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  • Title: [Echocardiographic study on systolic left ventricular posterior wall motion in patient with atrial septal defect].
    Author: Oki T, Fukuda N, Takemura H, Asai M, Murao A, Ohshima C, Bando S, Niki T, Mori H.
    Journal: J Cardiogr; 1982 Mar; 12(1):243-56. PubMed ID: 7119496.
    Abstract:
    Systolic motion of the left ventricular posterior wall (LVPW) was studied by M-mode and long-axis two-dimensional echocardiography in 35 patients (pts) with secundum type of atrial septal defect (ASD), comparing with that of 19 surgically closed ASD (post ASD), 27 with hypertrophic cardiomyopathy (HCM), 15 with old anteroseptal myocardial infarction (a-s MI) and 28 normal subjects. The results obtained were as follows: 1) Excursion of LVPW (PWE) was significantly increased in the pts with ASD compared with normal subjects (P less than 0.001), but there was no significant difference in PWE between the pts with ASD and the pts with HCM or a-s MI. 2) Mean systolic posterior wall velocity (MPWVs) was significantly decreased in the pts with ASD compared with the pts with HCM (p less than 0.05). However, no significant difference could be found in MPWVs between the pts with ASD and a-s MI or normal subjects. 3) End-systolic thickening of LVPW was significantly increased in the pts with ASD compared with normal subjects (p less than 0.05), the pts with a-s MI (p less than 0.05) and the pts with post ASD (p less than 0.01), except for the pts with HCM. There was a significant difference in % end-systolic thickness of lVPW between the pts with ASD and the pts with a-s MI or post ASD (p less than 0:05). 4) Mid-systolic thickening and % mid-systolic thickening of LVPW were significantly increased in the pts with ASD compared with normal subjects, the pts with a-s MI, the pts with post ASD and the pts with HCM (p less than 0.01). This characteristic mid-systolic bulging of LVPW in the pts with ASD was coincident with early-systolic anterior motion of IVS. 5) Basal portion of LVPW indicated the marked inward contraction during end-systole in 30 of 35 pts (86%) with ASD. In these 30 pts, association of mitral valve (MV) prolapse was observed. 6) Following surgical closure of ASD in 19 pts, MV prolapse disappeared following normalization of excessive endsystolic contraction of the LVPW in 16 pts (functional MV prolapse). In 3 pts, however, posterior MV showed multiple abnormal echoes, indicating MV prolapse or mitral regurgitation (organic MV prolapse). In conclusion, these results suggested that mid-systolic bulging of LVPW in ASD is compensatory reaction for systolic anterior IVS motion, and that mechanism of MV prolapse in ASD is related to abnormal left ventricular geometry due to excessive inward contraction of basal portion of LVPW during end-systole.
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