“…Norman Chevers, a physician who, through meticulous postmortem examination of the aortic orifices and valves, noted that the “part of the ‘aortic’ orifice immediately below the valves” is liable to become generally rigid and contracted from inflammatory change,” offered the first of what would become many descriptions (and proposed etiologies) of the development of fibrous tissue and the resulting stenosis below the aortic valve [ 14 ]. A mere 2 years later, in 1844, a congenital etiology for aortic stenosis was first proposed, the thought being that a misshapen semilunar valve could be tied to an abnormality in development and, therefore, in the compositional texture of the valve [ 15 , 16 ].…”
Section: Sas Through the Centuriesmentioning
confidence: 99%
“…Other possible complications include mitral chord rupture or papillary muscle rupture with secondary mitral regurgitation or pulmonary edema [ 61 ]. Balloon valvuloplasty of valvular aortic stenosis in human patients was first reported in 1983 and has since become common practice in the treatment of this related disease [ 15 ]. However, neither species responds to balloon valvuloplasty as a method of treatment for SAS, in contrast to other forms of congenital valvular stenosis.…”
Subvalvular aortic stenosis (SAS) is the most common congenital heart disease (CHD) in dogs and is also prevalent in human children. A fibrous ridge below the aortic valve narrows the left ventricular outflow tract (LVOT) and increases blood flow velocity, leading to devastating side effects in diseased patients. Due to the similarities in presentation, anatomy, pathophysiology, cardiac development, genomics, and environment between humans and dogs, canine SAS patients represent a critical translational model of human SAS. Potential adverse outcomes of SAS include arrhythmias, left-sided congestive heart failure, endocarditis, exercise intolerance, syncope, and sudden cardiac death. The greatest divergence between canine and human SAS clinical research has been the standard of care regarding treatment of these outcomes, with pharmacological intervention dominating best practices in veterinary medicine and surgical intervention comprising the standard practice for human SAS patients. Regardless of the species, the field has yet to identify a treatment option to prevent disease progression or permanently remove the fibrous ridge, but historical leaps in SAS research support a continued translational approach as the most promising method for achieving this goal.
“…Norman Chevers, a physician who, through meticulous postmortem examination of the aortic orifices and valves, noted that the “part of the ‘aortic’ orifice immediately below the valves” is liable to become generally rigid and contracted from inflammatory change,” offered the first of what would become many descriptions (and proposed etiologies) of the development of fibrous tissue and the resulting stenosis below the aortic valve [ 14 ]. A mere 2 years later, in 1844, a congenital etiology for aortic stenosis was first proposed, the thought being that a misshapen semilunar valve could be tied to an abnormality in development and, therefore, in the compositional texture of the valve [ 15 , 16 ].…”
Section: Sas Through the Centuriesmentioning
confidence: 99%
“…Other possible complications include mitral chord rupture or papillary muscle rupture with secondary mitral regurgitation or pulmonary edema [ 61 ]. Balloon valvuloplasty of valvular aortic stenosis in human patients was first reported in 1983 and has since become common practice in the treatment of this related disease [ 15 ]. However, neither species responds to balloon valvuloplasty as a method of treatment for SAS, in contrast to other forms of congenital valvular stenosis.…”
Subvalvular aortic stenosis (SAS) is the most common congenital heart disease (CHD) in dogs and is also prevalent in human children. A fibrous ridge below the aortic valve narrows the left ventricular outflow tract (LVOT) and increases blood flow velocity, leading to devastating side effects in diseased patients. Due to the similarities in presentation, anatomy, pathophysiology, cardiac development, genomics, and environment between humans and dogs, canine SAS patients represent a critical translational model of human SAS. Potential adverse outcomes of SAS include arrhythmias, left-sided congestive heart failure, endocarditis, exercise intolerance, syncope, and sudden cardiac death. The greatest divergence between canine and human SAS clinical research has been the standard of care regarding treatment of these outcomes, with pharmacological intervention dominating best practices in veterinary medicine and surgical intervention comprising the standard practice for human SAS patients. Regardless of the species, the field has yet to identify a treatment option to prevent disease progression or permanently remove the fibrous ridge, but historical leaps in SAS research support a continued translational approach as the most promising method for achieving this goal.
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