Po-02-100 late menarche onset and the risk of cardiac events after the onset of adolescence in women with long qt syndrome
Women with congenital long-QT syndrome (LQTS) experience increased risk of cardiac events (CE) after the onset of adolescence, possibly due to effects of sex hormones on the potassium ion channels. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: May Goldenberg, David T. Huang, Mehmet K. Aktas, Kristina Cutter, Bonnie MacKecknie, Rebecca Horn, Scott McNitt, Wojciech Zareba, Arwa Younis Source Type: research
Po-02-068 non-invasive, bloodless estimation of serum potassium from icm ecg waveforms
Safe and effective titration of guideline directed medical therapy (GDMT) drugs for patients with heart failure, requires frequent monitoring of serum potassium (K+) levels. This is especially applicable to renin-angiotensin-aldosterone system inhibitors and β-blockers, which carry the potential to cause hyperkalemia, if not monitored carefully. Monitoring of serum K+ requires expensive and invasive blood draws. Latest recommendations call for titration of GDMT drugs as frequently as every 1 to 2 weeks, requiring more frequent blood draws. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Sierra Mulrine, Abhijit Kadrolkar Source Type: research
Mp-470543-009 light-gated potassium channels shorten the action potential and suppress premature excitation without arrhythmogenic risk
Prolonged ventricular action potentials (AP) and premature excitation (PVE) can lead to deadly arrhythmias. Optogenetics, involving manipulation of cardiac electrophysiology with light-gated ion channels is an emerging, transformative anti-arrhythmic technology. Newly discovered potassium (K+)-selective channels may be optimal for AP shortening and suppression of PVE, however their advantage over current cation-nonselective or anion-selective channels has not been explored. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Ahmed Ramadan, Matthew R. Stoyek, Andries Leemisa, Sara A. Rafferty, Patrick Boyle, Franziska Schneider-Warme, T. Alexander Quinn Source Type: research
Mp-470543-003 high-throughput screen identifies evacetrapib as candidate drug to treat long qt syndrome type 2
Congenital Long QT Syndrome (LQTS) can result in fatal cardiac arrhythmias. The main pharmacological treatment includes beta-blockers; however, while effective at reducing cardiac events, beta-blockers do not treat underlying mechanisms of the disease, and patients occasionally experience breakthrough cardiac events or side effects. Genetic variants in the voltage gated potassium ion channel (Kv11.1) are the second leading cause of LQTS, and approximately 90% cause defective intracellular transport (trafficking) of Kv11.1 protein to the cell surface membrane. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Christian Egly, Tri Do, Yehuda Wexler, Harel Grinstein, Brian P. Delisle, Lior Gepstein, Bjorn C. Knollmann Source Type: research
Bs-469619-003 granular variant-specific features improve kcnh2-long qt syndrome risk stratification
Long QT syndrome (LQTS) is a lethal arrhythmia syndrome, frequently caused by rare loss-of-function variants in the potassium channel encoded by KCNH2. Variant-based risk stratification is complicated by heterogenous clinical data, incomplete penetrance, and low-throughput functional data. While variant-specific functional data can assist with variant classification, whether functional data can assist with prediction of outcomes is unknown. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Matthew O'Neill, Chai-ann Ng, Takanori Aizawa, Luca Sala, Sahej Bains, Isabelle Denjoy, Annika Winbo, Rizwan Ullah, Qianyi Shen, Chek-ying Tan, Krystian Kozek, Loren Vanags, Devyn Mitchell, Alex Shen, Yuko Wada, Asami Kashiwa, Lia Crotti, Federica Dagradi Source Type: research
En-482891-004 aav9-mediated kcnh2-suppression-replacement gene therapy prolongs the pathologically shortened qt/apd in short qt syndrome type 1 rabbit models
Short QT syndrome type 1 (SQT1) is an inherited channelopathy with gain-of-function variants in the KCNH2-encoded Kv11.1 potassium channel, which conducts the IKr current essential for the cardiac action potential (AP). Patients with SQT1 have a shortened AP and are susceptible to ventricular arrhythmias, which can ultimately lead to sudden cardiac death (SCD). (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Saranda Nimani, Sahej Bains, Nicolo Alerni, Lucilla Giammarino, Andr ás Horváth, Julien Louradour, Miriam Barbieri, Olgica Beslac, Manuel Egle, David Tester, Nicolas Christoforou, Lluis Matas, Ruben Lopez, Stefanie Perez-Feliz, Changsung J. Kim, Wei Zho Source Type: research
Po-05-003 empagliflozin shortened the prolonged action potential duration in human induced pluripotent stem cell-derived cardiomyocytes with thin filament hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is a common, potentially genetic heart disease with an estimated prevalence of 1:500 that is characterized clinically by unexplained left ventricular hypertrophy. Concomitant QTc prolongation> 480 ms occurs in 13% of patients with HCM. Compared to controls, cardiomyocytes derived from HCM patients undergoing myectomy have a prolonged action potential duration (APD) related to increased late sodium and calcium currents and decreased repolarizing potassium currents. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Wei Zhou, Dan Ye, David Tester, John R. Giudicessi, Michael J. Ackerman Source Type: research
Po-05-170 hypercholesterolemia induces diastolic dysfunction and upregulates ikas in female but not male rabbits
Isoproterenol activates apamin-sensitive small conductance calcium-activated potassium (SK) current (IKAS) more in female than male rabbit ventricles. Hypercholesterolemic (HC) rabbits have cardiac sympathetic hyperinnervation and diastolic dysfunction. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Liyang Zhang, Xiao Liu, Anxhela Kote, Jae Hyung Cho, Joshua I. Goldhaber, Zhenhui Chen, James Tisdale, Robert J. Siegel, Peng-Sheng Chen Source Type: research
Po-05-191 aav9-mediated kcnq1-suppression-replacement gene therapy in transgenic rabbits with type 1 long qt syndrome (lqt1)
Type 1 long QT syndrome (LQT1) is caused by pathogenic variants in the KCNQ1-encoded Kv7.1 potassium channels which prolong the ventricular cardiomyocyte ’s (VCM) action potential duration (APD) and the clinical QT interval. During increased catecholamine exposure, patients with LQT1 exhibit paradoxical prolongation of the QT/APD. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Sahej Bains, Lucilla Giammarino, Julien Louradour, Saranda Nimani, Nicolo Alerni, David Tester, Changsung J. Kim, Nicolas Christoforou, Andras Horvath, Olgica Beslac, Gideon Koren, Michael Brunner, Daniela Casoni, Fabien Praz, Andreas Haeberlin, Gabriel B Source Type: research
Po-06-049 sex hormones and repolarization dynamics during the menstrual cycle in women treated with qt-prolonging drugs
Women with congenital and acquired long QT syndrome (LQTS) experience increased risk of cardiac events after the onset of adolescence, induced mainly by the modulating effects of sex hormones on the KCNH2 cardiac potassium channel. We hypothesized that the effect of sex hormones on cardiac ion channel function may modify propensity for ventricular tachyarrhythmia during the menstrual cycle in women who are treated with QT prolonging drugs. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Ilan Goldenberg, Emma Hassell, Aneliya San, Ahmed Shah, Wojciech Zareba, Scott McNitt, Kristina Cutter, Bonnie MacKecknie, Rebecca Horn, Mehmet K. Aktas Source Type: research
Po-ces-05 light-gated potassium channels shorten the action potential and suppress premature excitation without arrhythmogenic risk
Prolonged ventricular action potentials (AP) and premature excitation (PVE) can lead to deadly arrhythmias. Optogenetics, involving manipulation of cardiac electrophysiology with light-gated ion channels is an emerging, transformative anti-arrhythmic technology. Newly discovered potassium (K+)-selective channels may be optimal for AP shortening and suppression of PVE, however their advantage over current cation-nonselective or anion-selective channels has not been explored. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Ahmed Ramadan, Matthew R. Stoyek, Andries Leemisa, Sara A. Rafferty, Patrick Boyle, Franziska Schneider-Warme, T. Alexander Quinn Source Type: research
Po-ces-03 aav9-mediated kcnq1-suppression-replacement gene therapy in transgenic rabbits with type 1 long qt syndrome (lqt1)
Type 1 long QT syndrome (LQT1) is caused by pathogenic variants in the KCNQ1-encoded Kv7.1 potassium channels which prolong the ventricular cardiomyocyte ’s (VCM) action potential duration (APD) and the clinical QT interval. During increased catecholamine exposure, patients with LQT1 exhibit paradoxical prolongation of the QT/APD. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Sahej Bains, Lucilla Giammarino, Julien Louradour, Saranda Nimani, Nicolo Alerni, David Tester, Changsung J. Kim, Nicolas Christoforou, Andras Horvath, Olgica Beslac, Gideon Koren, Michael Brunner, Daniela Casoni, Fabien Praz, Andreas Haeberlin, Gabriel B Source Type: research
Po-ces-01 high-throughput screen identifies evacetrapib as candidate drug to treat long qt syndrome type 2
Congenital Long QT Syndrome (LQTS) can result in fatal cardiac arrhythmias. The main pharmacological treatment includes beta-blockers; however, while effective at reducing cardiac events, beta-blockers do not treat underlying mechanisms of the disease, and patients occasionally experience breakthrough cardiac events or side effects. Genetic variants in the voltage gated potassium ion channel (Kv11.1) are the second leading cause of LQTS, and approximately 90% cause defective intracellular transport (trafficking) of Kv11.1 protein to the cell surface membrane. (Source: Heart Rhythm)
Source: Heart Rhythm - May 1, 2024 Category: Cardiology Authors: Christian Egly, Tri Do, Yehuda Wexler, Harel Grinstein, Brian P. Delisle, Lior Gepstein, Bjorn C. Knollmann Source Type: research
Intercalating a potassium –aqua complex cation into an α-MoO3 layer without reducing molybdenum: a potential storage system
Chem. Commun., 2024, Advance Article DOI: 10.1039/D4CC01400F, CommunicationDebu Jana, Shalini Sanjay Mishra, Samar K. Das We have prepared a rod-shaped MoO3 material, [MoVI3O9{K(H2O)4}(CH3COO)] ·H2O intercalating potassium-aqua-complex acetate into its lamellar space,via a green aqueous synthesis; the compound acts as a potential storage system of alkali metal ions. To cite this article before page numbers are assigned, use the DOI form of citation above. The content of this RSS Feed (c) The Royal Society of Chemistry (Source: RSC - Chem. Commun. latest articles)
Source: RSC - Chem. Commun. latest articles - April 30, 2024 Category: Chemistry Authors: Debu Jana Source Type: research
Intercalating a potassium-aqua complex cation into an α-MoO < sub > 3 < /sub > layer without reducing molybdenum: a potential storage system
Chem Commun (Camb). 2024 Apr 30. doi: 10.1039/d4cc01400f. Online ahead of print.ABSTRACTWe have demonstrated a green aqueous synthesis of rod-shaped MoO3 material, [MoVI3O9{K(H2O)4}(CH3COO)]·H2O (2) intercalating potassium-aqua-complex acetate into its lamellar space, simply by ion-exchange of Co(II)-aqua-complex in compound [MoVI4O12(CH3COO)2{CoII(H2O)6}]·2H2O (1) by {K(H2O)4}+ in an aqueous solution of 1 and KCl. Compound 2 acts as a potential storage system of alkali metal ions.PMID:38686497 | DOI:10.1039/d4cc01400f (Source: Chemical Communications)
Source: Chemical Communications - April 30, 2024 Category: Chemistry Authors: Debu Jana Shalini Sanjay Mishra Samar K Das Source Type: research
