Carvedilol and thyroid hormones co-administration mitigates oxidative stress and improves cardiac function after acute myocardial infarction

2019 ◽  
Vol 854 ◽  
pp. 159-166 ◽  
Author(s):  
Vanessa Duarte Ortiz ◽  
Patrick Türck ◽  
Rayane Teixeira ◽  
Bruna Gazzi Lima-Seolin ◽  
Denise Lacerda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Thyroid Hormones ◽  
Cardiac Function

scholarly journals Urinary 1-Hydroxypyrene is Associated with Oxidative Stress and Inflammatory Biomarkers in Acute Myocardial Infarction

2014 ◽  
Vol 11 (9) ◽  
pp. 9024-9037 ◽  
Author(s):  
Fernando Freitas ◽  
Natália Brucker ◽  
Juliano Durgante ◽  
Guilherme Bubols ◽  
Rachel Bulcão ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Inflammatory Biomarkers

Stabilization of hypoxia inducible factor rather than modulation of collagen metabolism improves cardiac function after acute myocardial infarction in rats

2006 ◽  
Vol 8 (4) ◽  
pp. 347-354 ◽  
Author(s):  
Sebastian Philipp ◽  
Jan Steffen Jürgensen ◽  
Jens Fielitz ◽  
Wanja M. Bernhardt ◽  
Alexander Weidemann ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Hypoxia Inducible Factor ◽  
Collagen Metabolism

scholarly journals Galectin-3 and Cardiac Function in Survivors of Acute Myocardial Infarction

2013 ◽  
Vol 6 (3) ◽  
pp. 492-498 ◽  
Author(s):  
Robin A.P. Weir ◽  
Colin J. Petrie ◽  
C. Aengus Murphy ◽  
Suzanne Clements ◽  
Tracey Steedman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Galectin 3

Abstract 265: Uroetensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through Cystathionine-γ-Lyase (CSE)/Hydrogen Sulfide Pathway

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Hui Gong ◽  
Zhidan Chen ◽  
Xiaoyi Zhang ◽  
Jie Zhang ◽  
Yang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Erk Signaling ◽  
Cardiac Protection ◽  
Health Control ◽  
Cardiology Department ◽  
Apoptotic Protein ◽  
Induced Apoptosis ◽  
H2s Production

Plasma UII has been observed to be raised in patients with acute myocardial infarction, a lower UII response is associated with more severe injury of myocardium, suggesting a possible cardioprotective role for this peptide. In the present study, we studied plasma UII concentration of thirty patients admitted to the Cardiology Department with acute myocardial infartion.The results showed that plasma UII was sharply increased in patients compared to that in health control within one week after admission. We then explore whether UII could protect cardiomyocytes from injury induced by oxidative stress. Cultured cardiomyocyte were treated with H2O2 to induce oxidative stress, and the influence of UII on H2O2-induced apoptosis was observed. The results showed that UII pretreatment significantly reduced the number of TUNEL-positive cardiomyocytes induced by H2O2, and it partly abolished the upregulation of pro-apoptotic protein Bax and the down-regulation of anti-apoptotic protein Bcl-2. siRNA targeted to urotensin receptor (UT) greatly inhibited these effects. H2S has been reported to exert protective effect on cardiomyocytes, we detected the effect of UII on H2S production and CSE (Major H2S-producing enzyme) expressions in cardiomyocytes exposed to H2O2.The present data revealed that UII increased the H2S production by enhancing the expression of CSE by activating the ERK signaling in cardiomyocytes exposed to H2O2. Si-CSE or ERK inhibitor not only greatly inhibited the upregulation of CSE or the phosphorylation of ERK induced by UII but also reversed UII-induced-upregulation of H2S production and anti-apoptosis in cadiomyocytes exposed to H2O2. In conclusion, UII rapidly promoted the phosphorylation of ERK, increased CSE exression and induced H2S production, which in turn enhanced the p-ERK level to protect cardiomyocytes from apoptosis under ischemic or oxidative stress. The increased plasma UII level in patients may be critical for cardiac protection in patients at early-phase of acute myocardial infarction.

scholarly journals Study on oxidative stress and antioxidant level in patients of acute myocardial infarction before and after regular treatment

2015 ◽  
Vol 40 (2) ◽  
pp. 79-84 ◽  
Author(s):  
T Bashar ◽  
N Akhter
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Vitamin E ◽  
Plasma Vitamin ◽  
Regular Treatment ◽  
Before And After ◽  
The Difference ◽  
Plasma Vitamin E

In acute myocardial infarction (AMI), lack of oxygen delivery to myocardium leads to generation of reactive oxygen species (ROS) which play an important role in the pathogenesis of AMI. Endogenous anti-oxidants protect the myocardial tissues from the deleterious effect of free radical mediate injury. The study evaluates the extent of oxidative stress and antioxidant status against ROS in AMI patients and amelioration of oxidative stress after regular treatment and also assesses the association between oxidative stress and risk factors for atherosclerosis like dyslipidemia and diabetes mellitus (DM).The study was conducted on 72 AMI patients and age and sex matched 18 healthy controls. Patients were assigned to four groups, AMI without dyslipidemia or DM, with dyslipidemia, with DM and with both dyslipidemia and DM. Plasma malondialdehyde (MDA) and GSH content and vitamin E levels were determined on admission into hospital and on the 5th day of treatment. Plasma MDA level increased significantly (p<0.001) and erythrocyte GSH and plasma vitamin E levels were decreased (p<0.001) in all the groups of patients as compared to control. On the 5th day of regular treatment MDA level reduced (p<0.001) and GSH and vitamin E levels increased (p<0.001) in patients. The plasma MDA level was significantly higher (p<0.001) in patients with both dyslipidemia and DM or with only DM in comparison to patients without dyslipidemia and DM. The difference in the GSH level between patients with risk factors and without risk factors was not significant. It may be conclude that an imbalance exists between oxidant and antioxidant molecules in AMI patients which shift towards oxidative side and regular treatment restores this balance. There may be some association between oxidative stress in AMI and risk factors like dyslipidemia and diabetes mellitus.Bangladesh Med Res Counc Bull 2014; 40 (2): 79-84

scholarly journals Correlation of Triiodothyronine Level with In-Hospital Cardiac Function and Long-Term Prognosis in Patients with Acute Myocardial Infarction

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jianqing She ◽  
Jiahao Feng ◽  
Yangyang Deng ◽  
Lizhe Sun ◽  
Yue Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Survival Analysis ◽  
Cardiac Function ◽  
Thyroid Function ◽  
Major Adverse Cardiovascular Events ◽  
Free Triiodothyronine ◽  
Kaplan Meier ◽  
Significant Difference

Objective. The pathophysiologic mechanism of how thyroid function is related to the development and prognosis of acute myocardial infarction (AMI) remains under explored, and there has been a lack of clinical investigations. In this study, we investigate the relationship between triiodothyronine (T3) level and cardiac ejection fraction (EF) as well as probrain natriuretic peptide (NT-proBNP) on admission and subsequent prognosis in AMI patients. Methods. We measured admission thyroid function, NT-proBNP, and EF by echocardiography in 345 patients diagnosed with AMI. Simple and multiregression analyses were performed to investigate the correlation between T3 level and EF as well as NT-proBNP. Major adverse cardiovascular events (MACE), including new-onset myocardial infarction, acute heart failure, and cardiac death, were documented during the follow-up. 248 participants were separated into three groups based on T3 and free triiodothyronine (FT3) levels for survival analysis during a 2-year follow-up. Results. 345 patients diagnosed with AMI were included in the initial observational analysis. 248 AMI patients were included in the follow-up survival analysis. The T3 levels were found to be significantly positively correlated with EF (R square=0.042, P<0.001) and negatively correlated with admission NT-proBNP levels (R square=0.059, P<0.001), which is the same with the correlation between FT3 and EF (R square=0.053, P<0.001) and admission NT-proBNP levels (R square=0.108, P<0.001). Kaplan-Meier survival analysis revealed no significant difference with regard to different T3 or FT3 levels at the end of follow-up. Conclusions. T3 and FT3 levels are moderately positively correlated with cardiac function on admission in AMI patients but did not predict a long-time survival rate. Further studies are needed to explain whether longer-term follow-up would further identify the prognosis effect of T3 on MACE and all-cause mortality.

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