Page 266 - Clinical Small Animal Internal Medicine

234 Section 3 Cardiovascular Disease

an extent that it obstructs blood flow from getting out of majority of otherwise apparently healthy dogs when
VetBooks.ir the right heart during contraction. screened by Doppler echocardiography. However, aortic
or pulmonary insufficiency is typically well tolerated and
The natural history of PS is more benign than for SAS,
although patients may similarly suffer exercise intoler-
pulmonary valve dysplasia resulting in a predominantly
ance, syncope, sudden cardiac death, and right‐sided seldom of clinical significance. Rarely, cases of aortic or
congestive heart failure if the disease is severe. Dogs with regurgitant valve with severe insufficiency are detected,
PS do not appear to be at an increased risk for endocar- which may progress to cardiac decompensation.
ditis. Elevated right atrial pressure in the presence of a
PFO may allow shunting of blood across the atrial sep- Malformations of the Great Vessels
tum from right to left and the development of cyanosis
and secondary erythrocytosis. PFO is seen in ~30% of Vascular Ring Anomalies
dogs with PS as the atrial septum does not close normally Several malformations of the arterial system have been
at birth due to elevated right atrial pressure. If flow from described in animals; the most common clinical presen-
the right atrium to left atrium is substantial across a PFO, tation is a pediatric animal with dysphagia. The basic
the animal may have significant mixing of poorly pathophysiology of these malformations is an embryo-
oxygenated blood from the right atrium to the left and logic defect resulting from abnormal persistence or
clinical cyanosis. regression of fetal vascular structures (aortic arches),
ultimately leading to an abnormal spatial arrangement of
Mitral and Tricuspid Valve Stenosis the major intrathoracic arteries relative to the trachea
Mitral valve dysplasia (MVD) and TVD may result in ste- and esophagus. Clinical signs are the direct result of
nosis of these valves. Atrioventricular valve stenosis is extraluminal compression of the esophagus (resulting in
rare in small animals, but both mitral stenosis and tricus- megaesophagus, regurgitation, or aspiration pneumo-
pid stenosis are occasionally encountered in dogs and nia) and/or trachea (resulting in inspiratory stridor,
cats. These lesions lead to progressive atrial enlarge- coughing, or dyspnea). Persistence of the right aortic
ment, atrial arrhythmias, and congestive heart failure if arch is the most common vascular ring observed in small
left untreated. animals. Therapy is directed at surgical decompression
and transection of the offending structure, though
esophageal dysfunction may persist if not corrected at a
Regurgitant Valve Lesions
young age.
Mitral and Tricuspid Valve Dysplasia
Congenital malformations of the atrioventricular valves Cyanotic Heart Disease
are considered rare in dogs, but account for a greater
proportion of congenital heart disease in cats. Mitral Tetralogy of Fallot
valve dysplasia or TVD is a developmental abnormality Cyanotic heart disease is not common in small animals,
of valve formation, resulting in abnormal leaflet shape, but tetralogy of Fallot (ToF) is recognized in 2–6% of
attachment, and/or function. Animals with MVD or cases of CHD. ToF is the most common cyanotic CHD
TVD have pathology that typically results in regurgita- of humans and the four components of the tetralogy are
tion of the affected valve; however, a combination of ste- right ventricular outflow tract obstruction, right ven-
nosis and regurgitation may be encountered. Chronic tricular hypertrophy, VSD, and dextroposition of the
mitral valve regurgitation leads to left ventricular and aorta. The underlying pathophysiology of this defect is
left atrial volume overload and dilation in the setting of believed to result from incomplete rotation and faulty
MVD, which may lead to left‐sided congestive heart fail- partitioning of the developmental outflow tracts
ure. Similar progression may be seen in the right heart ( comprising the distal portions of the left and right
for TVD. Postmortem findings of dysplastic atrioven- ventricles and the proximal portion of the great ves-
tricular valves display fused and malformed leaflets with sels). In simple terms, the aorta receives more of the
shortened chordae tendineae. Direct attachment from embryologic tissue and aortic development occurs at
the papillary muscle to the valve is common. the expense of the pulmonary trunk. Therefore, the
ventricular septum cannot close because the aorta is
Aortic and Pulmonary Valve Dysplasia enlarged and deviated to the right. The result of right
Congenital defects of the semilunar valves typically ventricular outflow obstruction with a VSD is that
result in stenosis, as described above. In both SAS and deoxygenated blood is diverted to the systemic circula-
PS, regurgitation, or insufficiency, of the affected valve is tion, causing cyanosis, weakness, and collapse. Long‐
commonly observed by color Doppler imaging. standing sequelae include erythrocytosis and blood
Pulmonary valve insufficiency can even be seen in the hyperviscosity due to increased erythropoiesis.