نتایج جستجو برای: arrhythmogenicity

تعداد نتایج: 246  

2015
S C Salvage J H King K H Chandrasekharan D I G Jafferji L Guzadhur H R Matthews C L-H Huang J A Fraser

AIMS Cardiac ryanodine receptor mutations are associated with catecholaminergic polymorphic ventricular tachycardia (CPVT), and some, including RyR2-P2328S, also predispose to atrial fibrillation. Recent work associates reduced atrial Nav 1.5 currents in homozygous RyR2-P2328S (RyR2(S/S) ) mice with slowed conduction and increased arrhythmogenicity. Yet clinically, and in murine models, the Nav...

Journal: :Circulation research 2017
Joshua Mayourian Timothy J Cashman Delaine K Ceholski Bryce V Johnson David Sachs Deepak A Kaji Susmita Sahoo Joshua M Hare Roger J Hajjar Eric A Sobie Kevin D Costa

RATIONALE Myocardial delivery of human mesenchymal stem cells (hMSCs) is an emerging therapy for treating the failing heart. However, the relative effects of hMSC-mediated heterocellular coupling (HC) and paracrine signaling (PS) on human cardiac contractility and arrhythmogenicity remain unresolved. OBJECTIVE The objective is to better understand hMSC PS and HC effects on human cardiac contr...

Journal: :Journal of the American College of Cardiology 1984

2017
Gary Tse Sheung Ting Wong Vivian Tse Jie Ming Yeo

Brugada syndrome is a primary electrical disorder of the heart, predisposing affected individuals to potentially lethal, ventricular tachy-arrhythmias. A number of mechanisms have been identified as being important increasing the risk of these rhythms. Wavelength (λ) restitution has been suggested to predict the onset of action potential duration (APD) alternans in mouse Scn5a hearts modelling ...

Journal: :Circulation 2009
Hideyuki Kinoshita Koichiro Kuwahara Makoto Takano Yuji Arai Yoshihiro Kuwabara Shinji Yasuno Yasuaki Nakagawa Michio Nakanishi Masaki Harada Masataka Fujiwara Masao Murakami Kenji Ueshima Kazuwa Nakao

BACKGROUND Pharmacological interventions for prevention of sudden arrhythmic death in patients with chronic heart failure remain limited. Accumulating evidence suggests increased ventricular expression of T-type Ca(2+) channels contributes to the progression of heart failure. The ability of T-type Ca(2+) channel blockade to prevent lethal arrhythmias associated with heart failure has never been...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید