Peer-reviewed veterinary case report
Heart rate and ECG changes in dogs with chronic Ehrlichiosis
By Gianfranchesco Filippi, Mauricio et al.·Published in PloS one·2019·Department of Veterinary Clinics, Brazil·View original on PubMed →
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Original publication title: Evaluation of heart rate variability and behavior of electrocardiographic parameters in dogs affected by chronic Monocytic Ehrlichiosis.
- Species:
- dog
Plain-English summary
A group of 20 dogs with chronic Monocytic Ehrlichiosis (CME), a disease caused by a type of bacteria, showed serious heart issues, including a high rate of arrhythmias (irregular heartbeats). Common symptoms included loss of appetite, vomiting, fatigue, and heart murmurs. During a 28-day treatment period, 40% of these dogs sadly passed away. The study found significant changes in heart-related blood markers compared to healthy dogs, indicating that CME can lead to severe heart problems. Monitoring revealed that many of the affected dogs experienced various types of arrhythmias, suggesting a serious impact on their heart health.
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Abstract
Canine Monocytic Ehrlichiosis (CME) is a systemic disease prevalent in the entire world caused by the obligate intracellular bacteria Ehrlichia canis. The occurrence of myocarditis with a high prevalence of arrhythmias in dogs affected by this disease in the cytopenic phase has already been proven. This study aims to evaluate the concentrations of CK MB, cTnI and NT-proBNP in dogs affected by Ehrlichia canis in the chronic phase since the intense stimulation of the immune system can lead to myocarditis; to evaluate if the condition can lead to arrhythmic events and, if so, define their frequency and classification through conventional and ambulatory electrocardiogram tests (Holter method) for a period of 24 hours; to analyze heart rate variability in the time domain and whether the condition can lead to autonomic imbalance; and to determine the survival rate of affected dogs, identifying possible risk factors for mortality at this stage of the disease. For this purposes, we evaluated clinical, hematological and biochemical data, as well as the concentrations of cardiac biomarkers Creatine Kinase-MB (CK MB), Cardiac Troponin I (cTnI) and N-terminal pro-peptide natriuretic type B (NT-proBNP). We also analyzed conventional and ambulatory electrocardiography (24-hour Holter) and heart rate variability (HRV) in 20 dogs afflicted by cytopenic CME in the chronic phase of the disease (G1) and compared the results with a control group comprised of ten healthy dogs (G2). G1 was monitored during the treatment for 28 days, during which eight (8) of the 20 infected dogs died (40%). Anorexia, vomiting, fatigue, hypoalbuminemia, heart murmurs and increased concentrations of alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were common clinical signs. The mean concentrations of cTnI and CKMB were significant (0.24 ng / mL ± 0.5, 229 ± 205 IU / mL) in comparison to the control group (0.042 ± 0.07 ng / mL, 126 ± 46.12 IU / mL). No significant differences were observed between NT-proBNP concentrations in G1 (135.46 ± 29.7) and G2 (138.28 ± 19.77). Nine of the twenty dogs (45%) presented a high frequency of arrhythmias during 24-hour recording, ranging from first and second-degree atrioventricular block, ventricular and supraventricular ectopic events and sinus tachycardia. No sinus pause was observed. One dog had 120 episodes of unsustained ventricular tachycardia and two episodes of sustained ventricular tachycardia. The short-term and long-term HRV data, represented by SDNN (ms), SDANN (ms) and pnn50 (%) were also significant lower (83 ± 65, 56.05 ± 37.3 and 14.56 ± 20, respectively) in comparison to the healthy animals (268 ± 74.6, 168.3 ± 39.14 and 55.87 ± 12.8, respectively). These results suggest that cytopenic CME is characterized by an arrhythmogenic component and intense stimulation of the sympathetic autonomic nervous system in the heart, reflecting an imbalance in the activity of the ANS.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/31125348/