scholarly journals Myocardial Interstitial Fibrosis in Heart Failure

2018 ◽  
Vol 71 (15) ◽  
pp. 1696-1706 ◽  
Author(s):  
Arantxa González ◽  
Erik B. Schelbert ◽  
Javier Díez ◽  
Javed Butler
Keyword(s):  
Heart Failure ◽  
Interstitial Fibrosis ◽  
Myocardial Interstitial Fibrosis

scholarly journals Prognostic Impact of Myocardial Interstitial Fibrosis in Non-Ischemic Heart Failure

2011 ◽  
Vol 75 (11) ◽  
pp. 2605-2613 ◽  
Author(s):  
Tatsuo Aoki ◽  
Yoshihiro Fukumoto ◽  
Koichiro Sugimura ◽  
Minako Oikawa ◽  
Kimio Satoh ◽  
...  
Keyword(s):  
Heart Failure ◽  
Interstitial Fibrosis ◽  
Ischemic Heart ◽  
Prognostic Impact ◽  
Ischemic Heart Failure ◽  
Myocardial Interstitial Fibrosis

Heart failure in chronic kidney disease: the emerging role of myocardial fibrosis

2020 ◽  
Author(s):  
Gregorio Romero-González ◽  
Arantxa González ◽  
Begoña López ◽  
Susana Ravassa ◽  
Javier Díez
Keyword(s):  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Current Knowledge ◽  
Interstitial Fibrosis ◽  
Collagen Fibres ◽  
Fibrotic Tissue ◽  
Myocardial Interstitial Fibrosis ◽  
New Strategy

Abstract Heart failure (HF) is one of the main causes of morbidity and mortality in patients with chronic kidney disease (CKD). Decreased glomerular filtration rate is associated with diffuse deposition of fibrotic tissue in the myocardial interstitium [i.e. myocardial interstitial fibrosis (MIF)] and loss of cardiac function. MIF results from cardiac fibroblast-mediated alterations in the turnover of fibrillary collagen that lead to the excessive synthesis and deposition of collagen fibres. The accumulation of stiff fibrotic tissue alters the mechanical properties of the myocardium, thus contributing to the development of HF. Accumulating evidence suggests that several mechanisms are operative along the different stages of CKD that may converge to alter fibroblasts and collagen turnover in the heart. Therefore, focusing on MIF might enable the identification of fibrosis-related biomarkers and targets that could potentially lead to a new strategy for the prevention and treatment of HF in patients with CKD. This article summarizes current knowledge on the mechanisms and detrimental consequences of MIF in CKD and discusses the validity and usefulness of available biomarkers to recognize the clinical–pathological variability of MIF and track its clinical evolution in CKD patients. Finally, the currently available and potential future therapeutic strategies aimed at personalizing prevention and reversal of MIF in CKD patients, especially those with HF, will be also discussed.

Histomolecular fibrotic profile and an extent of the atrial and ventricular electroanatomical substrate in patients with atrial fibrillation and heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V Orshanskaya ◽  
V.S Orshanskaya ◽  
A.V Kamenev ◽  
L.B Mitrofanova ◽  
L.A Belyakova ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Plasma Level ◽  
Serum Level ◽  
Interstitial Fibrosis ◽  
Myocardial Interstitial Fibrosis ◽  
Relative Extent ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Abstract Background and purpose The aim of this pilot study was to investigate the association between an extent of the atrial and ventricular electroanatomical substrate, serum fibrotic biomarkers and histological and immune-histochemical myocardial characteristics in ipatients with atrial fibrillation and heart failure. Methods We prospectively analyzed electroanatomical ultra-high density bipolar maps (HDBM) in 72 patients with AF and CHF, who underwent circular pulmonary veins (PVs) isolation. LA areas outside PVs ostia with bipolar signals ≤0.75mV, associated with local conduction velocity delay were considered as EAS and measured. Relative area of low voltage zones in right (RV) and left ventricles (RV) with bipolar signals in range of 0,5–1,5 mV were also consistently measured. Endomyocardial biopsy samples were taken from low, mediate and high septal areas of RV; histological and immune-histochemical staining was performed and an extent of myocardial interstitial fibrosis (MIF) was calculated. Before the operation we measured plasma MMP2, MMP9, TIMP, MMPs/TIMPs, galectin 3 (Gal3), TGF, soluble ST2 and the cross-linked collagen I/III synthesis and degradation product levels. The patients were divided into groups according to their ejection fraction Simpson (EF) (groups 1: EF≥50%, groups 2: EF 40–49%, and groups 3: EF<40%). Results The data of electroanatomical mapping, serum biomarkers and myocardial expression are presented in the table. According to results of correlation analysis, an extent of LA EAS were correlated with Gal3 and PIIICP plasma level and Gal3 myocardial expression and MIF extent (Rs=0,40, 0,45 and 0,42 respectively). The relative extent of LV EAS was correlated with MMP9 serum level (Rs=0,38); LV volume (LVV) was correlated with sST2 serum level and RVV was correlated with CD 133 myocardial expression (Rs=0,42) (picture 1). The patients with lower EF had larger extent of the LA EAS, (group 3: 28±12.4% vs. 1: 17.7±11.6%, p=0.03), an extent of LV EAS and LVV (group 3: 8,4±4,5% vs. 1: 5,1±3,8% p=0.02; group 3 vs group 1 p=0,05 relatively),higher Gal3 plasma level (group 1: 7,1±2 vs. group 2: 8,9±1,5, p=0.05) and higher MIF extent (group 2: 134±56 vs. 3: 151±30 p=0.04) (picture 2). Conclusion Our data suggest that relative extent of LA EAS in patients with atrial fibrillation is associated with Gal3 plasma level and Gal3 myocardial expression; severity of myocardial remodeling is connected to CD 3/133 myocardial expression and myocardial interstitial fibrosis extent, especially in patients with HF with restricted LV ejection fraction. Funding Acknowledgement Type of funding source: None

Role of Inflammation, Viruses and Tissue Macrophages in the Development of Idiopathic Arrhythmia and Heart Failure

2016 ◽  
Vol 683 ◽  
pp. 487-492 ◽  
Author(s):  
Yuliya Rogovskaya ◽  
Roman Botalov ◽  
Vyacheslav Ryabov ◽  
Mariya Rebenkova ◽  
Rostislav Karpov ◽  
...  
Keyword(s):  
Heart Failure ◽  
Interstitial Fibrosis ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Viral Antigens ◽  
Myocardial Interstitial Fibrosis ◽  
Histological Criteria ◽  
Cardiotropic Viruses ◽  
Alternatively Activated

Endomyocardial biopsy is the gold standard in the diagnosis of myocardial pathology. Intravital study of endomyocardial samples offers the possibility to determine the morphological substrate and etiology of disease, to monitor the effectiveness of treatment. We studied morphological features, viral antigens, macrophages and specifically alternatively activated macrophages in endomyocardial biopsies of 25 patients with idiopathic arrhythmias and heart failure. Immunohistological study was performed to identify type of lymphocytes, macrophages and antigens of cardiotropic viruses. We observed the presence of alternatively activated macrophages in myocardium of patients with myocarditis and without it. We detected the presence of viral antigens in the myocardium of patients with myocardial fibrosis without of histological criteria myocarditis. Small focal infiltration of the myocardial CD68+ macrophages associated with heart failure and ventricular arrhythmias. The presence of virus antigens in myocardium associated with fewer myocardial stabilin-1+ macrophages [negative correlation]. On the other side small focal infiltration of stabilin-1+ macrophages correlated with severity of myocardial interstitial fibrosis [positive correlation]

scholarly journals Genetics of Myocardial Interstitial Fibrosis in the Human Heart and Association with Disease

2021 ◽  
Author(s):  
Victor Nauffal ◽  
Paolo Di Achille ◽  
Marcus D. R. Klarqvist ◽  
Jonathan W. Cunningham ◽  
James P. Pirruccello ◽  
...  
Keyword(s):  
Machine Learning ◽  
Heart Failure ◽  
Atrial Fibrillation ◽  
Human Heart ◽  
Iron Homeostasis ◽  
Interstitial Fibrosis ◽  
Association Studies ◽  
Interventricular Septum ◽  
Myocardial Interstitial Fibrosis ◽  
Myocardial T1

Myocardial interstitial fibrosis is a common thread in multiple cardiovascular diseases including heart failure, atrial fibrillation, conduction disease and sudden cardiac death. To investigate the biologic pathways that underlie interstitial fibrosis in the human heart, we developed a machine learning model to measure myocardial T1 time, a marker of myocardial interstitial fibrosis, in 42,654 UK Biobank participants. Greater T1 time was associated with impaired glucose metabolism, systemic inflammation, renal disease, aortic stenosis, cardiomyopathy, heart failure, atrial fibrillation and conduction disease. In genome-wide association analysis, we identified 12 independent loci associated with native myocardial T1 time with evidence of high genetic correlation between the interventricular septum and left ventricle free wall (r2g = 0.82). The identified loci implicated genes involved in glucose homeostasis (SLC2A12), iron homeostasis (HFE, TMPRSS6), tissue repair (ADAMTSL1, VEGFC), oxidative stress (SOD2), cardiac hypertrophy (MYH7B) and calcium signaling (CAMK2D). Transcriptome-wide association studies highlighted the role of expression of ADAMTSL1 and SLC2A12 in human cardiac tissue in modulating myocardial tissue characteristics and interstitial fibrosis. Harnessing machine learning to perform large-scale phenotyping of interstitial fibrosis in the human heart, our results yield novel insights into biologically relevant pathways for myocardial fibrosis and prioritize investigation of pathways for the development of anti-fibrotic therapies.

scholarly journals p90 ribosomal S6 kinase 3 contributes to cardiac insufficiency in α-tropomyosin Glu180Gly transgenic mice

2013 ◽  
Vol 305 (7) ◽  
pp. H1010-H1019 ◽  
Author(s):  
Catherine L. Passariello ◽  
Marjorie Gayanilo ◽  
Michael D. Kritzer ◽  
Hrishikesh Thakur ◽  
Zoharit Cozacov ◽  
...  
Keyword(s):  
Heart Failure ◽  
Transgenic Mice ◽  
Cardiac Function ◽  
Interstitial Fibrosis ◽  
Cardiac Insufficiency ◽  
S6 Kinase ◽  
Transgenic Expression ◽  
P90 Ribosomal S6 Kinase ◽  
Ribosomal S6 Kinase

Myocardial interstitial fibrosis is an important contributor to the development of heart failure. Type 3 p90 ribosomal S6 kinase (RSK3) was recently shown to be required for concentric myocyte hypertrophy under in vivo pathological conditions. However, the role of RSK family members in myocardial fibrosis remains uninvestigated. Transgenic expression of α-tropomyosin containing a Glu180Gly mutation (TM180) in mice of a mixed C57BL/6:FVB/N background induces a cardiomyopathy characterized by a small left ventricle, interstitial fibrosis, and diminished systolic and diastolic function. Using this mouse model, we now show that RSK3 is required for the induction of interstitial fibrosis in vivo. TM180 transgenic mice were crossed to RSK3 constitutive knockout ( RSK3−/−) mice. Although RSK3 knockout did not affect myocyte growth, the decreased cardiac function and mild pulmonary edema associated with the TM180 transgene were attenuated by RSK3 knockout. The improved cardiac function was consistent with reduced interstitial fibrosis in the TM180; RSK3−/− mice as shown by histology and gene expression analysis, including the decreased expression of collagens. The specific inhibition of RSK3 should be considered as a potential novel therapeutic strategy for improving cardiac function and the prevention of sudden cardiac death in diseases in which interstitial fibrosis contributes to the development of heart failure.

scholarly journals Crackle Pitch Rises Progressively during Inspiration in Pneumonia, CHF, and IPF Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Andrey Vyshedskiy ◽  
Raymond Murphy
Keyword(s):  
Heart Failure ◽  
Lung Volume ◽  
Interstitial Fibrosis ◽  
Lung Sounds ◽  
Lung Sound ◽  
Lung Volumes ◽  
Alternate Explanation ◽  
40 Hz

Objective. It is generally accepted that crackles are due to sudden opening of airways and that larger airways produce crackles of lower pitch than smaller airways do. As larger airways are likely to open earlier in inspiration than smaller airways and the reverse is likely to be true in expiration, we studied crackle pitch as a function of crackle timing in inspiration and expiration. Our goal was to see if the measurement of crackle pitch was consistent with this theory.Methods. Patients with a significant number of crackles were examined using a multichannel lung sound analyzer. These patients included 34 with pneumonia, 38 with heart failure, and 28 with interstitial fibrosis.Results. Crackle pitch progressively increased during inspirations in 79% of all patients. In these patients crackle pitch increased by approximately 40 Hz from the early to midinspiration and by another 40 Hz from mid to late-inspiration. In 10% of patients, crackle pitch did not change and in 11% of patients crackle pitch decreased. During expiration crackle pitch progressively decreased in 72% of patients and did not change in 28% of patients.Conclusion. In the majority of patients, we observed progressive crackle pitch increase during inspiration and decrease during expiration. Increased crackle pitch at larger lung volumes is likely a result of recruitment of smaller diameter airways. An alternate explanation is that crackle pitch may be influenced by airway tension that increases at greater lung volume. In any case improved understanding of the mechanism of production of these common lung sounds may help improve our understanding of pathophysiology of these disorders.

Sign in / Sign up

Export Citation Format

Share Document