scholarly journals Clinical and necropsy evaluation of endocardial fibroelastosis in a mixed-breed cat with left side heart failure

2022 ◽  
Author(s):  
T Yoshida ◽  
C Chieh-Jen ◽  
ASA Mandour ◽  
HAMM Hendawy ◽  
N Machida ◽  
...  
Keyword(s):  
Heart Failure ◽  
Respiratory Distress ◽  
Severe Congestive Heart Failure ◽  
Left Ventricular ◽  
Doppler Imaging ◽  
Endocardial Fibroelastosis ◽  
Ventricular Contractility ◽  
Mixed Breed ◽  
Fractional Shortening ◽  
Echocardiographic Findings

A two-month-old, male intact, mixed-breed cat weighing 0.6 kg was presented with respiratory distress and anorexia. From the transthoracic echocardiographic, reduced fractional shortening (FS) and increased endocardial echogenicity were recognised with severe congestive heart failure (CHF). The kitten was administered an antibiotic and pimobendane under oxygen supplementation in an ICU cage. However, the respiratory condition worsened and the cat died the next day, and the subsequent necropsy and histopathology examinations confirmed endocardial fibroelastosis (EFE). There is a lack of information regarding the antemortem cardiac function evaluated by tissue Doppler imaging (TDI) in EFE cases. We report on the echocardiographic findings including the TDI in the EFE cat with a concomitant necropsy and histopathology confirmation in this paper. The echocardiographic findings showed presence of a ventricular false tendon within the left ventricle, a decrease in the left ventricular contractility (FS 11.1%, and a marked CHF). In this case, the echocardiographic findings were consistent with the human counterpart. However, these findings were like those of dilated cardiomyopathy and, hence, non-specific to EFE. As a result, veterinarians should keep in mind that endocardial fibroelastosis might be a possible reason for respiratory distress resulting from CHF with a low fractional shortening in young cats.

DECREASED LEFT VENTRICULAR CONTRACTILITY AND VENTRICULAR-ARTERIAL MATCHING INDEX CORRELATION WITH N-TERMINAL PRO B-TYPE NATRIURETIC PEPTIDE IN HEART FAILURE

2015 ◽  
Vol 15 (02) ◽  
pp. 1540016 ◽  
Author(s):  
LIANG ZHONG ◽  
YI-JIA WANG ◽  
FEI-QIONG HUANG ◽  
DHANJOO GHISTA ◽  
RU-SAN TAN
Keyword(s):  
Heart Failure ◽  
Stroke Volume ◽  
Natriuretic Peptide ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Doppler Imaging ◽  
Ventricular Contractility ◽  
Arterial Elastance ◽  
Heart Failure Patients ◽  
Matching Index

This study is aimed to assess (1) Left ventricle (LV) contractile function and ventricular-arterial matching from echocardiography; (2) whether ventricular-arterial matching (VAM) is associated with N-terminal pro B-type natriuretic peptide (NT-proBNP), and stroke output in patients with heart failure. Normal subjects (n = 81) and heart failure patients (n = 80) underwent echocardiography, Doppler echocardiography and tissue Doppler imaging. Only heart failure patients underwent blood test for NT-proBNP. The LV contractility was calculated as dσ ⁎ /dt max = 3 × (dV/dt) max /2V m = 3 × V peak × (π × D2/4)/(2V m ), and the arterial elastance was calculated as Ea = SBP × 0.9/ SV , wherein V peak and D are peak velocity and diameter of LV outflow tract, Vm is myocardial volume, SBP is the systolic blood pressure and SV is stroke volume measured from LVOT. The VAM index was expressed as the ratio of LV contractility to arterial elastance (dσ ⁎ /dt max /Ea). We found that HF patients had (i) decreased dσ ⁎ /dt max (1.46 ± 0.73 versus 4.06 ± 1.06 s-1), (ii) increased Ea (2.90 ± 0.87 versus 1.81 ± 0.38 mmHg/mL), and (iii) attenuated ventricular-arterial matching index (0.66 ± 0.57 versus 2.38 ± 0.91 mL/mmHg⋅s) (all p < 0.001) compared with normal subjects. The VAM index was correlated inversely with NT-proBNP (r = -0.32, p < 0.05), but positively with the stroke volume (r = 0.85, p < 0.001). The VAM index of < 1.51 was able to clearly differentiate the failing heart from normal hearts (AUC = 0.959, Sensitivity = 0.911, Specificity = 0.905). Heart failure patients demonstrated impaired ventricular contractility, enhanced arterial stiffening, and attenuated ventricular-arterial matching index. The attenuated ventricular-arterial matching index value was associated with elevated NT-proBNP levels and lower cardiac output.

scholarly journals Myocardial work index: a marker of left ventricular contractility in pressure‐induced or volume overload‐induced heart failure

2021 ◽  
Author(s):  
Bálint Károly Lakatos ◽  
Mihály Ruppert ◽  
Márton Tokodi ◽  
Attila Oláh ◽  
Szilveszter Braun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Work Index

scholarly journals An Adult Mouse Model of Dilated Cardiomyopathy Caused by Inducible Cardiac-Specific Bis Deletion

2021 ◽  
Vol 22 (3) ◽  
pp. 1343
Author(s):  
Hye Hyeon Yun ◽  
Soon Young Jung ◽  
Bong Woo Park ◽  
Ji Seung Ko ◽  
Kyunghyun Yoo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Late Onset ◽  
Small Heat Shock Protein ◽  
Left Ventricular ◽  
Therapeutic Interventions ◽  
Ventricular Contractility ◽  
Knock Out ◽  
Multifunctional Protein ◽  
Cell Death Suppressor

BCL-2 interacting cell death suppressor (BIS) is a multifunctional protein that has been implicated in cancer and myopathy. Various mutations of the BIS gene have been identified as causative of cardiac dysfunction in some dilated cardiomyopathy (DCM) patients. This was recently verified in cardiac-specific knock-out (KO) mice. In this study, we developed tamoxifen-inducible cardiomyocyte-specific BIS-KO (Bis-iCKO) mice to assess the role of BIS in the adult heart using the Cre-loxP strategy. The disruption of the Bis gene led to impaired ventricular function and subsequent heart failure due to DCM, characterized by reduced left ventricular contractility and dilatation that were observed using serial echocardiography and histology. The development of DCM was confirmed by alterations in Z-disk integrity and increased expression of several mRNAs associated with heart failure and remodeling. Furthermore, aggregation of desmin was correlated with loss of small heat shock protein in the Bis-iCKO mice, indicating that BIS plays an essential role in the quality control of cardiac proteins, as has been suggested in constitutive cardiac-specific KO mice. Our cardiac-specific BIS-KO mice may be a useful model for developing therapeutic interventions for DCM, especially late-onset DCM, based on the distinct phenotypes and rapid progressions.

Importance of antioxidant and antiapoptotic effects of β-receptor blockers in heart failure therapy

2004 ◽  
Vol 287 (3) ◽  
pp. H1003-H1012 ◽  
Author(s):  
Keisuke Kawai ◽  
Fuzhong Qin ◽  
Junya Shite ◽  
Weike Mao ◽  
Shuji Fukuoka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Cardiac Pacing ◽  
Left Ventricular ◽  
Beneficial Effects ◽  
Myocyte Apoptosis ◽  
Adrenergic Blocking ◽  
Fractional Shortening

The present study was carried out to determine whether beneficial effects of carvedilol in congestive heart failure (CHF) are mediated via its β-adrenergic blocking, antioxidant, and/or α-adrenergic blocking action. Rabbits with heart failure induced by rapid cardiac pacing were randomized to receive subcutaneous carvedilol, metoprolol, propranolol plus doxazosin, or placebo pellets for 8 wk and compared with sham-operated rabbits without pacing. We found rapid cardiac pacing produced clinical heart failure, left ventricular dilation, and decline of left ventricular fractional shortening. This was associated with an increase in left ventricular end-diastolic pressure, decrease in left ventricular first derivative of left ventricular pressure, and myocyte hypertrophy. Tissue oxidative stress measured by GSH/GSSG was increased in the heart with increased oxidation product of mitochondrial DNA, 8-oxo-7,8-dihydro-2′-deoxyguanosine, increase of Bax, decrease of Bcl-2, and increase of apoptotic myocytes as measured by anti-single-stranded DNA monoclonal antibody. Administration of carvedilol and metoprolol, which had no effect in sham animals, attenuated cardiac ventricular remodeling, cardiac hypertrophy, oxidative stress, and myocyte apoptosis in CHF. In contrast, propranolol plus doxazosin, which has less antioxidant effects, produced smaller effects on left ventricular function and myocyte apoptosis. In all animals, GSH/GSSG correlated significantly with changes of left ventricular end-diastolic dimension ( r = −0.678, P < 0.0001), fractional shortening ( r = 0.706, P < 0.0001), and apoptotic myocytes ( r = −0.473, P = 0.0001). Thus our findings suggest antioxidant and antiapoptotic actions of carvedilol and metoprolol are important determinants of clinical beneficial effects of β-receptors in the treatment of CHF.

Cardiomyopathy, oxidative stress and impaired contractility in a rheumatoid arthritis mouse model

Heart ◽  
2018 ◽  
Vol 104 (24) ◽  
pp. 2026-2034 ◽  
Author(s):  
Gianluigi Pironti ◽  
Alex Bersellini-Farinotti ◽  
Nilesh M Agalave ◽  
Katalin Sandor ◽  
Teresa Fernandez-Zafra ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Heart Failure ◽  
Mouse Model ◽  
Posttranslational Modifications ◽  
Contractile Function ◽  
Joint Inflammation ◽  
Left Ventricular ◽  
Increased Risk ◽  
Fractional Shortening

ObjectivesPatients with rheumatoid arthritis (RA) display an increased risk of heart failure independent of traditional cardiovascular risk factors. To elucidate myocardial disease in RA, we have investigated molecular and cellular remodelling of the heart in an established mouse model of RA.MethodsThe collagen antibody-induced arthritis (CAIA) RA mouse model is characterised by joint inflammation and increased inflammatory markers in the serum. We used CAIA mice in the postinflammatory phase that resembles medically controlled RA or RA in remission. Hearts were collected for cardiomyocyte isolation, biochemistry and histology analysis.ResultsHearts from mice subjected to CAIA displayed hypertrophy (heart/body weight, mean±SD: 5.9±0.8vs 5.1±0.7 mg/g, p<0.05), fibrosis and reduced left ventricular fractional shortening compared with control. Cardiomyocytes from CAIA mice showed reduced cytosolic [Ca2+]i transient amplitudes (F/F0, mean±SD: 3.0±1.2vs 3.6±1.5, p<0.05) that was linked to reductions in sarcoplasmic reticulum (SR) Ca2+ store (F/F0, mean±SD: 3.5±1.3vs 4.4±1.3, p<0.01) measured with Ca2+ imaging. This was associated to lower fractional shortening in the cardiomyocytes from the CAIA mice (%FS, mean±SD: 3.4±2.2 vs 4.6%±2.3%, p<0.05). Ca2+ handling proteins displayed oxidation-dependent posttranslational modifications that together with an increase in superoxide dismutase expression indicate a cell environment with oxidative stress.ConclusionsThis study shows that inflammation during active RA has long-term consequences on molecular remodelling and contractile function of the heart, which further supports that rheumatology patients should be followed for development of heart failure.

Abstract 1604: Response to Cardiac Resynchronization Therapy Differs Between Patients With and Without Previous Right Ventricular Pacing

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Andrea M Thelen ◽  
Christopher L Kaufman ◽  
Kevin V Burns ◽  
Daniel R Kaiser ◽  
Aaron S Kelly ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Resynchronization Therapy ◽  
Systolic Function ◽  
Radial Strain ◽  
Left Ventricular ◽  
Doppler Imaging ◽  
Cardiac Resynchronization ◽  
Resynchronization Therapy ◽  
Peak Displacement

Background: Previous large studies on the effects of cardiac resynchronization therapy (CRT) in patients with heart failure have generally excluded patients previously paced from the right ventricle (RV). Previously RV paced patients (RVp) can exhibit an iatrogenic cause of dyssynchrony and reduced systolic function and thus, may respond differently to CRT than patients not previously RV paced (nRVp). The purpose of this study was to test the hypothesis that RVp patients have greater improvements in left ventricular systolic function, volumes, and dyssynchrony in response to CRT than nRVp. Methods: Standard echocardiograms with tissue Doppler imaging were performed before and after chronic CRT in RVp (n = 21, 16 male) and nRVp (n = 70, 54 male) heart failure patients. Ejection fraction (EF), left ventricular end diastolic (LVEDV) and systolic (LVESV) volumes were calculated using the biplane Simpson’s method. Longitudinal dyssynchrony was calculated as the standard deviation of time to peak displacement (TT-12) of 12 segments in the apical views. Using mid-ventricular short axis views and speckle-tracking methods, radial dyssynchrony (Rad dys ) was calculated as the maximal time difference between six myocardial segments for peak radial strain. Echo response was defined as ≥ 15% reduction in LVESV. Results are reported as mean ± SD. Results: Significant baseline differences (p < 0.05) were observed between groups (RVp vs. nRVp) for age (74 ± 13 vs. 67 ± 13 year), follow-up time (6.1 ± 1.8 vs. 4.6 ± 2.1 months), LVEDV (154.3±50.8 vs.185.3±56.9 mL), and a trend for LVESV (112.4 ± 40.6 vs. 134.9 ± 47 mL, p = 0 .05). No differences were observed for EF, etiology of heart failure, and dyssynchrony measures between groups at baseline. Echo response rate was significantly ( p < 0.05) greater in RVp (76%) than nRVp (57%). After adjusting for baseline differences, RVp had greater improvement in EF (14 ± 9 vs. 8 ± 7%, p < 0.05) and LVESV (−33 ± 18 vs. −20 ± 21%, p < 0.05). After adjustment for follow-up time, no difference was observed for change in dyssynchrony between groups. Conclusion: RVp patients upgraded to CRT exhibit greater improvements in systolic function and ventricular remodeling as compared to nRVp patients.

Abstract 306: Proinflammatory Prostaglandin E Impairs Adrenergic Contractility in Animal Hearts

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Yang K Xiang
Keyword(s):  
Heart Failure ◽  
Plasma Membrane ◽  
Calcium Signaling ◽  
Contractile Response ◽  
Left Ventricular ◽  
Prostaglandin E ◽  
Intracellular Camp ◽  
Ventricular Contractility ◽  
Adrenergic Stimulation ◽  
Phosphodiesterase 4

Introduction: Inflammation is a major risk factor for heart failure; inflammatory prostaglandin E is elevated in myocardium, and has been associated with development of heart failure via cardiac LV remodeling, but the mechanisms remain unclear. Hypothesis: We hypothesize that proinflammatory prostaglandin signaling might affect Left ventricular contractility by directly impairing β-adrenergic (βAR) signaling. Methods and Results: Pretreatment with Prostaglandin E impairs intracellular PKA phosphorylation of substrates in myocardium and cardiac contractile responses under β-adrenergic stimulation. Both prostaglandin E and β-adrenergic agonist isoproterenol induce intracellular cAMP activities in myocytes. However, the cAMP signal under prostaglandin stimulation is confined along the plasma membrane whereas the cAMP signal under isoproterenol stimulation is distributed throughout the cells, including the intracellular sarcoplasmic reticulum (SR), a calcium storage compartment critical for myocyte calcium signaling and contractile response. Interestingly, the prostaglandin E-induced cAMP signal is sufficient for PKA activation, leading phosphorylation and activation of phosphodiesterase 4 on the plasma membrane, a group of enzymes associated with membrane βARs for cAMP degradation. Moreover, pretreatment of prostaglandin E prevents dissociation of phosphodiesterase 4 from βAR induced by isoproterenol, a step necessary for cAMP diffusion from the plasma membrane to the intracellular SR. Together, prostaglandin E induces activation of phosphodiesterase 4 in βAR complex and prevents the cAMP diffusion from the plasma membrane to the SR under isoproterenol stimulation, and inhibits calcium signaling and contractile response in myocytes and animal hearts. Conclusions: This study provides a novel mechanism underlying the phosphodiesterase-mediated signaling crosstalk between two neurohormonal stimulation in myocardium under chronic conditions, and suggests that proinflammatory prostaglandin signaling may impair β-adrenergic contractile in the development of heart failure.

Abstract 17177: Furosemide Promotes Myocardial Fibrosis in Swine Heart Failure

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nisha Plavelil ◽  
Mark C Haigney ◽  
Robert E Goldstein ◽  
Michael Klein ◽  
Matie Shou ◽  
...  
Keyword(s):  
Heart Failure ◽  
Myocardial Fibrosis ◽  
Left Ventricular ◽  
Swine Model ◽  
Signaling Proteins ◽  
Ecm Remodeling ◽  
Animal Care ◽  
Pai 1 ◽  
Fractional Shortening

Introduction: Although frequently used in heart failure (HF), long-term furosemide exacerbates HF in a swine model. This paradoxical phenomenon may reflect furosemide-induced alterations in signaling proteins of the extracellular matrix (ECM) to increase fibrosis. Examination of the ECM may clarify how treatments like furosemide enhance the progression of HF. Hypothesis: The administration of furosemide increased inflammation and fibrosis of the heart, leading to accelerated HF deterioration in a swine model. Methods: After Institutional Animal Care and Use Committee (IACUC) approval, Yorkshire swine (N=10, 5 = furosemide, 5 = saline) were paced 3 to 5 weeks at 200 beats per minute to induce HF (left ventricular fractional shortening <16% on echocardiogram). Animals were treated with furosemide (1 mg/kg intramuscularly) or saline. Western Blot and histology with Masson’s trichrome stain were performed on transmural LV myocardium to quantify critical determinants of fibrosis. ANOVA with Tukey HSD correction and descriptive statistics were performed using SPSS with significance by α of 0.05; mean ± SEM. Results: The overall increase in ECM fibrosis in HF was clearly demonstrated on Masson’s trichrome histology associated with significant, uniform increase in signaling pathways leading to fibrosis associated with furosemide use. SMAD 2-HF Furosemide to Control (p<.05): HF Furosemide 0.266 ±.05, HF Saline 0.183±.02, Control 0.163±.01 ERK-all (p<.05): HF Furosemide 0.312±.02, HF Saline 0.209±.01,Control 0.149±.01 GDF-15-HF Furosemide to Control (p<.05): HF Furosemide 0.095 ±.00, HF Saline 0.073±.01, Control 0.062±.01 MMP-14-all (p<.05): HF Furosemide 0.451±.02, HF Saline 0.374±.03,Control 0.231±.02 TIMP-1-all (p<.05): HF Furosemide 0.184±.01, HF Saline 0.0135±.03,Control 0.033±.01 PAI-1-all (p<.05): HF Furosemide 0.105±.01, HF Saline 0.046±.01,Control 0.043±.00 Conclusions: Histologic and biochemical analysis showed worsening HF in furosemide-treated paced swine was associated with consistent increases in fibrosis and indices of adverse ECM remodeling. The diuretic intended to reduce water retention during HF appeared to enhance myocardial fibrosis, paradoxically accelerating pathological processes responsible for HF.

Sign in / Sign up

Export Citation Format

Share Document