In the developed world, rheumatic heart disease (RHD) accounts for less than 20% of
NVIE. In developing countries, RHD causes 50% of all cases (101,102). Over their lifetimes, 6%
of patients with RHD will develop IE usually of the mitral valve.
MVP makes up 30% of NVIE in younger adults. It has taken supplanted RHD as the
primary underlying condition for developing IE in this age group (101,103). Patients with the
type of MVP that has an insignificant degree of regurgitation, have a quite small risk of
developing IE. Additional risk factors for developing IE in MVP are thickened anterior mitral
leaflets and male sex greater than 45 years of age (100). Cases of MVP IE generally have
relatively lower rates of morbidity and mortality than other types of IE (104,105).
The term “degenerative cardiac lesions” describe a wide variety of abnormalities. These
include degenerative valvular disease (DVD) and postmyocardial infarction thrombi. All have
in common a roughend endocardium that promotes the development of a fibrin/platelet
thrombus. DVD accounts for 20% of all cases and 50% of cases of IE in patients who are older
than 60 years (106,107). Calcific aortic stenosis results from the deposition of calcium on either
a congenital bicuspid valve correlate previously normal valve damage by the cumulative
hemodynamic stresses that occur over a patient’s life span. Because of their age, these patients
have a high prevalence of associated illnesses, such as diabetes or chronic renal failure, which
contribute to their increased morbidity and mortality. Because the degree of stenosis is not
hemodynamically significant, this type of valvular lesion is often neglected for antibiotic
prophylaxis (108).
Excluding IVDA IE, 40% of NVIE infects only the mitral valve and 40% the aortic. The
right side of the heart is seldom involved except in cases of IVDA IE (109).
PVE accounts for approximately 10% of all cases of valvular infection and up to 26% in
those older than 60 years (60,110). The risk of infection is highest during the first three months
after implantation. At the end of one year of their placement, 1% to 3.1% had become infected.
The rate of infection goes down after this to be about 0.3% per year. Mechanical valves are
more susceptible to infection until their first year anniversary. After this, bioprosthetic valves
are at greater likelihood of developing IE due to the ongoing calcifications of their leaflets that
is caused by degeneration of the valvular tissue (111). The risk of developing PVE is 5% in the
10 years after their placement. Endothelialization of the sewing rings and struts of the valves
decreases but does not eliminate the risk of infection.
PMIE and infections of cardioverter–defibrillators and ventricular assist devices are very
similar in nature to PVE (112–115). Most cases of PMIE and IE of ventricular assist devices and
cardioverter–defibrillators occur within a few months of their placement. The implanted
material is “conditioned” by the deposition of fibrinogen, fibronectin laminin, and collagen.
This coagulum promotes the appearance of staphylococci. In addition both CoNS and
coagulase-positive staphylococci produce a biofilm that protects the infecting bacteria from
antibiotics as well as the host’s leukocytes. Unlike the situation in PVE,S. aureuspredominates
in early PMIE and CoNS in later infection (116). Infections of pacemakers most often involve
the generator pocket. There may be infection of the proximal leads (intravascular leads). True
PMIE is defined as infection of the leads at the point of contact with the endocardium. The
lifelong risk for an individual to develop PMIE is 0.5% (117,118).
A previous episode of IE is probably the most important predisposing condition for
development of valvular infection (119). The most important risk factor for recurrent IE is
IVDAIE, with 40% of these cases recurring. The recurrence rate of non IVDA IE is well less
than 10%.
Extracardiac Predisposing Factors
Chronic hemodialysis has become a significant risk factor for the development of IE (120).
Various types of infection are second only to coronary artery disease as the most common
cause of death in chronic renal failure. This vulnerability is due to the BSIs of infected dialysis
catheters, low albumin, excess iron stores that stimulate the growth of bacteria, metabolic
acidosis that impairs neutrophil function, accelerated calcification of the cardiac valves, and
the immunological dysfunction of chronic renal failure.
In addition, a variety of neoplasms, diabetes mellitus, liver disease, and the adminis-
tration of corticosteroids are becoming increasingly important predisposing conditions for the
Infective Endocarditis and Its Mimics in Critical Care 227