Myocarditis in dogs: What’s the clinical presentation, causes and outcome? | VETgirl Veterinary Continuing Education Podcasts

In this VETgirl online veterinary continuing education podcast, we discuss the clinical presentation, cardiovascular findings, etiology, and outcome of myocarditis in dogs. Myocarditis, or inflammation of the myocardium, is not well studied in dogs but can occur secondary to infectious and noninfectious etiologies. Infectious etiologies previously reported in dogs include trypanosomiasis, leishmaniasis, parvovirus, toxoplasmosis, neosporosis, borreliosis, ehrlichiosis, leptospirosis and bartonellosis. Drugs, toxins, immune-mediated disease, trauma, heat stroke, shock, and idiopathic account for the reported noninfectious causes. Definitive diagnosis requires histopathology, which would mean the need for endomyocardial biopsy in living patients – which I’ll admit, I’m scared to do – it’s not exactly a procedure without risk. As a result, antemortem histopathology is not commonly obtained in dogs and diagnosis is usually presumptive based on the subjective clinical picture. Standard criteria for antemortem diagnosis have not been established in dogs.

So, Lakhdhir et al out of Iowa State University and NCSU wanted to describe the clinical and diagnostic findings in dogs with both presumptive and confirmed myocarditis, as well as to identify etiologies and evaluate treatment, and report outcome in a study entitled Clinical presentation, cardiovascular findings, etiology, and outcome of myocarditis in dogs: 645 cases with presumptive antemortem diagnosis (26 confirmed postmortem) and 137 cases with postmortem diagnosis only (2004-2017). Importantly, the study population consisted of dogs that were not living in geographic regions endemic to Trypanosoma cruzi or Leishmania infantum (which is more commonly found in other countries outside of North America). The authors also hoped to propose criteria for antemortem diagnosis – so we can avoid those scary sounding endomyocardial biopsies! The study was retrospective from 2 academic institutions and looked at 2 groups: an antemortem and postmortem population of dogs. The antemortem population consisted of 64 dogs with high suspicion of myocarditis based on clinical presentation, laboratory findings and cardiopulmonary imaging, among others. Dogs with thoracic trauma were excluded. The postmortem population consisted of dogs with gross and histopathologic findings supportive of myocardial inflammation, and any special stains, cultures or other diagnostics that provided insight into etiology.

So, what did the authors find in this study? Let’s start with the antemortem population, where the mean age was 7.9 years, and median weight was 22.9 kilograms, but the ranges for these parameters were very wide – illustrating that myocarditis can occur in any age of dog. Breeds varied, with mixed breed and Labrador retrievers the most common – likely reflecting the commonality of these breeds as pets rather than a true breed association (although no control group existed for comparison). The most common clinical signs were lethargy and hyporexia, each occurring in over 2/3 of dogs. Gastrointestinal signs and tachypnea were also common. Only 21% of these dogs presented with a fever defined as rectal temperature > 102.5 degrees F. Numerous other physical examination findings were identified across cardiac, pulmonary, and orthopedic body systems, each occurring in less than 19% of dogs. Only 19% of dogs had heart murmurs. Hmmm, sounds like every dog presenting to me in the veterinary ER: ADR. The take-home point here is that dogs with myocarditis generally presented with a constellation of vague clinical signs, and a wide variety of physical abnormalities across various body systems.

Complete blood count (CBC) and serum chemistry findings were only somewhat insightful in these patients. Thrombocytopenia and/or neutrophilia was identified in over half of the dogs, with monocytosis and/or anemia occurring in just under half. Elevated ALT was identified in two-thirds of dogs, and elevated ALP in just over half. 54% were hypocalcemic, 45% were hypoalbuminemic, and 24% were azotemic.

Cardiac troponin I (cTnI), a serum biomarker for myocardial inflammation, was available on presentation for 29 of the dogs. cTnI was elevated (> 0.2 ng/mL) in all dogs – with median cTnI of 12.2 ng/mL and a range of 0.2-808 ng/mL. This reflects markedly elevated cardiac troponin I levels and a whole lot of myocardial inflammation! In dogs where cTnI was reassessed at some point, the cTnI was improved in 76% of cases. Electrocardiography findings varied but arrhythmias were extremely common, occurring in 91% of dogs. Tachyarrhythmias were more common than bradyarrhythmias, with ventricular tachycardia the most common, occurring in 46% of dogs. Echocardiographic abnormalities within 24 hours of presentation were predominantly decreased systolic function, left ventricular dilation, and changes in echogenicity of the myocardium. A small number of dogs (16%) had mild, hemodynamically insignificant pericardial effusion.

A variable number of dogs had additional diagnostic testing including urine culture, blood culture, synovial cultures, cytology (effusion or organ aspirates), abdominal ultrasound, thoracic radiographs, and/or infectious disease testing. 44% of dogs had postmortem examinations, of which 92% had confirmatory findings of myocarditis. 54% of these dogs had neutrophilic infiltrates, while 50% had lymphoplasmacytic infiltrates, which constituted the most common infiltrates identified (some had mixed infiltrates). 55% of the dogs in the antemortem group had a suspected infectious etiology based on ancillary diagnostic testing. These included bacterial sepsis (most common, occurred in 9 dogs), bacterial endocarditis, Toxoplasma, Neospora, Trypanosoma, Leptospira, Bartonella, and Dirofilaria. In 14 of the dogs, response to antibiotics or postmortem findings were highly supportive of an infectious etiology but a specific organism was not confirmed. So frustrating! 17% of cases were considered noninfectious with 8 being neoplastic, 2 rodenticide toxicities, and 1 immune-mediated hemolytic anemia. Of the neoplastic causes, 75% constituted extracardiac neoplasia via either neoplastic embolism or cardiac metastasis.

From a treatment standpoint, the most common therapies used in these patients were antibiotics, antiarrhythmic therapies, ancillary cardiac therapies (such as pimobendan, angiotensin-converting enzyme inhibitors, clopidogrel or furosemide), and immunosuppressive therapies. Median survival for the 41 (64%) dogs who were deceased at the time of publication was only 4 days duration. Myocarditis was considered related to patient death in 73% of these dogs – which is highly concerning and indicates that regardless of what the initial illness was, the cardiac manifestations were highly impactful on survival. Only 58% of dogs survived beyond 2 weeks, with a median survival in those dogs of only 81 days. The authors did detect a number of significant differences in the patient populations between the 2 primary institutions (Iowa State University and North Carolina State University), although many of these may simply reflect differences in clinician observation, laboratory machines, and clinician preferences. More infectious testing was submitted by North Carolina State University (We have less infectious disease in the midwest).

Dogs at North Carolina State University more commonly received sotalol, and more commonly received antibiotics; they also had longer survival times. Is this just coincidence? Probably not – in the univariate analysis, antibiotic treatment in general, doxycycline treatment, sotalol treatment, and infectious disease testing were associated with higher survival. (You know VETgirl’s stance – doxy for everything! Just kidding). Given the high incidence of neutrophilic myocarditis, bacterial sepsis, and ventricular arrhythmias in the population, these associations would make sense. It does suggest that sotalol may have superiority as an antiarrhythmic in this population over lidocaine, as there was no difference in frequency of use of these agents but only sotalol demonstrated survival benefit. In multivariate analysis, only sotalol treatment was predictive of survival beyond two weeks. Presence of pericardial effusion and azotemia were the only poor prognostic indicators in the multivariate analysis.

Reviewing the postmortem population of 137 dogs, the majority came from North Carolina State University. Myocarditis represented < 0.03% of total necropsy cases at the institutions involved. 59% were deemed infectious, of which 25% of these were extension of bacterial endocarditis into the myocardium. The most common myocardial infiltrates were again neutrophilic and lymphoplasmacytic. Only four cases had definitive infectious agents identified and these included intralesional bacteria, Dirofilaria, and blastomycosis.

So, what do we take away from this VETgirl podcast? Well, keep in mind that most of the prior data available on myocarditis in dogs is from populations predominantly affected by organisms like Trypanosoma cruzi (Chagas disease) which is endemic to the southwest United States, particularly Texas. This study illustrates the likelihood that the majority of dogs with myocarditis outside of this region (or at least in the midwest and southeast) may have vastly different etiologies of myocarditis, particularly in the form of bacterial disease. Given the relatively high frequency of bacterial disease/sepsis in dogs in general, myocarditis may be occurring with much greater frequency than we have suspected to this point, and may obviate the need for testing for some of the more exotic tick-borne, protozoal, or other infectious organisms in such cases where bacterial disease is clearly evident. The study also illustrates survival benefits of certain therapies like antibiotics and sotalol that emphasize the role of bacterial sepsis in causing myocarditis in many dogs, and the importance of controlling tachyarrhythmias in these dogs (VETgirl’s stance – never tolerate a HR > 170-180 in a dog!). What about viral myocarditis, which is common in humans, you ask? This study involved cases where limited viral testing was performed – however, a recent study did identify viral nucleic acids in a significant number of dogs with myocardial disorders and arrhythmias. So, it is likely that viral myocarditis does occur with some frequency in dogs – sounds like a great area for future study.

Finally, the authors did propose a diagnostic criteria algorithm for antemortem diagnosis of myocarditis modeled after the Duke criteria for diagnosis of endocarditis. The listener is referred to the manuscript for the complete list of proposed criteria and combinations of major and minor criteria considered supportive of myocarditis, but in basic terms the major criteria consisted of cardiac troponin I > 1 ng/mL and positive infectious disease culture, serology or PCR. Minor criteria included fever, new heart murmur, specific CBC alterations, ventricular arrhythmias, decreased left ventricular function or altered appearance on echocardiogram, and presence of pericardial effusion. When in doubt, don’t forget to have myocarditis on your radar!

1. Lakhdhir S, Viall A, Alloway E. Clinical presentation, cardiovascular findings, etiology, and outcome of myocarditis in dogs: 645 cases with presumptive antemortem diagnosis (26 confirmed postmortem) and 137 cases with postmortem diagnosis only (2004-2017). J Vet Cardiol 2020:30,44-56.

Today’s VETgirl online veterinary CE podcast is sponsored by IndeVets, who’s on a mission to make veterinary medicine better. IndeVets is hiring qualified vets to become a part of their team. Skip the off-hour call and office politics and get back to the medicine as an associate with great benefits! This isn’t a relief gig. IndeVets wants to rid the vet industry of burnout and over-working and empower vets to take control of when and where they want to work, so they can enjoy life outside of the clinic and be a better vet inside it. Go to IndeVets.com to learn more and apply.

Leave a Reply

Your email address will not be published. Required fields are marked *