Concomitant Aortic Root Replacement With Anterior Konno Annular Enlargement

2020 ◽  
Vol 11 (5) ◽  
pp. 630-635
Author(s):  
Brian E. Kogon

The need for concomitant aortic annular enlargement and aortic root replacement may be necessary in situations of multilevel left ventricular outflow tract obstruction and/or prior aortic or aortic valve surgery, particularly in the setting of congenital heart disease. It can be extremely tedious and fraught with numerous complications. Major challenges include bleeding in difficult-to-reach areas and the potential need for subsequent operations. This article describes a technique of concomitant aortic annular enlargement and aortic root replacement that minimizes the risk of significant blood loss and facilitates future surgery should it be necessary.

2002 ◽  
Vol 90 (7) ◽  
pp. 806-809 ◽  
Author(s):  
Sarah Gelehrter ◽  
Gail Wright ◽  
Tamera Gless ◽  
Achiau Ludomirsky ◽  
Richard Ohye ◽  
...  

2019 ◽  
Vol 30 (3) ◽  
pp. 439-442 ◽  
Author(s):  
Tetsuro Uchida ◽  
Yoshinori Kuroda ◽  
Kimihiro Kobayashi ◽  
Mitsuaki Sadahiro

Abstract An extensive infection of the native aortic or prosthetic valve beyond the aortic annulus could be complicated with various types and degrees of tissue destruction. The left ventricular–aortic discontinuity resulting from extensive infective endocarditis often necessitates pericardial reconstruction of the left ventricular outflow tract and subsequent aortic root replacement. Furthermore, if the membranous ventricular septum is involved with infective tissue destruction, communication between the left ventricle and right atrium, known as a Gerbode defect, and complete atrioventricular block could occur. Surgical reconstruction of these complex pathologies is challenging, with high mortality and morbidity. Herein, we present a rare case of prosthetic valve endocarditis complicated with both left ventricular–aortic discontinuity and an acquired Gerbode defect. At the time of surgery, left ventricular outflow tract reconstruction and the technically more demanding aortic root replacement were considered inevitable because of extensive tissue destruction. However, we performed circumferential left ventricular outflow tract reconstruction with a xenopericardial patch and supra-annular aortic valve replacement using the Solo Smart bovine pericardial stentless valve as a technically less demanding alternative to aortic root replacement. The postoperative course was uneventful, and the patient is well 1 year postoperatively, without valvular dysfunction and recurrent infection.


2019 ◽  
Author(s):  
Aldo Córdova-Palomera ◽  
James R. Priest

ABSTRACTCongenital heart disease is the most common birth defect in newborns and the leading cause of death in infancy, affecting nearly 1% of live births. A locus in chromosome 4p16, adjacent to MSX1 and STX18, has been associated with atrial septal defects (ASD) in multiple European and Chinese cohorts. Here, genotyping data from the UK Biobank was used to test for associations between this locus and congenital heart disease in adult survivors of left ventricular outflow tract obstruction (n=164) and ASD (n=223), with a control sample of 332,788 individuals, and a meta-analysis of the new and existing ASD data was performed.The results show an association between the previously reported markers at 4p16 and risk for either ASD or left ventricular outflow tract obstruction, with effect sizes similar to the published data (OR between 1.27-1.45; all p<0.05). Differences in allele frequencies remained constant through the studied age range (40-70 years), indicating that the variants themselves do not drive lethal genetic defects. Meta-analysis shows an OR of 1.35 (95% CI: 1.25-1.46; p<10−4) for the association with ASD.The findings show that the genetic associations with ASD can be generalized to adult survivors of both ASD and left ventricular lesions. Although the 4p16 associations are statistically compelling, the mentioned alleles confer only a small risk for disease and their frequencies in this adult sample are the same as in children, likely limiting their clinical significance. Further epidemiological and functional studies may elicit factors triggering disease in interaction with the risk alleles.


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