Effects of relaxin on experimentally-induced myocardial infarction. Is this hormone a natural shield against cardiovascular ischemic disease?

Relaxin 2000 ◽  
2001 ◽  
pp. 153-157
Author(s):  
Mario Bigazzi ◽  
Daniele Bani ◽  
Tatiana Bani Sacchi
Keyword(s):  
Myocardial Infarction ◽  
Ischemic Disease ◽  
Experimentally Induced

Mendelian Randomization Focused Analysis of Vitamin D on the Secondary Prevention of Ischemic Stroke

Stroke ◽  
2021 ◽  
Author(s):  
Yap-Hang Chan ◽  
C. Mary Schooling ◽  
Jie Zhao ◽  
Shiu-Lun Au Yeung ◽  
Jo Jo Hai ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Vitamin D ◽  
Ischemic Stroke ◽  
Risk Score ◽  
Genetic Risk ◽  
Odds Ratio ◽  
Mendelian Randomization ◽  
De Novo ◽  
Genetic Risk Score ◽  
Ischemic Disease

Background and Purpose: Experimental studies showed vitamin D (Vit-D) could promote vascular regeneration and repair. Prior randomized studies had focused mainly on primary prevention. Whether Vit-D protects against ischemic stroke and myocardial infarction recurrence among subjects with prior ischemic insults was unknown. Here, we dissected through Mendelian randomization any effect of Vit-D on the secondary prevention of recurrent ischemic stroke and myocardial infarction. Methods: Based on a genetic risk score for Vit-D constructed from a derivation cohort sample (n=5331, 45% Vit-D deficient, 89% genotyped) via high-throughput exome-chip screening of 12 prior genome-wide association study–identified genetic variants of Vit-D mechanistic pathways ( rs2060793 , rs4588 , and rs7041 ; F statistic, 73; P <0.001), we performed a focused analysis on prospective recurrence of myocardial infarction (MI) and ischemic stroke in an independent subsample with established ischemic disease (n=441, all with prior first ischemic event; follow-up duration, 41.6±14.3 years) under a 2-sample, individual-data, prospective Mendelian randomization approach. Results: In the ischemic disease subsample, 11.1% (n=49/441) had developed recurrent ischemic stroke or MI and 13.3% (n=58/441) had developed recurrent or de novo ischemic stroke/MI. Kaplan-Meier analyses showed that genetic risk score predicted improved event-free survival from recurrent ischemic stroke or MI (log-rank, 13.0; P =0.001). Cox regression revealed that genetic risk score independently predicted reduced risk of recurrent ischemic stroke or MI combined (hazards ratio, 0.62 [95% CI, 0.48–0.81]; P <0.001), after adjusted for potential confounders. Mendelian randomization supported that Vit-D is causally protective against the primary end points of recurrent ischemic stroke or MI (Wald estimate: odds ratio, 0.55 [95% CI, 0.35–0.81]) and any recurrent or de novo ischemic stroke/MI (odds ratio, 0.64 [95% CI, 0.42–0.91]) and recurrent MI alone (odds ratio, 0.52 [95% CI, 0.30–0.81]). Conclusions: Genetically predicted lowering in Vit-D level is causal for the recurrence of ischemic vascular events in persons with prior ischemic stroke or MI.

scholarly journals Commentary: Chest pain evaluation in the emergency department

CJEM ◽  
1999 ◽  
Vol 1 (01) ◽  
pp. 62
Author(s):  
Tim Allen
Keyword(s):  
Myocardial Infarction ◽  
Chest Pain ◽  
Practice Patterns ◽  
Clinical Problem ◽  
Regional Hospital ◽  
Improve Performance ◽  
Ischemic Disease ◽  
Admission Rates ◽  
Pain Evaluation ◽  
Thunder Bay

In this issue, Dr. David Mutrie illustrates both the utility of departmental care protocols and the caution we must take in drawing conclusions from them. The latter point is particularly important if one wishes to apply these conclusions to other institutions.The Thunder Bay Regional Hospital (TBRH), in Ontario, established simple guidelines for the management of patients with chest pain. Following the implementation of these guidelines, Mutrie reports shorter chest pain assessment times and reduced admission rates for non-myocardial infarction and non-unstable angina patients, without any obvious increase in inappropriate discharge of patients with ischemic disease. Can we therefore conclude that the guidelines were responsible for these improvements and that this set of guidelines would similarly improve performance in other emergency departments? The answer, unfortunately, is No. The fact is, the establishment of any organized approach to a clinical problem tends to improve performance. This is perhaps a sad reflection on “individual” practice patterns, but it is true nonetheless.

Exendin-4 Ameliorates Cardiac Remodeling in Experimentally Induced Myocardial Infarction in Rats by Inhibiting PARP1/NF-κB Axis in A SIRT1-Dependent Mechanism

2020 ◽  
Vol 20 (4) ◽  
pp. 401-418 ◽  
Author(s):  
Refaat A. Eid ◽  
Samah A. Alharbi ◽  
Attalla Farag El-kott ◽  
Samy M. Eleawa ◽  
Mohamed Samir Ahmed Zaki ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Remodeling ◽  
Dependent Mechanism ◽  
Experimentally Induced

Altered profiles of gene expression in curcumin-treated rats with experimentally induced myocardial infarction

2010 ◽  
Vol 61 (2) ◽  
pp. 142-148 ◽  
Author(s):  
Dongsheng Hong ◽  
Xiaowei Zeng ◽  
Wei Xu ◽  
Jing Ma ◽  
Yinghui Tong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Experimentally Induced

scholarly journals Pathomorphological changes in experimentally induced canine myocardial infarction

1988 ◽  
Vol 11 (3) ◽  
pp. 149-157
Author(s):  
T. Tomaru ◽  
Y. Uchida ◽  
T. Sugimoto
Keyword(s):  
Myocardial Infarction ◽  
Canine Myocardial Infarction ◽  
Experimentally Induced

Effects of transient increased afterload during experimentally induced acute myocardial infarction in dogs

1985 ◽  
Vol 55 (5) ◽  
pp. 566-570 ◽  
Author(s):  
Haim Hammerman ◽  
Robert A. Kloner ◽  
Kevin J. Alker ◽  
Frederick J. Schoen ◽  
Eugene Braunwald
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Experimentally Induced

Supplementation of squalene attenuates experimentally induced myocardial infarction in rats

2007 ◽  
Vol 105 (4) ◽  
pp. 1390-1395 ◽  
Author(s):  
K.H. Sabeena Farvin ◽  
S. Hari Senthil Kumar ◽  
R. Anandan ◽  
Suseela Mathew ◽  
T.V. Sankar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Experimentally Induced

scholarly journals Mast cells regulate myofilament calcium sensitization and heart function after myocardial infarction

2016 ◽  
Vol 213 (7) ◽  
pp. 1353-1374 ◽  
Author(s):  
Anta Ngkelo ◽  
Adèle Richart ◽  
Jonathan A. Kirk ◽  
Philippe Bonnin ◽  
Jose Vilar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Mast Cells ◽  
Cardiac Function ◽  
Cardiac Remodeling ◽  
Molecular Mechanisms ◽  
Troponin I ◽  
Heart Function ◽  
Ischemic Disease ◽  
Cardiomyocyte Contractility ◽  
The Impact

Acute myocardial infarction (MI) is a severe ischemic disease responsible for heart failure and sudden death. Inflammatory cells orchestrate postischemic cardiac remodeling after MI. Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key roles for mast cells (MCs) in postischemic cardiac remodeling. Because c-Kit mutations affect multiple cell types of both immune and nonimmune origin, we addressed the impact of MCs on cardiac function after MI, using the c-Kit–independent MC-deficient (Cpa3Cre/+) mice. In response to MI, MC progenitors originated primarily from white adipose tissue, infiltrated the heart, and differentiated into mature MCs. MC deficiency led to reduced postischemic cardiac function and depressed cardiomyocyte contractility caused by myofilament Ca2+ desensitization. This effect correlated with increased protein kinase A (PKA) activity and hyperphosphorylation of its targets, troponin I and myosin-binding protein C. MC-specific tryptase was identified to regulate PKA activity in cardiomyocytes via protease-activated receptor 2 proteolysis. This work reveals a novel function for cardiac MCs modulating cardiomyocyte contractility via alteration of PKA-regulated force–Ca2+ interactions in response to MI. Identification of this MC-cardiomyocyte cross-talk provides new insights on the cellular and molecular mechanisms regulating the cardiac contractile machinery and a novel platform for therapeutically addressable regulators.

scholarly journals Biochemical Studies on the Protective Effect of Betaine on Mitochondrial Function in Experimentally Induced Myocardial Infarction in Rats

2007 ◽  
Vol 53 (6) ◽  
pp. 671-681 ◽  
Author(s):  
Balaraman Ganesan ◽  
Rangasamy Rajesh ◽  
Rangasamy Anandan ◽  
Nanjappan Dhandapani
Keyword(s):  
Myocardial Infarction ◽  
Protective Effect ◽  
Mitochondrial Function ◽  
Biochemical Studies ◽  
Experimentally Induced
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