Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
We analysed contact with physicians, hospital care and actual prescriptions for medication recommended in international guidelines, referring to beta-blockers, ACE inhibitors or angiotensin II receptor blockers, P2Y12-antiplatelet agents, acetylsalicylic acid and statins, one year after myocardial infarction.
|
31371116 |
2020 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Transforming growth factor (TGF)-β1 contributed to angiotensin II (Ang II)-mediated collagen accumulation after myocardial infarction (MI).
|
31147455 |
2019 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
We determined the effects of spermidine in a model of MI, Sprague-Dawley rats with permanent ligation of the left anterior descending artery, and in cultured neonatal rat cardiomyocytes (NRCs) exposed to angiotensin II (Ang II).
|
31077347 |
2019 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
RDN reduced sympathetic nerve activity and release of B-type natriuretic peptide (BNP) and Angiotensin II (AngII) in the MI+ RDN group but not in the simple MI group.
|
31127792 |
2019 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Knockdown MALAT1 ameliorated MI-impaired cardiac function and prevented AngII-induced fibroblast proliferation, collagen production, and α-SMA expression in cardiac fibroblasts.
|
30146700 |
2019 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Here we describe the use a highly selective TG2 small-molecule inhibitor to test the efficacy of TG2 inhibition as an anti-fibrotic therapy for heart failure employing two different in vivo models of cardiac fibrosis: Progressively induced interstitial cardiac fibrosis by pressure overload using angiotensin II infusion: Acutely induced focal cardiac fibrosis through myocardial infarction by ligation of the left anterior descending coronary artery (AMI model).
|
29795262 |
2018 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Cav3 was experimentally confirmed as a direct target of miR-22, containing two seed binding sites in its 3'-untranslated region, and miR-22 was demonstrated to be significantly upregulated in the ischemic border zone in mice after myocardial infarction and in neonatal rat CFs pretreated with angiotensin II. miR-22 overexpression increased CFs proliferation, and collagen and α-smooth muscle actin levels in CFs, while the knockdown of endogenous miR-22 decreased CFs numbers.
|
29486470 |
2018 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Angiotensin-Converting Enzyme Inhibitors Provide Better Long-Term Survival Benefits to Patients With AMI Than Angiotensin II Receptor Blockers After Survival Hospital Discharge.
|
30130974 |
2018 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Enzyme-linked immunosorbent assay (ELISA) analysis showed that QLQX significantly reduced the levels of angiotensin II (AngII), brain natriuretic peptides (BNP), creatinine (CRE), cystatin C (CysC), tumor necrosis factor (TNF)-α, interleukin (IL)-6, microalbuminuria (MAU), and neutrophil gelatinase-associated lipocalin (NGAL) in plasma induced by myocardial infarction.
|
30068867 |
2018 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
In the present study, we used biochemical and histological approaches to examine the effects of FP on MI-induced cardiac fibrosis and the related mechanisms in a rat MI model and in angiotensin II- (Ang II-) treated rat cardiac fibroblasts (CFs).
|
30050588 |
2018 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
In this work, we analyzed the differences of the vasoconstriction induced by angiotensin II (Ang II) in the absence and presence of valsartan (200 nM) on the aortic rings of male and female Wistar rats at 2, 4, 24, and 48 hours and 1, 2, 3, and 4 weeks after induction of MI.
|
29040151 |
2018 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Angiotensin II receptor blocker reverses heart failure by attenuating local oxidative stress and preserving resident stem cells in rats with myocardial infarction.
|
30210678 |
2018 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
In addition, pretreatment with the AngII vaccine exerts neuroprotective effects in a cerebral ischemia model and cardioprotective effects in a myocardial infarction model.
|
29556794 |
2018 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
For the nonpersistent group, the percentage of switchers to angiotensin II-receptor blockers ranged from 27.6% (RD) to 42.2% (MI) and the restarters ranged from 15.0% (HF) to 18.1% (group without indication).
|
29943849 |
2018 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Increase in inflammatory cytokines synthesis coincides with activation of microglia within PVN of angiotensin II-induced hypertensive model and myocardial infarction-induced heart failure model.
|
26874752 |
2017 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
This study tested the hypothesis that Postcon attenuates the perivascular and interstitial fibrosis after myocardial infarction through modulating angiotensin II-activated fibrotic cascade.
|
28501115 |
2017 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Multiple trials over the past several years have examined the effects of both angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) in the treatment of left ventricular dysfunction, both acutely after myocardial infarction and in chronic heart failure.
|
28982370 |
2017 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
A peptide vaccine targeting angiotensin II attenuates the cardiac dysfunction induced by myocardial infarction.
|
28266578 |
2017 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Randomized, active controlled parallel group trials were included if they compared CCBs with α-blockers, β-blockers, angiotensin II receptor blockers, angiotensin-converting enzyme inhibitors, or diuretics, had a follow-up of ≥6 months, and had assessments of blood pressure (BP) and CV events [all-cause death, CV death, major CV events (myocardial infarction, MI; congestive heart failure, CHF; stroke; and CV death), MI, stroke, or CHF] in patients with baseline systolic/diastolic BP ≥140/≥90 mm Hg with either concomitant previous stroke and/or CAD.
|
26588586 |
2017 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Elastase-2, an angiotensin II-generating enzyme, contributes to increased angiotensin II in resistance arteries of mice with myocardial infarction.
|
28222221 |
2017 |
Myocardial Infarction
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Angiotensinogen-M235T as a risk factor for myocardial infarction in Asian populations: a genetic association study and a bioinformatics approach.
|
27586550 |
2016 |
Myocardial Infarction
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
In conclusion, the T174M polymorphism in the AGT gene may be related to an increased risk of MI.
|
25966146 |
2015 |
Myocardial Infarction
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
No associations were detected between AGT M235T and the risk of MI in total population and Caucasians.
|
23283824 |
2014 |
Myocardial Infarction
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Anterior localization of the infarct (p=0.008), leucocyte count at admission (p=0.040), global left ventricular longitudinal strain (p=0.021) and MM genotype of AGT (p=0.024) were independent predictors of ventricular remodelling after myocardial infarction.
|
23283822 |
2014 |
Myocardial Infarction
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
In East Asian group, significant association was found between AGT M235T polymorphism and risk of MI (for dominant model: OR=1.79; 95% CI=1.04-3.06; for recessive model OR=2.01; 95% CI=1.21-3.36; for additive model OR=1.79; 95% CI=1.14-2.86) as well as BI (for dominant model: OR=1.66; 95% CI=1.22-2.27; for recessive model OR=1.78, 95% CI=1.29-2.46; for additive model: OR=1.64, 95% CI=1.34-2.00), while the M235T polymorphism did not impact the risk of MI in total population and other ethnicity.
|
23933419 |
2013 |