Left ventricular remodeling in preclinical experimental mitral regurgitation of dogs

Dillon, A. Ray; Dell’Italia, Louis J.; Tillson, Michael; Killingsworth, Cheryl R.; Denney, Thomas S.; Hathcock, John T.; Botzman, L.

doi:10.1016/j.jvc.2012.01.012

Cited by 25 publications

(24 citation statements)

References 42 publications

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“…However, clinical staging may not adequately reflect intrinsic myocardial condition and structural changes, because guidelines for the classification of heart failure are based on clinical signs 18. Because the clinical signs of DMVD develop slowly over a period of years, they are often recognized only after cardiac remodeling has already occurred 19. Several studies in dogs with experimentally induced mitral valve insufficiency showed severe myocardial degeneration (e.g., myofibrillar loss, increased perinuclear space, and hypertrophy) in the LV as early as 4 months after induction of mild mitral regurgitation 10, 20, 21.…”

Section: Discussionmentioning

confidence: 99%

Pathologic Manifestations on Surgical Biopsy and Their Correlation with Clinical Indices in Dogs with Degenerative Mitral Valve Disease

Lee

Mizuno

et al. 2015

Veterinary Internal Medicne

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BackgroundEvaluation of myocardial function is clinically challenging in dogs with degenerative mitral valve disease (DMVD). Although myocardial dysfunction is caused by pathologic degeneration, histopathologic progression is poorly understood.ObjectivesTo characterize myocardial and pulmonary pathologic changes according to severity in dogs with naturally occurring DMVD, and to investigate whether or not pathologic degeneration is reflected by traditional clinical indices.AnimalsOne hundred and seventeen dogs with naturally occurring DMVD.MethodsProspective observational study. Biopsied left atrium (LA), left ventricle (LV), and lung were evaluated histologically, and an attempt was made to correlate pathologic findings with clinical indices.ResultsSevere myocardial changes were observed in all International Small Animal Cardiac Health Council classes. In the lung, heart failure cell levels were significantly increased in class III patients (P < .0001). In a paired comparison, the LA showed significantly more severe degeneration than the LV, including myocardial fatty replacement, immune cell infiltration, and interstitial fibrosis (P < .0001). In contrast, myocardial cells were more hypertrophied in the LV than in the LA (P < .0001). Left ventricular end‐diastolic dimension (LVEDd) was associated with fatty replacement (P = .033, R 2 = 0.584) and myocardial vacuolization (P = .003, R 2 = 0.588) in the LA.Conclusions and Clinical ImportanceIn DMVD, although severe pathologic changes may be evident even in early stages, there may be pathologic discrepancy between the LA and the LV. Myocardial degeneration may be reflected by clinical indices such as LVEDd and EF.

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Section: Discussionmentioning

confidence: 99%

Pathologic Manifestations on Surgical Biopsy and Their Correlation with Clinical Indices in Dogs with Degenerative Mitral Valve Disease

Lee

Mizuno

et al. 2015

Veterinary Internal Medicne

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“…The triggering event of these geometrical and structural changes is the increase of end-diastolic pressure and hence end-diastolic wall stress due to the volume overload (19). The leaking valve causes regurgitation of the stroke volume into the low-pressure atrium during systole.…”

Section: Natural History Of the Diseasementioning

confidence: 99%

“…The LV end-diastolic (EDV) and end-systolic volume (ESV) increase, and the total stroke volume (SV) increase, but the forward stroke volume decreases. The increased wall stress initiates a continuation of collagen loss and myocyte stretch (19). The result is increased end-diastolic LV diameter, and cardiac output is up to 30% less than the baseline output.…”

Section: Natural History Of the Diseasementioning

confidence: 99%

“…Below these endothelial layers lies a thin layer consisting of collagen fibers, elastic fibers and fibroblasts; on the atrial side there is also smooth muscle. Between the two layers are the spongiosa and the fibrosa layers (19). With the progression of the disease, the endothelium proliferates, and the number of fibroblasts increases; there are areas where the endothelial layer is damaged, exposing the basement membrane or the collagen matrix.…”

Section: Pathomorphology and Pathohystologic Changes In Mmvdmentioning

confidence: 99%

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Myxomatous Mitral Valve Disease in Dogs - an Update and Perspectives

Petrič

2015

Macedonian Veterinary Review

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“…Although in the whole heart cells are electrically connected and thus the myocardium should behave as a functional syncytium, a remarkable similarity of the electrical interaction with external field has been observed in isolated myocytes and whole hearts of neonatal rats (Gomes et al, 2001(Gomes et al, , 2002. Increase in cell length is known to occur in some physiological (pregnancy; Virgen-Ortiz et al, 2009) and pathophysiological conditions, such as mitral insufficiency (Dillon et al, 2012), spontaneous arterial hypertension (R.A. Bassani, unpublished results), dilated cardiomyopathy (Kaistura et al, 1995), and familial hypertrophic cardiomyopathy (Brouwer et al, 2011). Cardiac hypertrophy has been considered an independent factor associated with increased risk of arrhythmia and sudden death (Bender et al, 2012;Reinier et al, 2011), particularly in the case of hypertrophic cardiomyopathy (Brouwer et al, 2011).…”

Section: Cell Lengthmentioning

confidence: 99%

The influence of cell dimensions on the vulnerability of ventricular myocytes to lethal injury by high-intensity electrical fields

Goulart¹,

Oliveira²,

Bassani³

et al. 2012

RBEB

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Application of high intensity electric fields (HIEF) to the myocardium is commonly used for cardiac defibrillation/cardioversion. Although effective at reversing life-threatening arrhythmias, HIEF may cause myocyte damage due to membrane electropermeabilization. In this study, the influence of cell length and width on HIEF-induced lethal injury was analyzed in isolated rat cardiomyocytes in parallel alignment with the field. The field-induced maximum variation of membrane potential (∆V max ) was estimated with the Klee-Plonsey model. The studied myocyte population was arranged in two group pairs for comparison: the longest vs. the shortest cells, and the widest vs. narrowest cells. Threshold field intensity was significantly lower in the longest vs. shortest myocytes, whereas cell width influence was not significant. The threshold ∆V max was comparable in all groups. Likewise, a significant leftward shift of the lethality curve (i.e., relationship of the probability of lethality vs. field intensity) of the longest cells was observed, evidencing greater sensitivity to HIEF-induced damage. However, the lethality curve as a function of ∆V max was similar in all groups, confirming a prediction of the Klee-Plonsey model. The similar results for excitation and injury at threshold and HIEF stimulation, respectively, indicate that: a) the effect of cell length on the sensitivity to the field would be attributable to differences in field-induced membrane polarization that lead to excitation or lethal electroporation; b) the Klee-Plonsey model seems to be reliable for analysis of cell interaction with HIEF; c) it is possible that increased cell length in hypertrophied hearts enhances myocyte fragility upon defibrillation/cardioversion.

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Left ventricular remodeling in preclinical experimental mitral regurgitation of dogs

Cited by 25 publications

References 42 publications

Pathologic Manifestations on Surgical Biopsy and Their Correlation with Clinical Indices in Dogs with Degenerative Mitral Valve Disease

Pathologic Manifestations on Surgical Biopsy and Their Correlation with Clinical Indices in Dogs with Degenerative Mitral Valve Disease

Myxomatous Mitral Valve Disease in Dogs - an Update and Perspectives

The influence of cell dimensions on the vulnerability of ventricular myocytes to lethal injury by high-intensity electrical fields

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