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  • Title: [Ventricular septal defect and aortic regurgitation-pathophysiological aspects and therapeutic consequences].
    Author: Schmaltz AA, Schaefer M, Hentrich F, Neudorf U, Brecher AM, Asfour B, Urban AE.
    Journal: Z Kardiol; 2004 Mar; 93(3):194-200. PubMed ID: 15024586.
    Abstract:
    The development of aortic regurgitation (AI) is a rare but serious complication of subaortic ventricular septal defects (VSD). Over a period of 5 years we observed VSD-related AI in 24 patients, a frequency of 4.5% of all isolated VSD's encountered during that time frame. The location of the defects was in the infundibular septum in 59%, it was perimembranous in 25% and in the trabecular septum in 16%. Hemodynamically the defects were small except for 2 where the Q(p)/Q(s) ratio was > 2. Of the 24 pts, 16 had surgical closure of their VSD accompanied in 9 by aortic valvuloplasty. AI was caused by elongation or defect of the right coronary leaflet in 42%, of the noncoronary leaflet in 25% and a combination of both, in 8%. In 6 pts with infundibular VSD absence of part of the aortic valve ring above the defect was the underlying mechanism for AI. Postoperatively AI was improved to moderate in one pt and to none to trivial in 15. LV end-diastolic diameter decreased significantly in all pts operated. Pathogenetic mechanisms for the development of AI are a deficiency in the aorto-infundibular junction with prolaps of the right-or non-coronary leaflet, deficiency of the valve supporting structures including the valve ring as well as suction of the already elongated leaflet into the VSD with further damage to the antiregurgitant mechanism of the semilunar valve at risk. In perimembranous VSD's, late AI is probably related to turbulent flow through the adjacent LVOT. Surgical closure of isolated VSD's with a location immediately beneath the aortic valve is indicated regardless of their size to prevent the development of AI. If AI has occurred, VSD closure including aortic valvuloplasty improves the amount of regurgitation and normalizes LV enddiastolic dimension.
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