IE occurs as at least twice as often in men as in women. This differential increases over
the years. The incidence ratio of men to women ranges up to 9/1 at 50 to 60 years of age (68).
There has been a marked increase in cases of HCIE, IVDA IE, and PVE accounting for
22%, 36%, and 16%, respectively, of all cases (5,69). This reflects a significant increase in
staphylococcal/HCBSI coupled with a significant decrease in IE caused by S. viridans (70,71).
Cardiac Predisposing Factors
Pathogenesis
Any discussion of the predisposing factors to the development of IE needs to begin with a
basic understanding of the pathogenesis of this disease. Although there are many types of
valvular infections, they all share a common developmental pathway. First, there must be a BSI
with an organism with the ability to infect the endocardium. Then, the pathogen must adhere
to the endocardial surface. Finally, it needs to invade the underlying tissue (72).
In subacute IE, a pre-existing platelet fibrin thrombus (nonbacterial thrombotic
endocarditis, NBTE) is the site of attachment for the circulating bacteria. As discussed
above, certain organisms, especiallyS. aureus, are able to attach to the endothelium by
producing microthrombi. In CCU/HCIE, NBTE develops in one of three possible ways (73):
- When blood flows over a distorted valve, it loses its laminar characteristics. These
rheological changes affect the function of the endocardium (27). Leukocytes adhere
more readily to it and platelets become more reactive when in contact with it.
The surface of the valve becomes coated with fibrin. Small vegetations result. These
increase the degree of turbulence and so accelerate the formation of NBTE. - Garrison and Freedman developed a rabbit model of IE (74). First they produced
NBTE by scarring the valves of the animal’s right ventricle by means of a catheter
inserted in the femoral vein. The resultant thrombus was then infected by S. aureus
that was injected through the catheter. As the infection progressed, the adherent
bacteria were covered by successive layers of deposit fibrin. The superficial
organisms are metabolically active; those that live deep within the NBTE are quite
indolent. Within the thrombus, there is a tremendous concentration of organisms
(10
9
colony forming units per gram of tissue) (75). From this safe haven, the bacteria
are able to reseed the bloodstream in a continuous manner, the characteristic
continuous bacteremia of IE. In the CCU, insertion of a Swan–Ganz catheter
reproduces quite closely this experimental model. - The Jet and Venturi effects may play an important part in both the development and
site of the NBTE (76). When blood flows from a high-pressure area to a lower
pressure one, its laminar flow is disrupted and an NBTE develops at the low-
pressure sink side of the orifice. For example, in mitral insufficiency, NBTE is found
in the atrial surface of the valve and in aortic insufficiency on the ventricular side. In
the case of a ventricular septal defect, the NBTE forms on the right ventricular side.
An NBTE may also form at the site of the right ventricle that lies directly opposite the
septal defect. The endocardium of this area may be damaged by the force of the jet of
blood hitting it (Mac Callums patch) (77).
Table 4 Changing Patterns of IE Since 1966
Marked increase in the incidence of acute IE
Rise of HCIE, IVDA and prosthetic valve IE
a. Change in the underlying valvular pathology: rheumatic heart disease<20% of cases
b. MVP 30% of cases
c. Prosthetic valve endocarditis 10%–20% of cases
d. 50% of elderly patients have calcific aortic stenosis
These changes are due to:
a. The "graying" of patients (excluding cases of IVDA IE, 55% of patients>60 yr of age)
b. The increased numbers of vascular procedures
Abbreviations: IE, infective endocarditis; HCIE, health care associated IE; IVDA, intravenous
drug user; MVP, mitral valve prolapse.
224 Brusch