Page 134 - Small Animal Internal Medicine, 6th Edition
P. 134

106    PART I   Cardiovascular System Disorders


            definitive diagnosis and genetic counseling to breeders can     because of the orientation of the aortic arch. The murmur
            be difficult.                                        typically is heard over the carotid arteries as well and, in
  VetBooks.ir  pressure  overload  and  resulting  concentric  hypertrophy.   severe  cases,  sometimes  even  radiates  to  the  calvarium.
              The severity of the stenosis determines the degree of LV
                                                                 Aortic regurgitation can produce a diastolic murmur at the
            Coronary perfusion is easily compromised in animals with
            severe  LV hypertrophy.  Myocardial  capillary density can   left base or may be inaudible. Other common physical exam-
                                                                 ination findings in dogs with moderate to severe stenosis
            become inadequate as hypertrophy progresses. Furthermore,   include weak and late-rising femoral pulses (pulsus parvus et
            the high systolic wall tension, along with coronary narrow-  tardus), although concurrent severe aortic regurgitation can
            ing, can cause systolic flow reversal in small coronary arter-  increase the arterial pulse strength. There may be evidence
            ies.  These factors contribute to  intermittent myocardial   of pulmonary edema or arrhythmias.
            ischemia and secondary fibrosis. Clinical sequelae include   In mild cases, a soft, poorly radiating ejection murmur at
            arrhythmias, syncope, and sudden death. Many animals with   the left and sometimes right heart base may be the only
            SAS also have aortic or mitral valve regurgitation because of   abnormality found on physical examination. Low-grade
            related malformations or secondary changes; this imposes an   functional LV outflow murmurs that are not associated with
            additional volume overload on the LV. Left-sided CHF devel-  SAS are common in normal Greyhounds, other sighthounds,
            ops in some cases. Animals with SAS are thought to be at   and Boxers; presence of such physiologic flow murmurs can
            higher risk for aortic valve endocarditis because of jet lesion   complicate diagnosis of SAS.
            injury to the underside of the valve (see p. 132 and Figs. 6.5
            and 6.6).                                            Diagnosis
                                                                 Radiographic abnormalities (see  Table 5.2) can be subtle,
            Clinical Features                                    especially in animals with mild SAS. The LV can appear
            Most patients with SAS are asymptomatic on initial presen-  normal or enlarged; mild to moderate LA enlargement is
            tation. Clinical signs of fatigue, exercise intolerance or exer-  more likely with severe SAS or concurrent MR. Poststenotic
            tional weakness, syncope, or sudden death occur in about   dilation in the ascending aorta can cause a prominent cranial
            one third of dogs with SAS. Low-output signs can result from   waist in the cardiac silhouette (especially on a lateral view)
            severe outflow obstruction, tachyarrhythmias, or sudden   and cranial mediastinal widening. The ECG often is normal,
            reflex bradycardia and hypotension resulting from the acti-  although evidence of LV hypertrophy (left axis deviation) or
            vation of ventricular mechanoreceptors. Signs of left-sided   enlargement (tall R waves) can be present. Depression of the
            CHF can develop, usually in conjunction with concurrent   ST segment in leads II and aVF can occur from myocardial
            mitral or aortic regurgitation, other cardiac malformations,   ischemia or  secondary  to hypertrophy;  exercise  induces
            or acquired endocarditis. Dyspnea is the most commonly   further ischemic ST-segment changes in some animals. Ven-
            reported sign in cats with SAS.                      tricular tachyarrhythmias are common.
              The characteristic murmur of SAS is a harsh systolic ejec-  Echocardiography reveals the extent of LV hypertrophy
            tion murmur heard near the aortic valve area at the left heart   and subaortic narrowing. A discrete tissue ridge below the
            base, with or without a precordial thrill. This murmur often   aortic  valve is evident in many animals with moderate to
            radiates equally or more loudly to the right heart base   severe disease (Fig. 5.5). Increased LV subendocardial


















                     A                                         B


                          FIG 5.5
                          Right parasternal long-axis (A) and subcostal (B) echocardiographic images from a
                          3-month-old male Rottweiler with severe subaortic stenosis. Note the ridge of tissue
                          causing a tunnel-like defect (arrow) below the aortic valve, creating a fixed outflow tract
                          obstruction. Color Doppler reveals turbulent, high-velocity flow through the left ventricular
                          outflow tract and ascending aorta in systole (B), as well as mild aortic insufficiency (A).
                          Ao, Aorta; LA, left atrium; LV, left ventricle.
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