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.

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.