scholarly journals How does the Extracellular Matrix Change in the Setting of Heart Failure?

2018 ◽  
Vol 6 (3) ◽  
pp. 102-109
Author(s):  
Amerikos Argyriou
Keyword(s):  
Heart Failure ◽  
Extracellular Matrix ◽  
Degradation Products ◽  
Internal Communication ◽  
Matrix Proteins ◽  
Reduced Ejection Fraction ◽  
Functional Changes ◽  
Metalloproteinase Inhibitors

The Extracellular Matrix is a dynamic entity, showing constant degradation and deposition while providing the framework for the cardiomyocytes and interstitial proteins to lie on. Its function is important for the proper myocyte alignment within the heart and for internal communication from cell to matrix. Dysregulation of the remodeling process resulting in the breakdown of collagen by matrix metalloproteinases is a hallmark of heart failure pathophysiology and produces functional changes encompassing all matrix proteins. Several etiologies with distinct mechanisms ultimately bring about signs of heart exhaustion such as reduced ejection fraction, reduced compliance and ventricular dilatation. Discussed in this paper is the role of inflammation, collagen cross-linking and of myofibroblasts in matrix dysfunction and the mechanisms with which these changes occur in heart failure. Understanding extracellular protein roles within this context would allow for specific drug targeting and thus prevention of heart failure in the early stages of the disease. More studies must be conducted to discover the specific matrix proteins and cytokines that modulate the pathological remodeling process. Serum biomarkers of extracellular degradation products, selective metalloproteinase inhibitors and a personalized treatment approach with a revisal of the current classification of heart failure are topics requiring further exploration.

scholarly journals Extracellular Matrix in Cardiac Tissue Mechanics and Physiology: Role of Collagen Accumulation

2021 ◽  
Author(s):  
Kristen LeBar ◽  
Zhijie Wang
Keyword(s):  
Heart Failure ◽  
Mechanical Properties ◽  
Extracellular Matrix ◽  
Pressure Overload ◽  
Volume Overload ◽  
Tissue Mechanics ◽  
Functional Changes ◽  
Collagen Accumulation ◽  
Heart Failure Progression

The extracellular matrix (ECM) forms a mesh surrounding tissue, made up of fibrous and non-fibrous proteins that contribute to the cellular function, mechanical properties of the tissue and physiological function of the organ. The cardiac ECM remodels in response to mechanical alterations (e.g., pressure overload, volume overload) or injuries (e.g., myocardial infarction, bacterial infection), which further leads to mechanical and functional changes of the heart. Collagen, the most prevalent ECM protein in the body, contributes significantly to the mechanical behavior of myocardium during disease progression. Alterations in collagen fiber morphology and alignment, isoform, and cross-linking occur during the progression of various cardiac diseases. Acute or compensatory remodeling of cardiac ECM maintains normal cardiac function. However, chronic or decompensatory remodeling eventually results in heart failure, and the exact mechanism of transition into maladaptation remains unclear. This review aims to summarize the primary role of collagen accumulation (fibrosis) in heart failure progression, with a focus on its effects on myocardial tissue mechanical properties and cellular and organ functions.

Prognostic role of myocardial work in patients with heart failure and reduced ejection fraction treated by sacubitril/valsartan

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
E Galli ◽  
Y Bouali ◽  
C Laurin ◽  
A Gallard ◽  
A Hubert ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Rank Test ◽  
Reduced Ejection Fraction ◽  
Non Invasive ◽  
Patients With Heart Failure ◽  
Increase Risk ◽  
Echocardiographic Examination ◽  
Constructive Work

Abstract Background The non-invasive assessment of myocardial work (MW) by pressure-strain loops analysis (PSL) is a relative new tool for the evaluation of myocardial performance. Sacubitril/Valsartan is a treatment for heart failure with reduced ejection fraction (HFrEF) which has a spectacular effect on the reduction of cardiovascular events (MACEs). Purposes of this study were to evaluate 1) the short and medium term effect of Sacubitril/Valsartan treatment on MW parameters; 2) the prognostic value of MW in this specific group of patients. Methods 79 patients with HFrEF (mean age: 66±12 years; LV ejection fraction: 28±9%) were prospectively included in the study and treated with Sacubitril/Valsartan. Echocardiographic examination was performed at baseline, and after 6- and 12-month of therapy with Sacubitril/Valsartan. Results Sacubitril/Valsartan significantly increased global myocardial constructive work (CW) (1023±449 vs 1424±484 mmHg%, p<0.0001) and myocardial work efficiency (WE) [87 (78–90) vs 90 (86–95), p<0.0001]. During FU (2.6±0.9 years), MACEs occurred in 13 (16%) patients. After correction for LV size, LVEF and WE, CW was the only predictor of MACEs (Table 1). A CW<910 mmHg (AUC=0.81, p<0.0001, Figure 1A) identified patients at particularly increase risk of MACEs [HR 11.09 (1.45–98.94), p=0.002, log-rank test p<0.0001] (Figure 1 B). Conclusions In patients with HFrEF who receive a comprehensive background beta-blocker and mineral-corticoid receptor antagonist therapy, Sacubitril/Valsartan induces a significant improvement of myocardial CW and WE. In this population, the estimation of CW before the initiation of Sacubitril/Valsartan therapy allows the prediction of MACEs. Funding Acknowledgement Type of funding source: None

scholarly journals Refining the Role of Left Atrial Strain in Heart Failure with Reduced Ejection Fraction

2021 ◽  
Author(s):  
Alessandro Malagoli ◽  
Luca Rossi ◽  
Alessia Zanni ◽  
Concetta Sticozzi ◽  
Massimo Francesco Piepoli ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Left Atrial ◽  
Left Atrial Strain ◽  
Reduced Ejection Fraction ◽  
Atrial Strain

Clinico-pharmacological aspects of metoprolol use

2013 ◽  
Vol 10 (4) ◽  
pp. 80-83
Author(s):  
G S Anikin ◽  
I M Chernova ◽  
V G Vinokurov
Keyword(s):  
Heart Failure ◽  
Coronary Artery Disease ◽  
Review Article ◽  
Metoprolol Tartrate ◽  
Metoprolol Succinate ◽  
Treatment Of Hypertension ◽  
Cardiovascular Pathologies ◽  
Artery Disease

Over the years b-blocker metoprolol is one of the commonly prescribed drugs for the treatment of various cardiovascular pathologies . The following review article discusses the classification of b-blockers , and pharmacokinetics of two metoprolol forms available on the market today: metoprolol tartrate (Vasocardin, Corvitolum, Egilok ) and metoprolol succinate (Betaloc ZOK). The role of metoprolol in the treatment of hypertension, coronary artery disease and heart failure is described here as well.

An analysis of culmination in Dictyostelium using prestalk and stalk-specific cell autonomous markers

Development ◽  
1991 ◽  
Vol 111 (3) ◽  
pp. 779-787 ◽  
Author(s):  
K.A. Jermyn ◽  
J.G. Williams
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Dictyostelium Discoideum ◽  
Tube Formation ◽  
Matrix Proteins ◽  
Specific Cell ◽  
Primary Role ◽  
Fusion Genes ◽  
Spore Mass

The ecmA (pDd63) and ecmB (pDd56) genes encode extracellular matrix proteins of the slime sheath and stalk tube of Dictyostelium discoideum. Using fusion genes containing the promoter of one or other gene coupled to an immunologically detectable reporter, we previously identified two classes of prestalk cells in the tip of the migrating slug; a central core of pstB cells, which express the ecmB gene, surrounded by pstA cells, which express the ecmA gene. PstB cells lie at the position where stalk tube formation is initiated at culmination and we show that they act as its founders. As culmination proceeds, pstA cells transform into pstB cells by activating the ecmB gene as they enter the stalk tube. The prespore region of the slug contains a population of cells, termed anterior-like cells (ALC), which have the characteristics of prestalk cells. We show that the ecmA and ecmB genes are expressed at a low level in ALC during slug migration and that their expression in these cells is greatly elevated during culmination. Previous observations have shown that ALC sort to surround the prespore cells during culmination (Sternfeld and David, 1982 Devl Biol. 93, 111–118) and we find just such a distribution for pstB cells. We believe that the ecmB protein plays a structural role in the stalk tube and its presence, as a cradle around the spore head, suggests that it may play a further function, perhaps in ensuring integrity of the spore mass during elevation. If this interpretation is correct, then a primary role of anterior-like cells may be to form these structures at culmination. We previously identified a third class of prestalk cells, pstO cells, which lie behind pstA cells in the slug anterior and which appeared to express neither the ecmA nor the ecmB gene. Using B-galactosidase fusion constructs, which give more sensitive detection of gene expression, we now find that these cells express the ecmA gene but at a much lower level than pstA cells. We also show that expression of the ecmA gene becomes uniformly high throughout the prestalk zone when slugs are allowed to migrate in the light. Overhead light favours culmination and it may be that increased expression of the ecmA gene in the pst ‘O’ region is a preparatory step in the process.

Abstract 354: The Role of the Liver Heart Axis During Cardiac Remodeling

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Soichiro Usui ◽  
Shin-ichiro Takashima ◽  
Kenji Sakata ◽  
Masa-aki Kawashiri ◽  
Masayuki Takamura
Keyword(s):  
Heart Failure ◽  
Insulin Resistance ◽  
Cardiac Remodeling ◽  
Pressure Overload ◽  
Normal Subjects ◽  
Serum Levels ◽  
Lung Weight ◽  
Reduced Ejection Fraction ◽  
Hepatic Expression

Background: Hepatokine selenoprotein P (SeP) contributes to insulin resistance and hyperglycemia in patients with type 2 diabetes. Although clinical studies suggest the insulin resistance is an independent risk factor of heart failure and inhibition of SeP protects the heart from ischemia reperfusion injury, the role of SeP in pathogenesis of chronic heart failure is not well understood. Objective: We examined the role of SeP in the regulation of cardiac remodeling in response to pressure overload. Methods and Results: We measured serum SeP levels in 22 patients for heart failure with reduced ejection fraction (HFrEF; LVEF<50%) and 22 normal subjects. Serum levels of SeP were significantly elevated in patients with HFrEF compared to in normal subjects (3.55 ± 0.43 vs 2.98 ± 0.43, p<0.01). To examine the role of SeP in cardiac remodeling, SeP knockout (KO) and wild-type (WT) mice were subjected to pressure overload (transverse aortic constriction (TAC)) for 2 weeks. The mortality rate following TAC was significantly decreased in SeP KO mice compared to WT mice (22.5 % in KO mice (n=40) vs 52.3 % in WT mice (n=39) p<0.01). LV weight/tibial length (TL) was significantly smaller in SeP KO mice than in WT mice (6.75 ± 0.24 vs 8.33 ± 0.32, p<0.01). Lung weight/TL was significantly smaller in SeP KO than in WT mice (10.46 ± 0.44 vs 16.38 ± 1.12, p<0.05). Interestingly, hepatic expression of SeP in WT was significantly increased by TAC. To determine whether hepatic overexpression of SeP affects TAC-induced cardiac hypertrophy, a hydrodynamic injection method was used to generate mice that overexpress SeP mRNA in the liver. Hepatic overexpression of SeP in SeP KO mice lead to a significant increase in LV weight/TL and Lung weight/TL after TAC compared to that in other SeP KO mice. Conclusions: These results suggest that serum levels of SeP were elevated in patients with heart failure with reduced ejection fraction and cardiac pressure overload induced hepatic expression of SeP in mice model. Gene deletion of SeP attenuated cardiac hypertrophy and dysfunction in response to pressure overload in mice. SeP possibly plays a pivotal role in promoting cardiac remodeling through the liver-heart axis.

HFrEF other treatment: revascularization

ESC CardioMed ◽  
2018 ◽  
pp. 1881-1884
Author(s):  
Eric Velazquez ◽  
Mark C. Petrie
Keyword(s):  
Quality Of Life ◽  
Heart Failure ◽  
Coronary Artery Disease ◽  
Controlled Clinical Trial ◽  
Randomized Controlled Clinical Trial ◽  
Common Cause ◽  
Reduced Ejection Fraction ◽  
Artery Disease

Although coronary artery disease is the most common cause of heart failure with reduced ejection fraction (HFrEF), the role of revascularization as a treatment strategy to improve survival, reduce morbidity, and enhance the quality of life has only begun to be investigated in recent years. To date, a sole randomized controlled clinical trial has been completed. This chapter summarizes what is currently known and what is unknown with respect to revascularization for the treatment of HFrEF.

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