scholarly journals Concentric cardiac remodeling and hypertrophy as predictors of superimposed preeclampsia in women with chronic hypertension

2022 ◽  
Vol 226 (1) ◽  
pp. S444
Author(s):  
Elizabeth Seagraves ◽  
Carole Barake ◽  
Dana Baraki ◽  
Thomas Donaldson ◽  
Alfred Abuhamad ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Chronic Hypertension

scholarly journals miR-154-5p Functions as an Important Regulator of Angiotensin II-Mediated Heart Remodeling

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Que Wang ◽  
Xiaoxue Yu ◽  
Lin Dou ◽  
Xiuqing Huang ◽  
Kaiyi Zhu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Remodeling ◽  
Structural Changes ◽  
Molecular Mechanisms ◽  
Heart Function ◽  
Left Ventricular ◽  
Cardiomyocyte Hypertrophy ◽  
Left Ventricular Myocardium ◽  
Chronic Hypertension ◽  
Arylsulfatase B

Chronic hypertension, valvular heart disease, and heart infarction cause cardiac remodeling and potentially lead to a series of pathological and structural changes in the left ventricular myocardium and a progressive decrease in heart function. Angiotensin II (AngII) plays a key role in the onset and development of cardiac remodeling. Many microRNAs (miRNAs), including miR-154-5p, may be involved in the development of cardiac remolding, but the underlying molecular mechanisms remain unclear. We aimed to characterize the function of miR-154-5p and reveal its mechanisms in cardiac remodeling induced by AngII. First, angiotensin II led to concurrent increases in miR-154-5p expression and cardiac remodeling in adult C57BL/6J mice. Second, overexpression of miR-154-5p to a level similar to that induced by AngII was sufficient to trigger cardiomyocyte hypertrophy and apoptosis, which is associated with profound activation of oxidative stress and inflammation. Treatment with a miR-154-5p inhibitor noticeably reversed these changes. Third, miR-154-5p directly inhibited arylsulfatase B (Arsb) expression by interacting with its 3′-UTR and promoted cardiomyocyte hypertrophy and apoptosis. Lastly, the angiotensin type 1 receptor blocker telmisartan attenuated AngII-induced cardiac hypertrophy, apoptosis, and fibrosis by blocking the increase in miR-154-5p expression. Moreover, upon miR-154-5p overexpression in isolated cardiomyocytes, the protective effect of telmisartan was partially abolished. Based on these results, increased cardiac miR-154-5p expression is both necessary and sufficient for AngII-induced cardiomyocyte hypertrophy and apoptosis, suggesting that the upregulation of miR-154-5p may be a crucial pathological factor and a potential therapeutic target for cardiac remodeling.

scholarly journals 63: Perinatal outcomes associated with abnormal cardiac remodeling measured by echocardiography during pregnancy in women with treated chronic hypertension

2018 ◽  
Vol 218 (1) ◽  
pp. S47
Author(s):  
Anne M. Ambia ◽  
Jamie L. Morgan ◽  
Scott W. Roberts ◽  
C. Edward Wells ◽  
David B. Nelson ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Perinatal Outcomes ◽  
Chronic Hypertension

Perinatal outcomes associated with abnormal cardiac remodeling in women with treated chronic hypertension

2018 ◽  
Vol 218 (5) ◽  
pp. 519.e1-519.e7 ◽  
Author(s):  
Anne M. Ambia ◽  
Jamie L. Morgan ◽  
C. Edward Wells ◽  
Scott W. Roberts ◽  
Monika Sanghavi ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Perinatal Outcomes ◽  
Chronic Hypertension

Prevention of angiotensin II-induced cardiac remodeling by angiotensin-(1–7)

2007 ◽  
Vol 292 (2) ◽  
pp. H736-H742 ◽  
Author(s):  
Justin L. Grobe ◽  
Adam P. Mecca ◽  
Melissa Lingis ◽  
Vinayak Shenoy ◽  
Tonya A. Bolton ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cardiac Remodeling ◽  
Cardiac Tissue ◽  
Interstitial Fibrosis ◽  
Chronic Hypertension ◽  
Ang Ii ◽  
Myocyte Hypertrophy ◽  
Chronic Infusion

Cardiac remodeling, which typically results from chronic hypertension or following an acute myocardial infarction, is a major risk factor for the development of heart failure and, ultimately, death. The renin-angiotensin system (RAS) has previously been established to play an important role in the progression of cardiac remodeling, and inhibition of a hyperactive RAS provides protection from cardiac remodeling and subsequent heart failure. Our previous studies have demonstrated that overexpression of angiotensin-converting enzyme 2 (ACE2) prevents cardiac remodeling and hypertrophy during chronic infusion of angiotensin II (ANG II). This, coupled with the knowledge that ACE2 is a key enzyme in the formation of ANG-(1–7), led us to hypothesize that chronic infusion of ANG-(1–7) would prevent cardiac remodeling induced by chronic infusion of ANG II. Infusion of ANG II into adult Sprague-Dawley rats resulted in significantly increased blood pressure, myocyte hypertrophy, and midmyocardial interstitial fibrosis. Coinfusion of ANG-(1–7) resulted in significant attenuations of myocyte hypertrophy and interstitial fibrosis, without significant effects on blood pressure. In a subgroup of animals also administered [d-Ala7]-ANG-(1–7) (A779), an antagonist to the reported receptor for ANG-(1–7), there was a tendency to attenuate the antiremodeling effects of ANG-(1–7). Chronic infusion of ANG II, with or without coinfusion of ANG-(1–7), had no effect on ANG II type 1 or type 2 receptor binding in cardiac tissue. Together, these findings indicate an antiremodeling role for ANG-(1–7) in cardiac tissue, which is not mediated through modulation of blood pressure or altered cardiac angiotensin receptor populations and may be at least partially mediated through an ANG-(1–7) receptor.

Loss of distensibility in cerebral arteries with chronic hypertension and vasospasm after subarachnoid hemorrhage

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S557-S557
Author(s):  
Takeshi Kondoh ◽  
Seiji Nakajima ◽  
Akitsugu Morishita ◽  
Haruo Yamashita ◽  
Eiji Kohmura ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Chronic Hypertension

GIP advanced cardiac remodeling after LAD ligation leading to improved left-ventricular function

2018 ◽  
Author(s):  
A Dieckerhoff ◽  
J Möllmann ◽  
M Schwarz ◽  
E Liehn ◽  
S Diebold ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Ventricular Function ◽  
Cardiac Remodeling ◽  
Left Ventricular

Echocardiographic Evaluation of Cardiac Remodeling After Surgical Closure of Ventricular Septal Defect in Different Age Group

2017 ◽  
Vol 2 (2) ◽  
pp. 69-74
Author(s):  
Mohammad Aminullah ◽  
Fahmida Akter Rima ◽  
Asraful Hoque ◽  
Mokhlesur Rahman Sazal ◽  
Prodip Biswas ◽  
...  
Keyword(s):  
Ventricular Septal Defect ◽  
Ejection Fraction ◽  
Cardiac Remodeling ◽  
Septal Defect ◽  
Left Ventricular ◽  
Age Group ◽  
Surgical Closure ◽  
Group A ◽  
Group B ◽  
Fractional Shortening

Background: Cardiac remodeling is important issue after surgical closure of ventricular septal defect.Objective: The purpose of the present study was to evaluate cardiac remodeling by echocardiography by measuring the ejection fraction, fractional shortening, left ventricular internal diameter during diastole (LVIDd) and left ventricular internal diameter during systole (LVIDs) after surgical closure of ventricular septal defect in different age group. Methodology: This prospective cohort studies was conducted in the Department of Cardiac Surgery at National Institute of Cardiovascular Disease (NICVD), Dhaka. Patient with surgical closure of VSD were enrolled into this study purposively and were divided into 3 groups according to the age. In group A (n=10), patients were within the age group of 2.0 to 6.0 years; age of group B (n=8) patients were 6.1-18.0 years and the group C (n=6) aged range was 18.1-42.0 years. Echocardiographic variables such as ejection fraction, fractional shortening, LVIDd, LVIDs were taken preoperatively and at 1st and 3rd month of postoperative values. Result: A total number of 24 patients was recruited for this study. The mean ages of all groups were 12.60±12.09. After 1 month ejection fraction were decreased by 5.97%, 6.71% and 5.66% in group A, group B and group C respectively. After 3 months ejection fraction were increased by 6.13%, 5.13% and 5.14% in group A, group B and group C respectively. After 1 month fractional shortening were decreased by 13.55%, 9.30% and 9.09% in group A, group B and group C respectively. After 3 months fractional shortening were increased by 7.23%, 7.35% and 4.55% in group A, group B and group C respectively. After 1 month LVIDd were increased by 1.97%, 1.91% and 1.32% in group A, group B and group C respectively. After 3 months LVIDd were decreased by 10.84%, 9.89% and 7.34% in group A, group B and group C respectively. After 1 month LVIDs were increased by 2.19%, 2.86% and 1.98% in group A, group B and group C respectively. After 3 months LVIDs were decreased by 11.68%, 10.97% and 8.87% in group A, group B and group C respectively.Conclusion: Cardiac remodeling occurred after surgical closure of ventricular septal defect and remodeling were more significant in younger age group. Journal of National Institute of Neurosciences Bangladesh, 2016;2(2):69-74

199-LB: Low Prevalence of Small-for-Gestational-Age in Women with Type 1 Diabetes and Chronic Hypertension

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 199-LB
Author(s):  
SARIT HELMAN ◽  
TAMARRA JAMES-TODD ◽  
FLORENCE M. BROWN
Keyword(s):  
Type 1 Diabetes ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Chronic Hypertension ◽  
Low Prevalence
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