Genetic Complexity of Sinoatrial Node Dysfunction [PDF]
Frontiers in Genetics, 2021 The pacemaker cells of the cardiac sinoatrial node (SAN) are essential for normal cardiac automaticity. Dysfunction in cardiac pacemaking results in human sinoatrial node dysfunction (SND).
Michael J. Wallace +16 more
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The role of the calcium and the voltage clocks in sinoatrial node dysfunction. [PDF]
Yonsei Med J, 2011 Recent evidence indicates that the voltage clock (cyclic activation and deactivation of membrane ion channels) and Ca2+ clocks (rhythmic spontaneous sarcoplasmic reticulum Ca2+ release) jointly regulate sinoatrial node (SAN) automaticity.
Joung B, Chen PS, Lin SF.
europepmc +9 more sources
Possible sinoatrial node dysfunction in a 6-month-old domestic shorthair cat [PDF]
Journal of Feline Medicine and Surgery Open ReportsCase summary A 6-month-old male entire domestic shorthair cat was presented to the ophthalmology department for nasolacrimal duct cannulation and flushing, and castration under general anaesthesia.
Florence Hillen, Laurent Locquet
doaj +4 more sources
Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation [PDF]
JCI Insight, 2022 Loss-of-function (LOF) variants in SCN1B, encoding the voltage-gated sodium channel β1/β1B subunits, are linked to neurological and cardiovascular diseases. Scn1b-null mice have spontaneous seizures and ventricular arrhythmias and die by approximately 21
Roberto Ramos-Mondragon +13 more
doaj +6 more sources
Pharmacologic Approach to Sinoatrial Node Dysfunction. [PDF]
Annu Rev Pharmacol Toxicol, 2021 The spontaneous activity of the sinoatrial node initiates the heartbeat. Sino-atrial node dysfunction (SND) and sick sinoatrial (sick sinus) syndrome are caused by the heart's inability to generate a normal sinoatrial node action potential. In clinical practice, SND is generally considered an age-related pathology, secondary to degenerative fibrosis ...
Mesirca P +6 more
europepmc +7 more sources
Digenic heterozygous mutations of KCNH2 and SCN5A induced young and early‐onset long QT syndrome and sinoatrial node dysfunction [PDF]
Annals of Noninvasive Electrocardiology, 2022 Introduction Long QT syndrome (LQTS) is a life‐threatening inherited channelopathy, and prolonged QT intervals easily trigger malignant arrhythmias, especially torsades de pointes and ventricular fibrillation.
Zhe Yang +10 more
doaj +4 more sources
Emerging Signaling Regulation of Sinoatrial Node Dysfunction. [PDF]
Curr Cardiol Rep, 2023 PURPOSE OF REVIEW: The sinoatrial node (SAN), the natural pacemaker of the heart, is responsible for generating electrical impulses and initiating each heartbeat.
Zheng M, Erhardt S, Cao Y, Wang J.
europepmc +5 more sources
Fibrosis: a structural modulator of Sinoatrial Node physiology and dysfunction [PDF]
Frontiers in Physiology, 2015 Heart rhythm is initialized and controlled by the Sinoatrial Node (SAN), the primary pacemaker of the heart. The SAN is a heterogeneous multi-compartment structure characterized by clusters of specialized cardiomyocytes, enmeshed within strands of ...
Thomas A Csepe +4 more
doaj +4 more sources
Mechanisms of Sinoatrial Node Dysfunction in Heart Failure With Preserved Ejection Fraction. [PDF]
Circulation, 2022 Background: The ability to increase heart rate during exercise and other stressors is a key homeostatic feature of the sinoatrial node (SAN). When the physiological heart rate response is blunted, chronotropic incompetence limits exercise capacity, a common problem in patients with heart failure with preserved ejection fraction
Mesquita T +11 more
europepmc +5 more sources
Lithium-Induced Sinoatrial Node Dysfunction. [PDF]
Cureus, 2021 Lithium is a common mood-stabilizing drug for manic patients. We describe a case of sinoatrial node dysfunction in a patient with serum lithium levels within the therapeutic range. Given the symptomology and severity of the patient’s illness, after placing a permanent pacemaker, the patient was discharged on the preadmission dose of lithium.
Sarangi A, Javed S, Paul T, Amor W.
europepmc +5 more sources