Related Experiment Videos
[Echocardiographic manifestations of nonrheumatic aortic regurgitation]
Abstract:
Recently, the frequency of nonrheumatic aortic regurgitation (AR) has apparently increased, accompanied by a decrease in frequency of rheumatic fever. The purpose of the present study was to ascertain the echocardiographic features of nonrheumatic AR. We had 24 surgically- or autopsy-proven cases of nonrheumatic AR admitted during a two year period. These were 10 cases of infective endocarditis (IE), five with ventricular septal defect of type I, three with syphilis, and two with prosthetic valve malfunctions, and the remainder five were difficult to diagnose clinically. These five were three men and two women, whose ages ranged from 40 to 67 years and averaged 50 years, and their final diagnoses were annulo-aortic ectasia (AAE), Behcet's disease, and the aortitis syndrome (Takayasu's arteritis), and two other cases were of unknown etiology. The echocardiographic manifestations were compared with the operative, autopsy, and pathological findings. Echocardiographically, there were few or no increased intensities of aortic valvular echoes, and aortic roots had a tendency to dilate, leading to the failure of coaptation of valve leaflets, for a relative lack of valvular surface area to cross-sectional area of the aortic ring. Three of the five had flail aortic valves and three had associated MVP. Three were diagnosed as floppy aortic valves at the time of surgery. Excised valves revealed little hyperplasia or sclerosis grossly. Fibrinoid necrosis or mucoid degeneration were noted by light microscopy. Some specimens of aortic walls also revealed cystic medial necrosis or disruption of elastic fibers. All these findings were based on degenerative processes of connective tissue, and not on inflammatory processes. These pathological findings and the coexistence of mitral valve prolapse (MVP), which were not regarded as coincidental, suggest that connective tissue fragility--congenital or acquired--may play an important role in the genesis of nonrheumatic AR.