healed, Small, or Discrete
Vegetations
• Does not involve a major
portion of the tensor apparatus
• How:
– Closure of small defects of the
anterior or posterior leaflet using
autologus or bovine pericardium
or direct suturing
– Small vegetations might be
stripped off the chordae
tendineae

52. Surgical Approach
• Mitral Valve Endocarditis:
– Major destructions:
• Major challenge for repair
• Options:
– Replacement for all but small
vegetations : there is a risk of PVE in
the setting of active infection
– Debridement of infected tissue >
Sliding annuloplasty to reconstruct
commissural areas
– Partial leaflet resection and/or
pericardial patch replacement might
be needed
– Suture annuloplasty is preferable to
prosthetic ring.
– Biodegradable rings have also been
used in active infection setting and has
been shown to be safe

53. Surgical Approach
• Abscesses:
– When found: should be completely evacuated and
surrounded tissue debrided:
– Atrioventricular/ventriculoarterial discontinuity is
an important issue

54. Mitral Valve IE with Ring Abscess

55. Mitral Valve IE with Ring Abscess

56. Mitral Valve IE with Ring Abscess

57. Aortic Valve IE with Abscess

58. Aortic Valve IE with Abscess

59. Aortic Valve IE with Abscess

60. Choice of Devices
• Aortic Valve:
– Allograft
– Other devices also have good outcome
– When aortic root replacement is considered, allograft is not
superior to other choices
• Tricuspid:
– Repair
– Allograft
• Mitral:
– Repair
– If not possible then Mechanical Valve
• Recurrent Infections:
– Cardiac Transplant

61. Post Operative Considerations
• Vasoplegia
• Diuresis and PEEP for Early Extubation
• Renal Function
• Antibiotics
• Persistent Fever and Sepsis Despite
Satisfactory Operation