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Bacterial endocarditis in patients with aortic stenosis, pulmonary stenosis, or ventricular septal defect.
Circulation 1993 Februrary
BACKGROUND: All of the 2,401 patients with aortic stenosis (AS), pulmonary stenosis (PS), or ventricular septal defect (VSD) admitted to the First Natural History Study of Congenital Heart Defects between 1958 and 1965 were eligible for the Second Natural History Study. Most patients with severe defects were managed surgically, and most with mild defects were managed medically. Final examination in the first study was carried out 8 years after admission.
METHODS AND RESULTS: For AS, the incidence rate of bacterial endocarditis (BE) was 27.1 per 10,000 person-years. The incidence rate was 15.7 per 10,000 person-years for those managed medically and 40.9 per 10,000 person-years for those managed surgically. Most patients managed surgically had severe AS, and severity was more important to the risk of BE than the method of management. For PS, only one of the 592 patients with PS experienced BE. For VSD, the incidence rate of BE was 14.5 per 10,000 person-years. Size of the VSD was not associated with risk of BE. The risk of BE before closure of the VSD was more than twice that after surgery.
CONCLUSIONS: The incidence rate of BE was nearly 35-fold the population-based rate. The increased incidence in patients with AS after valvotomy was a function of severity of the defect and not a function of surgery. Presence of aortic regurgitation in patients with AS did not increase the risk of developing BE. Surgical closure of VSD lowered the risk of BE.
METHODS AND RESULTS: For AS, the incidence rate of bacterial endocarditis (BE) was 27.1 per 10,000 person-years. The incidence rate was 15.7 per 10,000 person-years for those managed medically and 40.9 per 10,000 person-years for those managed surgically. Most patients managed surgically had severe AS, and severity was more important to the risk of BE than the method of management. For PS, only one of the 592 patients with PS experienced BE. For VSD, the incidence rate of BE was 14.5 per 10,000 person-years. Size of the VSD was not associated with risk of BE. The risk of BE before closure of the VSD was more than twice that after surgery.
CONCLUSIONS: The incidence rate of BE was nearly 35-fold the population-based rate. The increased incidence in patients with AS after valvotomy was a function of severity of the defect and not a function of surgery. Presence of aortic regurgitation in patients with AS did not increase the risk of developing BE. Surgical closure of VSD lowered the risk of BE.
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