1. Infectious Endocarditis
-prevention, diagnosis, treatment.
ESC Guidelines 2015.
Tomasz Fabiszak

3. Why IE is a problem?
The mortality due to IE have decreased, but this disease still carries a poor prognosis and a high mortality.

4. Why IE is a problem?
IE is not a uniform disease, but presents in a variety of different forms, varying according to:
the initial clinical manifestation,
the underlying cardiac disease (if any),
the microorganism involved,
the presence or absence of complications,
underlying patient characteristics.

5. Why IE is a problem? IE requires a collaborative approach involving:
primary care physicians,
cardiologists,
surgeons,
microbiologists,
infectious disease specialists,
neurologists,
neurosurgeons,
radiologists,
pathologists.

6. Definition Endovascular infection, which may include:
the structure of the heart (valves, endocardial wall)
large vessels of the chest (patent ductus arteriosus, coarctation of the aorta, arteriovenous fistula)
foreign material placed in the cavities of the heart (valvular prostheses, intracardiac electrodes, surgically created vascular connections)

7. Non-infected vegetation (nonbacterial thrombotic endocarditis)
Definition
The most characteristic part of the disease is vegetation- various size formation, composed of platelets, fibrin and red blood cells, mixed with bacteria and inflammatory cells.
Abnormal blood flow
Endothelial damage
Non-infected vegetation (nonbacterial thrombotic endocarditis)
I E
Bacteria

8. Epidemiology
3-10/ /year
The peak incidence (14,5/ /y) years of age
Male > Female - 2:1
Older > younger
Female have a worse prognosis and undergo valve surgery less frequently than their male counterparts.

9. Changing Epidemiology of Native Valve Infective Endocarditis Distribution of the number of cases of native valve infective endocarditis in non-intravenous drug users during the study period.
Rev Esp Cardiol. 2011;64: Vol. 64 

11. Classification ACTIVE RECURRENCE RELAPSE REINFECTION
IE with persistent fever and positive blood cultures, or
Active inflammatory morphology found at surgery, or
Patient still under antibiotic therapy, or
Histopathological evidence of active IE
Repeat episode of IE caused by the same microorganism < 6 months after the initial episode
Infection with the different microorganism
Repeat episode of IE caused by the same microorganism > 6 months after the initial episode

12. Predispositions
mitral valve prolapse- the most common cause of IE on native valve in adults (risk 3,5-8,2%)
rheumatic valvular disease- 7-18% of IE (F-mitral valve, M-aortic valve)
congenital heart disease % young adults, 9% adults (patent ductus arteriosus, VSD, bicuspid aortic valve, coarctation of the aorta)
no risk factors %

13. Etiology Streptococci - 50-70% of NVE Staphylococci -25% of NVE
Enterococci- 10% of NVE
Gram-negative bacilli [HACEK]
Haemophilus parainfluenzae,
H. aphrophilus,
H. paraphrophilus,
H. influenzae,
Actinobacillus actinomycetemcomitans,
Cardiobacterium hominis,
Eikenella corrodens,
Kingella kingae,
K. denitrificans
Other: bacterias, fungi, rickettsiae,
mycobacteria, mycoplasma,
chlamydia.

14. Etiology

15. Pathophysiology Inflammatory process
Proliferation and destruction of the valves
Leaflet perforation, papilary muscle rapture
Abscesses, fistulas
Penetration into the myocardium- AV-conductions disorders

16. IE - prevention Antibiotic prophylaxis limited to pts:
with the highest risk of IE
undergoing the highest risk dental procedure
Good oral hygiene and regular dental review more important than antibiotic prophylaxis
Aseptic measures – mandatory for venous catherization and invasive procedures

23. Diagnosis Clinical features Echocardiography Microbiological diagnosis
Diagnostic criteria and their limitations

24. IE - Symptoms

25. Symptoms Fever - 80 - 90% Shivers - 40 - 75% Sweating - 25%
Lack of apetite %
Weight Loss %
Malaise %
Headaches
Muscles, joints, back- aches
Confusion

26. Signs Heart murmur (new) - 80 - 90%
Peripheral embolism % (arteries of the brain, Valsalva’s sinus, mesenteric artery, splenic artery, coronary arteries, pulmonary artery, vasa vasorum)
Strokes %
Splenomegaly %
Osler’s nodes %
Janeway lesions %
Petechiae %
Roth's spots %
Clubbed fingers %

27. Janeway lesions 
Non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms.
Pathologically, the lesion is described to be a microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis.
caused by septic emboli which deposit bacteria, forming microabscesses.
Janeway lesions are distal, flat, ecchymotic, and painless.

29. Osler's nodes
Painful, red, raised lesions found on the hands and feet.
Result from the deposition of immune complexes.
Osler's nodes and Janeway lesions are similar, but Osler's nodes present with tenderness and are of immunologic origin

31. Splinter haemorrhage

32. Roth's spots
Retinal hemorrhages with white or pale centers composed of coagulated fibrin.
They are typically observed via fundoscopy (using an ophthalmoscope to view inside the eye) or slit lamp exam.
Usually caused by immune complex mediated vasculitis often resulting from bacterial endocarditis.

33. Roth’s spots

34. WARNING Roth's spots may also be observed with: Leukemia DM
Pernicious anaemia
Ischemic events
HIV retinopathy

35. Conjunctival haemorrhages

36. Clubbed fingers

37. Right-sided endocarditis
Cough
Chest pain
Dyspnoea
Hemoptysis
Lung infarction, lung abscess, pneumothorax
Occasionally, extensive damage to the lungs, leading to RDS (respiratory distress syndrome)
% of IE in drug abused persons

38. Lab findings Inflammation parameters: Anaemia Erythrocyturia CRP OB
LEU
Gamma-Globulins
Anaemia
Erythrocyturia

40. Blood cultures
DIAGNOSIS
ECHO IE

49. Venous blood culture: At least 3x Separated by at least 1 hour
Each time with a different injection site
ml blood into tubes with liquid medium (aerobic bacteria), and semi-solid (anaerobic bacteria)
If possible, before the start of antibiotic therapy
If antibiotic therapy was started, 3 days after its discontinuation
The probability of (+) culture depends on the quality of blood and prior antibiotic therapy (in Poland % of blood cultures are negative)

52. Transesophageal (TEE)
ECHO
Transthoracic (TTE)
Transesophageal (TEE)
reveals vegetations in about 50% of the patients ( %)
reveals vegetations on native valve in about 90-94% of the patients
reveals vegetations on prostetic valve in about % of the patients

54. (e.g. frailty, immunosuppression, renal or pulmonary diseaase)

55. Antimicrobial therapy
General principles:
Blood culture guided
I.v.
Therapy duration:
2-6 weeks for native valve IE
6-8 weeks for prosthetic valve IE
Empirical therapy
Negative blood cultures
the patient’s condition is poor

61. Indications for surgery
Heart failure
Uncontrolled infection
Prevention of embolism
Emergency = within 24 hrs
Urgent = a few days
Elective = after 1-2 weeks

62. Indications for surgery

63. Indications for surgery

64. Indications for surgery

66. Right-sided infective endocarditis
Right-sided IE accounts for 5–10% of cases of IE
May occur in patients with a PPM, ICD, central venous catheter, or CHD, this situation is most frequently observed in IVDAs
Tricuspid valve is the usual site of infection in IVDAs, pulmonary and eustachian valve infection may also be observed
Diagnostic features include respiratory symptoms and fever
TTE is of major value in these patients
Despite relatively low in-hospital mortality, right-sided IE has a high risk of recurrence in IVDAs and a conservative approach to surgery is recommended in this group

68. Outcomes after discharge and long-term prognosis
The risk of recurrence amongst survivors of IE varies between 2.7 and 22.5%.
Progressive HF can occur as a consequence of valve destruction, even when infection is healed
Long-term survival is 60–90% at 10 years
Relapse- Repeat episode of IE caused by the same microorganism < 6 months after the initial episode
Reinfection- Infection with the different microorganism, repeat episode of IE caused by the same microorganism > 6 months after the initial episode

70. Infective endocarditis on pacemakers and implantable defibrillators
One of the most difficult forms of IE to diagnose
Must be suspected in the presence of frequently misleading symptoms, particularly in elderly patients
Blood cultures are positive in 77% of cases
Staphylococci are the most frequent pathogens
The Duke criteria are difficult to apply in these patients because of low sensitivity
In the majority of patients must be treated by prolonged antibiotic therapy and device removal (4-6 weeks)
Infective endocarditis on pacemakers and implantable defibrillators is
associated with high mortality

71. Infective endocarditis on pacemakers and implantable defibrillators
Blood cultures – 3 or more
Lead-tip culture at CIED explantation
TTE not sensitive enough -> go for TOE / ICE
Suspected CDRIE with +ve cultures, but –ve ECHO -> radiolabelled leukocyte scintigraphy and 18F-FDG PET/CT scanning

72. Infective endocarditis on pacemakers and implantable defibrillators
Indications for hardware removal*:
Definite CDRIE (+prolonged antibiotic therapy)
Presumably isolated pocket infection
Occult infection w/o another apparent source of infection
NVE/PVE + no evidence of associated device infection ??
*Percutaneous extraction preferred even with vegetations >10 mm

73. Thank you for your attention