Case 1. Worsening Mitral Valve Disease or Not?
Signalment
Eleven-year-old MC dachshund.
Chief Concern
Acute-onset dyspnea in last 24 hours.
History
Heart murmur known to be present for >3 years. Echocardiogram two years ago identified myxomatous mitral valve disease with normal left atrial size (ACVIM stage B1). Routine recheck echocardiogram eight months ago: unchanged.
New-onset dyspnea (severe/catastrophic at admission). Thoracic radiographs suggestive of pulmonary edema but heart size well within normal limits. Hospitalization and treatment (furosemide IV, O2 supplementation) with resolution of signs. Further evaluation to investigate discrepancy between congestive heart failure (CHF) and normal heart size.
Physical Exam (36 Hours after Admission)
Bright, alert, responsive dog breathing comfortably. Regular heart rhythm, 140 beats/minute. Grade IV/VI systolic left apical murmur. Pulse strong and synchronous.
Diagnostic Test Results
An echocardiogram confirmed changes indicating degenerative mitral valve disease but with limited secondary changes: no left ventricular enlargement, and mild left atrial enlargement (LA:Ao=1.7:1). Review of thoracic radiographs: interpretation unchanged.
Analysis and Conclusion
Discrepancy between heart failure and mild/moderate heart disease can be explained by transient intravascular volume overload, sudden worsening of heart disease (e.g., chordal rupture), or theoretically, insufficient pulmonary lymphatic drainage. In this case, despite careful history-taking, it was only later (after 24 h of hospitalization) that the owner’s spouse indicated having given the dog potato chips as a snack the day before the onset of dyspnea. No salty snack foods have been given since then, and there has been no recurrence of clinical signs.
Learning Point
Excessive sodium ingestion can be associated with congestive heart failure in dogs with moderate or marked disease. Identifying it is important: the prognosis is better than with deterioration of the primary disorder, and treatment can be increased temporarily rather than permanently.
Case 2. Cough plus Murmur: to Treat or Not to Treat?
Signalment
Eleven-year-old FS cocker spaniel.
Chief Concerns
Chronic cough; exercise intolerance; dyspnea; inappetence.
History
Cough x five months, worse last few weeks; exercise intolerance x one year; increase in respiratory effort (weeks); waxing-waning appetite x six weeks.
Physical Exam
Quiet, alert, responsive, inquisitive dog. Body weight=26.4 kg; body condition score=9/9. Mildly increased respiratory effort at rest and with exercise; no respiratory distress, no upper respiratory noise. Recurrent, moist cough. Left apical systolic grade IV/VI heart murmur. Respiratory sinus arrhythmia @ 90 beats/minute with fair, synchronous pulse. Unremarkable abdominal palpation.
Diagnostic Test Results
Thoracic radiographs (two views): difficult to interpret due to superimposed body fat; cardiac silhouette appears WNL; pulmonary pattern appears WNL but cannot rule out pulmonary edema (vs. superimposed fat). Echocardiogram: degenerative mitral valve disease causing moderate mitral regurgitation, with mild/moderate left atrial enlargement (LA:Ao=1.9:1). Doppler arterial blood pressure: 150 mm Hg systolic. Complete blood count, serum biochemistry profile, urinalysis, abdominal ultrasound examination: no significant abnormalities of note.
Analysis and Conclusion
The principal diagnostic question is whether or not this animal has pulmonary edema; knowing this will directly influence treatment (diuretic if yes, no diuretic if no) and prognosis. The thoracic radiographs are ambiguous because of the opacifying effect of superimposed body fat. The echocardiogram is of limited help, because with moderate left atrial enlargement, pulmonary edema is possible (stage C), but so is the compensated, preclinical state (stage B2). The dog’s increased respiratory effort, along with exercise intolerance, and weak pulse (from interposed SQ fat) can be attributed to obesity. Similarly, the decreased appetite may be a manifestation of selective taste rather than of longstanding illness, given the dog’s body condition score and lack of any evidence of anorexia-inducing illnesses on the tests performed to date. Therefore, the remaining information must be considered: the respiratory sinus arrhythmia, absence of sinus tachycardia, absence of respiratory distress, and inquisitive demeanor of the dog make CHF very unlikely. Treatment of suspected (+/- further testing for) primary airway disease are most appropriate.
Learning Point
The dilemma of whether respiratory signs are due to primary respiratory disease or to CHF is a common conundrum in coughing dogs with mitral valve disease. Thoracic radiographs and the echocardiogram are most useful for resolving this dilemma. Additionally, specific physical exam findings and historical elements can be very helpful, as in this case.
Case 3. Is It Boxer Cardiomyopathy/Arrhythmogenic Cardiomyopathy? If So, Do I Treat?
Signalment
Eight-year-old MC boxer dog.
Chief Concerns
Arrhythmia noted as incidental finding.
History
Active dog, no current health concerns, no medication. Arrhythmia noted on annual physical exam.
Physical Exam
Bright, alert, responsive, comfortable dog. Heart rate=170 beats/minute when calm and corresponding pulse rate=120/minute; heart rhythm=irregular, with single premature beats and occasional (1–2/minute) bursts of 3–5 premature beats with weak or absent corresponding pulse. Comfortable respirations. Normal heart sounds. Unremarkable abdominal palpation, cutaneous examination, and rest of physical exam.
Diagnostic Test Results
Electrocardiogram: normal sinus rhythm with single, paired and triplet monomorphic premature ventricular complexes (PVCs). Echocardiogram, thoracic radiographs, complete blood count, serum biochemistry profile, abdominal ultrasound exam: unremarkable.
Analysis and Conclusion
The diagnosis of arrhythmogenic cardiomyopathy (also called arrhythmogenic right ventricular cardiomyopathy, boxer cardiomyopathy, and familial ventricular arrhythmias of boxers) is one of exclusion: the presence of ventricular arrhythmias with no detectable primary cardiac or systemic cause is diagnostic. Holter monitoring can be undertaken when a dog is experiencing syncope, in order to document whether an arrhythmia is occurring during the episodes; or to establish a baseline number of PVCs prior to starting treatment (but realizing that normal day-to-day fluctuations of >80% in number of PVCs is expected irrespective of treatment). In this case, the dilemma is whether to begin antiarrhythmic treatment, typically with sotalol 1–3 mg/kg PO q 12 h, in the absence of clinical signs. Empirically, the occurrence of pairs and triplets of PVCs has been interpreted to mean a higher grade of ventricular arrhythmia (and to justify starting sotalol), but supportive proof is lacking.
Learning Point
Either treating or not treating is acceptable in subclinical arrhythmogenic cardiomyopathy, and a discussion with the owner can draw on the owner’s wishes and abilities regarding twice-daily medication administration and the owner’s beliefs and philosophy regarding pre-emptive but uncertain treatment of an irreversible condition. The known reduction in PVCs associated with omega-3 fatty acid treatment in this disease (though no proof of reduction in future syncope nor of prolongation in lifespan) can prompt treatment with DHA 497 mg/dog+EPA 780 mg/dog PO q 24 h.