Mutations in the genes encoding cardiac ion channels may contribute in life-threatening arrhythmias in patients with hypertrophic cardiomyopathy

2021 ◽  
Vol 69 ◽  
pp. 85-86
Author(s):  
E. Zaklyazminskaya ◽  
N. Chakova ◽  
S. Komissarova ◽  
S. Niyazova ◽  
A. Shestak ◽  
...  
Keyword(s):  
Ion Channels ◽  
Hypertrophic Cardiomyopathy ◽  
Cardiac Ion Channels ◽  
Genes Encoding ◽  
Life Threatening

Abstract 62: The Coxsackie Virus B3 modulates Cardiac Ion Channels

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Guiscard Seebohm ◽  
Katja Steinke ◽  
Ulrike Henrion ◽  
Nicole Ettischer ◽  
Frank Sachse ◽  
...  
Keyword(s):  
Ion Channels ◽  
Cardiac Cells ◽  
Coxsackie Virus ◽  
Cardiac Ion Channels ◽  
Increased Risk ◽  
Chronic Myocarditis ◽  
Life Threatening ◽  
The Common ◽  
In Silico Analyses

Infections with coxsackieviruses of type B (CVB) induce severe forms of acute and chronic myocarditis that are often accompanied by ventricular arrhythmias. The mechanisms underlying the development of virus-induced, life-threatening arrhythmia, remain largely elusive. Here, we show time-dependent CVB3-induced modulation of the cardiac ion channels Kv7.1, hERG1 and CaV1.2 in vitro. Channel protein localizations within cells and plasma membrane abundance are altered in infected mouse cardiac cells. In silico analyses of infected human myocytes suggest increased risk of arrhythmogenesis. These modifications are attenuated by the common Asian polymorphism KCNQ1-P448R, a genetic determinant preventing coxsackievirus-induced effects in vitro. This study provides a previously unknown explanation for the development of arrhythmias in enteroviral myocarditis, which will help to develop therapeutic strategies for arrhythmia treatment.

scholarly journals Hyperkalemia Induced Brugada Phenocopy: A Rare ECG Manifestation

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Muhammad Ameen ◽  
Ghulam Akbar ◽  
Naeem Abbas ◽  
Ghazi Mirrani
Keyword(s):  
Ion Channels ◽  
Ventricular Arrhythmias ◽  
Cardiac Conduction ◽  
St Segment Elevation ◽  
Electrolyte Disturbances ◽  
Cardiac Ion Channels ◽  
St Segment ◽  
Life Threatening ◽  
Severe Hyperkalemia ◽  
Brugada Pattern

Brugada syndrome (BrS) is an inherited disorder of cardiac ion channels characterized by peculiar ECG findings predisposing individuals to ventricular arrhythmias, syncope, and sudden cardiac death (SCD). Various electrolyte disturbances and ion channels blocking drugs could also provoke BrS ECG findings without genetic BrS. Clinical differentiation and recognition are essential for guiding the legitimate action. Hyperkalemia is well known to cause a wide variety of ECG manifestations. Severe hyperkalemia can even cause life threatening ventricular arrhythmias and cardiac conduction abnormalities. Most common ECG findings include peaked tall T waves with short PR interval and wide QRS complex. Since it is very commonly encountered disorder, physicians need to be aware of even its rare ECG manifestations, which include ST segment elevation and Brugada pattern ECG (BrP). We are adding a case to the limited literature about hyperkalemia induced reversible Brugada pattern ECG changes.

scholarly journals Mechanisms and Alterations of Cardiac Ion Channels Leading to Disease: Role of Ankyrin-B in Cardiac Function

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 211 ◽  
Author(s):  
Holly C. Sucharski ◽  
Emma K. Dudley ◽  
Caullin B.R. Keith ◽  
Mona El Refaey ◽  
Sara N. Koenig ◽  
...  
Keyword(s):  
Ion Channels ◽  
Cardiac Function ◽  
Cell Biology ◽  
Sinus Node ◽  
Conduction Block ◽  
Cardiac Ion Channels ◽  
Life Threatening ◽  
Ankyrin B ◽  
Normal Cardiac Function

Ankyrin-B (encoded by ANK2), originally identified as a key cytoskeletal-associated protein in the brain, is highly expressed in the heart and plays critical roles in cardiac physiology and cell biology. In the heart, ankyrin-B plays key roles in the targeting and localization of key ion channels and transporters, structural proteins, and signaling molecules. The role of ankyrin-B in normal cardiac function is illustrated in animal models lacking ankyrin-B expression, which display significant electrical and structural phenotypes and life-threatening arrhythmias. Further, ankyrin-B dysfunction has been associated with cardiac phenotypes in humans (now referred to as “ankyrin-B syndrome”) including sinus node dysfunction, heart rate variability, atrial fibrillation, conduction block, arrhythmogenic cardiomyopathy, structural remodeling, and sudden cardiac death. Here, we review the diverse roles of ankyrin-B in the vertebrate heart with a significant focus on ankyrin-B-linked cell- and molecular-pathways and disease.

scholarly journals Twenty single-nucleotide polymorphisms in four genes encoding cardiac ion channels

2002 ◽  
Vol 47 (4) ◽  
pp. 208-212 ◽  
Author(s):  
H. Iwasa ◽  
M. Kurabayashi ◽  
R. Nagai ◽  
Y. Nakamura ◽  
T. Tanaka
Keyword(s):  
Ion Channels ◽  
Single Nucleotide Polymorphisms ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Cardiac Ion Channels ◽  
Genes Encoding

Extraction of Auditory Information by Modulation of Neuronal Ion Channels

2018 ◽  
pp. 272-300
Author(s):  
Leonard K. Kaczmarek
Keyword(s):  
Ion Channels ◽  
Neuronal Firing ◽  
Auditory Information ◽  
Auditory Neurons ◽  
Complex Sound ◽  
Medial Nucleus ◽  
Rapid Changes ◽  
Genes Encoding ◽  
Kinetics Of ◽  
Trapezoid Body

All neurons express a subset of over seventy genes encoding potassium channel subunits. These channels have been studied in auditory neurons, particularly in the medial nucleus of the trapezoid body. The amplitude and kinetics of various channels in these neurons can be modified by the auditory environment. It has been suggested that such modulation is an adaptation of neuronal firing patterns to specific patterns of auditory inputs. Alternatively, such modulation may allow a group of neurons, all expressing the same set of channels, to represent a variety of responses to the same pattern of incoming stimuli. Such diversity would ensure that a small number of genetically identical neurons could capture and encode many aspects of complex sound, including rapid changes in timing and amplitude. This review covers the modulation of ion channels in the medial nucleus of the trapezoid body and how it may maximize the extraction of auditory information.All neurons express a subset of over seventy genes encoding potassium channel subunits. These channels have been studied in auditory neurons, particularly in the medial nucleus of the trapezoid body. The amplitude and kinetics of various channels in these neurons can be modified by the auditory environment. It has been suggested that such modulation is an adaptation of neuronal firing patterns to specific patterns of auditory inputs. Alternatively, such modulation may allow a group of neurons, all expressing the same set of channels, to represent a variety of responses to the same pattern of incoming stimuli. Such diversity would ensure that a small number of genetically identical neurons could capture and encode many aspects of complex sound, including rapid changes in timing and amplitude. This review covers the modulation of ion channels in the medial nucleus of the trapezoid body and how it may maximize the extraction of auditory information.

scholarly journals Anesthetic Challenges in the Management of Intracranial Aneurysm Clipping in a Patient with Hypertrophic Cardiomyopathy

2020 ◽  
Author(s):  
Sakshi Duggal ◽  
Priyanka Khurana ◽  
Pragati Ganjoo ◽  
Nilima Das
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Perioperative Complications ◽  
Artery Aneurysm ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Anterior Communicating Artery ◽  
Drug Selection ◽  
Aneurysm Clipping ◽  
Left Ventricular Outflow ◽  
Life Threatening

AbstractAneurysmal surgeries are high-risk procedures due to potential for occurrence of fatal perioperative complications. This risk is exaggerated in the presence of co-existing hypertrophic cardiomyopathy (HCM). It involves asymmetrical hypertrophy of left ventricle with mitral valve dysfunction, leading to left ventricular outflow tract obstruction. Various perioperative factors may precipitate this obstruction resulting in life-threatening consequences. We report the management of a patient with HCM undergoing anterior communicating artery aneurysm clipping and discuss the anesthetic concerns. Comprehensive approach with careful drug selection, vigilant monitoring, and preparedness for complications enabled patient safety and a good neurological outcome.

Acute O2 sensing through HIF2α-dependent expression of atypical cytochrome oxidase subunits in arterial chemoreceptors

2019 ◽  
Vol 13 (615) ◽  
pp. eaay9452 ◽  
Author(s):  
Alejandro Moreno-Domínguez ◽  
Patricia Ortega-Sáenz ◽  
Lin Gao ◽  
Olalla Colinas ◽  
Paula García-Flores ◽  
...  
Keyword(s):  
Ion Channels ◽  
Carotid Body ◽  
Acute Hypoxia ◽  
Mechanistic Explanation ◽  
Nerve Fibers ◽  
Adaptive Responses ◽  
Glomus Cells ◽  
Adult Mice ◽  
Genes Encoding ◽  
Regulation Of Breathing

Acute cardiorespiratory responses to O2 deficiency are essential for physiological homeostasis. The prototypical acute O2-sensing organ is the carotid body, which contains glomus cells expressing K+ channels whose inhibition by hypoxia leads to transmitter release and activation of nerve fibers terminating in the brainstem respiratory center. The mechanism by which changes in O2 tension modulate ion channels has remained elusive. Glomus cells express genes encoding HIF2α (Epas1) and atypical mitochondrial subunits at high levels, and mitochondrial NADH and reactive oxygen species (ROS) accumulation during hypoxia provides the signal that regulates ion channels. We report that inactivation of Epas1 in adult mice resulted in selective abolition of glomus cell responsiveness to acute hypoxia and the hypoxic ventilatory response. Epas1 deficiency led to the decreased expression of atypical mitochondrial subunits in the carotid body, and genetic deletion of Cox4i2 mimicked the defective hypoxic responses of Epas1-null mice. These findings provide a mechanistic explanation for the acute O2 regulation of breathing, reveal an unanticipated role of HIF2α, and link acute and chronic adaptive responses to hypoxia.

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