Bacterial Endocarditis in the Antibiotic Era

Since the introduction of penicillin therapy for bacterial endocarditis in 1944 there have been 228 patients with this disease at the Massachusetts General Hospital. In 53 instances it was of the acute form, and in 175 it was subacute. The immediate outcome and the ultimate fate of these patients have been studied. Acute bacterial endocarditis remains an ominous and often fatal disease. In only 21 patients was the presence of an acute bacterial infection on the heart valve recognized before death; 8 of these survived. Even when the disease was recognized clinically, death often ensued before an adequate antibiotic program could be instituted. In the subacute group 119 patients (68 per cent) recovered and 56 (32 per cent) died. Postmortem examination in 48 of the 56 revealed that the principal cause of death in one half the cases was either rupture of a mycotic aneurysm or valve cusp or an embolus to a cerebral or coronary vessel. In the postmortem group the presence of bacterial endocarditis was unsuspected in 25. Therefore the "cure rate" in those actually treated was 79 per cent. Of the 119 patients who recovered, 60 patients have been followed for 5 years with a 69 per cent survival rate, and 23 for 10 years with 49 per cent survival. Only 1 patient has been " lost." The principal cause of death in the years after cure of bacterial endocarditis has been congestive failure. In the 119 original survivors, 16 had a high degree of aortic regurgitation, clearly augmented by their disease in 8 instances and necessitating a Hufnagel valve in 5. Embolic episodes unrelated to active infection occurred later in 9 patients, and arterial aneurysms were found at a later date in 2. A recurrence of bacterial endocarditis from 6 months to 10 years after the original infection occurred in 10 patients (8.5 per cent), 8 of whom again had Streptococcus viridans infection and were rescued, whereas 2 had Staphylococcus aureus and succumbed. Postmortem examination was done in 17 patients with healed bacterial endocarditis who later died. In 12 of the 17 cases a severe degree of structural damage was found to be the result of the healing process. These alterations were responsible for a variety of special syndromes now recognized as peculiar to the antibiotic era. Notable in this group was aortic regurgitation of unusually high degree, frequently associated with left ventricular failure and angina pectoris. In other instances the abrupt onset of congestive failure heralded the rupture of a weakened valve cusp. Some patients were never well again, and their insidious decline and ultimate death resulted from one or more factors including valve distortion, diffuse myocardial injury, and occasionally a reactivation of rheumatic fever. Finally, in a few instances a fatal embolus occurred. In concluding this survey of bacterial endocarditis in the antibiotic era, 3 special features remain for further study and clarification. First in importance is the prevention of rheumatic and possibly of congenital heart disease, thereby eradicating the cardiac lesions most susceptible to bacterial invasion. Second, the protection of patients with these lesions during dental and other surgical procedures is vital; although the currently recommended programs for this purpose seem adequate in the majority of instances, the optimal antibiotic dosage and the duration of administration remain to be settled. Third, the emergence in recent years of increasing numbers of organisms resistant to presently available antibiotics poses a most serious and urgent problem.