Abstract 13171: Cellular Basis of Angiotensin-(1-7) Produced Augmentation on Left Ventricular Contractile Function in Heart Failure

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Xiaowei Zhang ◽  
Heng-Jie Cheng ◽  
Peng Zhou ◽  
Tiankai Li ◽  
Wei-Min Li ◽  
...  
Keyword(s):  
Heart Failure ◽  
Enzyme Inhibitor ◽  
Contractile Function ◽  
Heart Diseases ◽  
Cardiovascular Effects ◽  
Fold Increase ◽  
Left Ventricular ◽  
Inotropic Effects ◽  
Cardiac Depression ◽  
Hoe 140

Background: Accumulating evidence suggests that Angiotensin (A)-(1-7) exhibits cardiovascular effects that are in opposition to that of AII, thus providing protection against heart diseases. However, the exact means by which A-(1-7) affords cardioprotection are unclear. Its direct cardiac effect is not well understood. We previously showed that in heart failure (HF), AII decreases left ventricle (LV) contractility. Whether A-(1-7) may antagonize AII-induced cardiac depression, thereby contributing to its beneficial actions in HF remains to be determined. We assessed the hypothesis that A-(1-7) may produce positive modulation on [Ca 2+ ] i regulation and LV and myocyte contraction via A-(1-7) receptors, coupled with nitric oxide (NO)/bradykinin (BK)-mediated mechanism. Methods: We measured LV contractility changes after A-(1-7) (650 ng/kg, iv), which produced a 20-fold increase in plasma A-(1-7) levels, mimicking the elevations caused by angiotensin-converting enzyme inhibitor therapy in HF, and compared myocyte contractile, [Ca 2+ ] i transient ([Ca 2+ ] iT ) and I Ca,L responses to A-(1-7) (10 -5 M) in 14 rats with isoproterenol induced HF (3 months after 170 mg/kg sq for 2 days). In the subsets of cell contractile study, myocytes were pretreated to inhibit NO synthase (L-NAME, 10 -5 M), BK (HOE 140, 10 -6 M) or A-(1-7) receptor [D-Ala 7 ]-A-(1-7), 10 -5 M) followed with A-(1-7) exposure. Results: Compared with baseline, after A-(1-7), E ES (47%, 1.0 vs 0.68 mmHg/μl) and M SW (49%, 94.3 vs 62.8 mmHg) were increased, indicating enhanced LV contractility. In HF myocytes, A-(1-7) increased myocyte percent shortening (28%, 6.8% vs 5.3%), the velocity of contraction (31%, 106.4 vs 74.5 μm/sec) and relengthening (41%, 74.7vs 50.1 μm/sec) accompanied by significantly-increased [Ca 2+ ] iT (27%, 0.19 vs 0.15 pA/pF) and I Ca,L (24%, 6.3 vs 5.1pA/pF). L-NAME increased, HOE 140 decreased, and A-(1-7) receptor blockade prevented myocyte contractile responses to A-(1-7). Conclusion: In HF, clinically-relevant concentrations of A-(1-7) counteracted AII-induced cardiac depression, increased [Ca 2+ ] iT and I Ca,L , and produced positive inotropic effects in both LV and myocytes. These effects are coupled with A-(1-7) receptors and involve activation of NO/BK pathways.

Abstract 5248: Direct Cardiac Effect and Cellular Mechanism of Angiotensin-(1–7) in Heart Failure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Che-Ping Cheng ◽  
Peng Zhou ◽  
Heng-Jie Cheng ◽  
Michael Cross ◽  
William C Little
Keyword(s):  
Heart Failure ◽  
Enzyme Inhibitor ◽  
Cardiac Contractility ◽  
Cell Voltage ◽  
Fold Increase ◽  
Cardiac Effect ◽  
Inotropic Effects ◽  
Cardiac Depression ◽  
Hoe 140 ◽  
Myocyte Contractility

Angiotensin-(1–7) {A-(1–7)} plays an important role in counteracting various actions of angiotensin II (AII) in the heart. However, its effect on cardiac contractility remains controversial. We previously demonstrated that in heart failure (HF), AII decreases left ventricle (LV) contractility. Whether A-(1–7) may antagonize AII-induced cardiac depression, thereby contributing to the beneficial actions of angiotensin-converting enzyme inhibitor (ACEI) therapy in HF, remains undefined. We assessed the hypothesis that A-(1–7) may produce positive modulation on Ca 2+ current (I Ca,L ) and increase LV and myocyte contractility via A-(1–7) receptors, acting through nitric oxide (NO)/bradykinin (BK)-mediated mechanism. We measured LV contractility changes after A-(1–7) (650 ng/kg, iv), which produced more than a 20-fold increase in plasma A-(1–7) levels, mimicking the elevations caused by ACEI in HF patients, and compared myocyte contractile and I Ca,L responses to A-(1–7) (10 −5 M) in 12 rats with isoproterenol (ISO)-induced HF (3 months after 170 mg/kg sq for 2 days). LV contractility was measured by pressure-volume analysis. I Ca,L was measured using whole-cell voltage clamp technique. In additional contractile studies, myocytes were pretreated to inhibit either NO synthase (L-NAME, 10 −5 M), BK (HOE 140, 10 −6 M) or A-1–7 receptor (D-Ala 7 ]-A-(1–7), 10 −5 M) followed with A-(1–7) exposure. Compared with baseline , after A-(1–7), E ES (44%, 1.1 vs 0.74 mmHg/μl) and M sw (37%, 91.2 vs 66.5 mmHg) were increased, indicating enhanced LV contractility. In HF myocytes, A-(1–7) increased myocyte percent shortening (28%, 7.3% vs 5.7%), the velocity of cell contraction (31%, 110.4 vs 84.2 μm/sec) and relengthening (41%, 71.8 vs 51.1 μm/sec) accompanied by significantly-increased peak I Ca,L (21%, 6.3±0.2 vs 5.2±0.2 pA/pF). L-NAME increased, HOE 140 decreased, and A-(1–7) receptor blockade prevented myocyte contractile responses to A-(1–7). In HF, clinically-relevant concentrations of A-(1–7) counteracted AII-induced cardiac depression, increased I Ca,L , and produced positive inotropic effects in both LV and myocytes. These effects are coupled with A-(1–7) receptors and involve activation of NO/BK pathways.

Abstract 820: Autoregulation of CGRP Expression via β 2 -Adrenoreceptor Signaling in Intrinsic Cardiac Adrenergic Cells

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Vince Nguyen ◽  
Ignatius Gerardo Zarraga ◽  
Saurabh Rastogi ◽  
Yochai Birnbaum ◽  
Barry Uretsky ◽  
...  
Keyword(s):  
Gene Expression ◽  
Contractile Function ◽  
Cardiovascular Effects ◽  
Fold Increase ◽  
Left Ventricular ◽  
Mrna Levels ◽  
Opioid Agonist ◽  
Double Labeling ◽  
Adult Rat ◽  
Δ Opioid Receptor

Background : Calcitonin gene-related peptide (CGRP) is a neuropeptide with broad salutary cardiovascular effects. Mechanisms underlying cardiac CGRP regulation are poorly understood. The intrinsic cardiac adrenergic (ICA) cell is a novel cardiac neuroendocrine cell that expresses the δ-opioid receptor. We have shown that δ-opioid stimulation of ICA cells induces epinephrine liberation exerting an infarct-size limiting effect via β 2 -adrenoreceptor (β 2 -AR) stimulation. In this study we hypothesize that ICA cells synthesize and release CGRP which is involved in myocardial function and that CGRP gene expression can be autoregulated by epinephrine released from the ICA cell or regulated exogenously via β 2 -AR agonist. Methods and Results : In situ hybridization coupled with immunofluorescent double labeling localized CGRP mRNA expression exclusively to ICA cells in explanted human left ventricular tissue. To determine whether δ-opioid-enhanced epinephrine release from ICA cells autoregulates CGRP gene expression, isolated and cultured (for 2-weeks) adult rat ICA cells were treated with δ-opioid agonist DPDPE (0.1 μM for 1h) in the absence and presence of the β 2 -AR antagonist ICI-118551 (ICI, 10 μM). DPDPE induced 4-fold increase in CGRP mRNA at 6h post DPDPE-treatment by real-time PCR. This effect was abolished in the presence of ICI. To confirm the epinephrine-β 2 -AR signaling pathway, exogenous epinephrine was applied (0.1 μM for 1h) to ICA cells in the absence and presence of ICI (10 μM). Epinephrine induced 16-fold increase in CGRP mRNA levels at 6h post-treatment. This effect was completely abolished in the presence of ICI. To determine whether endogenous CGRP release from ICA cells exerts tonic modulation on myocyte contractile function, we studied the interaction between ICA cells and myocytes in ICA cell-myocyte co-culture model using a ratio fluorescent spectrometer. Application of CGRP-receptor antagonist CGRP 8 –37 (0.2 μM) reduced myocyte [Ca 2+ ]i transients by 30 ± 5%. Conclusion s: ICA cells exclusively express CGRP gene in human and animal hearts. Robust and sustained CGRP gene-expression can be induced via β 2 -AR signaling through autocrine epinephrine positive feedback or pharmacological β 2 -AR stimulation.

Abstract 3361: Progressive Left Ventricle, Myocyte Dysfunction, and Heart Failure in the Lethality of Anthrax Toxin in Conscious Dogs

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Che-Ping Cheng ◽  
Satoshi Masutani ◽  
Heng-Jie Cheng ◽  
Michael Cross ◽  
Chun-Xian Zhang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Pathologic Finding ◽  
Primary Role ◽  
Similar Time ◽  
Reduced Ejection Fraction ◽  
Cardiac Depression

Background . Bacillus anthracis ( BA ) infection is a cause of human and animal disease and associated with biowarfare. Although circulatory shock related to anthrax lethal toxin (LeTx) may play a primary role in lethality due to BA infection, its mechanisms are unclear. Methods . Six chronically-instrumented conscious dogs were assigned to receive a bolus injection of LeTx (10 ml saline with equivalent doses PA/LF, about 0.265 mg/kg, iv, n = 2) or saline (10 ml, iv, n = 4). Hemodynamic, left ventricular (LV) systolic and diastolic responses were determined periodically until 96 hours (h) in both groups. LV biopsies were performed at about 98H (before death). Isolated myocyte contractile function and histopathological alterations were determined. Results . Compared with control, in LeTx-treated animals, there were progressive decreases in LV contractility and slowed LV relaxation during the transition from LV dysfunction to heart failure (HF) over 96–98H. The cardiac depression was apparent about 6 – 8H after LeTx, but progressed through the subsequent 72–98H. At 72H after LeTx, heart rate (LeTx:129vsControl:95 bpm), LV end-diastolic pressure (P) (21vs9 mmHg), and the time constant of relaxation (40.9vs29.7 ms) were increased with markedly reduced ejection fraction, stroke volume (SV, 8.4vs15.8 ml), and end-systolic P (92vs118 mmHg). Moreover, LV contractility was decreased 49% (E ES , 4.1vs8.2 mmHg/ml and M SW , 44.9vs88.9 mmHg) with rightward shifts of LV P-V loops. At 96H, M SW , SV, and EF were further decreased accompanied by the development of severe HF. Pathologic finding of LV dilatation was associated with significantly increased length of LV myocytes (201±11vs122±13 μm). In LeTx-treated myocytes, there were about 46% reductions in cell contraction (79.0±9.7vs146.2±11.4 μm/s) and relaxation, respectively. LeTx produced lethality in dogs 4 days after LeTx treatment with similar time courses to those previously reported in man. Conclusions . LeTx causes direct and time-dependent progressive decrease in LV contractility, slow relaxation, cardiomyocyte dysfunction, LV, and myocyte remodeling and leads to HF, which suggests that the heart could be the primary target for the action of LeTx and plays an important role in lethality due to BA infection.

Abstract 1876: Functional Effect of Chronic Urotensin II Receptor Antagonist on L-Type Ca 2+ Current in Mouse Model of Progressive Heart Failure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Peng Zhou ◽  
Heng-Jie Cheng ◽  
Michael Cross ◽  
Michael F Callahan ◽  
Bridget Brosnihan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Receptor Antagonist ◽  
Weight Ratio ◽  
Heart Association ◽  
Cell Voltage ◽  
Fold Increase ◽  
Left Ventricular ◽  
Lv Function ◽  
List Type ◽  
Urotensin Ii

Voltage-gated Ca 2+ channels play fundamental roles in the regulation of cardiac function by various neurotransmitters. Recently, we have shown that urotensin II (UII), a potent vasoconstrictor, inhibits L-type Ca 2+ current (I Ca,L ) and produces negative inotropic action. In heart failure (HF), the UII-mediated pathway is upregulated, suggesting a therapeutic value of UII receptor antagonist (UII-ANT) for HF. However, the role and mechanism of chronic UII-ANT in HF is unclear. We tested the hypothesis that chronic UII-ANT may improve cardiac I Ca,L , preventing β-adrenergic deregulation on I Ca,L and limit HF progression. We examined plasma levels of norepinephrine (NE), left ventricular (LV) function, and myocyte I Ca,L responses to isoproterenol (ISO) in 3 age-matched groups of mice: HF (n = 7), 2 months after ISO (150 mg/kg sq for 2 days); HF/UII-ANT (n = 11), 1 month after receiving ISO, then urantide, a potent UII-ANT (10 −5 M/kg/day, sq via implanted osmotic mini pump), given for 1 month; and Controls (n = 7). I Ca,L was measured using whole-cell voltage clamp technique. Compared with controls, ISO-treated mice progressed to HF with 4.7-fold increase in plasma NE (18975 vs 4066 pg/ml) and LV dilatation associated with increased myocyte length (ML, 155 vs120 μm) and heart-to-body weight ratio (H/BW, 7.6 vs 5.5 g/kg). Stroke volume (SV, 30.3 vs 61.4 μl) and ejection fraction (EF, 39% vs 60%) were decreased. Compared with normal myocytes, in HF myocytes, I Ca,L was reduced (50%, 3.7 ± 0.2 vs 7.4 ± 0.2 pA/pF), and I Ca,L response to β-AR stimulation (ISO, 10 −8 M) was attenuated (11% vs 35%) (p < 0.01). In HF/UII-ANT mice, plasma NE (5148 pg/ml), SV (57.9 μl), and EF (57%) returned close to control levels with retained normal ML (124 μm) and H/BW (5.9 g/kg). Moreover, compared with controls, in HF/UII-ANT mice, ISO caused similar increases in the peak I Ca,L (32% vs 35%). Chronic UII-ANT treatment normalizes LV L-type Ca 2+ channel basal function and β-adrenergic regulation, leading to regression of LV and myocyte dysfunction and remodeling in mice with ISO-induced HF. This research has received full or partial funding support from the American Heart Association, AHA National Center.

Abstract 16574: Heart Failure Biomarkers (NT-proBNP, Gal-3, sST2) Correlate With Right Ventricular Systolic Pressure and Provide Insight to Poor CRT Response: A BIOCRT Substudy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Roderick C Deaño ◽  
Jackie Szymonifka ◽  
Qing Zhou ◽  
Jigar H Contractor ◽  
Zachary Lavender ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Fold Increase ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Cardiac Transplant ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Crt Response

Objective: Patients with heart failure (HF) and pulmonary hypertension (PH) have worse outcomes after cardiac resynchronization therapy (CRT). The relationship of circulating HF biomarkers and right ventricular systolic pressure (RVSP) may provide insight to the mechanism between PH and poor CRT response. Methods: In 90 patients (age 65 ± 13, 78% male, EF 26 ± 8%, RVSP 44 ± 12 mmHg) undergoing CRT, we measured baseline RVSP by echocardiography and obtained peripheral blood samples drawn at the time of device implantation. We measured levels of established and emerging HF biomarkers (Table 1). CRT non-response was defined as no improvement of adjudicated HF Clinical Composite Score at 6 months. Major adverse cardiac event (MACE) was defined as composite endpoint of death, cardiac transplant, left ventricular assist device, and HF hospitalization within 2 years. Results: There were 34% CRT non-responders and 27% had MACE. Per 1 unit increase in log-transformed RVSP, there was an 11-fold increase risk of having CRT non-response (odd ratio [OR] 11.0, p=0.01) and over 5-fold increase of developing 2-year MACE (hazard ratio [HR] 5.8, p=0.02). When comparing patients with severe PH (RVSP>60 mmHg) to those without PH (RVSP < 35 mmHg), there was an 8-fold increase in CRT nonresponse (OR 8.4, p=0.03) but no difference in MACE (p=NS). RVSP was correlated with increased biomarker levels of myocardial stretch and fibrosis, but not myocardial necrosis (Table 1). Conclusions: Higher RVSP is associated with greater rates of CRT non-response and adverse clinical outcomes. The mechanistic association between severe PH and CRT nonresponse may be explained by the biomarker profile reflective of myocardial wall stretch and fibrosis.

scholarly journals Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications

2021 ◽  
Vol 12 ◽  
Author(s):  
Ke Si ◽  
Chijing Wei ◽  
Lili Xu ◽  
Yue Zhou ◽  
Wenshan Lv ◽  
...  
Keyword(s):  
Heart Failure ◽  
Vascular Inflammation ◽  
Cardiovascular Effects ◽  
Daily Practice ◽  
Left Ventricular ◽  
Therapeutic Interventions ◽  
Current Evidence ◽  
Free Oxygen Radical ◽  
Positive Role ◽  
Therapeutic Implications

The association between hyperuricemia and cardiovascular disease (CVD) has been reported and studied in the past two decades. Xanthine oxidase (XO) induced uric acid (UA) serves as a risk factor and has the independent prognostic and functional impact of heart failure (HF), but whether it plays a positive role in the pathogenesis of HF has remained unclear. Growing evidence suggest the up-regulated XO avtivity and increased production of free oxygen radical (ROS) correspondingly are the core pathogenesis of HF with hyperuricemia, which results in a whole cluster of pathophysiologic cardiovascular effects such as oxidative stress, endothelial dysfunction, vascular inflammation, left ventricular (LV) dysfunction as well as insulin resistance (IR). The use of XO inhibition represents a promising therapeutic choice in patients with HF due to its dual effect of lowering serum UA levels as well as reducing ROS production. This review will discuss the pathophysiologic mechanisms of hyperuricemia with HF, the targeted therapeutic interventions of UA lowering therapies (ULT) with XO inhibition and mechanism underlying beneficial effects of ULT. In addition, the review also summarizes current evidence on the role of ULT in HF and compares CV risk between allopurinol and febuxostat for practical and clinical purposes. Guidelines and implementation of CV risk management in daily practice will be discussed as well.

scholarly journals Positive Inotropic Effects of ATP Released via the Maxi-Anion Channel in Langendorff-Perfused Mouse Hearts Subjected to Ischemia-Reperfusion

2021 ◽  
Vol 9 ◽  
Author(s):  
Hiroshi Matsuura ◽  
Akiko Kojima ◽  
Yutaka Fukushima ◽  
Yu Xie ◽  
Xinya Mi ◽  
...  
Keyword(s):  
Contractile Function ◽  
Organic Anion ◽  
Left Ventricular ◽  
Transient Increase ◽  
Tyrode Solution ◽  
Inotropic Effects ◽  
Cl Channel ◽  
Short Period ◽  
Cl Channels ◽  
Normal Tyrode Solution

The organic anion transporter SLCO2A1 constitutes an essential core component of the ATP-conductive large-conductance anion (Maxi-Cl) channel. Our previous experiments using Langendorff-perfused mouse hearts showed that the Maxi-Cl channel contributes largely to the release of ATP into the coronary effluent observed during 10-min reperfusion following a short period (6 min) of oxygen-glucose deprivation. The present study examined the effect of endogenous ATP released via Maxi-Cl channels on the left ventricular contractile function of Langendorff-perfused mouse hearts, using a fluid-filled balloon connected to a pressure transducer. After the initial 30-min stabilization period, the heart was then perfused with oxygen-glucose-deprived Tyrode solution for 6 min, which was followed by a 10-min perfusion with oxygenated normal Tyrode solution in the absence and presence of an ATP-hydrolyzing enzyme, apyrase, and/or an adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). In the absence of apyrase and DPCPX, the left ventricular developed pressure (LVDP) decreased from a baseline value of 72.3 ± 7.1 to 57.5 ± 5.5 mmHg (n = 4) at the end of 6-min perfusion with oxygen-glucose-deprived Tyrode solution, which was followed by a transient increase to 108.5 ± 16.5 mmHg during subsequent perfusion with oxygenated normal Tyrode solution. However, in the presence of apyrase and DPCPX, the LVDP decreased to the same degree during 6-min perfusion with oxygen-glucose-deprived Tyrode solution, but failed to exhibit a transient increase during a subsequent perfusion with oxygenated normal Tyrode solution. These results strongly suggest that endogenous ATP released through Maxi-Cl channels contributes to the development of transient positive inotropy observed during reperfusion after short-period hypoxia/ischemia in the heart.

scholarly journals Effect of Acute Hyperglycemia on Left Ventricular Contractile Function in Diabetic Patients with and without Heart Failure: Two Randomized Cross-Over Studies

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e53247 ◽  
Author(s):  
Roni Nielsen ◽  
Helene Nørrelund ◽  
Ulla Kampmann ◽  
Hans Erik Bøtker ◽  
Niels Møller ◽  
...  
Keyword(s):  
Heart Failure ◽  
Contractile Function ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Acute Hyperglycemia

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.

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