scholarly journals Adiponectin Ameliorates Endotoxin-Induced Acute Cardiac Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Yoshio Watanabe ◽  
Rei Shibata ◽  
Noriyuki Ouchi ◽  
Takahiro Kambara ◽  
Koji Ohashi ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Contractile Function ◽  
Myocardial Dysfunction ◽  
Systolic Dysfunction ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Systemic Delivery ◽  
Lv Dysfunction ◽  
Soluble Tnf Receptor

Background. Obesity is a risk factor for cardiovascular disease. Increasing evidence suggests that reduced levels of the adipocyte-derived plasma protein adiponectin are associated with an increased cardiovascular risk. Here, we examined the effects of adiponectin on lipopolysaccharide- (LPS-) induced acute cardiac injuryin vivo.Methods and Results. A single dose of LPS (10 mg/kg) was intraperitoneally injected into wild-type (WT) and adiponectin-knockout (APN-KO) mice. Following LPS administration, APN-KO mice had exacerbation of left ventricular (LV) systolic dysfunction compared with WT mice. Administration of LPS to WT and APN-KO mice led to an increased expression of inflammatory cytokines including TNF-αand IL-6 in the heart, but the magnitude of this induction was greater in APN-KO mice compared to WT mice. Systemic delivery of an adenoviral vector expressing adiponectin (Ad-APN) improved LPS-induced LV dysfunction in APN-KO mice, and this effect was accompanied by the reduced expression of TNF-αand IL-6 in the heart. Administration of etanercept, a soluble TNF receptor abolished the reduced LV contractile function in response to LPS in APN-KO mice.Conclusion. These results suggest that adiponectin protects against LPS-induced acute cardiac injury by suppressing cardiac inflammatory responses, and could represent a potential therapeutic target in sepsis-associated myocardial dysfunction.

β-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger

2011 ◽  
Vol 111 (5) ◽  
pp. 1242-1248 ◽  
Author(s):  
Damien Vitiello ◽  
Julien Boissière ◽  
Grégory Doucende ◽  
Sandrine Gayrard ◽  
Anne Polge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Troponin I ◽  
Ex Vivo ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Strenuous Exercise ◽  
Lv Dysfunction ◽  
Cardiac Fatigue

Prolonged strenuous exercise (PSE) induces transient left ventricular (LV) dysfunction. Previous studies suggest that β-adrenergic pathway desensitization could be involved in this phenomenon, but it remains to be confirmed. Moreover, other underlying mechanisms involving oxidative stress have been recently proposed. The present study aimed to evaluate the involvement of both the β-adrenergic pathway and NADPH oxidase (Nox) enzyme-induced oxidative stress in myocardial dysfunction in rats following PSE. Rats were divided into 4 groups: controls (Ctrl), 4-h exercised on treadmill (PSE), and 2 groups in which Nox enzyme was inhibited with apocynin treatment (Ctrl APO and PSE APO, respectively). We evaluated cardiac function in vivo and ex vivo during basal conditions and isoproterenol stress. GSH/GSSG ratio, cardiac troponin I (cTnI) release, and lipid peroxidation (MDA) were evaluated. PSE induced a decrease in LV developed pressure, intrinsic myocardial contractility, and relaxation associated with an increase in plasma cTnI release. Our in vivo and ex vivo results demonstrated no differences in myocardial response to isoproterenol and of effective dose 50 between control and PSE rats. Interestingly, the LV dysfunction was reversed by apocynin treatment. Moreover, apocynin prevented cellular oxidation [GSH/GSSG ratio: PSE APO rats vs. PSE rats in arbitrary units (au): 1.98 ± 0.07 vs. 1.35 ± 0.10; P < 0.001]. However, no differences in MDA were observed between groups. These data suggest that myocardial dysfunction observed after PSE was not due to β-adrenergic receptor desensitization but could be due to a signaling oxidative stress from the Nox enzyme.

Abstract 13928: Subclinical Myocardial Dysfunction With Coronavirus Disease 2019

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Jordan B Strom ◽  
Lila M Martin ◽  
Sarah E Fostello ◽  
James D Chang ◽  
Connie W Tsao ◽  
...  
Keyword(s):  
Left Ventricular Systolic Dysfunction ◽  
Myocardial Dysfunction ◽  
Systolic Dysfunction ◽  
Global Longitudinal Strain ◽  
Cardiac Injury ◽  
Multivariable Analysis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Multicenter Studies ◽  
Ventricular Ejection Fraction

Background: Coronavirus disease 2019 (COVID-19) is associated with cardiac injury and overt myocardial dysfunction. However, whether COVID-19 is associated with subclinical myocardial dysfunction is unknown. Methods: We evaluated patients hospitalized for COVID-19 referred for transthoracic echocardiography (TTE), between March 17 and May 22, 2020, with a left ventricular ejection fraction (LVEF) ≥ 50%. Controls in a 1:1 ratio were selected from patients receiving TTE during the same month. Global longitudinal strain (GLS) was used to assess the association of COVID-19 and subclinical myocardial disease. Results: Among 99 patients (49 cases, 50 controls), average GLS was significantly reduced in cases vs. controls (mean ± SD, -14.8 ± 4.0% vs. -21.1 ± 4.0%, p < 0.0001). A total of 82.8% of cases vs. 7.1% of controls had an average GLS below normal (> 18%; p < 0.0001), which persisted despite multivariable adjustment ( Table ). Among COVID-19 patients with a prior TTE, absolute average GLS decreased 3.2% (p = 0.008) despite no change in LVEF (p = 0.41). Average GLS was reduced in non-survivors compared with survivors (p = 0.04), though only septal wall thickness (p = 0.03) was associated with in-hospital mortality on multivariable analysis. Conclusions: Among hospitalized patients receiving TTE, COVID-19 is independently associated with subclinical left ventricular systolic dysfunction in the vast majority of patients, and subclinical LV dysfunction is associated with survival. The clinical implications of these findings should be evaluated in future longitudinal multicenter studies.

Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage

2006 ◽  
Vol 105 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Nader Banki ◽  
Alexander Kopelnik ◽  
Poyee Tung ◽  
Michael T. Lawton ◽  
Daryl Gress ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Recovery Rate ◽  
Time Course ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Lv Function ◽  
Ventricular Systolic Dysfunction ◽  
Lv Dysfunction

Object Subarachnoid hemorrhage (SAH) has been associated with cardiac injury and left ventricular (LV) dysfunction. The incidence and natural history of neurocardiogenic injury after SAH remains poorly understood. The objective of this study was to describe the incidence, time course, recovery rate, and segmental patterns of LV dysfunction after SAH. Methods Echocardiography was performed three times over a 7-day period in 173 patients with SAH. The incidence of global (ejection fraction [EF] < 50%) and segmental (any regional wall-motion abnormality [RWMA]) LV dysfunction was measured. The time course of LV dysfunction was determined by comparing the prevalence of LVEF less than 50% and RWMA at 0 to 2, 3 to 5, and 6 to 8 days after SAH. The recovery rate was defined as the proportion of patients with partial or complete normalization of function. The distribution of RWMAs among 16 LV segments was also determined. An LVEF less than 50% was found in 15% of patients, and 13% had an RWMA with a normal LVEF. There was a trend toward increased dysfunction at 0 to 2 days after SAH, compared with 3 to 8 days after SAH. Recovery of LV function was observed in 66% of patients. The most frequently abnormal LV segments were the basal and middle ventricular portions of the anteroseptal and anterior walls. The apex was rarely affected. Conclusions Left ventricular systolic dysfunction occurs frequently after SAH and usually improves over time. The observed segmental patterns of LV dysfunction often do not correlate with coronary artery distributions.

scholarly journals Reversible Myocardial Injury and Intraventricular Thrombus Associated with Aluminium Phosphide Poisoning

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Abdelkader Jalil El Hangouche ◽  
Hala Fennich ◽  
Oumaima Alaika ◽  
Taoufiq Dakka ◽  
Zaineb Raissouni ◽  
...  
Keyword(s):  
Cardiovascular Magnetic Resonance ◽  
Magnetic Resonance ◽  
Transthoracic Echocardiography ◽  
Left Ventricular Systolic Dysfunction ◽  
Myocardial Dysfunction ◽  
Systolic Dysfunction ◽  
Cardiac Injury ◽  
Symptomatic Treatment ◽  
Left Ventricular ◽  
Aluminium Phosphide

Aluminium phosphide (ALP) is widely used as a fumigant pesticide. In case of ALP poisoning, it is responsible for myocardial dysfunction, related to toxic myocarditis, and hemodynamic disorders. We report a case of a 28-year-old female who had intentionally ingested ALP and was admitted with cardiogenic shock. The transthoracic echocardiography (TTE) at the time of admission showed severe global myocardial hypokinesia with the presence of a giant left ventricular thrombus. Cardiovascular magnetic resonance (CMR) revealed extensive toxic myocarditis with a left ventricular systolic dysfunction. All cardiac lesions were reversible after symptomatic treatment, within 6 months. We aim, by reporting this case, to evidence the complete reversibility of cardiac injury due to aluminium phosphide poisoning documented by transthoracic echocardiography and cardiovascular magnetic resonance.

Escherichia coli LPS-induced LV dysfunction: role of toll-like receptor-4 in the adult heart

2002 ◽  
Vol 282 (6) ◽  
pp. H2316-H2323 ◽  
Author(s):  
Shintaro Nemoto ◽  
Jesus G. Vallejo ◽  
Pascal Knuefermann ◽  
Arunima Misra ◽  
Gilberto Defreitas ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Lv Function ◽  
Toll Like Receptor ◽  
Wild Type ◽  
Toll Like Receptor 4 ◽  
Lv Dysfunction ◽  
Dimensional Echocardiography

The precise molecular mechanisms responsible for sepsis-induced myocardial dysfunction remain undefined. Toll-like receptor-4 (TLR-4) engages lipopolysaccharide (LPS) and activates signaling pathways leading to the expression of proinflammatory cytokines implicated in myocardial dysfunction. We determined whether TLR-4 was necessary for LPS-induced myocardial dysfunction in vivo. The effects of LPS on left ventricular (LV) function were studied in mice with defective TLR-4 signaling (C3H/HeJ, TLR-4 deficient) and wild-type mice (C3HeB/FeJ). Mice ( n = 5/group) were injected with LPS or diluent, and LV function was examined by using two-dimensional echocardiography and conductance catheters. LPS significantly decreased all indexes of LV function in wild-type mice when compared with controls; LV function was not depressed in the LPS-treated TLR-4-deficient mice relative to controls. LPS increased myocardial nitric oxide synthase-2 expression and cGMP only in wild-type mice. This study suggests that TLR-4 mediates the LV dysfunction that occurs in LPS-induced shock. Therefore, TLR-4 might be a therapeutic target for attenuating the effects of LPS on the heart.

Abstract 13423: Pharmacologic Inhibition of the NLRP3 Inflammasome Improves Left Ventricular Dysfunction after Severe Ischemic and Non-Ischemic Injury

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Carlo Marchetti ◽  
Stefano Toldo ◽  
Jeremy Chojnacki ◽  
Eleonora Mezzaroma ◽  
Salvatore Carbone ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Ischemia Reperfusion Injury ◽  
Interstitial Fibrosis ◽  
Ischemia Reperfusion ◽  
Systolic Dysfunction ◽  
Cardiac Injury ◽  
Ischemic Injury ◽  
Left Ventricular ◽  
Lv Dysfunction ◽  
Vehicle Treatment

Introduction: The formation of the NLRP3 inflammasome during injury to the heart amplifies the inflammatory response and mediates further damage. An inhibitor of the NLRP3 inflammasome was shown to reduce ischemia/reperfusion injury in the mouse. Hypothesis: We hypothesize that the NLRP3 inflammasome inhibitor would limit left ventricular (LV) dysfunction following severe ischemic (non-reperfused myocardial infarction [MI]) and non-ischemic (doxorubicin-induced) injury to heart. Methods: Adult male CD-1 male mice underwent permanent ligation of the left anterior descending coronary artery to induce a large non-reperfused MI (ischemic model) or injection of doxorubicin 10mg/kg to induce LV systolic dysfunction (non-ischemic model). The NLRP3 inflammasome inhibitor (16673-34-0, 100 mg/kg) or vehicle (N=6-8 per each group) were administered intraperitoneally daily for 7 days. Transthoracic echocardiography was performed to measure LV end-diastolic diameter (EDD) and LV fractional shortening (FS). We used Masson’s Trichrome stain to measure infarct size (ischemic model) or interstitial fibrosis (non-ischemic model). Results: Permanent coronary ligation led to a large non-reperfused MI and a significant increase in LVEDD and a reduction in LVFS (ischemic model). When compared with vehicle, treatment with the NLRP3 inflammasome inhibitor significantly limited LV enlargement (4.53±0.14 vs vehicle 4.95±0.04mm, P=0.006) and limited systolic dysfunction after AMI (Figure). A significant increase in interstitial fibrosis and reduction in LVFS was seen after doxorubicin treatment (non-ischemic model), and treatment with the inhibitor significantly reduced interstitial fibrosis (0.73%±0.14 vs vehicle 3.35%±0.83, P=0.001) and preserved LVFS (Figure). Conclusion: Inhibition of the NLRP3 inflammasome using a small molecule, 16673-34-0, reduces cardiac injury and limits LV systolic dysfunction following ischemic and non-ischemic injury.

Functional significance of inflammatory mediators in a murine model of resuscitated hemorrhagic shock

2005 ◽  
Vol 288 (3) ◽  
pp. H1272-H1277 ◽  
Author(s):  
Jesus G. Vallejo ◽  
Shintaro Nemoto ◽  
Masakuni Ishiyama ◽  
Bi Yu ◽  
Pascal Knuefermann ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Murine Model ◽  
Inflammatory Mediators ◽  
Functional Significance ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Lv Function ◽  
Sham Operation ◽  
Lv Dysfunction

The mechanisms that underlie the development of myocardial dysfunction after resuscitated hemorrhagic shock (HS) are not known. Recent studies suggest that systemic activation of inflammatory mediators may contribute to cellular dysfunction and/or cell death in various organs, including the heart. However, the precise role that inflammatory mediators play in the heart in the setting of resuscitated HS is not known. Accordingly, the purpose of the present study was to use a well-defined murine model of resuscitated HS to characterize the functional significance of inflammatory mediators in the heart in vivo. Mice were subjected to sham operation or resuscitated HS. Left ventricular (LV) function was assessed by two-dimensional echocardiography 6 h after resuscitation. Myocardial TNF, IL-1β, and IL-6 proteins were measured 1 and 6 h after resuscitation. To determine the role of TNF in HS-induced LV dysfunction, mice were treated with a soluble TNF receptor antagonist (etanercept) before HS or at the time of resuscitation. LV fractional shortening was significantly depressed ( P < 0.05) in resuscitated HS mice (28 ± 1.5%) compared with sham controls (35.8 ± 1.0%). TNF and IL-1β levels were significantly increased ( P < 0.05) in resuscitated HS mice. Pretreatment with etanercept abrogated resuscitated HS-induced LV dysfunction, whereas treatment at the time of resuscitation significantly attenuated, but did not abrogate, LV dysfunction. Together, these data suggest that TNF plays a critical upstream role in resuscitated HS-induced LV dysfunction; however, once the deleterious consequences of reperfusion injury are initiated, TNF contributes to, but is not necessary for, the development of LV dysfunction.

scholarly journals AB0422 LEFT VENTRICULAR ABNORMALITIES IN SYSTEMIC LUPUS ERYTHEMATOSUS PATIENTS FOLLOWED BY SEQUENTIAL ECHOCARDIOGRAPHY

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1510.1-1511
Author(s):  
T. Kuga ◽  
M. Matsushita ◽  
K. Tada ◽  
K. Yamaji ◽  
N. Tamura
Keyword(s):  
Lupus Erythematosus ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Monocyte Count ◽  
Lv Dysfunction ◽  
Group A ◽  
Group B ◽  
Lv Diastolic Dysfunction ◽  
Group D

Background:Cardiovascular disease (CVD) is detected in up to 50% of systemic lupus erythematosus (SLE) patients1and major cause of death2. Even clinically silent SLE patients can develop left ventricular (LV) diastolic dysfunction3. Proper echocardiographic follow up of SLE patients is required.Objectives:To clarify how the prevalence of LV abnormalities changes over follow-up period and identify the associated clinical factors, useful in suspecting LV abnormalities.Methods:29 SLE patients (24 females and 5 men, mean age 52.8±16.3 years, mean disease duration 17.6±14.5 years) were enrolled. All of them underwent echocardiography as the baseline examination and reexamined over more than a year of follow-up period(mean 1075±480 days) from Jan 2014 to Sep 2019. Patients complicated with pulmonary artery hypertension, deep venous thrombosis or pulmonary embolism and underwent cardiac surgery during the follow-up period were excluded. Left ventricular(LV) systolic dysfunction was defined as ejection fraction (EF) < 50%. LV diastolic dysfunction was defined according to ASE/EACVI guideline4. LV dysfunction (LVD) includes one or both of LV systolic dysfunction and LV diastolic function. Monocyte to HDL ratio (MHR) was calculated by dividing monocyte count with HDL-C level.Prevalence of left ventricular abnormalities was analysed at baseline and follow-up examination. Clinical characteristics and laboratory data were compared among patient groups as follows; patients with LV dysfunction (Group A) and without LV dysfunction (Group B) at the follow-up echocardiography, patients with LV asynergy at any point of examination (Group C) and patients free of LV abnormalities during the follow-up period (Group D).Results:At the baseline examination, LV dysfunction (5/29 cases, 13.8%), LV asynergy (6/29 cases, 21.7%) were detected. Pericarditis was detected in 7 patients (24.1%, LVD in 3 patients, LV asynergy in 2 patients) and 2 of them with subacute onset had progressive LV dysfunction, while 5 patients were normal in echocardiography after remission induction therapy for SLE. At the follow-up examination, LV dysfunction (9/29 cases, 31.0%, 5 new-onset and 1 improved case), LV asynergy (6/29 cases, 21.7%, 2 new-onset and 2 improved cases) were detected. Though any significant differences were observed between Group A and Group B at the baseline, platelet count (156.0 vs 207.0, p=0.049) were significantly lower in LV dysfunction group (Group A) at the follow-up examination. Group C patients had significantly higher uric acid (p=0.004), monocyte count (p=0.009), and MHR (p=0.003) than Group D(results in table).Conclusion:LV dysfunction is progressive in most of patients and requires regular follow-up once they developed. Uric acid, monocyte count and MHR are elevated in SLE patients with LV asynergy. Since MHR elevation was reported as useful marker of endothelial dysfunction5, our future goal is to analyse involvement of monocyte activation and endothelial dysfunction in LV asynergy of SLE patients.References:[1]Doria A et al. Lupus. 2005;14(9):683-6.[2]Manger K et al. Ann Rheum Dis. 2002 Dec;61(12):1065-70.[3]Leone P et al. Clin Exp Med. 2019 Dec 17.[4]Nagueh SF et al. J Am Soc Echocardiogr. 2016 Apr;29(4):277-314.[5]Acikgoz N et al. Angiology. 2018 Jan;69(1):65-70.Numbers are median (interquartile range), Mann-Whitney u test were performed, p value less than 0.05 was considered statistically significant.Disclosure of Interests: :None declared

scholarly journals Changes in mechanics of septal and lateral walls in patients with left bundle-branch block are related to extent of systolic dysfunction

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
K Kupczynska ◽  
KA Nguyen ◽  
E Surkova ◽  
CH Palermo ◽  
F Sambugaro ◽  
...  
Keyword(s):  
Left Bundle Branch Block ◽  
Systolic Dysfunction ◽  
Lateral Wall ◽  
Left Ventricular ◽  
Public Institution ◽  
Healthy Controls ◽  
Bundle Branch Block ◽  
Funding Sources ◽  
Lv Dysfunction ◽  
Artery Disease

Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): Karolina Kupczynska was supported by research grant awarded by the Club 30 of the Polish Cardiac Society Background Left bundle branch block (LBBB) affects left ventricular (LV) mechanics and promotes systolic dysfunction. Purpose To analyse myocardial work (MW) and myocardial work efficiency (MWE) of the septal and LV lateral wall in healthy controls and LBBB patients with various degrees of LV dysfunction using non-invasive method. Methods Our study involved 102 healthy controls (mean age 41.5 ± 15.7 years, 45% male) and 58 LBBB patients without coronary artery disease (mean age 65 ± 13 years, 60% male) divided into 3 groups based on their LVEF: preserved (n= 27), mid-range (n= 16) and reduced (n= 15). Myocardial work parameters were estimated in septal and lateral wall by LV pressure-strain loop obtained by echocardiography. Results There were no differences between septal and lateral MW and MWE in healthy controls (p = NS). We found lower septal MW in comparison to lateral MW (p &lt; 0.0001), but there were no differences in MWE (p = NS) in LBBB patients with preserved LVEF. Patients with LBBB and mid-range or reduced LVEF had lower MW (p &lt; 0.0001 in both subgroups) and lower MWE (p = 0.002 and p = 0.0001, respectively) in septum compared with lateral wall. There was a progressive decrease in septal MW and MWE with the occurring of LBBB and the worsening of LVEF (figure A). Interestingly in healthy controls there was significantly lower lateral MW but higher MWE in comparison to group with LBBB and preserved LVEF. We did not detect differences between LBBB groups with preserved and mid-range LVEF, but patients with reduced LVEF had significant reduction in terms of lateral MW and MWE (figure B). Conclusions Impairment in septal myocardial work escalated according to the appearance of LBBB and LVEF loss. Septal dysfunction was compensated by the effective myocardial work of the lateral wall in LBBB patients with preserved and mid-range LVEF. Mechanical dysfunction of the lateral wall was associated with severely reduced LVEF. Abstract Figure.

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