Role Of Atrium Research Articles

The role of atria in ventricular fibrillation after continuous-flow left ventricular assist device implantation in ovine model.

This study attempted to explore the hemodynamics and potential mechanisms driving pulmonary circulation in status of ventricular fibrillation (VF) following continuous-flow left ventricular assist device (CF-LVAD) implantation. An ovine CF-LVAD model was built in small-tailed Han sheep, with the pump speed set as 2,400 rpm. VF was induced following ventricular tachycardia using a temporary pacemaker probe to stimulate the right and left ventricular free walls. The central venous pressure (CVP), pump flow (PF), pulmonary artery flow (PAF) and other major indicators were observed and recorded after VF. Low-flow systemic and pulmonary circulation could be sustained for 60 min under VF with sinus atrial rhythm after CF-LVAD implantation. The CVP gradually increased. The mean PF declined from 1.80 to 1.20 L/min, and the mean PAF decreased from 1.62 L/min to 0.87 L/min. Under VF with atrial fibrillation, the systemic and pulmonary circulation couldn't be sustained. The CVP jumped from the 5 mmHg baseline to 12 mmHg, the mean PF rapidly decreased from 3.45 L/min to 0.79 L/min, and the PAF declined from 3.94 L/min to 0.77 L/min. The atrial rhythm and function might be essential for the circulation maintenance in patients with VF after CF-LVAD implantation.

Atrial AMP-activated protein kinase is critical for prevention of dysregulation of electrical excitability and atrial fibrillation.

Metabolic stress is an important cause of pathological atrial remodeling and atrial fibrillation. AMPK is a ubiquitous master metabolic regulator, yet its biological function in the atria is poorly understood in both health and disease. We investigated the impact of atrium-selective cardiac AMPK deletion on electrophysiological and structural remodeling in mice. Loss of atrial AMPK expression caused atrial changes in electrophysiological properties and atrial ectopic activity prior to the onset of spontaneous atrial fibrillation. Concomitant transcriptional downregulation of connexins and atrial ion channel subunits manifested with delayed left atrial activation and repolarization. The early molecular and electrophysiological abnormalities preceded left atrial structural remodeling and interstitial fibrosis. AMPK inactivation induced downregulation of transcription factors (Mef2c and Pitx2c) linked to connexin and ion channel transcriptional reprogramming. Thus, AMPK plays an essential homeostatic role in atria, protecting against adverse remodeling potentially by regulating key transcription factors that control the expression of atrial ion channels and gap junction proteins.

Kv1.1 potassium channel subunit deficiency alters ventricular arrhythmia susceptibility, contractility, and repolarization.

Epilepsy‐associated Kv1.1 voltage‐gated potassium channel subunits encoded by the Kcna1 gene have traditionally been considered absent in heart, but recent studies reveal they are expressed in cardiomyocytes where they could regulate intrinsic cardiac electrophysiology. Although Kv1.1 now has a demonstrated functional role in atria, its role in the ventricles has never been investigated. In this work, electrophysiological, histological, and gene expression approaches were used to explore the consequences of Kv1.1 deficiency in the ventricles of Kcna1 knockout (KO) mice at the organ, cellular, and molecular levels to determine whether the absence of Kv1.1 leads to ventricular dysfunction that increases the risk of premature or sudden death. When subjected to intracardiac pacing, KO mice showed normal baseline susceptibility to inducible ventricular arrhythmias (VA) but resistance to VA under conditions of sympathetic challenge with isoproterenol. Echocardiography revealed cardiac contractile dysfunction manifesting as decreased ejection fraction and fractional shortening. In whole‐cell patch‐clamp recordings, KO ventricular cardiomyocytes exhibited action potential prolongation indicative of impaired repolarization. Imaging, histological, and transcript analyses showed no evidence of structural or channel gene expression remodeling, suggesting that the observed deficits are likely electrogenic due to Kv1.1 deficiency. Immunoblots of patient heart samples detected the presence of Kv1.1 at relatively high levels, implying that Kv1.1 contributes to human cardiac electrophysiology. Taken together, this work describes an important functional role for Kv1.1 in ventricles where its absence causes repolarization and contractility deficits but reduced susceptibility to arrhythmia under conditions of sympathetic drive.

Prediction of major bleeding in patients receiving DOACs for venous thromboembolism: A prospective cohort study

BackgroundIn the direct oral anticoagulants (DOACs) era, extended anticoagulation is an attractive strategy after venous thromboembolism (VTE). The role of currently available bleeding risk scores for VTE patients treated with DOACs in clinical practice is undefined. MethodsConsecutive patients with VTE were included in a prospective multicenter cohort at the initiation of treatment with DOACs. The role of ATRIA, HAS-BLED, Kuijer, ORBIT, RIETE and VTE-BLEED scores in predicting major bleeding (ISTH definition) while on DOAC treatment was assessed. ResultsOverall, 1034 patients were included and followed for one year or until the end of treatment or the occurrence of major bleeding. During study period, 26 major bleedings occurred in 25 patients (2.8% patient-year). Anemia, bleeding history and creatinine clearance <60 ml/min were significant predictors of major bleedings.The predictive value of bleeding risk scores was modest. In the 12-month study period, ORBIT (HR intermediate-high vs. low risk patients 3.62, 95% CI 1.65–7.94 and c-statistics 0.645, 95% CI 0.523–0.767) and VTE-BLEED (HR high vs. low 16.11, 95% CI 2.18–119.09 and c-statistics 0.674, 95% CI 0.593–0.755) score significantly predicted major bleeding. The lowest incidence of major bleeding (0.3%) was observed in the low-risk category of VTE-BLEED, while the highest (7.1%) in the high-risk category of ORBIT. ConclusionsIn a real-life cohort of patients with VTE treated with DOACs, the predictive value of currently available bleeding risk scores was modest and not statistically different. Whether these scores can be used for decision making on anticoagulation should be assessed in management studies.

Role of atrium in automaticity of the sinus node.

As the electrical source of hearts, sino-atrial node cells (SANCs) play significant roles in rhythmic firings. Due to the complex structure and function of SANCs, electrical interactions of SAN and its surrounding atrium has not yet been fully understood. The aim of the present study is to investigate effects of coupling conductance between SAN and atrial cells as well as the ectopic beats in atrium on automaticity of the SAN by computer simulation methods. On the basis of a dynamic mathematical single cell model considering the heterogeneity of central and peripheral SANCs, a two-dimensional inhomogeneous tissue slice including SAN and atrium was developed. The operator splitting method was used to integrate the tissue model. The results demonstrated that the coupling conductance between SAN and atrium had effects on the direction of spontaneous action potential conduction in SAN. Weak coupling resulted in a shift of the earliest pacemaker site from central to peripheral SANCs. Additionally, the ectopic beat-induced excitation in atrium was found to be able to enter into and overdrive suppress the automaticity of SAN. Even if the ectopic beat was delivered after the spontaneous firing had started in central SANCs, the spontaneous conduction toward the periphery could also be suppressed by the retrograde activation from the entering atrial depolarization wave. These findings suggested a direct link between sinus node dysfunction and atrial arrhythmias, and therefore were helpful in explaining the role of atrium in sinus node dysfunction.

Investigation of the synchronization of the sinoatrial node upon stimulation from atria

The excitation of the sinoatrial node from frog heart atria has been experimentally investigated. Potentials were measured by means of microelectrodes introduced in pacemaker cells of the sinoatrial node. It has been found that atria can modulate the rhythm of the sinoatrial node due to electric and electromechanical actions, among which the electromechanical action is more important. Specific transient processes accompanying the establishment of the stationary rhythm have been studied. A mathematical model of the transient processes of achieving the rhythm of the sinoatrial node is proposed on the basis of Diophantine methods. The calculations performed using the mathematical model satisfactorily agree with the experimental results. The stabilizing role of atria in forming the rhythm of the sinoatrial node is revealed.

Dopamine 4-sulfate : Effects on isolated perfused rat heart and role of atria

We studied the effects of sulfate conjugate of dopamine on the isolated perfused rat heart (Langendorff preparation). In the experimental group, we removed atria from half number of the hearts. In the hearts with intact atria, dopamine 4-sulfate significantly improved the DT (developed tension), +dT/dt max (maximal rate of contraction), -dT/dt max (maximum rate of relaxation) over baseline values. But when atria were removed, dopamine 4-sulfate had no effect on the mechanical functions of heart. We analysed the effluent perfusate for the free and conjugated catecholamines. In the control group (no drug), and when atria were excised, the free catecholamine levels were negligible. But when the atria were kept intact, the effluent contained significant amount of free dopamine (DA), and norepinephrine (NE). These data suggested that dopamine sulfate had no direct effect on the ventricular muscle of rat heart, but was converted within the atrial tissues into free catecholamines which might be responsible for the positive inotropic actions.

Role of atrium in closure of mitral valve in man.

ARTICLESRole of atrium in closure of mitral valve in manA Zaky, E Steinmetz, and H FeigenbaumA Zaky, E Steinmetz, and H FeigenbaumPublished Online:01 Dec 1969https://doi.org/10.1152/ajplegacy.1969.217.6.1652MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 217Issue 6December 1969Pages 1652-1659 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.217.6.1652PubMed5353040History Published online 1 December 1969 Published in print 1 December 1969 Metrics