Browsing by Author "Wan, Juyi"
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Item type:Item, Concomitant SK current activation and sodium current inhibition cause J wave syndrome(2018-11-15) ;Chen, Mu ;Xu, Dong-Zhu ;Wu, Adonis Z. ;Guo, ShuaiWan, JuyiThe mechanisms of J wave syndrome (JWS) are incompletely understood. Here, we showed that the concomitant activation of small-conductance calcium-activated potassium (SK) current (I-KAS) and inhibition of sodium current by cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (CyPPA) recapitulate the phenotypes of JWS in Langendorff-perfused rabbit hearts. CyPPA induced significant J wave elevation and frequent spontaneous ventricular fibrillation (SVF), as well as sinus bradycardia, atrioventricular block, and intraventricular conduction delay. I-KAS activation by CyPPA resulted in heterogeneous shortening of action potential (AP) duration (APD) and repolarization alternans. CyPPA inhibited cardiac sodium current (I-Na) and decelerated AP upstroke and intracellular calcium transient. SVFs were typically triggered by short-coupled premature ventricular contractions, initiated with phase 2 reentry and originated more frequently from the right than the left ventricles. Subsequent I-KAS blockade by apamin reduced J wave elevation and eliminated SVF. beta-Adrenergic stimulation was antiarrhythmic in CyPPA-induced electrical storm. Like CyPPA, hypothermia (32.0 degrees C) also induced J wave elevation and SVF. It facilitated negative calcium-voltage coupling and phase 2 repolarization alternans with spatial and electromechanical discordance, which were ameliorated by apamin. These findings suggest that I-KAS activation contributes to the development of JWS in rabbit ventricles.Item type:Item, Skin sympathetic nerve activity precedes the onset and termination of paroxysmal atrial tachycardia and fibrillation(2017-07-01) ;Uradu, Andrea ;Wan, Juyi ;Doytchinova, Anisiia ;Wright, Keith C.Lin, Andrew Y. T.BACKGROUND Skin sympathetic nerve activity (SKNA) is useful for estimating sympathetic tone in humans. OBJECTIVE The purpose of this study was to test the hypotheses that (1) increased SKNA is associated with the onset and termination of paroxysmal atrial tachycardia (AT) and atrial fibrillation (AF) and (2) sinoatrial node response to SKNA is reduced in patients with more frequent AT or AF episodes. METHODS SKNA and electrocardiogram were recorded in 11 patients (4 men and 7 women; average age 66 +/- 10 years), including 3 patients with AT (11 +/- 18 episodes per patient) and 8 patients with AF (24 +/- 26 episodes per patient). RESULTS The average SKNA (aSKNA) 10 seconds before AT onset was 1.07 +/- 0.10 mu V and 10 seconds after termination was 1.27 6 0.10 mV; both were significantly (P = .032 and P < .0001) higher than that during sinus rhythm (0.97 +/- 0.09 mu V). The aSKNA 10 seconds before AF onset was 1.34 +/- 0.07 mu V and 10 seconds after termination was 1.31 +/- 0.07 mu V; both were significantly (P < .0001) higher than that during sinus rhythm (1.04 +/- 0.07 mu V). The aSKNA before onset (P < .0001) and after termination (P < .0011) was higher in AF than in AT. The sinus rate correlated (P < .0001) with aSKNA in each patient (average r = 0.74; 95% confidence interval 0.65-0.84). The r value in each patient negatively correlated with the number of AT and AF episodes (r = -0.6493; 95% confidence interval -0.8990 to -0.08073; P = .0306). CONCLUSION Increased SKNA was observed both at the onset and termination of AT and AF. Patients with more frequent AT and AF episodes had a weak correlation between sinus rate and aSKNA, suggesting sinoatrial node remodeling by tachycardia.