Prosthetic Valve Endocarditis

I.  Overview of Prosthetic Valves and Complications
Two basic types of prosthetic valves, mechanical vs bioprosthetic (usually heterografts from porcine or bovine tissue). 
Advantage of mechanical valves is their durability (generally last 20-30 years), but at the cost of higher risk of thrombosis necessitating lifelong anticoagulation.  Advantage of bioprosthetic valves is that in the absence of other risk factors, long-term anticoagulation is not needed, but this comes at the cost of much less durability (~30% of porcine valves fail within 10-15 years).

Complications

1. Thrombosis and Bleeding - account for the majority of complications of mechanical valves.  In the absence of anticoagulation, risk of systemic embolization per year on warfarin is ~1.0%, 2.2% on ASA, and 4% with nothing.  Mitral valve is approximate twice the risk as aortic valve.  Generally, goal INR is 2.5 to 3.5 for MVR and AVR if any other risk factors present (A-fib, prior thromboembolic event, LV dysfunction, hypercoagulable state); 2-3 is ok with AVR without any other risk factors.   Valve thrombosis can be a catastrophic event, leading to valvular obstruction and acute heart failure.  Systemic embolization can obviously cause CVAs and such.  Treatment is generally thrombolysis +/- surgery.
2. Structural Failure – as above, more common with bioprosthetic valves, and can present with signs of valvular regurgitation and heart failure. 
3. Endocarditis – bigtime concern with prosthetic valves and can be devastating.  See below for more.
4. Hemolytic anemia – due to shearing of RBCs across mechanical valves, usually mild, can see schistocytes.  Can be severe – especially as a presentation of valve failure.

 

 

II. Grading of Murmur Severity
  Grade 1 – barely audible murmur, heard under the best conditions
  Grade 2 – standard audible murmur
  Grade 3 – very loud murmur
  Grade 4 – palpable thrill
  Grade 5 – palpable thrill and loud enough to be heard with the stethoscope partly off the chest
  Grade 6 – palpable thrill and loud enough to be heard without the stethoscope
So remember that anything with a palpable thrill is automatically grade 4 or higher.

 

 

III.  Etiologies and Basic Management of Acute Mitral Regurgitation
Native Valve – Etiologies of Acute MR:

1. Flail leaflet – due to Mitral valve prolapse, endocarditis, or trauma
2. Chordae tendinae rupture – due to trauma, spontaneous rupture, endocarditis, acute rheumatic fever
3. Papillary muscle rupture – trauma or MI

Prosthetic Valve:

1. Tissue valve leafleft rupture – due to degenerating calcification or endocarditis
2. Valve thrombosis
3. Paravalvular regurgitation due to infection or suture rupture

Basically, you get an acute rise in LA volume/pressure leading to pulmonary edema and usually signs of right heart failure as well.  Blood ejected from the LV goes backwards and thus limits effective forward flow.  Unfortunately, with cardiogenic shock that ensures, you get a compensatory vasoconstriction and increase in SVR which worsens the MR. 
Treatment acutely centers around afterload reduction with nitroprusside being the drug of choice (unless hypotensive), and inotropes such as dobutamine can be helpful too.  Mechanical assistance from a balloon pump is often necessary until the definitive treatment of surgical valve repair/replacement (which unfortunately still carries a very high mortality of ~50% for acute MR).

 

 

IV. Prosthetic Valve Endocarditis
Highest risk is during the 1st three months after surgery, then risk falls gradually.  Risk is likely equal between AVR and MVR.  The risk is equal for mechanical vs bioprosthetic valves during the 1st year, but afterwards, bioprosthetic valves are at higher risk (due to the leaflets experiencing age-related alterations in surface characteristics that predispose to infection).

 

Microbiology

Early PVE (within ~2 months) – usually due to direct intraop contamination or early hematogenous spread after surgery.
# 1= Staphylococci – both Staph aureus and Coag-negative staph
Also: Culture negative endocarditis and fungal endocarditis
Late PVE (after ~2 months) – begins to resemble the microbiology of native valve endocarditis (NVE).
# 1 = Staphylococci (still) - S.aureus and coag negative staph
But also: Strep viridans and Enterococci, and still culture-negative endocarditis
Clinically, presents with signs/symptoms similar to NVE, but with a higher rate of invasive infections leading to new/changing murmurs, CHF, conduction abnormalities, and embolic events.

 

• Early infection (<60 days): typically secondary to intraoperative contamination
  • Microbiology:
    • Staph aureus (40%)
    • Coag neg staph (20%)
    • Cx neg (20%)
    • Fungal (10%
• Late infection: pathophysiology more similar to native valve endocarditis (adherence to platelet-fibrin thrombi on valve), as foreign material has become endothelialized
  • Of note, bioprosthetic valves are at greater risk of late infection, given degenerative changes that occur on surface
  • Microbiology:
    • Coag neg staph (20%)
    • Staph aureus (15%)
    • Enterococcus (10%)
    • Strep viridans (10%)

A Few General Principles of PVE
1) TEE >> TTE for sensitivity of endocarditis (this difference is much more magnified than it is for NVE), as well as demonstrating signs of invasive infection which is more common with PVE.
2) Antibiotic regimens are generally the same for PVE as for NVE, with the notable exception of Staphylococci which involves multiple drug regimens (Vanc/Nafcillin + Gentamicin + Rifampin).  The regimen for culture-negative endocarditis is also different, and treatment durations tend to be longer for PVE vs NVE as well (minimum of 6 weeks).   Antibiotics alone, however frequently fail to clear PVE.
3) Given the higher rate of invasive infection and antibiotic failure, surgery plays a much more prominent role in PVE than in NVE.  Have a low threshold for calling your CT surgery colleagues.
Diagnostically, aside from TTE being highly insensitive, diagnosis still relies on the Duke Criteria as for NVE.
** Empiric antibiotic regimen for PVE in a hemodynamically unstable patient: Vancomycin + Cefepime(or Carbapenem) + Gentamicin **

Indications for Surgery in PVE – the first 4 are similar to the indications as for NVE
1)      Heart failure due to valve dysfunction
2)      Invasive infection causing abscess, conduction abnormalities, dehiscence, etc
3)      Recurrent or persistent bacteremia/emboli despite appropriate abxs

In addition, surgery is generally recommended when the following pathogens are implicated, due to the fact that it is virtually impossible to clear with antimicrobials alone.

1)      Staph aureus – carries up to a 70% mortality in PVE with abxs alone
2)      Gram negative bacilli especially Pseudomonas
3)      Fungal infections (similar to NVE, where surgery is generally indicated as well)
4)      Multiresistant Enterococci

 

 

Treatment

• Abx therapy: requires combination therapy, to prevent resistance to rifampin
  • Methicillin (or vancomycin)
  • Rifampin: to penetrate biofilm and kill bacteria adherent to foreign material
  • Aminoglycoside (or fluoroquinolone) for at least two weeks
• Indications for surgery:
• Heart failure, valve dehiscence, worsening regurgitation, abscess
• Persistent bacteremia or recurrent emboli (>2 episodes) despite appropriate antibiotic therapy
• Relapsing infection
• Certain microbes: Staph aureus (due to high recurrence rate), fungi, GNR

 

(Christopher Woo MD, 1/13/11)

(Chanu Rhee MD, 12/10/10)