Alterations in mitochondrial DNA content in canine heart failure
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Background
Heart failure is the most common lethal consequence of cardiovascular abnormalities in the dog population. In humans, the abundance of mtDNA content plays a crucial role in the pathogenesis of different types of cardiovascular diseases such as ischemic heart disease, dilated cardiomyopathy, and congestive HF. Changes in mtDNA copy number could indicate the extent of mtDNA damage, serving as a potential biomarker for mitochondrial function and a predictor of several cardiovascular disease risks in humans. However, evidence regarding the alterations in mtDNA content in canine heart failure remains poorly explored. This study aims to determine the peripheral blood mitochondrial DNA content in healthy dogs and those experiencing acute heart failure.
Results
A total of thirty client-owned dogs, aged between 5 and 15 years, were selected for the study. The dogs were categorized into two groups: a healthy group (HT, n = 15) and a heart failure group (HF, n = 15). A comprehensive evaluation was performed on all dogs, involving physical examination, thoracic radiography, and transthoracic echocardiographic assessment. Additionally, three milliliters of blood were collected for hematology, blood chemistry profiles, and mitochondrial DNA (mtDNA) analysis. The monocyte levels were found to be significantly higher in the heart failure group (HF) than in the healthy group (HT). Furthermore, parameters such as blood urea nitrogen (BUN), creatinine, vertebral heart score (VHS), and vertebral left atrial size (VLAS) showed significant elevation in the HF group (p-value < 0.05). Echocardiographic measurements, including left ventricular internal dimension at end-diastole (LVIDd), left atrium (LA), left atrial to aortic root ratio (LA/Ao), end-diastolic volume (EDV), end-systolic volume (ESV), and left ventricular mass, were also notably higher in the HF group compared to the healthy group (p-value < 0.05). Moreover, the mtDNA content was significantly higher in the HF group than in the healthy group (p-value < 0.05).
Conclusion
In the context of decompensated HF, the occurrence of tissue hypoxia might instigate cellular damage, consequently resulting in the release of mtDNA. This phenomenon potentially explains the observed higher mtDNA content in the HF group in comparison to the healthy group.
