scholarly journals The Role of Anti-Inflammatory Cytokines in Heart Failure

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Rachel Pathimagaraj
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Immune Complex ◽  
Therapeutic Potential ◽  
Innate Immune ◽  
Sterile Inflammation ◽  
Ischaemia Reperfusion Injury ◽  
Pyrin Domain

Coronary occlusion promotes a state of ischaemia that results in myocardial infarction; it  is  a  major  cause  of  mortality  accounting  for  one  hospital  admission  every  three minutes. At the site of infarct, sterile inflammation is initiated due to pro-inflammatory secretions from cardiac and innate immune cells. The focus of this review is to explore the role of a newly discovered innate immune complex, the nod-like receptor family pyrin domain containing 3 inflammasome. This review discusses the potential of this immune  complex  in  decreasing  the  proportion  of  functional  myocardium  during ischaemia   and   ischaemia-reperfusion   injury.   Due   to   the   central   role   of   this inflammasome  in  promoting  cardiac  dysfunction  following  an  acute  myocardial infarction,  the  risk  of  port-infarction  heart  failure  increases.  With  an  intention  of highlighting the importance of improving current management of patients with acute myocardial  infarction,  this  review  addresses  novel  therapeutic  agents  that  have demonstrated  cardioprotective  outcomes  in  recent  studies.  This  follows  discussion concerning the therapeutic potential of these agents, intending to form the basis of heart failure therapy.

scholarly journals Status of Prostacycline-Thromboxane System and Platelet Functional Activities in Patients with Acute Myocardial Infarction Depending on Stages of Heart Failure

2015 ◽  
Vol 26 (2) ◽  
pp. 83-87
Author(s):  
AFM Sakhawat Hossain ◽  
Brindaban Biswas ◽  
Md Alfazzaman ◽  
Mohammad Mohsin ◽  
Md Mujibur Rahman
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
New England ◽  
Medical Institute ◽  
Functional Activities ◽  
The Status ◽  
Platelet Functions

Among possible pathogenic and adaptive mechanism of acute myocardial infarction and development of its complications, the system of prostanoids, particularly prostacycline-thromboxane system is of prime importance. But many questions relating the role of prostacycline-thromboxane system in pathogenesis of myocardial infarction associated with heart failure have studied insufficiently. The objective of this work is to study the ststus of prostacycline-thromboxane system in patients of acute myocardial infarction associated with heart failure and its correlation with the platelet functions depending on stages of heart failure. This study was performed in the department of Internal Medicine in Kharkov State Medical Institute, Ukraine in 1985-89. 120 patients with acute myocardial infarction leading to heart failure were studied. The status of prostacycline-thromboxane was considered by the level of stable metabolites of prostacycline and thromboxane - A2 as 6-keto-PGF and TXB2 respectively in venous plasma. 6-Keto-PGF-1a and TXB2 levels were determined by Radio-immunological method with the help of kits manufactured by the English Firm "New England Nuclear". To determine the platelet aggregation properties, the instrument "Bian-120" transmitter was used. It was established clinically that prostacycline- thromboxane activation depends on clinical features of myocardial infarction, i.e. its localization, depth, extension or affected size of MI, first attack or re-infarction. Maximum changes of prostacycline thromboxane system took place in extensive myocardial infarction which was expressed in increased level of TXB2 and significant change of prostanoid imbalance ratio. Parameters of platelet aggregation function and prostacycline thromboxane system were interrelated during heart failure, which were expressed by their changes in aggregation diagram.Medicine Today 2014 Vol.26(2): 83-87

scholarly journals Using human genetics to understand the causes and consequences of circulating cardiac troponin I in the general population

2020 ◽  
Author(s):  
Marta R Moksnes ◽  
Helge Røsjø ◽  
Anne Richmond ◽  
Magnus N Lyngbakken ◽  
Sarah E Graham ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
General Population ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Mendelian Randomization ◽  
Cardiac Troponin I ◽  
Health Study

AbstractCirculating cardiac troponin proteins are associated with structural heart disease and predict incident cardiovascular disease in the general population. However, the genetic contribution to cardiac troponin I (cTnI) concentrations and its causal effect on cardiovascular phenotypes is unclear. We combine data from two large population-based studies, the Trøndelag Health Study and the Generation Scotland Scottish Family Health Study and perform a genome-wide association study of high-sensitivity cTnI concentrations with 48 115 individuals. We further used two-sample Mendelian randomization to investigate the causal effects of circulating cTnI on acute myocardial infarction and heart failure.We identified 12 genetic loci (8 novel) associated with cTnI concentrations. Associated protein-altering variants highlighted putative functional genes: CAND2, HABP2, ANO5, APOH, FHOD3, TNFAIP2, KLKB1 and LMAN1. Phenome-wide association tests in 1283 phecodes and 274 continuous traits in UK Biobank showed associations between a polygenic risk score for cTnI and cardiac arrhythmias, aspartate aminotransferase 1 and anthropometric measures. Excluding individuals with a known history of comorbidities did not materially change associations with cTnI. Using two-sample Mendelian randomization we confirmed the non-causal role of cTnI in acute myocardial infarction (5 948 cases, 355 246 controls). We found some indications for a causal role of cTnI in heart failure (47 309 cases and 930 014 controls), but this was not supported by secondary analyses using left ventricular mass as outcome (18 257 individuals).Our findings clarify the biology underlying the heritable contribution to circulating cTnI and support cTnI as a non-causal biomarker for acute myocardial infarction and heart failure development in the general population. Using genetically informed methods for causal inference of cTnI helps inform the role and value of measuring cTnI in the general population.

Abstract 414: Putative Role of MicroRNA-143 in Modulating Natriuretic Peptide Signaling via Down-regulation of the Expression of Natriuretic Peptide Receptor 3

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Juan Wang ◽  
Lee L Wong ◽  
Arthur M Richards ◽  
Yei-Tsung Chen
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Natriuretic Peptide ◽  
Therapeutic Potential ◽  
Cardiac Cells ◽  
Luciferase Reporter ◽  
Natriuretic Peptide Receptor ◽  
Down Regulation ◽  
Peptide Receptor

Cardiac natriuretic peptides (NPs) play important roles in the regulation of intravascular blood volume and vascular tone. Among other clearance mechanisms, bio-active circulating NPs are removed by the clearance receptor, Natriuretic Peptide Receptor 3 (NPR3). We hypothesized that the level of NPR3 could be modulated by microRNAs (miRNAs) resulting in changes in the bioactivity of NPs. We have previously reported a cluster of miRNAs potentially regulating NPR3 expression. To extend these findings, expression of the microRNAs concerned was examined in multiple platforms, including plasma from a clinical heart failure cohort, in the rat myocardial infarction model, and in a human cardiac derived cell line subjected to hypoxic challenge. Results: miR-143 was up-regulated in peripheral blood in heart failure patients compared with controls. The binding of miR-143 to the 3’UTR of NPR3 m RNA was verified by luciferase reporter assay. Antagomir-based silencing of miR-143 enhanced NPR3 expression in human derived cardiac cells. Elevation of miR-143 and down-regulation of NPR3 levels were observed in hypoxia treated cells and in the myocardium from the rat myocardial infarction model. Taken together, these findings suggest miR-143 may be involved in the down-regulation of NPR3 which in turn may provide more cardiac protective bioactivity from NPs in heart failure, myocardial hypoxic stress and in myocardial infarction. In summary, NPR3 is negatively regulated by miR-143, pointing to the therapeutic potential of miR-143 to beneficially enhance NP responses.

Acute myocardial infarction and heart failure: Role of apoptosis

2006 ◽  
Vol 38 (11) ◽  
pp. 1834-1840 ◽  
Author(s):  
Antonio Abbate ◽  
Rossana Bussani ◽  
Mitesh S. Amin ◽  
George W. Vetrovec ◽  
Alfonso Baldi
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction
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