Atrial fibrillation is associated with atrial remodeling, in which connexin 43 (Cx43) and cell hypertrophy play important roles. In this study, apelin-13, an aliphatic peptide, was used to explore the protective effects of the adenosine monophosphate-activated protein kinase (AMPK)/mTOR signaling pathway on Cx43 expression and autophagy, using murine atrial HL-1 cells. The expression of Cx43, AMPK, B-type natriuretic peptide (BNP) and pathway-related proteins was detected by Western blot analysis. Cellular fluorescence imaging was used to visualize Cx43 distribution and the cytoskeleton. Our results showed that the Cx43 expression was significantly decreased in HL-1 cells treated with angiotensin II but increased in cells additionally treated with apelin-13. Meanwhile, apelin-13 decreased BNP expression and increased AMPK expression. However, the expression of Cx43 and LC3 increased by apelin-13 was inhibited by treatment with compound C, an AMPK inhibitor. In addition, rapamycin, an mTOR inhibitor, promoted the development of autophagy, further inhibited the protective effect on Cx43 expression and increased cell hypertrophy. Thus, apelin-13 enhances Cx43 expression and autophagy via the AMPK/mTOR signaling pathway, and serving as a potential therapeutic target for atrial fibrillation., Yifan Chen, Xi Qiao, Lijun Zhang, Xuewen Li, Qinghua Liu., and Obsahuje bibliografii
We have examined the changes of intercellular electrical coupling protein connexin-43 (Cx43) and of PKC-ε in heart atria of diabetic rats and/or after the treatment with triiodothyronine (T3 ). Diabetes was induced in Wistar-Kyoto rats by streptozotocin (50 mg/kg, i.v.) and atria were examined after 5 (acute stage) and 10 (chronic stage) weeks. T 3 (10 μg/100 g/day) was applied via a gastric tube for the last 10 days prior to the end of the experiments to non-diabetic and to the half of diabetic rats. Expression and phosphorylated status of Cx43, as well as expression of PKC-ε , were analyzed by Western blots using mouse monoclonal anti-Cx43 and rabbit polyclonal anti-PKC-ε antibodies. We found that the Cx43 expression was significantly increased after the treatment with T3 and in the acute diabetes. Both in diabetes and after T3 treatment the phosphorylation of Cx43 isoforms was markedly suppressed compared to the non-diabetic and T3-untreated controls. Such a down-regulation was less pronounced in diabetic rats after the T3-treatment. The expression of atrial PKC-ε was increased in diabetic rats. This increase was suppressed after T3 administration and the expression was decreased in T3-treated non-diabetic rats. We suggest that the reduced Cx43 phosphorylation in diabetic and hyperthyroid rats can deteriorate a cell-to-cell coupling and consequently facilitate a development of atrial tachyarrhythmia in diabetic or hyperthyroid animals., M. Mitašíková ... [et al.]., and Obsahuje seznam literatury
Spontaneous depolarization similar to that from the sinus node was documented from the myocardial sleeves of pulmonary veins (PV) after isolation procedures. It was then hypothesized that sinus node-like tissue is present in the PVs of humans. Based on a number of features, the myocar dium of myocardial sleeves (MS) is highly arrhythmogenic. Membrane potentials originating from MS are invariably recordable at the PVs ostia in patients with atrial fibrillation (AF) and delayed conduction around the PVs ostia may play a role in re-e ntry process responsible for the initiation and maintenance of AF. Diagnostic and therapeutic evidence of premature atrial beats induced in MS of PVs and resulting in launch of AF was detected by 3D electroanatomic method of monophasic action potential (MAP). MAP recording plays an important role in a di rect view of human myocardial electrophysiology under both physiological and pathological conditions. Its crucial importance lies in the fact that it enables the study of the action potential of myocardial cell in vivo and, therefore, the study of the dynamic relation of this potential with all the organism variables. The knowledge of pathological MAPs from PV myocardial sleeves can help us to confirm a diagnosis when finding the similar action potential morphology. MAP can be also used to evaluate the therap eutic efficiency of vagal nerves suppression, radiofrequency ablation or other treatment procedures in PVs myocardial sleeves as well as for post- treatment following up., O. Kittnar, S.-G. Yang, M. Mlček., and Obsahuje bibliografii a bibliografické odkazy
Fallotova tetralógia (ToF) je najčastejšou cyanotickou vrodenou srdcovou chybou. Liečba tohto ochorenia je kardiochirurgická – kompletná korekcia už v detskom veku. Bez chirurgického zákroku sa len 10 % pacientov dožívalo 3. decénia a iba 3–5 % pacientov sa dožívalo viac ako 40 rokov. Opisujeme prípad 69-ročného pacienta s anamnézou nekorigovanej Fallotovej tetralógie – z dôvodu odmietavého postoja k chirurgickému riešeniu, chronického srdcového zlyhávania NYHA III–IV a chronickej obličkovej choroby, ktorý bol prijatý na internú kliniku pre niekoľkodňové bolesti na hrudníku s edémami predkolení a ponámahovou dýchavicou pri minimálnej námahe. Echokardiografickým vyšetrením sa zistila stenóza pľúcnice, ťažká trikuspidálna insuficiencia, koncentrická hypertrofia stien oboch komôr, defekt komorového septa, dextropozícia aorty a veľký cirkulárny perikadiálny výpotok. RTG hrudníka potvrdil masívny pravostranný pleurálny výpotok. Liečbou diuretikami, antiarytmikom a po realizácii pleurálnej punkcie sa stav pacienta významne zlepšil a bol prepustený domov. V literatúre popísané prípady nekorigovanej ToF u starších pacientov boli asociované s hypertrofiou ľavej komory (HĽK) a hypoplastickou pulmonálnou artériou s pomalým vývojom subpulmonálnej obštrukcie, ktoré sme zistili aj u nášho pacienta. HĽK sa v prípade nekorigovanej ToF môže postupne vyvinúť a jej priaznivý účinok sa môže prejaviť až v dospelosti., Tetralogy of Fallot (ToF) is the most common cyanotic congenital heart defect. The actual treatment relies on cardio-surgery – complete correction within the infant age. Without surgery only 10 % of subjects survived 3rd decade and only 3–5 % of subjects were able to survive until their 40th. This particular paper is dedicated to case of a 69-years old male subject with positive history of uncorrected ToF due to his refusal of surgery, ischemic cardiac disease NYHA III–IV and chronic kidney failure. This subject was hospitalized within the department of internal medicine due to several days of chest pain connected with lower extremities oedemas and dyspnoeic syndrome after minimal physical load. Provided echocardiography revealed pulmonary artery stenosis, severe tricuspid insufficiency, concentric hypertrophy of ventricles, ventricular septal defect, dextroposition of aorta and severe pericardial effusion. Chest X-ray proved massive pleura effussion. The actual conditions of subject improved significantly after onset of diuretics, antiarrhytmics and providing of pleural punction. Subject has been discharged. Cases of ToF presented within available sources in older population were associated with left ventricular hypertrophy and hypoplastic pulmonary artery and slow subpulmonal obstruction development which also presented within our subject. Left ventricular hypertrophy has a potential to develop continuously and therefore its benefits can be visible within adult age., and Naďa Hučková, Katarína Sekurisová, Laura Slezáková, Katarína Kusendová, Andrej Zachar, Mária Szántová
Although atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice, precise mechanisms that lead to the onset and persistence of AF have not completely been elucidated. Over the last decade, outstanding progress has been made in understanding the complex pathophysiology of AF. The key role of ectopic foci in pulmonary veins as a trigger of AF has been recognized. Furthermore, structural remodeling was identified as the main mechanism for AF persistence, confirming predominant role of atrial fibrosis. Systemic inflammatory state, oxidative stress injury, autonomic balance and neurohormonal activation were discerned as important modifiers that affect AF susceptibility. This new understanding of AF pathophysiology has led to the emergence of novel therapies. Ablative interventions, renin-angiotensin system blockade, modulation of oxidative stress and targeting tissue fibrosis represent new approaches in tackling AF. This review aims to provide a brief summary of novel insights into AF mechanisms and consequent therapeutic strategies., B. Aldhoon ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Beside heart failure and metabolic syndrome, atrial fibrillation is termed the cardiovascular epidemic of the 21st century. Its increased morbidity and mortality is alarming. The present, most effective therapy of atrial fibrillation is catheter ablation. Successful ablation of atrial fibrillation prevents the occurrence and progression of electrical, structural and mechanic myocardium remodelling, improves function of the left ventricle, and prevents the risk of thrombembolism. Onset of sinus rhythm activates the reversal remodelling leading to wall reconstruction and atrium reduction. The paper reviews the technique and presents own experience with catheter ablation., R. Lábrová, J. Špinar, N. Honzíková., and Obsahuje bibliografii a bibliografické odkazy
Kardiomyopatie představuje heterogenní skupinu onemocnění srdečního svalu, provázenou poruchou srdeční funkce. Tachykardií indukovaná kardiomyopatie (TIC) je způsobena déle trvající tachykardií vedoucí k dilataci a systolické dysfunkci s klinickými projevy srdečního selhání, které jsou reverzibilní po normalizaci tepové frekvence. Diagnóza je obvykle stanovena retrospektivně po normalizaci tepové frekvence a následné úpravě funkce levé komory (LKS). Více než 100 let po prvním dokumentovaném případu (roku 1913 popsána u mladého nemocného s fibrilací síní a projevy srdečního selhání [25]) jsou nadále znalosti patofyziologických mechanizmů omezené. Mezi nejčastější arytmie odpovědné za TIC patří fibrilace síní [1,2], flutter síní [3], incesantní supraventrikulární tachykardie [4], komorová tachykardie (KT) [5] a frekventní komorové extrasystoly (KES) [6]. Vzhledem k potenciální reverzibilitě je proto rozpoznání TIC a včasný terapeutický zásah stěžejní. Mezi stávající možnosti léčby patří farmakoterapie a chirurgická či katetrová ablace., Cardiomyopathy is a heterogeneous group of diseases of heart muscle accompanied with impaired cardiac function. Tachycardia-induced cardiomyopathy (TIC) is caused by prolonged tachycardia leading to dilatation and systolic dysfunction with clinical manifestation of heart failure. This state is reversible after normalization of heart rate. The diagnosis is usually made retrospectively after normalization of heart rate and recovery of left ventricular function (LVF). More than 100 years after the first documented case (described in 1913 in a young patient with atrial fibrillation and symptoms of heart failure [25]) is still limited knowledge of pathophysiological mechanisms. The most common arrhythmias responsible for the TIC include atrial fibrillation [1,2], atrial flutter [3], incessant supraventricular tachycardia [4], ventricular tachycardia (VT) [5] and frequent ventricular extrasystoles (VES) [6]. TIC detection and therapeutic intervention is crucial considering potential reversibility of tachycardia. Current options of treatment involve drug therapy and surgical or catheter ablation., and Jan Povolný