Imaging of Myocardial Fibrosis and Its Functional Correlates in Aortic Stenosis: A Review and Clinical Potential

Katbeh, Asim; Ondrúš, Tomáš; Barbato, Emanuele; Galderisi, Maurizio; Trimarco, Bruno; Camp, Guy Van; Vanderheyden, Marc; Pěnička, Martin

doi:10.1159/000493164

Cited by 13 publications

(8 citation statements)

References 61 publications

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“…In the conduction system, fibrosis causes bradyarrhythmia and heart block, a substantial cause of morbidity in the elderly (Csepe, Kalyanasundaram, Hansen, Zhao, & Fedorov, ; Kerola et al, ). Risk factors for cardiac fibrosis are diverse and include hypertension (Cuspidi, Ciulla, & Zanchetti, ), ischaemic heart disease (Hinderer & Schenke‐Layland, ), aortic stenosis (Bing et al, ; Katbeh et al, ), inherited cardiomyopathy (Gulati et al, ; Ho et al, ), diabetes (Russo & Frangogiannis, ), and ageing (Lu et al, ).…”

Section: Fibrosis: a Final Common Pathway Underlying Cardiac And Renamentioning

confidence: 99%

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IL‐11 in cardiac and renal fibrosis: Late to the party but a central player

Corden

Adami

Sweeney

et al. 2020

British J Pharmacology

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Fibrosis is a pathophysiological hallmark of cardiorenal disease. In the heart, fibrosis leads to contractile dysfunction and arrhythmias; in the kidney, it is the final common pathway for many diseases and predicts end‐stage renal failure. Despite this, there are currently no specific anti‐fibrotic treatments available for cardiac or renal disease. Recently and unexpectedly, IL‐11 was found to be of major importance for cardiorenal fibroblast activation and fibrosis. In mouse models, IL‐11 overexpression caused fibrosis of the heart and kidney while genetic deletion of Il11ra1 protected against fibrosis and preserved organ function. Neutralizing antibodies against IL‐11 or IL‐11RA have been developed that have anti‐fibrotic activity in human fibroblasts and protect against fibrosis in murine models of disease. While IL‐11 biology has been little studied and, we suggest, largely misunderstood, its autocrine activity in myofibroblasts appears non‐redundant for fibrosis, which offers new opportunities to better understand and potentially target cardiorenal fibrosis.

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Section: Fibrosis: a Final Common Pathway Underlying Cardiac And Renamentioning

confidence: 99%

“…hypertension (Cuspidi, Ciulla, & Zanchetti, 2006), ischaemic heart disease (Hinderer & Schenke-Layland, 2019), aortic stenosis (Bing et al, 2019;Katbeh et al, 2018), inherited cardiomyopathy (Gulati et al, 2013;Ho et al, 2010), diabetes (Russo & Frangogiannis, 2016), and ageing (Lu et al, 2017).…”

mentioning

confidence: 99%

IL‐11 in cardiac and renal fibrosis: Late to the party but a central player

Corden

Adami

Sweeney

et al. 2020

British J Pharmacology

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“…Strain parameters, however, are known to be correlated with EF and brosis [28][29][30][31]. Therefore, we tried to control for these effects by using propensity score matching between ICM and DCM patients.…”

Section: Discussionmentioning

confidence: 99%

CMR-derived myocardial strain analysis differentiates ischemic and dilated cardiomyopathy - A propensity score-matched study

Vietheer

Lehmann

Unbehaun

et al. 2021

Preprint

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Purpose Left ventricular (LV) longitudinal, circumferential, and radial motion can be measured using feature tracking of cardiac magnetic resonance (CMR) images. The aim of our study was to detect differences in LV mechanics between patients with dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) who were matched using a propensity score-based model. Methods Between April 2017 and October 2019, 1224 patients were included in our CMR registry, among them 141 with ICM and 77 with DCM. Propensity score matching was used to pair patients based on their indexed end-diastolic volume (EDVi), ejection fraction (EF), and septal T1 relaxation time. Feature tracking provided six parameters for global longitudinal, circumferential, and radial strain with corresponding strain rates. Results Propensity score matching yielded 72 patients in each group (DCM mean age 58.6 ± 11.6 years, 15 females; ICM mean age 62.6 ± 13.2 years, 11 females, p = 0.084 and 0.44 respectively; LV-EF 32.2 ± 13.5% vs. 33.8 ± 12.1%, p = 0.356; EDVi 127.2 ± 30.7 ml/m² vs. 121.1 ± 41.8 ml/m², p = 0.251; native T1 values 1165 ± 58 ms vs. 1167 ± 70 ms, p = 0.862). There was no difference in global longitudinal strain between DCM and ICM patients (-10.9 ± 5.5% vs. -11.2 ± 4.7%, p = 0.72), whereas in DCM patients there was a significant reduction in global circumferential strain (-10.0 ± 4.5% vs. -12.2 ± 4.7%, p = 0.002) and radial strain (17.1 ± 8.51 vs. 21.2 ± 9.7%, p = 0.039). Conclusion Our data suggest that ICM and DCM patients have inherently different myocardial mechanics, even if phenotypes are similar. The ability to discriminate these two conditions may aid in developing additional prognostic and therapeutic strategies in the future.

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“…A fibrous cap structure of carotid artery plaques is associated with a worse prognosis, and recent clinical trials have validated the significance of plaque composition as a marker for the clinical management of atherosclerosis using various imaging methods [94,95]. In the case of AVS, myocardial fibrosis is indicative of clinical outcomes and survival post valve replacement [96], and combined use of cardiac magnetic resonance and echocardiography has been proposed to assess myocardial fibrosis and left-ventricular dysfunction as a measure to determine the timing of aortic valve replacement [97].…”

Section: Clinical Implications Of Fibrosismentioning

confidence: 99%

Fibroblasts and Their Pathological Functions in the Fibrosis of Aortic Valve Sclerosis and Atherosclerosis

Singh

Torzewski

2019

Biomolecules

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Cardiovascular diseases, such as atherosclerosis and aortic valve sclerosis (AVS) are driven by inflammation induced by a variety of stimuli, including low-density lipoproteins (LDL), reactive oxygen species (ROS), infections, mechanical stress, and chemical insults. Fibrosis is the process of compensating for tissue injury caused by chronic inflammation. Fibrosis is initially beneficial and maintains extracellular homeostasis. However, in the case of AVS and atherosclerosis, persistently active resident fibroblasts, myofibroblasts, and smooth muscle cells (SMCs) perpetually remodel the extracellular matrix under the control of autocrine and paracrine signaling from the immune cells. Myofibroblasts also produce pro-fibrotic factors, such as transforming growth factor-β1 (TGF-β1), angiotensin II (Ang II), and interleukin-1 (IL-1), which allow them to assist in the activation and migration of resident immune cells. Post wound repair, these cells undergo apoptosis or become senescent; however, in the presence of unresolved inflammation and persistence signaling for myofibroblast activation, the tissue homeostasis is disturbed, leading to excessive extracellular matrix (ECM) secretion, disorganized ECM, and thickening of the affected tissue. Accumulating evidence suggests that diverse mechanisms drive fibrosis in cardiovascular pathologies, and it is crucial to understand the impact and contribution of the various mechanisms for the control of fibrosis before the onset of a severe pathological consequence.

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Imaging of Myocardial Fibrosis and Its Functional Correlates in Aortic Stenosis: A Review and Clinical Potential

Cited by 13 publications

References 61 publications

IL‐11 in cardiac and renal fibrosis: Late to the party but a central player

IL‐11 in cardiac and renal fibrosis: Late to the party but a central player

CMR-derived myocardial strain analysis differentiates ischemic and dilated cardiomyopathy - A propensity score-matched study

Fibroblasts and Their Pathological Functions in the Fibrosis of Aortic Valve Sclerosis and Atherosclerosis

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