Relationship of postcontrast myocardial T1 value and delayed enhancement to reduced cardiac function and serious arrhythmia in dilated cardiomyopathy with left ventricular ejection fraction less than 35%

Tachi, Masaki; Amano, Yasuo; K, Inui; Takeda, Minako; Yamada, Fumi; Asai, Kuniya; Kumita, Shin‐ichiro

doi:10.1177/0284185115580840

Cited by 16 publications

(9 citation statements)

References 33 publications

(51 reference statements)

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“…The majority of studies evaluated the presence or absence of LGE by visual analysis. 4,6,7,10,[13][14][15][16][17][18][19][20]22,[24][25][26][27][28][29]30,32 Duration of follow-up ranged from 1 year to 5.3 years; mean follow up was 3 years. The majority of reports considered a composite arrhythmic end-point formed by sudden cardiac death and/or aborted cardiac arrest, sustained ventricular arrhythmias and/or appropriate ICD therapies.…”

Section: Study Characteristicsmentioning

confidence: 99%

Late Gadolinium Enhancement and the Risk for Ventricular Arrhythmias or Sudden Death in Dilated Cardiomyopathy

Marco

Anguera

Schmitt³

et al. 2017

JACC: Heart Failure

311

188

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Di Marco, A. et al. (2017) Late gadolinium enhancement and the risk for ventricular arrhythmias or sudden death in dilated cardiomyopathy: systematic review and meta-analysis. JACC: Heart Failure, 5(1), pp. 28-38. (doi:10.1016/j.jchf.2016.09.017) This is the author's final accepted version.There may be differences between this version and the published version. You are advised to consult the publisher's version if you wish to cite from it.http://eprints.gla.ac.uk/133553/ Background: Risk stratification for SCD in DCM needs to be improved.

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Section: Study Characteristicsmentioning

confidence: 99%

Late Gadolinium Enhancement and the Risk for Ventricular Arrhythmias or Sudden Death in Dilated Cardiomyopathy

Marco

Anguera

Schmitt³

et al. 2017

JACC: Heart Failure

311

188

View full text Add to dashboard Cite

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“…Therefore, further study on the internal mechanism of HF pathology and explore the effective means to block the mechanism, will provide valuable basic research information for clinical treatment of HF. Indeed, certain mutations often induce HF with cardiac arrhythmia that is considered as the potential trigger of sudden cardiac death 62 63 . Thus, both the effective prognostic determination and appropriate cardiac care depend on accurate molecular and genetic diagnoses and therapy.…”

Section: Discussionmentioning

confidence: 99%

Autophagy inhibition of hsa-miR-19a-3p/19b-3p by targeting TGF-β R II during TGF-β1-induced fibrogenesis in human cardiac fibroblasts

Zou

Wang

Gao

et al. 2016

Sci Rep

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Transforming growth factor-β1 (TGF-β1) plays an important role on fibrogenesis in heart disease. MicroRNAs have exhibited as crucial regulators of cardiac homeostasis and remodeling in various heart diseases. MiR-19a-3p/19b-3p expresses with low levels in the plasma of heart failure patients. The purpose of our study is to determine the role of MiR-19a-3p/19b-3p in regulating autophagy-mediated fibrosis of human cardiac fibroblasts. We elucidate our hypothesis in clinical samples and human cardiac fibroblasts (HCF) to provide valuable basic information. TGF-β1 promotes collagen I α2 and fibronectin synthesis in HCF and that is paralleled by autophagic activation in these cells. Pharmacological inhibition of autophagy by 3-methyladenine decreases the fibrotic response, while autophagy induction of rapamycin increases the response. BECN1 knockdown and Atg5 over-expression either inhibits or enhances the fibrotic effect of TGF-β1 in experimental HCF. Furthermore, miR-19a-3p/19b-3p mimics inhibit epithelial mesenchymal transition (EMT) and extracellular matrix (ECM) prodution and invasion of HCF. Functional studies suggest that miR-19a-3p/19b-3p inhibits autophagy of HCF through targeting TGF-β R II mRNA. Moreover, enhancement of autophagy rescues inhibition effect of miR-19a-3p/19b-3p on Smad 2 and Akt phosphorylation through TGF-β R II signaling. Our study uncovers a novel mechanism that miR-19a-3p/19b-3p inhibits autophagy-mediated fibrogenesis by targeting TGF-β R II.

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“…10). More importantly, the occurrence and extent of LGE have been associated with a worse clinical outcome, in particular with impaired ventricular filling and systolic function [83][84][85] and with life-threatening arrhythmias [86][87][88]. A recent study found that galectin-3 predicted the presence and extent of replacement fibrosis at cardiac CMR in a cohort of patients with DCM [89], consistently with the causal role of galectin-3 in the determination of myocardial fibrosis and remodelling.…”

Section: Late Gadolinium Enhancementmentioning

confidence: 94%

Myocardial interstitial remodelling in non-ischaemic dilated cardiomyopathy: insights from cardiovascular magnetic resonance

et al. 2015

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Myocardial remodelling involves not only the myocytes, but also non-myocyte cells and the extracellular matrix, which constitutes around 6 % of the normal heart and includes fluid, collagen and glycoproteins. In non-ischaemic dilated cardiomyopathy (DCM), the cardiac interstitium increases as a result of diffuse interstitial (microscopic) fibrosis, post-necrotic replacement (macroscopic) fibrosis or myocardial oedema. The activation of the renin-angiotensin-aldosterone system is a major determinant of fibroblasts activation and collagen deposition, with the transforming growth factor β as the downstream signal mediator. Endomyocardial biopsy still represents the current reference method for interstitial and replacement myocardial fibrosis assessment, but cardiovascular magnetic resonance (CMR) allows in vivo detection of macroscopic fibrosis with post-contrast late enhancement imaging. Moreover, recent pre- and post-contrast T1 mapping techniques provide a quantitative estimation of myocardial interstitial remodelling, with potential diagnostic and prognostic clinical utility. Here, we review the pathophysiological mechanisms of myocardial interstitial remodelling in DCM, its non-invasive characterization with biomarkers and with CMR, as well as the most recent studies about their clinical utility.

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Relationship of postcontrast myocardial T1 value and delayed enhancement to reduced cardiac function and serious arrhythmia in dilated cardiomyopathy with left ventricular ejection fraction less than 35%

Cited by 16 publications

References 33 publications

Late Gadolinium Enhancement and the Risk for Ventricular Arrhythmias or Sudden Death in Dilated Cardiomyopathy

Late Gadolinium Enhancement and the Risk for Ventricular Arrhythmias or Sudden Death in Dilated Cardiomyopathy

Autophagy inhibition of hsa-miR-19a-3p/19b-3p by targeting TGF-β R II during TGF-β1-induced fibrogenesis in human cardiac fibroblasts

Myocardial interstitial remodelling in non-ischaemic dilated cardiomyopathy: insights from cardiovascular magnetic resonance

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