Endocarditis: the problems remain and multiply.

In 1920 Sir Thomas Horder (1) in a discourse upon endocarditis pointed out that the relative importance of a number of factors in the pathological process was unknown. The factors he mentioned were the primary focus of infection, the lowered tissue resistance, the damaged endothelium and the infecting agent. In spite of the development of a number of animal models of infective endocarditis, 59 years after Horder's comments we still are struggling to clarify the problems he raised. Furthermore, within the past decade we have been presented with new problems: who should receive antibiotic prophylaxis to prevent the development of endocarditis, which patients who had developed endocarditis should receive treatment with one antibiotic, which patient should receive two antibiotics, and is oral therapy feasible; what is the best antimicrobial prophylactic program to utilize at the time of cardiac surgery and for how tong; which patients with endocarditis should undergo surgery as treatment of the endocarditis and when; which patient with endocarditis of a prosthetic heart valve could be treated adequately by medical means? The reader may be astonished that I pose these problems. The initial reaction of many individuals would be to say "There are guidelines for all of these problems. You are raising dead issues." There have been detailed studies of the clinical aspects of infective endocarditis (2--4). These studies have shown that although antibiotic therapy of endocarditis has improved in the last three decades, patient survival, morbidity and mortality in this disease are still significant. In truth, we do not know what the primary focus of infection has been in a significant proportion of cases of endocarditis. We teach the "jet stream" theory as a major contributory factor in endocarditis. But we cannot explain why some individuals with mitral insufficiency develop endocarditis and others do not. The same problem to a greater extent is true in regard to individuals with hypertrophic subaortic stenosis and the "floppy mitral" valve syndrome. Who should receive antibiotic prophylaxis to prevent the development of infective endocarditis? The American Heart Association has developed guidelines which have been revised in the last few years on the basis of experimental studies using a rabbit model (5). We know that transient bacteremia is a common event with 60--85% of individuals sustaining a transient bacteremia after dental extraction, but bacteremia also occurs after tooth brushing, while chewing hard candy, and after a bowel movement. It is possible to identify predisposing events at best in 35% of episodes of endocarditis. Approximately 35o/0 of patients presenting with endocarditis have no prior history of underlying heart disease and would not be candidates for dental prophylaxis (3, 4). Only 20o/o of patients who have known heart disease remember to tell the dentist of that fact (6). Finally, endocarditis due to Streptococcus viridans is decreasing and endocarditis due to Streptococcus faecalis, Staphylococcus aureus, Staphylococcus epidermidis and other agents are on the rise (3, 4). Given these facts it seems quite apparent that the problem of the antibiotic prophylaxis to prevent endocarditis is far from solved. Which patient should be treated with one agent and which with two? Everyone will agree that true enterococcal