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

Sharykin, A.S.; Badtieva, Victoriya; Trunina, I.I.; Османов, И. М.

doi:10.15829/1728-8800-2019-6-126-135

Cited by 9 publications

(5 citation statements)

References 49 publications

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“…Exposure to air pollution contributes to adverse remodeling and worsening myocardial fibrosis [10,11,13,62], degenerative and fibrotic lesions in the myocardium [63]. The myocardial hypertrophy commonly observed in high performance athletes may degenerate in fibrosis remodeling [64]. Furthermore, the severity extent in which fibrosis affects the cardiac function can be submitted to the interaction with multiple factors, such as, genetic conditions [65], gender [66] and ageing [67].…”

Section: Discussionmentioning

confidence: 99%

The Effects of Fibrotic Cell Type and Its Density on Atrial Fibrillation Dynamics: An In Silico Study

Palacio

Ugarte

Sáiz

et al. 2021

Cells

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Remodeling in atrial fibrillation (AF) underlines the electrical and structural changes in the atria, where fibrosis is a hallmark of arrhythmogenic structural alterations. Fibrosis is an important feature of the AF substrate and can lead to abnormal conduction and, consequently, mechanical dysfunction. The fibrotic process comprises the presence of fibrotic cells, including fibroblasts, myofibroblasts and fibrocytes, which play an important role during fibrillatory dynamics. This work assesses the effect of the diffuse fibrosis density and the intermingled presence of the three types of fibrotic cells on the dynamics of persistent AF. For this purpose, the three fibrotic cells were electrically coupled to cardiomyocytes in a 3D realistic model of human atria. Low (6.25%) and high (25%) fibrosis densities were implemented in the left atrium according to a diffuse fibrosis representation. We analyze the action potential duration, conduction velocity and fibrillatory conduction patterns. Additionally, frequency analysis was performed in 50 virtual electrograms. The tested fibrosis configurations generated a significant conduction velocity reduction, where the larger effect was observed at high fibrosis density (up to 82% reduction in the fibrocytes configuration). Increasing the fibrosis density intensifies the vulnerability to multiple re-entries, zigzag propagation, and chaotic activity in the fibrillatory conduction. The most complex propagation patterns were observed at high fibrosis densities and the fibrocytes are the cells with the largest proarrhythmic effect. Left-to-right dominant frequency gradients can be observed for all fibrosis configurations, where the fibrocytes configuration at high density generates the most significant gradients (up to 4.5 Hz). These results suggest the important role of different fibrotic cell types and their density in diffuse fibrosis on the chaotic propagation patterns during persistent AF.

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Section: Discussionmentioning

confidence: 99%

The Effects of Fibrotic Cell Type and Its Density on Atrial Fibrillation Dynamics: An In Silico Study

Palacio

Ugarte

Sáiz

et al. 2021

Cells

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“…Such changes do not disrupt the myocardium global function, but in fibro-modified areas there is a regional dysfunction, manifested as changes in stress and longitudinal gradient in the myocardium, and LV end-diastolic volume and relative wall thickness are significantly higher in these cases, than those in athletes without myocardial fibrosis. Fibrosis is more often observed in myocardial hypertrophy, because the latter is often combined with apoptosis and necrosis of cardiomyocytes, the loss of which is compensated by an excessive collagen deposition and fibroblast accumulation [9].…”

Section: Discussionmentioning

confidence: 99%

“…It should be noted, that blood pressure is at a higher level during exercise, than in everyday circumstances, and hypertension in athletes is not uncommon, therefore all of these combine to cause myocardial fibrosis [9].…”

Section: Discussionmentioning

confidence: 99%

Features of cardiac remodeling depending on the mode of training session

Malakhova

Syvolap

Potapenko

2020

ZMJ

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Різні види фізіологічної адаптації серця в атлетів формуються залежно від специфіки спортивної діяльності. У спортсменів, які тренуються в циклічних, насамперед аеробних видах спорту (біг на довгі дистанції, лижний спорт, плавання), здебільшого розвивається дилятація порожнини лівого шлуночка (ЛШ) із пропорційним збільшенням товщини його стінок.Якщо у тренуванні переважають статичні або ізометричні навантаження (важкоатлети, єдиноборці, метальники), у спортсменів розвивається концентрична гіпертрофія зі збільшенням товщини стінки ЛШ без зміни розміру його порожнини. Але зміни геометрії серця в атлетів не обмежуються тільки ексцентричною та концентричною гіпертрофією ЛШ.Мета роботи -вивчення особливостей ремоделювання серця спортсменів залежно від спрямованості тренувального процесу (витривалість, швидкість, сила).

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“…В настоящее время не вызывает сомнений, что основным патогенетическим субстратом ЖА у больных НКМП является диффузный фиброз миокарда [26,27]. Сложная цепь клеточного ремоделирования с исходом в фиброз предсердий лежит и в основе ФП [28].…”

Section: фп и вероятность возникновения клинически значимых жт в будущемunclassified

Clinical Predictors of Occurrence of Ventricular Tachyarrhythmias in Patients with Reduced Left Ventricle Ejection Fraction. Results of Single-Center Prospective Study

et al. 2021

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Aim To evaluate the diagnostic significance of clinical and demographic parameters for predicting a 2-year probability of ventricular tachyarrhythmias (VT) in patients with chronic heart failure and reduced left ventricular ejection fraction (CHFrLVEF).Material and methods This single-center, prospective cohort study included 175 patients with CHFrLVEF who were implanted with a cardioverter defibrillator (CD). The endpoint was a CD-detected episode of VT. Patients were followed up for 2 years with visits at 3, 12, and 24 months after CD implantation.Results The primary endpoint was observed in 43 (24.4 %) patients at an average of 20.9 months (95 % confidence interval (CI), 20–21.9). The 2-year risk of fatal ventricular arrhythmias increased with detection of unstable VT (one-factor analysis, odds ratio (OR), 4.2; 95 % CI, 1.1–16.5; р=0.041; multifactor analysis, OR, 6.3; 95 % CI, 1.5–26.3; р=0.012) and with ischemic CHFrLVEF origin (one-factor analysis, OR, 2.2; 95 % CI, 1.1–4.5; p=0.021; multifactor analysis, OR, 2.5; 95 % CI, 1.2–5.1; р=0.018). In the presence of any type of atrial fibrillation (AF) in patients with non-ischemic CHFrLVEF, the probability of VT increased threefold (one-factor analysis, OR, 2.97; 95 % CI, 1.02–8.8; р=0.047; multifactor analysis, OR, 3.5; 95 % CI, 1.1–10.9; р=0.032).Conclusion The presence of ischemic heart disease and unstable VT paroxysms can be included in the number of important clinical predictors of VT in patients with CHFrLVEF. In patients with non-ischemic CHF, the presence of AF is associated with a high risk of VT.

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

Cited by 9 publications

References 49 publications

The Effects of Fibrotic Cell Type and Its Density on Atrial Fibrillation Dynamics: An In Silico Study

The Effects of Fibrotic Cell Type and Its Density on Atrial Fibrillation Dynamics: An In Silico Study

Features of cardiac remodeling depending on the mode of training session

Clinical Predictors of Occurrence of Ventricular Tachyarrhythmias in Patients with Reduced Left Ventricle Ejection Fraction. Results of Single-Center Prospective Study

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