American heart journal · 1998
Are high-velocity tricuspid and pulmonary regurgitation endocarditis risk substrates?
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Dodo H, Perloff J K, Child J S, Miner P D, Pegues D A
Аннотация
BACKGROUND: A major predisposing cause of infective endocarditis is a susceptible cardiac substrate characterized by high-velocity turbulent flow. However, the risk incurred by high-pressure, high-velocity regurgitation across inherently normal pulmonary and tricuspid valves has not hitherto been examined.
METHODS AND RESULTS: This study focused on 186 adult patients with congenital heart disease who had pulmonary vascular disease and inherently normal right-sided pulmonary and tricuspid valves. The observation period was approximately 1646 patient-years. Exclusion criteria were coexisting lesions that might have served as independent risk substrates for infective endocarditis. High-velocity turbulent pulmonary and tricuspid regurgitation were identified and quantified by color flow imaging and continuous wave Doppler echocardiography. Diagnoses of infective endocarditis were based on established clinical and laboratory criteria. Tricuspid regurgitation was moderate to severe in 80 patients and mild or absent in 106 patients. Pulmonary regurgitation was moderate to severe in 84 patients and mild or absent in 102 patients. With the exception of a single habitual intravenous drug abuser, no patient, irrespective of the degree of high-velocity turbulent pulmonary or tricuspid regurgitation, had infective endocarditis.
CONCLUSIONS: High-velocity turbulent flow across inherently normal pulmonary and tricuspid valves rendered incompetent by pulmonary hypertension may represent a relatively low-risk or no-risk substrate for infective endocarditis.
METHODS AND RESULTS: This study focused on 186 adult patients with congenital heart disease who had pulmonary vascular disease and inherently normal right-sided pulmonary and tricuspid valves. The observation period was approximately 1646 patient-years. Exclusion criteria were coexisting lesions that might have served as independent risk substrates for infective endocarditis. High-velocity turbulent pulmonary and tricuspid regurgitation were identified and quantified by color flow imaging and continuous wave Doppler echocardiography. Diagnoses of infective endocarditis were based on established clinical and laboratory criteria. Tricuspid regurgitation was moderate to severe in 80 patients and mild or absent in 106 patients. Pulmonary regurgitation was moderate to severe in 84 patients and mild or absent in 102 patients. With the exception of a single habitual intravenous drug abuser, no patient, irrespective of the degree of high-velocity turbulent pulmonary or tricuspid regurgitation, had infective endocarditis.
CONCLUSIONS: High-velocity turbulent flow across inherently normal pulmonary and tricuspid valves rendered incompetent by pulmonary hypertension may represent a relatively low-risk or no-risk substrate for infective endocarditis.