Infectious heart diseases

Jiri Bonaventura, MD
Department of Cardiology, Charles University in Prague,
2nd Faculty of Medicine and Motol University Hospital,
Prague, Czech Republic
 Infectious diseases of the heart

• Infective endocarditis
• Myocarditis
• Pericarditis
Infective endocarditis
 Epidemiology
• IE is a relatively rare but serious disease with
high mortality despite the improvement in dg.
and th.
• Estimated annual incidence 3-10/100 000
• The profile of patients and pathogens has
changed over time (rheumatic fever x PM/ICD)
• Predisposing factors:
• prosthetic valves
• elderly patients with degenerated valves
• i.v. drug users
• i.v. catheters, pacemaker electrodes
 Classification
• (Acute x subacute/ lenta)

• NVE - native valve endocarditis

• PVE - prosthetic valve endocarditis
• IVDU - intravenous drug users
• IE on PM / ICD electrodes
 Classification

• Relapse - repeat IE within 6 months and proven

identical pathogen
• Reinfection, - new microorganism, or the same
species but > 6 months

• Early PVE - within 1 year (usually aggressive

nosocomial infection of sewing material)
• Late PVE - > 1 year after surgery/implantation
 Pathophysiology
• IE is rare in healthy individuals despite common
bacteremia (dental procedures, toothbrushing…)
x
• Any injury to endocardial surface (degenerative
changes, impact of catheters, electrodes,
prosthetic materials…) → endocardial damage,
exposing EC matrix → factor III, platelet activation,
fibrin-platelet (sterile) vegetation → increase risk
of bacterial seeding
 NVE
• Rheumatic valvular disease – usually mitral valve
followed by the aortic valve
• Congenital heart disease - patent ductus
arteriosus, ventricular septal defect, tetralogy of
Fallot (TOF), any native or surgical high-flow lesion
• Mitral valve prolapse
• Degenerative heart disease
• aortic stenosis in elderly ,bicuspid valve, Marfan
syndrome, rarely syphilitic disease
• mitral regurgitation
 Clinical presentation

• Variable!
• Fever (95%), signs of systemic disease (nausea,
weight loss….)
• Heart murmur (85%)
• Septic embolization (20-50%)
- brain, kidneys, spleen
- pulmonary
• Peripheral microembolization less common
 Diagnostic testing
Blood cultures
• 3 sets (aero + anaerobe) at different times + from diff. sites
• 85-90% - streptococci, staphylococci, enterococci
• 10% culture negative
• (usually due to previous ATB th.)
• less commonly HACEK (Haemophilus, Actinobacillus,
Cardiobacterium, Eikenella, Kingella )
• Fungi – Candida, Aspergillus
• Intracellular pathogens: Coxiella, Bartonella, Chlamydia,
Mycoplasma, Legionella, Trephonema
 Diagnostic testing
Echocardiography

• TTE - low sensitivity (40-60%)

• TEE - sensitivity 90 - 100%
• vegetations / abscess / new prosthetic valve
dehiscence = specific
• new regurgitation / obstruction = not specific
 Duke
criteria (IE
probability)

ESC guidelines
2015
Duke criteria (IE probability)
 Treatment
• ATB therapy

• Surgery - performed in high-risk patients

• Age/comorbidities/PVE/DM
• Complicated IE (heart failure, shock…)
• High-risk agents (S.aureus, fungi…), ATB
failure
• TTE/TEE high-risk morphology parameters –
risk of embolisation
 Antibiotics
• beta-lactam (penicillin, cefalosporin)

• glykopeptide (vancomycine)
• aminoglykosides (gentamicin)
• rifampicin in PVE

Fungi – ATB centre expert consult

 Antibiotics
• Streptococci: PEN/CEF + GENTA, (VANCO)
• Enterococci: like streptococci, PEN resist. common
• Staphylococci: MET/OXA + GENTA
• Empiric therapy - should focus on S. aureus
• HACEK/early PVE/fungi - require expert ATB consult
• PVE - prolonged (min. 6w) + RIFAMPIN
 Antibiotics
• Usually 4-6 weeks (regardless of surgery)
• No fever and decrease in CRP are good markers
of th. success, TTE follow-up (< 2weeks) necessary

• Cessation of therapy in case of:

• normal CRP (1w), favourable TTE, no
embolisation (2w), absence of focus for
potential reinfection
 Surgery

• progressive heart failure (emergency in shock)

• signs of ATB th. failure - continuous fever,
abscess, vegetation, valve dehiscence…
• embolization potential (> 10 mm)
 PVE
• 1% / 1 yr / patient
• risk: mechanical similar to biological (later!)
• most common manifestation – valve regurgitation
• long-term sterilisation rare - surgery likely !!!

• early PVE = aggressive pathogens in sewing

material, rapidly spreading into surroundings
• late PVE = NVE like
 PM/ICD IE
• IE anywhere on/close to electrodes
• S. aureus most likely
• Electrode withdrawal necessary (embolisation
during withdrawal common, rarely clinically
significant)
 IVDU
• Most commonly Tricuspid valve
• S. aureus, pseudomonas, G-, fungi, polymicrobial
• Fever, septic pulmonary embolisation (cough,
hemoptysis, pulmonary abscesses, …)
• Mortality < 10% , but high likelihood of
recurrence, surgery common
 Prevention
• Restrictive approach
• High risk patients only
• Prosthetic valve implant
• Previous IE
• Congenital Heart Disease patients
• High-risk procedures (dental)
Myocarditis
 Overview
• Inflammatory disease of the myocardium with a
wide range of clinical presentations, from subtle
to devastating
• Usually manifests in otherwise healthy person
• Wide variety of infectious organisms,
autoimmune disorders and exogenous agents

• Acute phase (0-2wks): direct cytotoxic effect +

cell mediated cytotoxicity
• Chronic phase (>2wks): mainly autoimmune
 Etiology
• “Idiopathic” in 50% of cases
• Viruses - Enterovirus, Coxsackie A,B, Adenovirus,
Parvovirus B19, Influenza, CMV,EBV, HCV, HIV…
• Bacterial - streptococci, TBC, diptheria, Borrelia,
Chlamydia, Mycoplasma
• Fungi – Aspergillus, Candida
•Protozoa – Trypanosoma cruzii
• Drugs - anthracyclines, cocaine
• Rheumatic fever
• Autoimmune disorders – SLE, Sarcoidosis, Sjögren
sy, Churg-Strauss sy, Wegeners granulomatosis,
„giant-cell“ myocarditis
 Clinical presentation
• flu-like symptomes, arthralgias, malaise, fever
• pharyngitis, tonsillitis, upper respiratory tract
infection
• Chest pain, sweats, dyspnea, palpitations
• Signs of heart failure, cardiogenic shock
• Syncope or sudden cardiac death due to underlying
ventricular arrhythmias or AV block)
 Diagnostic workup
• Complete blood count, erythrocyte
sedimentation rate level, CRP, rheumatologic
screening, cardiac biomarkers (TnI, TnT)
• Viral antibody titers - rarely indicated, low
specificity and delayed rising, no impact on
therapeutic decisions
• ECG - nonspecific - sinus tachycardia, ST-T
changes, AV blocks
• Echocardiography (TTE) - to estimate
dysfunction and rule-out other causes
 Diagnostic workup
• CAG (coronary angiography)- rule-out CAD
• MRI (late gadolinium enhancement) - extent
of inflammation and cellular edema, nonspecific
• EMB (endomyocardial biopsy) - routine use
rarely helpful, mandatory in rapidly progressive
HF to rule-out giant-cell myocarditis
 Treatment
• Standard HF treatment (ACEi, BB, ARB,
diuretics, inotropics,…IABP, LVAD in shock)
• Avoid physical stress (several months)
• Routine use of immunosuppression not
recommended
• Immunosuppression used in giant-cell
myocarditis or in systemic autoimmune disease
(SLE, RA…)
 Follow-up
• Ongoing, chronic inflammation may cause DCM
(dilated cardiomyopathy) and subsequent HF
• Patients with a history of myocarditis should be
monitored at 1-3 months interval initially, with
gradual return of physical activity
• Any evidence of residual cardiac dysfunction
should be treated in the same manner as for
chronic HF
 Prognosis
• Patients who survive fulminant myocarditis
generally have good prognosis
• Most patients with mild symptoms recover
completely without any residual cardiac
dysfunction, although up to 30% develop DCM
• 90% of patients with giant-cell myocarditis die or
undergo Tx in 6 months
Pericarditis
 Acute pericarditis
• is an inflammation of the pericardium characterized by
chest pain, pericardial friction rub, and serial ECG
changes
• Pain
• usually precordial or retrosternal with referral to the
trapezius ridge, neck, left shoulder, or arm
• quality is usually pleuritic, range from sharp, dull,
aching, burning, or pressing,
• intensity varies, is worse during inspiration, when
lying flat, or during swallowing and with body
motion, it may be relieved by leaning forward while
seated
 Clinical presentation
• Intermittent fever
• dyspnea/tachypnea (!myocarditis, pericarditis,
and cardiac tamponade)
• cough, dysphagia
• Any form of pericardial inflammation may
cause effusion

Myocarditis ↔ myopericarditis
Pericarditis ↔ perimyocarditis
 Etiology
• Idiopathic causes - about 50%, likely viral
• Infectious
• Viral – enterovirus,echovirus, parvovirus, EBV, HIV…
• bacterial, TBC, mycotic (Candida)
• Inflammatory disorders - RA, SLE, scleroderma,
rheumatic fever, Reiter sy, dermatomyositis
• Metabolic – renal failure, hypothyroidism,
• Cardiovascular disorders - acute MI, Dressler
syndrome,
• Iatrogenic – postpericardiotomic sy, catheterization
• Neoplasms – adjacent / secondary / paraneoplastic
• Drugs, Irradiation
• Trauma, Pneumonia, Pulmonary infarction…
 Diagnostic workup

• ECG changes
• chest radiograph (enlarged if effusion >250ml)
• TTE (effusion), CT (calcification), MRI
• Laboratory studies (Complete blood count, ESR,
CRP, cardiac TnI/TnT, electrolytes, BUN,
creatinine, thyroid hormones + specific (RF...))
• CAG ?
 Treatment
• If specific cause revealed, treat accordingly (ATB)
• Idiopathic or viral treated for symptom relief
• NSAIDs in full dose for 7-14 days (600-800 mg
ibuprofen /day), consider PPI as gastric
protection
• Colchicine (recurrence or beyond 14 days, 1
mg/day)
• Corticosteroids - not for initial therapy, unless
specific therapy (autoimmune) or no response to
NSAIDs + colchicine
• Pericardiocentesis – large effusions, cardiac
tamponade
 Treatment
Surgical therapy

• usually when recurrence or large effusions

• pericardial window
• pericardectomy - in constrictive pericarditis
 Complications
• The most common complication of idiopathic
acute pericarditis is recurrence, 15 -30 %

Constrictive pericarditis
• Acute and subacute forms of pericarditis may
deposit fibrin → pericardial effusion → further
pericardial inflammation, chronic fibrotic
scarring, calcification, and restricted cardiac
filling
 Complications
Cardiac tamponade

•especially in acute pericardial hemorrhage or

large chronic malignant effusions
•accumulation of fluid in the pericardial space
•resulting in reduced ventricular filling and
subsequent hemodynamic compromise
•medical emergency
 Complications
Cardiac tamponade

• Symptoms vary with the acuteness and underlying

cause
• Dyspnea, tachycardia, tachypnea, hypotension
• Elevated jugular venous pressure
• Pulsus paradoxus
• chest pain, fever, dysphoria
Thank You.