Common acquired cardiac diseases of the dog include those that are caused by valvular defects, myocardial failure, infectious
reasons, as a result of arrhythmias, and parasitism.
The most common cardiac disease in dogs is valvular insufficiency caused by abnormal aging of the valves of the heart. Approximately
30% of dogs at age 13 are clinically affected. On necropsy, 90% of dogs at 13 have evidence of valvular degeneration. The
disease also can be referred to as chronic myxomatous valvular degeneration, mitral valve disease, chronic valve disease,
and endocardiosis. Breeds affected include Poodles, Yorkshire Terriers, Chihuahuas, and other small dogs, but the most commonly
affected is the Cavalier King Charles Spaniel (CKCS). CKCS are known to be affected severely, often at quite a young age.
The mitral valve is most commonly affected with CVD, but lesions can be seen on the other cardiac valves, as well. Valve leaflets
are thickened and nodular, and the chordae tendinae can be thickened and elongated. Chordae may also rupture, causing flail
or prolapse of the valvular leaflet. The consequence of valvular degeneration is insufficiency. In the case of the mitral
valve, chronic significant insufficiency causes an increase in left atrial pressure, and atrial enlargement results. When
the left atrium enlarges to a certain point, blood backs up into the pulmonary veins, and pulmonary edema develops. As the
disease progresses, myocardial failure may also result.
The most significant physical exam characteristic of valvular degeneration is a heart murmur. Because the most common valve
affected is the mitral valve, the most common murmur is systolic and located at the left apex. A right-sided murmur may also
be ausculted, and it may be from tricuspid regurgitation or radiation of the mitral murmur. If the aortic valve is affected,
a diastolic murmur may be detected. Generally, the intensity of the murmur correlates with severity of disease, but this is
not exclusively true. Pulmonary edema results in respiratory distress and/or coughing, and in severe cases, is detected by
the presence of crackles in the lung fields. Mild to moderate edema cannot typically be ausculted, so clear lung sounds do
not rule out the presence of fluid.
Radiographic changes vary also with severity of the valve disease. With severe disease, the most common signs are left atrial
and auricular enlargement and left ventricular enlargement. As the disease progresses to left-sided congestive heart failure,
pulmonary edema can be seen. Some dogs will also develop ascites and/or pleural effusion as a consequence of right-sided failure.
Valvular insufficiency is seen on color Doppler evaluation of the valve. Other echocardiographic findings include thickened
valves, cardiac chamber enlargement, and flail or prolapsing valve leaflets.
There is some debate about the use of ACE inhibitors prior to the development of CHF, but at the author's institution, it
is believed that treatment of CVD is effective after signs of congestive heart failure have developed. Treatment consists
of stabilizing the patient with diuretics, primarily injectable furosemide. Long-term treatment includes oral furosemide,
ACE inhibitors such as enalapril or benazepril, and pimobendan, a positive inotrope and venodilator. Renal values must be
monitored serially to follow changes in BUN, creatinine, and electrolytes. Though highly effective at treating CHF and improving
quality of life, some cardiologists will reserve pimobendan until there are signs of refractory congestive heart failure,
i.e. doses of furosemide greater than 2 mg/kg PO q 8 h, because it has been shown to deteriorate valve function in long-term
use. Other diuretics such as spironolactone and hydrochlorothiazide can be used to help manage signs of fluid overload. When
arrhythmias such as atrial fibrillation result from CVD, antiarrhythmics are indicated. The most common antiarrhythmic used
in this case is digoxin. Digoxin slows the heart rate by slowing the electrical impulse through the atrioventricular node.
It also has positive inotropic effects, so it is useful when concurrently treating congestive heart failure. Because the therapeutic
range of the digoxin dose overlaps with the toxic dose, it must be prescribed and monitored carefully. Signs of digoxin toxicity
range from mild—inappetance and diarrhea—to fatal arrhythmias. Digoxin blood levels must be done 7-14 days after starting
it at six to eight hours post-pill until an appropriate range is reached, and then every 3-4 months. Other antiarrhythmics
have negative inotropic effects, and should be used with caution when treating a patient in active CHF.
Surgical repair or replacement of the mitral valve, while standard in humans, has been attempted in dogs, but unfortunately,
it is not widely available; it is highly cost-prohibitive; requires intensive open heart surgery with cardiac bypass; and
results are discouraging.
The end result of valve disease is often euthanasia due to refractory congestive heart failure, but some patients die suddenly
as a result of a fatal arrhythmia. Endocarditis has not been associated with CVD. Rarely, the left atrium may perforate, or
rupture, as a result of a jet lesion. This allows blood to leak from the atrium into the pericardium. Many of these patients
die as a result of both sudden blood loss and compression of the heart by the pericardial effusion. Pericardiocentesis may
be attempted, but because the defect in the left atrial wall still exists, it is risky. CPR for a patient with left atrial
perforation is contraindicated, as the compressions will force more blood from the heart into the pericardial space, and may
actually rupture the pericardium.