Myocardial fibrosis: why image, how to image and clinical implications

Bing, Rong; Dweck, Marc R

doi:10.1136/heartjnl-2019-315560

Cited by 89 publications

(62 citation statements)

References 58 publications

(50 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“… 4 Fibrosis is a common final pathway in chronic myocardial disease, including in diastolic heart failure. 5 In adults with heart failure with preserved ejection fraction (HFpEF), myocardial fibrosis is intrinsically linked to ventricular stiffness and adverse remodelling. 6 In Fontan patients, liver fibrosis is recognised as a nearly ubiquitous and time-dependent end-organ complication of the circulation and may be worsened in the setting of diastolic dysfunction and elevated Fontan pressure.…”

Section: Introductionmentioning

confidence: 99%

Myocardial fibrosis, diastolic dysfunction and elevated liver stiffness in the Fontan circulation

et al. 2020

View full text Add to dashboard Cite

IntroductionSingle ventricle diastolic dysfunction and hepatic fibrosis are frequently observed in patients with a Fontan circulation. The relationship between adverse haemodynamics and end-organ fibrosis has not been investigated in adolescents and young adults with Fontan circulation.MethodsProspective observational study of Fontan patients who had a cardiac catheterisation. Cardiac MRI with T1 mapping was obtained to measure extracellular volume (ECV), a marker of myocardial fibrosis. Hepatic magnetic resonance elastography was performed to assess liver shear stiffness. Serum biomarkers of fibrosis including matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) were measured. Very high ECV was defined as >30% and elevated serum biomarkers as >75th percentile for each biomarker.Results25 Fontan patients (52% female) with mean age of 16.3±6.8 years were included. Mean ECV was 28%±5%. There was a significant correlation between ECV and systemic ventricular end-diastolic pressure (r=0.42, p=0.03) and between ECV and liver stiffness (r=0.45, p=0.05). Patients with elevated ECV demonstrated elevations in MMPs and TIMPs. Similarly, patients with elevated MMPs and TIMPs had greater liver stiffness compared with patients with normal levels of these biomarkers.ConclusionsIn Fontan patients, cardiac magnetic resonance evidence of myocardial fibrosis is associated with diastolic dysfunction, increased liver stiffness and elevated circulating biomarkers of fibrosis. These findings suggest the presence of a profibrotic milieu, with end-organ implications, in some patients with Fontan circulation.

show abstract

Section: Introductionmentioning

confidence: 99%

Myocardial fibrosis, diastolic dysfunction and elevated liver stiffness in the Fontan circulation

et al. 2020

View full text Add to dashboard Cite

show abstract

“…По сравнению с другими органами, сердце имеет ограниченную регенеративную способность после его повреждения. Процессы репарации миокарда при его ишемии включают в себя апоптоз поврежденных кардиомиоцитов с последующей заменой фиброзной рубцовой тканью, которая способствует сохранению функциональной целостности миокарда [6,9].…”

Section: патологическая анатомия и физиология фиброза миокардаunclassified

“…Помимо кардиомиоцит-ориентированного представления о сердечной недостаточности (СН), в настоящее время принято считать, что изменения в экстрацеллюлярном матриксе (ЭЦМ) и коронарной микроциркуляции также играют важную роль в развитии патологического структурного ремоделирования миокарда и фиброза, которое патофизиологически определяет механизм развития ХСН. Фибротическое ремодели рование миокарда, которое характеризуется избыточным отложением белков ЭЦМ сердечными фибробластам, является основополагающим в развитии ХСН [6][7][8][9]. Повышение плотности и, соответ ственно, ри гидности ЭЦМ снижает сократительную способность миокарда и, таким образом, ускоряет прогрессирование СН [10].…”

unclassified

Biomarkers of myocardial fibrosis and their genetic regulation in patients with heart failure

Печерина

Kutikhin

2020

Russ J Cardiol

View full text Add to dashboard Cite

Currently, the development of chronic heart failure (CHF) is considered from the perspective of pathological structural remodeling of myocardium and fibrosis. Despite the widespread use of molecular genetic markers in clinical practice, only a small number of them are used to evaluate remodeling processes, as well as to predict potential complications associated with heart failure (HF). In addition, the relationship between many biomarkers with instrumental and histological confirmation of myocardial fibrosis has not yet been determined. Myocardial fibrosis remains quite debatable and controversial subject, which actualizes the further study of this direction. The discovery of pathogenetic and diagnostic markers of myocardial fibrosis could contribute to the development of targeted therapy. Of particular interest is the search for possible pathogenetic markers, since this is relevant for clinical practice.

show abstract

“…Cardiac fibrosis is a common attribute of myocardial diseases of different etiology such as ischaemic cardiomyopathy and myocardial infarction, dilated cardiomyopathy, aortic stenosis, hypertrophic cardiomyopathy, and myocarditis [2]. Fibrosis is shown to be a predictor of adverse outcomes, including heart failure, ventricular arrhythmias, sudden cardiac death and all-cause mortality [3].…”

Section: Introductionmentioning

confidence: 99%

Myocardial Fibrosis in a 3D Model: Effect of Texture on Wave Propagation

2020

View full text Add to dashboard Cite

Non-linear electrical waves propagate through the heart and control cardiac contraction. Abnormal wave propagation causes various forms of the heart disease and can be lethal. One of the main causes of abnormality is a condition of cardiac fibrosis, which, from mathematical point of view, is the presence of multiple non-conducting obstacles for wave propagation. The fibrosis can have different texture which varies from diffuse (e.g., small randomly distributed obstacles), patchy (e.g., elongated interstitional stria), and focal (e.g., post-infarct scars) forms. Recently, Nezlobinsky et al. (2020) used 2D biophysical models to quantify the effects of elongation of obstacles (fibrosis texture) and showed that longitudinal and transversal propagation differently depends on the obstacle length resulting in anisotropy for wave propagation. In this paper, we extend these studies to 3D tissue models. We show that 3D consideration brings essential new effects; for the same obstacle length in 3D systems, anisotropy is about two times smaller compared to 2D, however, wave propagation is more stable with percolation threshold of about 60% (compared to 35% in 2D). The percolation threshold increases with the obstacle length for the longitudinal propagation, while it decreases for the transversal propagation. Further, in 3D, the dependency of velocity on the obstacle length for the transversal propagation disappears.

show abstract

Myocardial fibrosis: why image, how to image and clinical implications

Cited by 89 publications

References 58 publications

Myocardial fibrosis, diastolic dysfunction and elevated liver stiffness in the Fontan circulation

Myocardial fibrosis, diastolic dysfunction and elevated liver stiffness in the Fontan circulation

Biomarkers of myocardial fibrosis and their genetic regulation in patients with heart failure

Myocardial Fibrosis in a 3D Model: Effect of Texture on Wave Propagation

Contact Info

Product

Resources

About