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1 ys a critical role in the pathophysiology of arrhythmogenesis.
2 atherosclerosis, thrombosis, vasomotion, and arrhythmogenesis.
3 ance, and enhanced susceptibility to induced arrhythmogenesis.
4 ssion of Cx40 have been implicated in atrial arrhythmogenesis.
5 sympathetic response that may play a role in arrhythmogenesis.
6 of RyR2 and how this contributes to cardiac arrhythmogenesis.
7 r may reduce SR Ca content and contribute to arrhythmogenesis.
8 ty of ion channel subunit genes that promote arrhythmogenesis.
9 acute stress may have served to promote this arrhythmogenesis.
10 polarizations, known cellular mechanisms for arrhythmogenesis.
11 coupling, which is an important mechanism of arrhythmogenesis.
12 (LQTS), a condition associated with enhanced arrhythmogenesis.
13 factor in triggering cardiac enlargement and arrhythmogenesis.
14 function, peripheral vascular resistance and arrhythmogenesis.
15 tribution of the autonomic nervous system to arrhythmogenesis.
16 nfluence electrophysiological properties and arrhythmogenesis.
17 cal link between contractile dysfunction and arrhythmogenesis.
18 physiology and the fundamental mechanisms of arrhythmogenesis.
19 positions of fibrotic tissues contribute to arrhythmogenesis.
20 nation of fibrillation without shock-induced arrhythmogenesis.
21 sms of dyslipidaemias contribute directly to arrhythmogenesis.
22 CO pretreatment was confounded by refractory arrhythmogenesis.
23 morphogenesis, congenital heart disease and arrhythmogenesis.
24 sion observed and will have implications for arrhythmogenesis.
25 divergent effects on atrial and ventricular arrhythmogenesis.
26 findings may have important implications in arrhythmogenesis.
27 ogy, which could favor a matrix conducive to arrhythmogenesis.
28 tion potential recovery may provide clues to arrhythmogenesis.
29 prevented the induction of inflammation and arrhythmogenesis.
30 II/RyR2 overactivation and calcium-dependent arrhythmogenesis.
31 lum into the cytosol, contributing to atrial arrhythmogenesis.
32 inadequate solutions to specifically address arrhythmogenesis.
33 upling in scar tissue may be responsible for arrhythmogenesis.
34 ckdown of FKBP5 was sufficient to enhance AF arrhythmogenesis.
35 e SG may be intimately involved in malignant arrhythmogenesis.
36 nts undergoing gene therapy and could impact arrhythmogenesis.
37 n suggested to contribute to dysfunction and arrhythmogenesis.
38 authors investigate the influence of EAT on arrhythmogenesis.
39 electromechanical heterogeneities, promoting arrhythmogenesis.
40 paired cytosolic Ca(2+) buffering and atrial arrhythmogenesis.
41 leukocytes and fibroblasts can contribute to arrhythmogenesis.
42 ure by modulating inflammation, fibrosis and arrhythmogenesis.
43 ardiac pathologies and is strongly linked to arrhythmogenesis.
44 y a critical role in myocardial ischemia and arrhythmogenesis.
45 Strong evidence implicates SDB in cardiac arrhythmogenesis.
46 patients with SCVF and assess their role in arrhythmogenesis.
47 echanisms involved in atrial and ventricular arrhythmogenesis.
48 the mitofusins may impact on post-MI cardiac-arrhythmogenesis.
49 experimentally observed EADs and EAD-related arrhythmogenesis.
50 Ms) and determine its contribution to atrial arrhythmogenesis.
51 ations, a known mechanism of Ca(2+)-mediated arrhythmogenesis.
52 d with altered Ca(2+) cycling and subsequent arrhythmogenesis.
53 thylation might play an important role in AF arrhythmogenesis.
54 ives rise to a vulnerable period for mechano-arrhythmogenesis.
55 the molecular mechanisms associated with AF arrhythmogenesis.
56 CG) as an additional important biomarker for arrhythmogenesis.
57 arization alternans (RA) are associated with arrhythmogenesis.
58 ensin II-induced gap junction remodeling and arrhythmogenesis.
59 substrate for sex- and age-dependent cardiac arrhythmogenesis.
60 to predict long QT syndrome prolongation and arrhythmogenesis.
61 c nervous system modulation by RDN on atrial arrhythmogenesis.
62 in repolarization, a substrate that promotes arrhythmogenesis.
63 tion system (CCS) development, and increased arrhythmogenesis.
64 system is an important determinant of atrial arrhythmogenesis.
65 one-dependent predisposition to postischemia arrhythmogenesis.
66 s remodeling on atrial electrophysiology and arrhythmogenesis.
67 modulation of cardiac electrophysiology and arrhythmogenesis.
68 onsequent wavebreak, have been implicated in arrhythmogenesis.
69 of ROS and whether ROS played a role in the arrhythmogenesis.
70 nimals, acute blockade of O-GlcNAc inhibited arrhythmogenesis.
71 cts may play a critical role in EAD-mediated arrhythmogenesis.
72 s to study electrophysiologic remodeling and arrhythmogenesis.
73 n of ion channels as a mechanism for cardiac arrhythmogenesis.
74 ral architecture and is a key contributor to arrhythmogenesis.
75 istent INa and EADs) promotes reflection and arrhythmogenesis.
76 nregulated in heart failure and functions in arrhythmogenesis.
77 ity has been previously implicated in atrial arrhythmogenesis.
78 er to elucidate the role of I(K1) in cardiac arrhythmogenesis.
79 expense of (1) increasing the likelihood of arrhythmogenesis; (2) activating hypertrophic, apoptotic
80 upports the involvement of autoantibodies in arrhythmogenesis, a large-panel autoantibody screening w
81 s the cellular basis for QT prolongation and arrhythmogenesis after reversal of the direction of acti
82 optimized platform in a tachycardic model of arrhythmogenesis, an aspect of cardiac electrophysiology
84 hermore, AV-Shunt(Gap27) showed less cardiac arrhythmogenesis and cardiac hypertrophy index compared
85 itochondrial metabolism in the mechanisms of arrhythmogenesis and contractile dysfunction in cardiac
87 n prior to challenge protected mdx mice from arrhythmogenesis and death, while mdx:utr mice displayed
88 l cell arrays, the tissue's vulnerability to arrhythmogenesis and dynamic behaviour of re-entrant exc
89 To determine the role of IP3R2 in atrial arrhythmogenesis and ECC, we generated IP3R2-deficient m
90 of RyR2s by ROS contributes to CG-dependent arrhythmogenesis and examine the relevant sources of ROS
92 ases of cardiac sympathetic outflow, cardiac arrhythmogenesis and impairment in cardiac function in r
93 fibroblasts reduces cardiac fibrosis, blunts arrhythmogenesis and improves diastolic function in HFpE
94 Left atrial (LA) fibrosis is associated with arrhythmogenesis and increased risk of ischaemic stroke;
95 ave been postulated to contribute to cardiac arrhythmogenesis and injury during ischemia/reperfusion.
96 nt implications for SOCE-mediated signaling, arrhythmogenesis and intercellular mechanical and electr
97 shown by WT hearts, these findings attribute arrhythmogenesis and its modification by flecainide and
98 tion of the native immune response in atrial arrhythmogenesis and its therapeutic potential as a targ
99 These results not only implicate FoxO1 in arrhythmogenesis and lusitropy but also demonstrate that
102 fects associated with cardiac injury, namely arrhythmogenesis and progression into heart failure.
104 channels at S2814 plays an important role in arrhythmogenesis and sudden cardiac death in mice with h
105 are at increased risk of developing cardiac arrhythmogenesis and sudden cardiac death; however, the
106 ave been associated with a high incidence of arrhythmogenesis and sudden death in several cardiac dis
107 Myocardial ischemia, an important factor for arrhythmogenesis and sudden death, may affect the induci
109 rovide important insights into mechanisms of arrhythmogenesis and suggest that conditional lineage ab
110 highlight the importance of EAD alternans in arrhythmogenesis and suggests that ectopic beats may not
112 rical stability; yet, it reduced ventricular arrhythmogenesis and susceptibility to SCD (mortality ra
113 eralization contributes significantly to DMD arrhythmogenesis and that selective inhibition may provi
115 analyze how HCM-specific remodeling promotes arrhythmogenesis and to develop a personalized strategy
116 te a role for the FKBP5-deficiency in atrial arrhythmogenesis and to establish FKBP5 as a negative re
117 iew summarizes the role of SG in ventricular arrhythmogenesis and updates the novel targeting of SG f
118 r, the mechanisms underlying Pitx2 modulated arrhythmogenesis and variable effectiveness of antiarrhy
119 istic link between SQT3 mutations and atrial arrhythmogenesis, and potential ion channel targets for
121 pertrophic factors, are implicated in atrial arrhythmogenesis, and Walras additionally in cardiomyocy
124 ects of anger and other negative emotions on arrhythmogenesis, are important areas of future investig
125 s in myocardial structure, can contribute to arrhythmogenesis around the region of myocardial injury.
128 -wave alternans, known to be associated with arrhythmogenesis, as well as increasing inducibility of
129 Neural dysregulation is central to atrial arrhythmogenesis associated with endurance exercise trai
130 Investigations on the role of Na(v)1.5 in arrhythmogenesis associated with its functional polymorp
131 xcess of PCs promotes triggered activity and arrhythmogenesis at lower levels of stress than VMs.
132 APD prolongation form a potent substrate for arrhythmogenesis at the isthmus/BZ of chronically infarc
133 tivating site in cardiac Ca(2+) handling and arrhythmogenesis before and during beta-adrenergic recep
134 not only molecular and cellular mechanism of arrhythmogenesis but also more complex mechanisms at the
135 ncoupling induced by acute ischemia enhances arrhythmogenesis, but it may also protect the heart by l
136 ent alternans (CTA) has a recognized role in arrhythmogenesis, but its origin is not yet fully unders
137 vity is known to be important in ventricular arrhythmogenesis, but there is little information on the
138 mitochondrial Ca(2+) handling is involved in arrhythmogenesis by modulating diastolic sarcoplasmic re
139 y seem to be protected from systolic mechano-arrhythmogenesis by near-simultaneous restoration of res
140 groups, and reperfusion-provoked ventricular arrhythmogenesis, cardiac damage markers, and signaling
143 To date, information on the role of NCX in arrhythmogenesis derived from models with increased NCX
145 These findings suggest that stress-related arrhythmogenesis due to the WTC tragedy was not restrict
148 ntiation could result in three mechanisms of arrhythmogenesis: focal ectopy, heart block, and reentry
149 re) and interictal (between seizure) cardiac arrhythmogenesis following SE using continuous electroca
155 coupling, the role of the t-tubules in such arrhythmogenesis has not previously been considered.
156 tochondrial SK (mito-SK) channels to cardiac arrhythmogenesis, however, remains incompletely understo
157 Papillary muscles have been implicated in arrhythmogenesis; however, their role in post-infarction
158 xpression, sinus node dysfunction and atrial arrhythmogenesis, illustrating how spatiotemporally defi
159 whether right heart disease promotes atrial arrhythmogenesis in a rat model of pulmonary hypertensio
160 ved the way for an improved understanding of arrhythmogenesis in a wide spectrum of life-threatening
162 olonged RRC allows for late-systolic mechano-arrhythmogenesis in acute ischemia, involving contributi
163 ors (RyR2s) is hypothesized to contribute to arrhythmogenesis in AF, but the molecular mechanisms are
164 igated how overactive HRAS activity triggers arrhythmogenesis in atrial-like cardiomyocytes (ACMs) de
166 wave initiation, potentially accounting for arrhythmogenesis in CPVT linked to mutations in CASQ2.
168 o contribute to the increased propensity for arrhythmogenesis in diseased myocardium, although a caus
169 gically activated kinase that contributes to arrhythmogenesis in heart disease models, is a candidate
175 n the progression of cardiac dysfunction and arrhythmogenesis in high-output heart failure; furthermo
176 ing the process of wavefront propagation and arrhythmogenesis in human atria, technical concerns and
177 eness to physiological stress contributes to arrhythmogenesis in human carriers of the R14del mutatio
178 ver minutes, but investigating its impact on arrhythmogenesis in humans is experimentally challenging
181 e we investigated mechanisms of KCNE3-linked arrhythmogenesis in Kcne3(-/-) mice using real-time qPCR
183 plasma membrane-related pathways involved in arrhythmogenesis in long QT syndrome, whereas proarrhyth
187 hether ion channel remodeling contributes to arrhythmogenesis in N-cadherin conditional knock-out (N-
188 cardial fibrosis is strongly associated with arrhythmogenesis in nonischemic cardiomyopathy, but its
190 s phenomenon may contribute significantly to arrhythmogenesis in patients with Brugada syndrome.
191 ole in the pathogenesis of heart failure and arrhythmogenesis in patients with ischemic cardiomyopath
196 al heterogeneities and thus to contribute to arrhythmogenesis in the long QT and Brugada syndromes.
198 peri-infarct zone contributes to ventricular arrhythmogenesis in the postmyocardial infarction settin
199 Vm and the shortened APD95 could facilitate arrhythmogenesis in the presence of underlying ischemia.
200 pathways that may contribute to ventricular arrhythmogenesis in the settings of HF-associated remode
201 nding of mechano-electrical contributions to arrhythmogenesis in this and other cardiac conditions.
204 sh it from the classic explanation of R-on-T arrhythmogenesis in which an exogenous PVC coincidentall
205 ce in regulating inflammation, fibrosis, and arrhythmogenesis in young and aged infarcted rabbits.
206 id-derived mediators that may play a part in arrhythmogenesis include phospholipids and leucotrienes
207 ingle-cell analysis revealed a substrate for arrhythmogenesis, including a complete absence of transi
208 analysis revealed an anatomic substrate for arrhythmogenesis, including a decrease and mislocalizati
209 that modulate atrial fibrosis and associated arrhythmogenesis, including atrial fibrillation (AF).
212 ated by the fact that cardiac excitation and arrhythmogenesis involve the three-dimensional ventricul
213 ce of the autonomic nervous system in atrial arrhythmogenesis is also supported by circadian variatio
214 vascularization, and the potential for fatal arrhythmogenesis is associated with the fetal cell-like
220 A popular biological model used to study arrhythmogenesis is the cultured cardiac cell monolayer,
222 se higher doses of digoxin may predispose to arrhythmogenesis, lower dose digoxin should be considere
223 peri-infarct zone, a potential substrate for arrhythmogenesis, may serve as a novel prognosticator an
224 [Ca(2+)](i) fluorescence imaging and mechano-arrhythmogenesis mechanisms were pharmacologically teste
225 that Cl- channels may contribute to cardiac arrhythmogenesis, myocardial hypertrophy and heart failu
227 ic substrates that underlie pathogenesis and arrhythmogenesis of arrhythmogenic right ventricular car
228 l a new general transcriptional mechanism of arrhythmogenesis of enhanced late sodium current caused
243 e essential for mechanistic understanding of arrhythmogenesis, since cells are subjected to rapid per
244 tress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and incr
245 ation is a critical component of ventricular arrhythmogenesis that can be noninvasively assessed with
246 yanodine receptors (RyR2) has been linked to arrhythmogenesis, the molecular mechanisms triggering re
247 rcoplasmic reticulum (SR) has been linked to arrhythmogenesis, the role played by SR Ca(2+) uptake re
248 mechanism suggests that fibroblasts promote arrhythmogenesis through direct electrical interactions
249 yte electrophysiology may contribute to this arrhythmogenesis through processes referred to as mechan
250 gen species (ROS), which could contribute to arrhythmogenesis through redox modification of cardiac r
251 we describe their relevance to mechanisms of arrhythmogenesis under different disease conditions, and
252 variation in myocyte orientations on cardiac arrhythmogenesis using 3D tissue electrophysiology simul
253 immunohistochemistry, and the potential for arrhythmogenesis was examined using programmed electrica
256 lasts (Fb) that modulate atrial fibrosis and arrhythmogenesis, we developed the first atrial Fb signa
257 be the relationship between excitability and arrhythmogenesis, we explored conditions for new wavelet
258 m our understanding of mechanisms underlying arrhythmogenesis, we extended this approach, identifying
259 annelopathy on cardiac electrophysiology and arrhythmogenesis, we generated a murine model of ODDD by
260 e spatial organization of repolarization and arrhythmogenesis were determined in a surrogate model of
262 sis-independent role of NT-GSDMD in ACMs and arrhythmogenesis, which involves ROS-driven mitochondria
263 ted with a low incidence of systolic mechano-arrhythmogenesis, while a vulnerable period emerged by p
264 e and its inflammatory milieu in influencing arrhythmogenesis with age is not clear, particularly in
265 tions produced multiple mechanisms of atrial arrhythmogenesis, with significant differences between t
266 rtant effect on atrial electrophysiology and arrhythmogenesis, with the overall response depending on