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CHAPTER 5   Congenital Cardiac Disease   107


            echogenicity (probably from fibrosis) is common in animals   recommended. Likewise, transvascular balloon dilation of
            with severe obstruction; systolic anterior motion of the ante-  the stenotic area can reduce the measured gradient in some
  VetBooks.ir  rior mitral leaflet and mid-systolic partial aortic valve closure   dogs; however, significant survival benefit has not been doc-
                                                                 umented with this procedure. More recently, a combined
            suggest concurrent dynamic LV outflow obstruction.
            Ascending aorta dilation, aortic valve thickening, and LA
                                                                 plasty followed by high-pressure balloon dilation has been
            enlargement with hypertrophy may also be seen. In mildly   valvuloplasty procedure involving cutting balloon valvulo-
            affected animals, 2-D and M-mode findings may be unre-  tried, with the goal of “scoring” (disrupting) the fibrous ring
            markable. Doppler echocardiography reveals systolic turbu-  to make the subvalvular region more amenable to balloon
            lence originating below the aortic valve and extending into   dilation. This procedure can reduce  LV pressure gradient
            the aorta, as well as high peak systolic outflow velocity (see   and appears to be safe, although serious complications can
            Fig. 5.5). Some degree of aortic or mitral regurgitation is   occur. However, some degree of re-stenosis is common by
            common. Spectral Doppler studies are used to estimate the   6 to 12 months postprocedure. As with other interventions
            stenosis severity by calculating the pressure gradient across   for SAS, long-term survival benefit of this combined cutting
            the LV outflow tract (between the LV and aorta). A pressure   and high-pressure balloon dilation procedure has not been
            gradient of  <50 mm Hg is defined as mild stenosis, 50 to   documented.
            80 mm Hg is moderate stenosis, and >80 mm Hg indicates   Medical therapy with a β-blocker has been advocated in
            severe stenosis. The LV outflow tract should be interrogated   patients with moderate to severe SAS, to reduce myocardial
            from more  than one position to achieve the best possible   oxygen demand and minimize the frequency and severity of
            alignment with blood flow. The subcostal (subxiphoid) posi-  arrhythmias. Animals with a high pressure gradient, marked
            tion usually yields the highest-velocity signals, although the   ST-segment depression, frequent ventricular premature
            left apical position is optimal in some animals. Doppler-  beats, or a history of syncope might be more likely to benefit
            estimated systolic pressure gradients in unanesthetized   from this therapy. Whether β-blockers prolong survival is
            animals are usually 40% to 50% higher than those recorded   unclear. Exercise restriction is advised for animals with mod-
            during cardiac catheterization under anesthesia.     erate to severe SAS. Prophylactic antibiotic therapy is recom-
              The Doppler-estimated aortic outflow velocity might be   mended for animals with SAS before any procedures with
            only equivocally high in animals with mild SAS, especially   the potential to cause bacteremia (e.g., dentistry) are done,
            with  suboptimal  Doppler beam alignment.  With optimal   although the efficacy of this practice in preventing endocar-
            alignment, aortic root velocities of less than 1.9 m/sec are   ditis is unclear.
            typical in normal unsedated dogs; velocities over approxi-  The prognosis in dogs and cats with severe stenosis (pres-
            mately 2.25 m/sec are generally considered abnormal. Peak   sure gradient > 80 mm Hg) is guarded. Median survival time
            velocities in the equivocal range between these values could   is approximately 4.5 years, with a bimodal age distribution
            indicate the presence of mild SAS, especially if other evidence   describing cause of death. Sudden death is more common in
            of disease exists, such as a subaortic ridge, aortic regurgita-  dogs younger than 3 years of age; overall, approximately 20%
            tion, or disturbed flow in the outflow tract or ascending   of dogs with SAS die suddenly. In contrast, infective endo-
            aorta with an abrupt increase in velocity. This mainly is of   carditis and CHF are more likely to develop later in life (8-10
            concern when selecting animals for breeding. In some breeds   years) in surviving dogs. Atrial and ventricular arrhythmias
            (e.g., Boxer, Golden Retriever, Greyhound), outflow veloci-  and worsened mitral regurgitation are complicating factors.
            ties in this equivocal range (1.8-2.25 m/sec) are common in   Dogs with mild stenosis (pressure gradient  < 50 mm Hg)
            normal dogs. This could reflect breed-specific variation in   could live a normal life span without clinical signs.
            LV outflow tract anatomy or response to sympathetic stimu-
            lation, rather than SAS. A limitation of using the estimated   PULMONIC STENOSIS
            pressure gradient to assess outflow obstruction severity is the
            dependence of this gradient on blood flow. Factors causing   Etiology and Pathophysiology
            sympathetic stimulation and increased cardiac output (e.g.,   PS is more common in small breeds of dogs. Some cases of
            excitement, exercise, fever) will increase outflow velocities,   valvular PS result from simple fusion of the valve cusps, but
            whereas myocardial failure, cardiodepressant drugs, and   valve dysplasia is more common. Dysplastic valve leaflets are
            other causes of reduced stroke volume will decrease recorded   variably thickened, asymmetric, and partially fused, with or
            velocities. Cardiac catheterization and angiocardiography   without a hypoplastic valve annulus. RV pressure overload
            rarely are used now to diagnose or quantify SAS, except in   leads to concentric hypertrophy, as well as secondary dila-
            conjunction with balloon dilation of the stenotic area.  tion of the RV. Severe ventricular hypertrophy promotes
                                                                 myocardial ischemia and its sequelae. Excessive muscular
            Treatment and Prognosis                              hypertrophy in the infundibular region below the valve can
            Several palliative surgical techniques have been attempted   create a dynamic subvalvular component to the stenosis.
            in dogs with severe SAS. Although some have reduced the   Other variants of PS, including supravalvular stenosis and
            LV systolic pressure gradient and possibly improved exer-  RV muscular partition (double-chamber RV), occur rarely.
            cise ability, because of high complication rates, expense,   Turbulence caused by high-velocity flow across the ste-
            and lack of a long-term survival advantage, surgery is not   notic orifice leads to poststenotic dilation in the main
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