scholarly journals Differential expression of embryonic epicardial progenitor markers and localization of cardiac fibrosis in adult ischemic injury and hypertensive heart disease

2013 ◽  
Vol 65 ◽  
pp. 108-119 ◽  
Author(s):  
Caitlin M. Braitsch ◽  
Onur Kanisicak ◽  
Jop H. van Berlo ◽  
Jeffery D. Molkentin ◽  
Katherine E. Yutzey
Keyword(s):  
Heart Disease ◽  
Differential Expression ◽  
Cardiac Fibrosis ◽  
Hypertensive Heart Disease ◽  
Ischemic Injury

Abstract P380: Common And Distinct Signatures Of Interstitial And Perivascular Fibrosis In Mouse Models Of Hypertensive Heart Disease

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Louise Thisted ◽  
Claudia Correia ◽  
Karin Jennbacken ◽  
Maria Wagberg ◽  
Franziska Wichern ◽  
...  
Keyword(s):  
Heart Disease ◽  
Mouse Models ◽  
Vascular Function ◽  
Cardiac Fibrosis ◽  
Interstitial Fibrosis ◽  
Severe Disease ◽  
Cardiac Contractility ◽  
Hypertensive Heart Disease ◽  
Light Sheet ◽  
Preclinical Research

Fibrosis is the hallmark of hypertensive heart disease and heart failure with preserved ejection fraction. Perivascular fibrosis impairs vascular function while interstitial fibrosis leads to compromised cardiac contractility. How these fibrosis types are represented in mouse models of hypertensive heart disease and to what extent the transcriptional signatures of cardiac fibrosis are defined by their location is unknown. Mice were dosed over 4 weeks with angiotensin II (AngII) alone or together with α 1 -adrenergic agonist phenylephrine (PE) and were characterized by echocardiography, light sheet imaging and fibrosis histology. While both groups developed systolic and diastolic dysfunction, hypertrophy and perivascular fibrosis, co-administration of PE resulted in a more severe disease phenotype and prevalent interstitial fibrosis, highlighting the benefits of this model in preclinical research. High-precision spatial transcriptomics based on laser capture microdissected perivascular and interstitial fibrotic areas revealed activation of distinct pro-fibrotic as well as cardioprotective pathways in the AngII+PE infusion model. Perivascular and interstitial fibrosis showed remarkable differences in global gene expression signatures, as demonstrated by high expression of osteochondrogenic genes and markers of secretory fibroblasts in perivascular fibrosis. A limited number of upregulated genes is shared between the fibrosis locations. These data collectively show the suitability of mouse models of hypertensive heart disease to study cardiac fibrosis and demonstrate how progression of fibrosis in mice is closely coupled to deteriorating cardiac dysfunction associated with highly distinct molecular signatures of perivascular and interstitial fibrosis.

scholarly journals Regression of Established Cardiac Fibrosis in Hypertensive Heart Disease

2017 ◽  
Vol 30 (11) ◽  
pp. 1049-1052 ◽  
Author(s):  
Karl T Weber ◽  
Yao Sun ◽  
Ivan C Gerling ◽  
Ramareddy V Guntaka
Keyword(s):  
Heart Disease ◽  
Cardiac Fibrosis ◽  
Hypertensive Heart Disease

Chronic administration of hexarelin attenuates cardiac fibrosis in the spontaneously hypertensive rat

2012 ◽  
Vol 303 (6) ◽  
pp. H703-H711 ◽  
Author(s):  
Xiangbin Xu ◽  
Fan Ding ◽  
Jinjiang Pang ◽  
Xue Gao ◽  
Rong-Kun Xu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Disease ◽  
Cardiac Fibrosis ◽  
Spontaneously Hypertensive Rat ◽  
Therapeutic Potential ◽  
Heart Diseases ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Spontaneously Hypertensive

Cardiac fibrosis is a hallmark of heart disease and plays a vital role in cardiac remodeling during heart diseases, including hypertensive heart disease. Hexarelin is one of a series of synthetic growth hormone secretagogues (GHSs) possessing a variety of cardiovascular effects via action on GHS receptors (GHS-Rs). However, the role of hexarelin in cardiac fibrosis in vivo has not yet been investigated. In the present study, spontaneously hypertensive rats (SHRs) were treated with hexarelin alone or in combination with a GHS-R antagonist for 5 wk from an age of 16 wk. Hexarelin treatment significantly reduced cardiac fibrosis in SHRs by decreasing interstitial and perivascular myocardial collagen deposition and myocardial hydroxyproline content and reducing mRNA and protein expression of collagen I and III in SHR hearts. Hexarelin treatment also increased matrix metalloproteinase (MMP)-2 and MMP-9 activities and decreased myocardial mRNA expression of tissue inhibitor of metalloproteinase (TIMP)-1 in SHRs. In addition, hexarelin treatment significantly attenuated left ventricular (LV) hypertrophy, LV diastolic dysfunction, and high blood pressure in SHRs. The effect of hexarelin on cardiac fibrosis, blood pressure, and cardiac function was mediated by its receptor, GHS-R, since a selective GHS-R antagonist abolished these effects and expression of GHS-Rs was upregulated by hexarelin treatment. In summary, our data demonstrate that hexarelin reduces cardiac fibrosis in SHRs, perhaps by decreasing collagen synthesis and accelerating collagen degradation via regulation of MMPs/TIMP. Hexarelin-reduced systolic blood pressure may also contribute to this reduced cardiac fibrosis in SHRs. The present findings provided novel insights and underscore the therapeutic potential of hexarelin as an antifibrotic agent for the treatment of cardiac fibrosis.

scholarly journals Estimation and determinants of direct medical costs of ischaemic heart disease, stroke and hypertensive heart disease: evidence from two major hospitals in Cameroon

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Leopold Ndemnge Aminde ◽  
Anastase Dzudie ◽  
Yacouba N. Mapoure ◽  
Jacques Cabral Tantchou ◽  
J. Lennert Veerman
Keyword(s):  
Diabetes Mellitus ◽  
Heart Disease ◽  
Ischaemic Stroke ◽  
Ischaemic Heart Disease ◽  
Economic Burden ◽  
Hypertensive Heart Disease ◽  
Haemorrhagic Stroke ◽  
Medical Costs ◽  
Communicable Diseases ◽  
Direct Medical Costs

Abstract Background Cardiovascular disease (CVD) is the largest contributor to the non-communicable diseases (NCD) burden in Cameroon, but data on its economic burden is lacking. Methods A prevalence-based cost-of-illness study was conducted from a healthcare provider perspective and enrolled patients with ischaemic heart disease (IHD), ischaemic stroke, haemorrhagic stroke and hypertensive heart disease (HHD) from two major hospitals between 2013 and 2017. Determinants of cost were explored using multivariate generalized linear models. Results Overall, data from 850 patients: IHD (n = 92, 10.8%), ischaemic stroke (n = 317, 37.3%), haemorrhagic stroke (n = 193, 22.7%) and HHD (n = 248, 29.2%) were analysed. The total cost for these CVDs was XAF 676,694,000 (~US$ 1,224,918). The average annual direct medical costs of care per patient were XAF 1,395,200 (US$ 2400) for IHD, XAF 932,700 (US$ 1600) for ischaemic stroke, XAF 815,400 (US$ 1400) for haemorrhagic stroke, and XAF 384,300 (US$ 700) for HHD. In the fully adjusted models, apart from history of CVD event (β = − 0.429; 95% confidence interval − 0.705, − 0.153) that predicted lower costs in patients with IHD, having of diabetes mellitus predicted higher costs in patients with IHD (β = 0.435; 0.098, 0.772), ischaemic stroke (β = 0.188; 0.052, 0.324) and HHD (β = 0.229; 0.080, 0.378). Conclusions This study reveals substantial economic burden due to CVD in Cameroon. Diabetes mellitus was a consistent driver of elevated costs across the CVDs. There is urgent need to invest in cost-effective primary prevention strategies in order to reduce the incidence of CVD and consequent economic burden on a health system already laden with the impact of communicable diseases.

QT dispersion and hypertensive heart disease in the elderly

2000 ◽  
Vol 18 (4) ◽  
pp. 461-464 ◽  
Author(s):  
Barbara Gryglewska ◽  
Tomasz Grodzicki ◽  
Danuta Czarnecka ◽  
Kalina Kaweoicka-Jaszcz ◽  
Józef Kocemba
Keyword(s):  
Heart Disease ◽  
Hypertensive Heart Disease ◽  
Qt Dispersion ◽  
The Elderly
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