Pathomorphology of the Heart Conduction System: Comparative Study during Increase in Left or Right Ventricular Afterload

Tverskaya, M. S.; Sukhoparova, V. V.; Karpova, V. V.; Kadyrova, M. Kh.; Klyuchikov, V. Yu.

doi:10.1007/s10517-011-1402-0

Cited by 6 publications

(1 citation statement)

References 4 publications

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“…RVH also contributes to mortality as a comorbid condition in a number of other syndromes, such as chronic obstructive pulmonary disease and scleroderma [4] [5]. Even without progressing to frank failure, progressive remodeling of the RV may generate a substrate for electrocardiographic abnormalities [6], which may contribute to the incidence of sudden cardiac death [7]. As such, improved understanding of molecular pathways that contribute to or modify RVH phenotypes may provide important clues towards novel therapies for PAH treatment.…”

Section: Introductionmentioning

confidence: 99%

Muscle RING Finger-1 Promotes a Maladaptive Phenotype in Chronic Hypoxia-Induced Right Ventricular Remodeling

et al. 2014

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Exposure to chronic hypoxia (CH) induces elevated pulmonary artery pressure/resistance, leading to an eventual maladaptive right ventricular hypertrophy (RVH). Muscle RING finger-1 (MuRF1) is a muscle-specific ubiquitin ligase that mediates myocyte atrophy and has been shown to play a role in left ventricular hypertrophy and altered cardiac bioenergetics in pressure overloaded hearts. However, little is known about the contribution of MuRF1 impacting RVH in the setting of CH. Therefore, we hypothesized that MuRF1 deletion would enhance RVH compared to their wild-type littermates, while cardiac-specific overexpression would reduce hypertrophy following CH-induced pulmonary hypertension. We assessed right ventricular systolic pressure (RVSP), right ventricle to left ventricle plus septal weight ratio (RV/LV+S) and hematocrit (Hct) following a 3-wk isobaric CH exposure. Additionally, we conducted dual-isotope SPECT/CT imaging with cardiac function agent 201Tl-chloride and cell death agent 99mTc-annexin V. Predictably, CH induced pulmonary hypertension, measured by increased RVSP, RV/LV+S and Hct in WT mice compared to normoxic WT mice. Normoxic WT and MuRF1-null mice exhibited no significant differences in RVSP, RV/LV+S or Hct. CH-induced increases in RVSP were also similar between WT and MuRF1-null mice; however, RV/LV+S and Hct were significantly elevated in CH-exposed MuRF1-null mice compared to WT. In cardiac-specific MuRF1 overexpressing mice, RV/LV+S increased significantly due to CH exposure, even greater than in WT mice. This remodeling appeared eccentric, maladaptive and led to reduced systemic perfusion. In conclusion, these results are consistent with an atrophic role for MuRF1 regulating the magnitude of right ventricular hypertrophy following CH-induction of pulmonary hypertension.

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Section: Introductionmentioning

confidence: 99%

Muscle RING Finger-1 Promotes a Maladaptive Phenotype in Chronic Hypoxia-Induced Right Ventricular Remodeling

et al. 2014

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Histoenzymological Characteristics of the Heart Conduction System: Comparative Study with Left or Right Ventricle Afterload

et al. 2013

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Histoenzymological changes, indicating inhibition of the main metabolic processes, were found in the conduction cardiomyocytes of the left ventricle and ventricular septum in experimental stenosis of the aorta. The histoenzymological changes in the conduction system of both ventricles and ventricular septum were similar in experimental stenosis of the pulmonary artery and indicated primarily activation of glycolysis. The histoenzymological profile of conduction cardiomyocytes differed little in cases when the increase of the pressure load was complicated or not complicated by the development of heart failure, particularly in pulmonary artery stenosis. The histoenzymological changes in the conduction system in response to increased afterload differed significantly from those in the contractile myocardium and correlated with the level of cellular functional activity and sensitivity to the regulatory and alterative exposure. These data attest to minor role of metabolic shifts in conduction cell injuries with increasing afterload, primarily, of the right ventricle.

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Effect of Natural Cytokine Complex on the Structure and Metabolism of the Cardiac Conduction System in the Myocardium under Normally and Increased Hemodynamic Load

et al. 2018

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Effect of natural complex of cytokines with activity of IL-1, IL-2, IL-6, TNF, MIF, and GTFβ on the structure and metabolism of conduction cardiomyocytes was assessed in the control and under acute experimental aortic stenosis. After systemic administration of the cytokine complex in the control, structural abnormalities were revealed in a relatively low number of conduction cardiomyocytes; their relative number increased in the left ventricle and interventricular septum. When the complex was administered against the background of aortic stenosis, morphological changes in the conduction system were seen in a significant number of cells with their plasma imbibition, especially in the left ventricle and interventricular septum. Systemic administration of the natural cytokine complex inhibited the major metabolic processes in the conduction system, both in the control and under conditions of sharply increased hemodynamic load. In conduction cardiomyocytes, deceleration of glycolysis and citric acid cycle, inhibition of oxidation of free fatty acids and their metabolites, and suppression of shuttle mechanisms and biosynthetic reactions were observed. Increased blood levels of cytokines, primarily of the proinflammatory ones, can cause structural and metabolic disturbances in the cardiac conduction system and promote the development of arrhythmias, especially in case of sharply increased hemodynamic load.

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Pathomorphology of the Heart Conduction System: Comparative Study during Increase in Left or Right Ventricular Afterload

Cited by 6 publications

References 4 publications

Muscle RING Finger-1 Promotes a Maladaptive Phenotype in Chronic Hypoxia-Induced Right Ventricular Remodeling

Muscle RING Finger-1 Promotes a Maladaptive Phenotype in Chronic Hypoxia-Induced Right Ventricular Remodeling

Histoenzymological Characteristics of the Heart Conduction System: Comparative Study with Left or Right Ventricle Afterload

Effect of Natural Cytokine Complex on the Structure and Metabolism of the Cardiac Conduction System in the Myocardium under Normally and Increased Hemodynamic Load

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