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• W2129028069 abstract "Cardiac fibrosis is the consequence of extracellular cardiac matrix remodeling resulting from pathological processes, including ischemia, stretch, inflammation, and neurohormonal activation. Fibrosis can be reparative or reactive. At the site of a transmural myocardial infarction, fibrotic scarring provides protective strength and prevents myocardial rupture. Diffuse reactive fibrosis occurs remotely from the ischemic scar. It is associated with myocyte hypertrophy and contributes to the detrimental process of remodeling, increased ventricular stiffness, tissue disarray with consequent contractile heterogeneity, reduced contractile reserve, and arrhythmogenic anisotropy. Although most commonly found in the setting of ischemic heart disease, where it acts as a precursor to heart failure (HF), the more diffuse type of fibrosis is also an essential feature of idiopathic dilated cardiomyopathy, diabetic cardiomyopathy, hypertensive heart disease, and hypertrophic cardiomyopathy (HCM). Cardiac fibrosis results in an accumulation of proteins including collagen in the extracellular space, damage that has previously been considered irreversible in many cardiovascular (CV) diseases. It is now emerging as an important novel target for future CV antifibrotic therapies.1,2 Promising therapeutic candidates include antihypertensive therapies, antialdosterone agents, anti-inflammatory and antioxidant agents, growth factor inhibitors, matricellular proteins, and key miRNAs, as well as cell therapy or genetic interventions. It is therefore important to noninvasively identify, measure, image, and monitor the degree of cardiac fibrosis to better understand its pathophysiology and select optimal patients for antifibrotic therapy trials. Furthermore, noninvasive surrogate end points such as circulating biomarkers or magnetic resonance and molecular imaging should allow for larger proof-of-concept clinical trials than previously possible with endomyocardial biopsies.Article see p 271Detection of cardiac fibrosis is based on the quantification of a diffuse excess of collagen fiber deposition in the interstitial space, as assessed by staining techniques. Fibrosis may also be monitored noninvasively using biochemical assessments at circulating levels of collagen substrates, …" @default.
• W2129028069 created "2016-06-24" @default.
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• W2129028069 date "2014-03-01" @default.
• W2129028069 modified "2023-10-09" @default.
• W2129028069 title "What Is Measured by Cardiac Fibrosis Biomarkers and Imaging?" @default.
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• W2129028069 doi "https://doi.org/10.1161/circheartfailure.114.001156" @default.
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