LEFT VENTRICULAR OUTFLOW TRACT OBSTRUCTIONS IN DOGS: WHAT WE KNOW AND DON'TKNOW

摘要

Left ventricular outflow tract (LVOT) obstructions are detected commonly in dogs with congenital heart disease and many of the anatomic variants documented in people have also been identified in canine patients. It is noteworthy that coarctation and interruption of the aorta as well as supravalvular aortic stenosis occur rarely in dogs and are worthy of only passing reference in the context of this presentation. Elastin deficiency, as occurs in humans with the Williams-Beurens syndrome and other nonsyndromic conditions resulting in supravalvular aortic stensosis, has not been documented in dogs.1 Congenital valvular aortic stenosis, most often manifested as a bicuspid or less commonly as a unicuspid aortic valve, is particularly common in humans isvery uncommon in dogs. Valvular aortic stenosis does occur in bull terriers and mini bull terriers but the nature of the valvular pathology is quite different from the human disorder in that the aortic leaflets of affected bull terriers are thickened andinflexible but usually are not fused with a normal tricuspid configuration. Fixed subvalvular aortic stenosis is a common disorder in dogs, comprising 20 to 25% of the congenital cardiac malformations recognized in dogs.3'4 In contrast, fixed subvalvular aortic stenosis (SAS) comprises about 6.5% of the defects found in adults with congenital heart disease. In both dogs and humans, SAS is sometimes found in association with pulmonic stenosis, mitral valve dysplasia, patent ductus arteriosus, ventricular septal and atrioventricular septal defects.5"7 Insight into these associations is beginning to emerge as the developmental interrelationships and co-dependencies of these different anatomic constituents of the growing heart are understood. Dynamic subvalvular aortic stenosis (DSAS) also occurs in humans and dogs, but the predominance of hypertrophic cardiomyopathy as the underlying disorder has not been conclusively established in dogs. Clarification of the etiology of DSAS is often confounded by theoccurrence of systolic anterior motion (SAM) together with the anatomic features of fixed SAS or in association with other anatomic derangements such as mitral valve dysplasia, pulmonic stenosis, and tetralogy of Fallot.9"13