By:  Merrilee T. Small, DVM, DACVIM (Cardiology)

History: 11/17/2016. Otis, a six-year-old, 57.7 kg MN Giant Schnauzer, presented to Western Branch Veterinary Hospital with a 2-3 day history of lethargy, dry cough and diarrhea. Otis was treated for heartworm disease at ~ 4 years of age, and an arrhythmia had been ausculted at routine physical exams since. He was fed  Diamond Naturals Lamb and Rice. A tachyarrhythmia with pulse deficits was ausculted on PE and he was promptly referred to The COVE's ER and Cardiology services. Otis was mentally dull/weak, tachycardic and arrhythmic on presentation. A gallop sound was present, most audible on the right. An electrocardiogram revealed atrial fibrillation with a ventricular response rate of 180-210 bpm. TFAST revealed mild pleural and trivial pericardial effusions and a subjectively hypocontractile heart. Labwork revealed creatinine 2.0 mg/dL ( 0.5-1.8mg/dL), total T4 < 0.5 ug/dL (0.8-3.5), TSH 1.86 ng/mL (0.0-0.6) and free T4 6 pmol/L (8-40). A diagnosis of dilated cardiomyopathy with severe systolic dysfunction and global cardiac enlargement was confirmed  by The COVE's Cardiology Department. He was stabilized and the following medical therapies were instituted:  pimobendan 15 mg PO TID, benazepril 30 mg PO q 24 hours, furosemide 120 mg PO TID, spironolactone 75 mg PO q 24 hours, diltiazem titrated from 15 mg TID to final dose of 90 mg PO TID based upon ECG monitoring, levothyroxine 0.3 mg PO BID, and fish oil supplement 1800 mg of the EPA component daily.

 

12/2016 - present: Otis' respiratory effort, cough, and exercise tolerance all improved following therapy. Ventricular response rate measured 150-160 on ECG, recorded at rechecks. As of this writing, Otis continues to enjoy a very high quality of life. His hypothyroidism is well controlled. He developed pleural effusion in September 2017 and is now on 160 mg furosemide PO TID and 50 mg hydrochlorothiazide PO BID in addition to his previous medications. A mild residual effusion is chronically present. Labwork is routinely monitored and he has a mild azotemia without electrolyte imbalance.

 

Discussion: Dilated cardiomyopathy (DCM) accounts for about 10% of cardiac disease in the dog. Males are affected more commonly than females. There are multiple causes of DCM in the dog. Doberman Pinschers, Boxers, Great Danes, English Cocker Spaniels and Giant breeds are predisposed to it, and genetics are likely the cause. A genetic link has been confirmed in Dobermans and Danes. Other potential causes include blood or myocardial taurine or L-carnitine deficiencies. Low plasma taurine levels have been documented in affected dogs on homemade, lamb/rice, and more recently some grain-free diets. Dietary history should be investigated in any atypical breed diagnosed with DCM. Myocarditis due to toxins or infectious disease is another potential cause of DCM. Endocrinopathies such as hypothyroidism and hypoadrenocorticism have been associated with systolic dysfunction. Pacing-induced cardiomyopathy occurs when a sustained heart rate of > 190-200 bpm (usually an arrhythmia) occurs over a period of several weeks. Alas, many cases of DCM are diagnosed as idiopathic.  

 

Affected dogs often present with signs of left, right, or biventricular heart failure, a soft cough (common in deep-chested dogs), and syncope. Prognoses vary with etiology and breed. Dobermans and Danes tend to experience rapidly progressive clinical courses, with the prognosis often only 4-10 months even with aggressive treatment. Other patients may have much more time. Unfortunately, sudden cardiac death due to ventricular arrhythmia is a complication that could significantly reduce life expectancy. 

 

Atrial fibrillation (AF) can be present in giant breed dogs without overt echocardiographic evidence of myocardial dysfunction. This is termed "lone atrial fibrillation." Most patients with lone AF develop systolic dysfunction or overt DCM over time. AF is more commonly associated with structural heart disease and occurs in ~ 45% of dogs with DCM. AF is typically permanent. Therefore, control of the ventricular response (VR) rate is targeted. The VR cannot be counted by auscultation alone, as not every electrical impulse will result in sufficient muscular contraction to generate a heart sound. ECG is necessary to document the VR. Optimal heart rate control (VR < 125 bpm on 24-hour Holter monitor at home) is positively associated with improved survival. The best rate control is achieved with a combination of diltiazem and digoxin. On ECGs performed in the hospital, a VR below 155 bpm appears to correspond to around 130 bpm at home. Optimized monitoring at home may be achieved with 24-hour Holter monitoring or through owner use of an Alivecor or Kardia veterinary monitor.

 

References available upon request.