Myocardial Fibrosis in Congenital Heart Disease

Rathod, Rahul H.; Powell, A.; Geva, Tal

doi:10.1253/circj.cj-16-0353

Cited by 40 publications

(26 citation statements)

References 54 publications

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“…Следует помнить, что нежизнеспособный миокард, который замещается фиброзной тканью отличается не только снижением диастолической функции, но и не способен к усилению сократительной способности в ответ на увеличение степени нагрузки, что особенно репрезентативно при проведении стресс-эхокардиографии (ЭхоКГ) с добутамином или ФН. Нагрузочные тесты нашли широкое применение не только в спортивной медицине, но и в диагностике коронарной ишемии у детей с врожденными пороками сердца: аномальное отхождение левой коронарной артерии от ствола легочной артерии, после операции артериального переключения, и перенесших болезнь Кавасаки [4].…”

Section: диагностика фиброзаunclassified

Myocardial fibrosis — a new component of heart remodeling in athletes?

Sharykin

Badtieva

Trunina

et al. 2019

Cardiovasc Ther Prev

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Section: диагностика фиброзаunclassified

Myocardial fibrosis — a new component of heart remodeling in athletes?

Sharykin

Badtieva

Trunina

et al. 2019

Cardiovasc Ther Prev

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“…There are two major CMR approaches for assessing myocardial fibrosis: Late gadolinium enhancement (LGE) imaging and T1 mapping/ECV fraction calculation. LGE identifies areas of discrete replacement fibrosis, with high sensitivity and specificity (13). …”

Section: Assessment Of Myocardial Fibrosismentioning

confidence: 99%

“…Disturbances in the balance between collagen production and degradation in the ECM, that led to expansion of collagens, cause myocardial fibrosis. Such derangement occurs either due to the death of cardiomyocytes, or because of stimuli that trigger elevated collagen synthesis (13). …”

Section: Introductionmentioning

confidence: 99%

Myocardial fibrosis in congenital and pediatric heart disease

Tian

Niu

2017

Experimental and Therapeutic Medicine

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Cardiac fibrosis is a common phenomenon in different types of heart diseases, such as ischemic heart disease, inherited cardiomyopathy mutations, diabetes, and ageing and is associated with morbidity and mortality. Increased accumulation of extracellular matrix (ECM) that impacts cardiac function, is the underlying cause of fibrotic heart disease. There are four different types of cardiac fibrosis, including, reactive interstitial fibrosis, replacement fibrosis, infiltrative interstitial fibrosis and endomyocardial fibrosis. They are involved in the activation and transformation of cardiac fibroblasts to myofibroblasts, which participate in ECM production and fibrotic process and several inflammatory pathways. Besides the ECM proteins, myofibroblasts also express smooth muscle α-actin, SM22 and caldesmon and other markers related to fibrotic process. Most commonly employed techniques to assess myocardial fibrosis include stress echocardiography, cardiac magnetic resonance imaging and positron emission tomography. Because of the involvement of renin-angiotensin-II-aldosterone system, transforming growth factor-β signaling and activin-linked kinase 5 in the mechanisms of cardiac fibrosis, these pathways and the involved proteins are useful as therapeutic targets. However, because of the importance of these pathways in many other physiological functions, their therapeutic targeting needs to be approached with caution.

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“…New promising cardiac imaging technologies, recently reviewed by Rathod et al, have allowed the identification of different types of myocardial fibrosis, including reactive interstitial fibrosis and replacement fibrosis (97). In particular, reactive interstitial fibrosis, which is characterized by a progressive chronic course of diffuse collagen deposition, may be found in patients with CHD.…”

Section: Regulation Of Fibrosismentioning

confidence: 99%

“…In particular, reactive interstitial fibrosis, which is characterized by a progressive chronic course of diffuse collagen deposition, may be found in patients with CHD. It occurs mainly after hypertension, aortic stenosis (AS), chronic heart insufficiency or shunts-cardiac pathologies that are also found in CHD patients (97). Therefore, the development of anti-fibrotic drugs may have tremendous therapeutic potential and ameliorate the clinical outcome of many CHD patients.…”

Section: Regulation Of Fibrosismentioning

confidence: 99%

MicroRNAs: pleiotropic players in congenital heart disease and regeneration

et al. 2017

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Congenital heart disease (CHD) is the leading cause of infant death, affecting approximately 4-14 live births per 1,000. Although surgical techniques and interventions have improved significantly, a large number of infants still face poor clinical outcomes. MicroRNAs (miRs) are known to coordinately regulate cardiac development and stimulate pathological processes in the heart, including fibrosis or hypertrophy and impair angiogenesis. Dysregulation of these regulators could therefore contribute (I) to the initial development of CHD and (II) at least partially to the observed clinical outcomes of many CHD patients by stimulating the aforementioned pathways. Thus, miRs may exhibit great potential as therapeutic targets in regenerative medicine. In this review we provide an overview of miR function and elucidate their role in selected CHDs, including hypoplastic left heart syndrome (HLHS), tetralogy of Fallot (TOF), ventricular septal defects (VSDs) and Holt-Oram syndrome (HOS). We then bridge this knowledge to the potential usefulness of miRs and/or their targets in therapeutic strategies for regenerative purposes in CHDs.

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Myocardial Fibrosis in Congenital Heart Disease

Cited by 40 publications

References 54 publications

Myocardial fibrosis — a new component of heart remodeling in athletes?

Myocardial fibrosis — a new component of heart remodeling in athletes?

Myocardial fibrosis in congenital and pediatric heart disease

MicroRNAs: pleiotropic players in congenital heart disease and regeneration

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