2016
DOI: 10.1186/s12917-015-0626-z
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Abstract: BackgroundDilated cardiomyopathy (DCM) and chronic mitral valve disease (CMVD) in dogs are associated with heart chamber enlargement, also of the left atrium. DCM is often accompanied by rhythm disturbances (mainly atrial fibrillation or ventricular arrhythmias). In CMVD, arrhythmias are observed less frequently. It is still unclear whether left atrial enlargement in these diseases results from volume overload or if it is also connected with other factors (e.g. rhythm disturbances).This study was conducted on … Show more

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Cited by 14 publications
(22 citation statements)
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“…The expression of various cardiomyocyte proteins in left atria of dogs is altered in heart failure, as was noted in this study and previous studies [6,[11][12][13]. Although the majority of studies on SERCA2 expression in heart failure point to a decrease in the protein level, in some studies, the expression levels of SERCA2 was found to be unaltered, similarly to our results [14,16].…”
Section: Discussionsupporting
confidence: 91%
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“…The expression of various cardiomyocyte proteins in left atria of dogs is altered in heart failure, as was noted in this study and previous studies [6,[11][12][13]. Although the majority of studies on SERCA2 expression in heart failure point to a decrease in the protein level, in some studies, the expression levels of SERCA2 was found to be unaltered, similarly to our results [14,16].…”
Section: Discussionsupporting
confidence: 91%
“…Each specimen was randomly assigned a number to allow a blinded examination. The specimens were stained with hematoxylin-eosin or Masson-Goldner trichrome methods and evaluated for interstitial and perivascular fibrosis, cardiomyocyte degeneration (including cardiomyocyte nuclei enlargement, loss of cross striation and altered cardiomyocyte structure), intramyocardial arterial narrowing and inflammatory infiltrates as described in our previous studies [11,12]. Each of the features was evaluated in 20 randomly chosen fields per slide (for interstitial fibrosis, cardiomyocyte degeneration and inflammatory infiltrates) or in at least 10 vessels per slide (for perivascular fibrosis and intramyocardial arterial narrowing).…”
Section: Methodsmentioning
confidence: 99%
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“…These findings might be explained by the progressive LA volume overload due to MR and remodeling and by an increase in LV filling pressures in the advanced phases of the disease. Specifically, LA remodeling includes adaptive and maladaptive processes, such as alterations in the composition of extracellular matrix with excessive fibroblast proliferation, and myocyte hypertrophy, necrosis, and apoptosis 45, 46. All of these ultrastructural changes significantly affect LA myocardial wall properties, such as relaxation and compliance, ultimately leading to the observed reduction of LA phasic functions assessed by STE 40, 47, 48.…”
Section: Discussionmentioning
confidence: 99%