glycogen and Atrial-Fibrillation

Topics: AMP-Activated Protein Kinases; Animals; Atrial Fibrillation; Disease Progression; Energy Metabolism; Glucose; Glycogen; Humans; Lipid Metabolism

Topics: Alcohol Drinking; Atrial Fibrillation; Binge Drinking; Calcium; Glycogen; Glycogen Synthase Kinase 3 beta; Holidays; Humans; Protein Kinase C; T-Lymphocytes; Up-Regulation

Topics: AMP-Activated Protein Kinase Kinases; Animals; Anti-Arrhythmia Agents; Arthritis, Experimental; Atrial Fibrillation; Atrial Remodeling; Female; Fibrosis; Glycogen; Heart Atria; Interleukin-6; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Protein Kinases; Rats, Wistar; Resveratrol; Tumor Necrosis Factor-alpha

Mitral stenosis (MS) has the highest incidence of atrial fibrillation (AF) in chronic rheumatic valvular disease. There are very few studies in isolated MS comparing histopathological changes in patients with sinus rhythm (SR) and AF.. To analyze the histological changes associated with isolated MS and compare between changes in AF and SR.. This was a prospective study in patients undergoing valve replacement surgery for symptomatic isolated MS who were divided into 2 groups, Group I AF (n = 13) and Group II SR (n = 10). Intra-operative biopsies performed from 5 different sites from both atria were analyzed for 10 histopathologic changes commonly associated with AF.. On multivariate analysis, myocytolysis (odds ratio [OR]: 1.48, P = 0.05) was found to be associated with AF, whereas myocyte hypertrophy (OR: 0.21, P = 0.003), and glycogen deposition (OR: 0.43, P = 0.002) was associated with SR. Interstitial fibrosis the commonest change was uniformly distributed across both atria irrespective of the rhythm.. In rheumatic MS, SR is associated with myocyte hypertrophy whereas AF is associated with myocytolysis. Endocardial inflammation is more common in left atrial appendage irrespective of rhythm. Interstitial fibrosis is seen in >90% of patients distributed in both the atria and is independent of the rhythm. Amyloid and Aschoff bodies are uncommon and the rest of the changes are uniformly distributed across both the atria.

Topics: Adolescent; Adult; Aged; Atrial Fibrillation; Biopsy; Cardiomegaly; Female; Fibrosis; Glycogen; Heart Atria; Heart Valve Prosthesis Implantation; Humans; Male; Middle Aged; Mitral Valve Stenosis; Multivariate Analysis; Odds Ratio; Prospective Studies; Rheumatic Heart Disease; Risk Factors; Young Adult

Previous studies of the goat heart subjected to prolonged atrial pacing induced sustained atrial fibrillation (AF). Structural changes included marked accumulation of glycogen in atrial myocytes.. In the present study, we hypothesized that glycogen deposition in canine atrial myocytes promotes paroxysmal forms of AF and is involved in fibrosis development in the later stages of AF.. In dogs under pentobarbital anesthesia, tissues were obtained from the right and left atrial appendages (LAA/RAA). Periodic acid Schiff (PAS) and Masson's trichrome staining of the LAA/RAA from normal dogs, and those subjected to atrial pacing induced AF for 48 h or 8 weeks determined glycogen and collagen concentrations, respectively, using morphometric analysis.. At baseline, there was a significant greater concentration of glycogen in the LAA than the RAA (P ≤ 0.05). Compared to the RAA, the LAA glycogen, was dense and locked against the intercalated discs. After pacing induced AF for 48 hours and 8 weeks there was a marked increase in glycogen deposition, significantly greater than in the baseline state (P ≤ 0.05). There was a similar and progressive increase in collagen concentrations in each group (P ≤ 0.05).. The differential in glycogen concentration, in conjunction with other factors, neural and electrophysiological, provide a basis for the greater propensity of the left atrium for paroxysmal AF, at baseline and 48 hours of pacing induced AF. The marked increase in collagen at 8 weeks of pacing provides a substrate for sustained AF. Evidence is presented linking glycogen accumulation and fibrosis as factors in the persistent forms of AF.

Topics: Animals; Atrial Appendage; Atrial Fibrillation; Disease Progression; Dogs; Female; Fibrosis; Glycogen; Heart Atria; Image Processing, Computer-Assisted; Male

Differentiation of foetal cardiomyocytes is accompanied by sequential actin isoform expression, i.e. down-regulation of the 'embryonic' alpha smooth muscle actin, followed by an up-regulation of alpha skeletal actin (alphaSKA) and a final predominant expression of alpha cardiac actin (alphaCA). Our objective was to detect whether re-expression of alphaSKA occurred during cardiomyocyte dedifferentiation, a phenomenon that has been observed in different pathologies characterized by myocardial dysfunction. Immunohistochemistry of alphaCA, alphaSKA and cardiotin was performed on left ventricle biopsies from human patients after coronary bypass surgery. Furthermore, actin isoform expression was investigated in left ventricle samples of rabbit hearts suffering from pressure- and volume-overload and in adult rabbit ventricular cardiomyocytes during dedifferentiation in vitro. Atrial goat samples up to 16 weeks of sustained atrial fibrillation (AF) were studied ultrastructurally and were immunostained for alphaCA and alphaSKA. Up-regulation of alphaSKA was observed in human ventricular cardiomyocytes showing down-regulation of alphaCA and cardiotin. A patchy re-expression pattern of alphaSKA was observed in rabbit left ventricular tissue subjected to pressure- and volume-overload. Dedifferentiating cardiomyocytes in vitro revealed a degradation of the contractile apparatus and local re-expression of alphaSKA. Comparable alphaSKA staining patterns were found in several areas of atrial goat tissue during 16 weeks of AF together with a progressive glycogen accumulation at the same time intervals. The expression of alphaSKA in adult dedifferentiating cardiomyocytes, in combination with PAS-positive glycogen and decreased cardiotin expression, offers an additional tool in the evaluation of myocardial dysfunction and indicates major changes in the contractile properties of these cells.

Topics: Actinin; Actins; Animals; Aortic Valve Insufficiency; Atrial Fibrillation; Biomarkers; Cell Dedifferentiation; Cells, Cultured; Coronary Artery Disease; Down-Regulation; Female; Glycogen; Goats; Humans; Myocardial Stunning; Myocytes, Cardiac; Protein Isoforms; Rabbits; Up-Regulation

Persistent atrial fibrillation (AF) has been associated with structural and electric remodeling and reduced contractile function.. To unravel mechanisms underlying reduced sarcoplasmic reticulum (SR) Ca(2+) release in persistent AF.. We studied cell shortening, membrane currents, and [Ca(2+)](i) in right atrial myocytes isolated from sheep with persistent AF (duration 129+/-39 days, N=16), compared to matched control animals (N=21). T-tubule density, ryanodine receptor (RyR) distribution, and local [Ca(2+)](i) transients were examined in confocal imaging.. Myocyte shortening and underlying [Ca(2+)](i) transients were profoundly reduced in AF (by 54.8% and 62%, P<0.01). This reduced cell shortening could be corrected by increasing [Ca(2+)](i). SR Ca(2+) content was not different. Calculated fractional SR Ca(2+) release was reduced in AF (by 20.6%, P<0.05). Peak Ca(2+) current density was modestly decreased (by 23.9%, P<0.01). T-tubules were present in the control atrial myocytes at low density and strongly reduced in AF (by 45%, P<0.01), whereas the regular distribution of RyR was unchanged. Synchrony of SR Ca(2+) release in AF was significantly reduced with increased areas of delayed Ca(2+) release. Propagation between RyR was unaffected but Ca(2+) release at subsarcolemmal sites was reduced. Rate of Ca(2+) extrusion by Na(+)/Ca(2+) exchanger was increased.. In persistent AF, reduced SR Ca(2+) release despite preserved SR Ca(2+) content is a major factor in contractile dysfunction. Fewer Ca(2+) channel-RyR couplings and reduced efficiency of the coupling at subsarcolemmal sites, possibly related to increased Na(+)/Ca(2+) exchanger, underlie the reduction in Ca(2+) release.

Topics: Actin Cytoskeleton; Animals; Atrial Fibrillation; Atrial Function, Right; Calcium Channels, L-Type; Calcium Signaling; Disease Models, Animal; Electrophysiologic Techniques, Cardiac; Female; Glycogen; Heart Atria; Membrane Potentials; Myocardial Contraction; Myocytes, Cardiac; Ryanodine Receptor Calcium Release Channel; Sarcolemma; Sarcoplasmic Reticulum; Sheep; Sodium-Calcium Exchanger; Time Factors

Experimental atrial fibrillation in intact rats significantly decreased the content of catecholamines in atrial adrenergic fibers and phosphorylase activity, which attests to enhanced glycogen consumption in the heart. These changes were specific of the fibrillating myocardium and atria, but were absent in the ventricles. Induced atrial fibrillation did not modify activities of SDH and monoamine oxidase in cardiac subdivisions. It was hypothesized that increased energy requirements in the atria during myocardial fibrillation led to activation of anaerobic metabolism.

Topics: Adrenal Glands; Adrenergic Fibers; Anaerobiosis; Animals; Atrial Fibrillation; Catecholamines; Glycogen; Male; Monoamine Oxidase; Myocardium; Phosphorylases; Rats; Rats, Wistar; Succinate Dehydrogenase

Prolonged atrial fibrillation (AF) results in electrical, structural, and gap-junctional remodeling. We examined the reversibility of the changes in (ultra)structure and gap junctions.. Four groups of goats were used: (1) sinus rhythm (SR), (2) 4 months' AF (4 mo AF), (3) 2 months' SR after 4 mo AF (2 mo post-AF), and (4) 4 months' SR after 4 mo AF (4 mo post-AF). Atria were characterized electrophysiologically, (ultra)structure was studied by light and electron microscopy, and structural and gap-junctional protein expression was studied by immunohistochemistry or Western blotting. The atrial effective refractory period had completely returned to normal values 2 mo post-AF. Induced AF episodes still lasted for minutes at 2 and 4 mo post-AF, compared with seconds in the SR group. Structural abnormalities were still present at 2 and 4 mo post-AF, although to a lesser extent. The increased atrial myocyte diameter was back to normal at 4 mo post-AF. The number of myocytes with severe myolysis had almost normalized 4 mo post-AF, whereas myocytes with mild myolysis remained significantly increased. Extracellular matrix area fraction after 4 mo AF was similar to SR. However, the extracellular matrix fraction per myocyte had increased after 4 mo AF and remained higher post-AF. Changes in expression of structural proteins were partially restored post-AF. The reduction of connexin 40 that was observed during AF was completely reversed at 4 mo post-AF.. Recovery from structural remodeling after 4 mo AF is a slow process and is still incomplete 4 mo post-AF. Several months post-AF, the duration of AF episodes is still prolonged (minutes).

Topics: Animals; Atrial Fibrillation; Cardiac Pacing, Artificial; Cell Size; Connexins; Disease Models, Animal; Disease Progression; Electrophysiologic Techniques, Cardiac; Gap Junctions; Glycogen; Goats; Heart Atria; Immunohistochemistry; Myocardium; Recovery of Function; Reference Values; Remission Induction

Topics: Adenosine Triphosphatases; Adolescent; Adult; Atrial Fibrillation; Biopsy; Female; Glycerolphosphate Dehydrogenase; Glycogen; Heart Atria; Histocytochemistry; Humans; Isocitrate Dehydrogenase; L-Lactate Dehydrogenase; Malate Dehydrogenase; Male; Middle Aged; Mitral Valve Insufficiency; Mitral Valve Stenosis; Myocardium; Myofibrils; Oxidoreductases; Rheumatic Heart Disease; Succinate Dehydrogenase