Chronic Mitral Valve Insufficiency Research Articles

MORPHOFUNCTIONAL FEATURES OF THE MYOCARDIUM IN ITS DIASTOLIC OVERLOAD

Relevance. Adaptation of the heart chambers to their volume overload, which increases with diastolic filling of the left ventricle (LV) or systolic regurgitation in the left atrium (LA) in case of mitral valve insufficiency leads to remodeling of the myocardium of these chambers. Longitudinal hypertrophy of cardiomyocytes (CMCs), realized by building up new sarcomeres at the end of existing myofibrils, is an adaptation mechanism in the early stages, but eventually turns into maladjustment, which leads to heart failure. Hypertrophied CMCs, damaged during decompensation, are replaced by connective tissue due to excessive activation of fibroblasts with deposition of the extracellular matrix, which is also an element of the myocardial remodeling. The progression of heart failure is also associated with a mismatch between blood supply and myocardial oxygen demand, since an increase in the size of the CMCs is accompanied by a rarefaction of the intramural network of microvessels. It is believed that the violation of the ratio of the size of the heart, angiogenesis and cardiac function are the basis for the transition of adaptive compensation of the heart to decompensation with the progression of heart failure.
 Objective: to study morphological changes in the myocardium of the LV and LA in patients with mitral valve insufficiency.
 Materials and methods. Macroscopically, the condition of the myocardium was studied on the material of 14 autopsies of patients who died of NdMK insufficiency. History of NdMK – from 3 months. up to 2.4±1.1 years. As a control, the hearts of 3 deaths without cardiopathology were studied. The material for light microscopy was pieces of myocardium from different segments of the left ventricle, as well as from the walls of the left ventricle, obtained during autopsy.Morphological (macroscopic, histological and electron microscopic), morphometric and statistical research methods were used.
 Results. With LV dilatation associated with chronic mitral valve insufficiency, lengthening of each CMCs provides an increase in the area of ​​the myocardial walls, and, accordingly, the size of the cavity of the corresponding chamber of the heart, which compensates to some extent for the increase in diastolic blood volume in the LV and systolic blood volume in the LA. However, the factor limiting this compensation mechanism is the deficiency of the myocardial microvasculature associated with limited capillary growth. The contradiction between the need for the myocardium to lengthen the CMCs and the inability of capillaries to provide them with oxygen leads to a breakdown in compensation with an increase in fibrotic changes. This is a factor limiting the further increase in the volume of the cavity.
 Conclusions. Overloading of the myocardium with volume leads to an increase in the length of the CMCs, on average, from 57.3±9.1 µm to 93.7±12.4 µm. The increase in the length of the CMCs is due to the increase in the number of sarcomeres from 43.7±8.4 to 62.5±14.5. The diameter of the CMCs in this case does not increase reliably. Overloading of the heart cavities with volume is often accompanied by desynchronization of the CMCs contraction, which leads to disruption of the integrity of the myocytic "working syncytium" and pronounced interstitial fibrosis.

Analysis of certain blood biochemical parameters in relation to oxidative stress in chronic mitral valve insufficiency of dogs with heart failure

Chronic mitral valve insufficiency (CMVI) is the most common acquired heart disease in dogs. In heart failure, the cellular oxygenation and metabolism are affected, which leads to the production of free radicals. Free radicals damage DNA, lipid and protein molecules in cells. In the present experiment, blood samples were collected from CMVI dogs with heart failure and were compared with the results obtained from healthy dogs. A significant increase in the levels of xanthine oxidase, AST, LDH and CK and decrease in the activity of catalase were noticed in CMVI dogs when compared to healthy dogs, which revealed overall cardiac and skeletal muscle damage in CMVI dogs. Results of biochemical parameters revealed an increase in urea level and decrease in sodium, potassium, and calcium levels in CMVI dogs as compared to control dogs, all of which indicate cardiac damage in dogs. Study on hematological parameters revealed a significant decrease in Hb, PCV, RBC and platelet counts and an increase in total WBC counts and percentage of neutrophils, decrease in percentage of the lymphocyte and monocyte in CMVI dogs than control. These results indicate secondary phenomenon to heart failure. The present research data indicates the usefulness of these biomarkers in the diagnosis and prognosis of CMVI with heart failure in dogs.

Late right ventricular performance after mitral valve repair assessed by exercise echocardiography

ObjectivesThe aim of the study was to evaluate the right ventricular (RV) performance during exercise in patients who underwent mitral valve repair for chronic mitral valve insufficiency relative to healthy individuals and to assess exercise capacity using a semisupine ergometer.MethodsWe studied 56 patients who underwent mitral valve repair for degenerative posterior mitral leaflet prolapse between 2005 and 2014 and a control group of 13 healthy individuals. Clinical data were collected prospectively, and echocardiographic measurements of RV function were obtained at rest and at peak exercise.ResultsOne-third of the study patients had RV systolic dysfunction as indicated by tricuspid annular plane excursion (TAPSE) at rest. Resting TAPSE was lower in the study group (16.7 ± 3.3 mm) than in the control group (24.4 ± 4.3 mm), p < 0.001. TAPSE increased in both groups during exercise and exercise was shown to have a significant main effect on TAPSE F(1, 52) = 80, p < 0.001. TAPSE increased more in the control group and an interaction was detected between the participant groups (study group vs. control group) and exercise, F(1, 52) = 24, p < 0.001. In the study group, Poor postoperative RV function was associated with preoperative left ventricular dilatation but was not correlated with impaired maximum exercise capacity.ConclusionsDespite the excellent clinical outcome during rest and exercise after mitral valve repair, our results suggest patients that have undergone mitral valve repair due to posterior leaflet prolapse have significantly reduced RV function at rest and during exercise compared to healthy controls at long-term follow-up, as measured by TAPSE.

Administration of Tolvaptan for Chronic Mitral Valve Insufficiency in a Dog with Hyponatremia

Administration of Tolvaptan for Chronic Mitral Valve Insufficiency in a Dog with Hyponatremia

Evaluation of Serum Symmetric Dimethylarginine Concentrations in Dogs with Chronic Mitral Valve Insufficiency

Evaluation of Serum Symmetric Dimethylarginine Concentrations in Dogs with Chronic Mitral Valve Insufficiency

Diagnostic value of echocardiographic indices and cardiac biomarkers in dogs with chronic mitral valve insufficiency

Diagnostic value of echocardiographic indices and cardiac biomarkers in dogs with chronic mitral valve insufficiency

Clinical Relevance of Cystatin C as a Renal Marker in Dogs with Chronic Mitral Valve Insufficiency

Cystatin C is a low molecular weight 13 kilodalton protein. It is known to be a more sensitive marker of glomerular filtration rate than creatinine in humans. The purpose of the present study was to demonstrate the changes of renal markers including cystatin C according to the severity of chronic mitral valve insufficiency (CMVI) and to investigate the clinical relevance of cystatin C as an early renal marker in dogs with CMVI. A retrospective study was performed to assess renal function according to International Small Animal Cardiac Health Council (ISACHC) system classification of heart failure in dogs with CMVI. Thirty seven dogs were divided into a group 1 (healthy dogs ; n = 10), a group 2 (ISACHC I ; n = 10) and a group 3 (ISACHC II-III ; n = 17). In all dogs, serum concentrations of bun (sUr), creatinine (sCr) and cystatin C (sCys-C) were measured with an automated analyzer. In dogs with CMVI, sCys-C concentrations were significantly correlated with sCr concentrations and were independent of age, BW, SBP, and sex. Renal dysfunction tended to occur more frequently as the severity of CMVI increases. In dogs with mild CMVI, only sCys-C concentrations were statistically higher than in healthy dogs. This study demonstrates the clinical relevance of sCys-C. sCys-C may be a valuable renal marker for early diagnosis of renal dysfunction in dogs with CMVI.

Evaluation of Plasma D-Dimer Concentration in Dogs with Chronic Mitral Valve Insufficiency

This study aimed to evaluate the plasma concentration of NT-proBNP in dogs with different stages of heart failure by chronic mitral valve insufficiency (CMVI). Fifty small-breed dogs with CMVI and 7 healthy control dogs without cardiac disease and critical systemic diseases were included in the study population. As a preliminary study, we compared the plasma concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP) and the echocardiographic parameters between dogs of the International Small Animal Cardiac Health Council (ISACHC) classes. Then, we evaluated the associations between NT-proBNP and echocardiographic parameters. Plasma NT-proBNP levels showed a significant difference among the ISACHC groups. In the comparison between echocardiographic parameters and NT-proBNP, NT-proBNP were found to be associated with left atrium/aorta (LA/AO), early diastolic transmitral flow (E) velocity, late diastolic transmitral flow (A) velocity, end diastolic volume index (EDVI). Our study found plasma NT-proBNP might be useful to predict the disease progression in dogs with CMVI.

Decreased Insulin Secretion in Dogs with Chronic Mitral Valve Insufficiency

Glucose metabolism abnormalities secondary to heart failure, including insulin resistance (IR) and impaired fasting glucose, have been gradually recognized as important prognostic factors in disease progression. However, to date, no study has investigated glucose abnormalities in dogs with chronic mitral valve insufficiency (CMVD). Thus, we hypothesized that glucose metabolism abnormalities due to heart failure may develop in dogs with CMVD. A prospective study was performed on 113 client-owned dogs with variable CMVD severities. Serum insulin, glucagon, fructosamine, and glucose concentrations were measured, and insulin resistance was determined using the homeostatic model assessment (HOMA) score. The serum insulin concentration had a significant inverse association with the heart failure severity. However, there was no significant association between the heart failure severity and fructosamine, HOMA score, and fasting blood glucose. Insulin, fructosamine, and HOMA had a significant positive association with body condition scores (BCS), whereas glucose had no association. This study found that insulin secretion in dogs with naturally occurring heart failure due to CMVD might be compromised as the disease worsens.

Clinical assessment of systolic myocardial deformations in dogs with chronic mitral valve insufficiency using two-dimensional speckle-tracking echocardiography

ObjectiveThe objective of this study was to clinically assess myocardial deformations in dogs with chronic mitral valve insufficiency (CMVI) using two-dimensional speckle-tracking echocardiography (2D-STE). Animals87 dogs with CMVI. MethodsDogs were placed into 1 of 3 classes, based on the International Small Animal Cardiac Health Council classification. In addition, 20 weight- and age-matched healthy dogs were enrolled as controls. The dogs were examined for myocardial deformations using 2D-STE, and strain and strain rate in the longitudinal, circumferential, and radial directions were evaluated. ResultsClass II and III dogs had higher circumferential strain than class I dogs (P = 0.002 and P = 0.001, respectively) and controls (P < 0.001 and P < 0.001, respectively). Class III dogs had higher radial strain than class I dogs (P = 0.001) and controls (P < 0.001). Class III dogs had higher radial strain rate than class I dogs (P = 0.006) and controls (P = 0.001). Other deformations, including longitudinal deformations, were not significantly different between classes of CMVI or between CMVI dogs and controls. ConclusionsIn the clinical progression of CMVI in dogs, myocardial deformations, as assessed by 2D-STE, differed according to myocardial contractile direction. Thus, assessments of multidirectional myocardial deformations may be important for better assessment of clinical cardiac function in dogs with CMVI.

Evaluation of homocysteine levels in dogs with chronic mitral valve insufficiency

Homocysteine is a nonessential amino acid that is biosynthesised through a multistep process from methionine, and can also be converted into cysteine (Chandler and Payne-James 2006, Rossi and others 2008)....

Decreased Systolic Function and Inadequate Hypertrophy in Large and Small Breed Dogs with Chronic Mitral Valve Insufficiency

Systolic dysfunction associated with chronic mitral valve insufficiency (CMVI) has been demonstrated in experimental animal models and large breed (LB) dogs but has been reported as an uncommon finding in small breed (SB) dogs with naturally occurring disease. It has been suggested the myocardial failure could be, in part, because of an insufficient increase in left ventricular mass. To test if SB and LB dogs with CMVI and moderate heart failure have systolic dysfunction and if they have adequate eccentric hypertrophy. Data from 38 SB and 18 LB dogs affected with CMVI were compared retrospectively with results from 2 groups of normal dogs (17 SB and 32 LB). Systolic function was investigated echocardiographically by using percentage fractional shortening (FS), the ratio between observed and expected end-systolic diameter (ESD/ESDe), and end-systolic volume index (ESVI). Left ventricular hypertrophy was estimated by using the ratio between the thickness of the left ventricular free wall and the radius in diastole (h/R). Both affected SB and LB dogs had a significantly increased FS and ESVI (FS% SB 45.6 + 8.04 versus 40.06 + 8.9, P < .05; FS% LB 33.64 + 8.61 versus 27.3 + 7.3 P < .05; ESVI SB 30.0 +/- 2.3 mL/m2 versus 21.18 +/- 13.9 mL/m2, P < .05; ESVI LB 83.22 +/- 43.84 mL/m2 versus 36.43 +/- 13.30 mL/m2 versus P < .001). The h/R in affected animals was decreased (0.53 +/- 0.11 versus 0.41 +/- 0.12, P < .05 SB; 0.47 +/- 0.11 versus 0.38 +/- 0.09, P < .05, LB). Data from this study indicate that dogs with moderate heart failure caused by CMVI have systolic dysfunction. Inadequate hypertrophy of the left ventricle may be, in part, responsible for this finding.

Decreased Systolic Function and Inadequate Hypertrophy in Large and Small Breed Dogs with Chronic Mitral Valve Insufficiency

Background: Systolic dysfunction associated with chronic mitral valve insufficiency (CMVI) has been demonstrated in experimental animal models and large breed (LB) dogs but has been reported as an uncommon finding in small breed (SB) dogs with naturally occurring disease. It has been suggested the myocardial failure could be, in part, because of an insufficient increase in left ventricular mass. Hypothesis: To test if SB and LB dogs with CMVI and moderate heart failure have systolic dysfunction and if they have adequate eccentric hypertrophy. Animals: Data from 38 SB and 18 LB dogs affected with CMVI were compared retrospectively with results from 2 groups of normal dogs (17 SB and 32 LB) Methods: Systolic function was investigated echocardiographically by using percentage fractional shortening (FS), the ratio between observed and expected end‐systolic diameter (ESD/ESDe), and end‐systolic volume index (ESVI). Left ventricular hypertrophy was estimated by using the ratio between the thickness of the left ventricular free wall and the radius in diastole (h/R). Results: Both affected SB and LB dogs had a significantly increased FS and ESVI (FS% SB 45.6 + 8.04 versus 40.06 + 8.9, P &lt; .05; FS% LB 33.64 + 8.61 versus 27.3 + 7.3 P &lt; .05; ESVI SB 30.0 ± 2.3 mL/m2 versus 21.18 ± 13.9 mL/m2, P &lt; .05; ESVI LB 83.22 ± 43.84 mL/m2 versus 36.43 ± 13.30 mL/m2 versus P &lt; .001). The h/R in affected animals was decreased (0.53 ± 0.11 versus 0.41 ± 0.12, P &lt; .05 SB; 0.47 ± 0.11 versus 0.38 ± 0.09, P &lt; .05, LB). Conclusions and Clinical Importance: Data from this study indicate that dogs with moderate heart failure caused by CMVI have systolic dysfunction. Inadequate hypertrophy of the left ventricle may be, in part, responsible for this finding.