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1 rophin deficient), the SSC was excessive and arrhythmogenic.
2 educing its slope, rendering the tissue less arrhythmogenic.
3 bition or genetic deletion of NOX2 prevented arrhythmogenic abnormalities in vivo during high stature
5 o 48 hours of exposure to the drug generated arrhythmogenic afterdepolarizations and >/=15-fold incre
6 al cardiac cells, in turn, is accompanied by arrhythmogenic afterdepolarizations thought to trigger t
7 omyocytes to spontaneous Ca(2+)-releases and arrhythmogenic afterdepolarizations, particularly upon e
9 problem differently making the prediction of arrhythmogenic and/or antiarrhythmic effects difficult.
10 ent of chemokines, extracellular matrix, and arrhythmogenic arrays confirmed the dysregulation of mul
12 us node dysfunction in CPVT, and whether the arrhythmogenic beats originate from the conduction syste
14 cteristic properties of TCWs are potentially arrhythmogenic by promoting both conduction block and re
15 oportion of A103V-CaM is sufficient to evoke arrhythmogenic Ca disturbances via ryanodine receptor 2
16 roportion of CPVT-CaM is sufficient to evoke arrhythmogenic Ca disturbances, whereas LQTS-CaMs do not
17 ains an effective inhibitor of RyR2-mediated arrhythmogenic Ca release even when cardiac sodium chann
20 itates spontaneous Ca(2+) release in form of arrhythmogenic Ca(2+) waves and spontaneous action poten
21 he myocyte level, PLN ablation converted the arrhythmogenic Ca(2+) waves evoked by high extracellular
24 lls were also more susceptible to developing arrhythmogenic Ca(2+) waves which might form the substra
25 waves and a larger fraction of waves (termed arrhythmogenic Ca(2+) waves) triggered APs and global Ca
27 ilies with somatic mosaicism associated with arrhythmogenic calmodulinopathy, and demonstrate dysregu
28 a release channels in the heart, but whether arrhythmogenic CaM mutants alter RyR2 function is not kn
29 This is in stark contrast to the actions of arrhythmogenic CaM mutations N54I, D96V, N98S, and D130G
30 growth and viability, yet the effect of the arrhythmogenic CaM mutations on cell viability, as well
34 milies, including hypertrophic, dilated, and arrhythmogenic cardiomyopathies and inherited arrhythmia
35 pping phenotype of dilated and left-dominant arrhythmogenic cardiomyopathies complicated by frequent
38 Desmoglein 2 gene (DSG2) mutations cause arrhythmogenic cardiomyopathy (AC) in human and transgen
50 cardiomyocytes, are the predominant cause of arrhythmogenic cardiomyopathy and can be identified in a
51 r early cardiac arrhythmias in patients with arrhythmogenic cardiomyopathy and cardiocutaneous syndro
52 as sarcomeric, force generation disease; and arrhythmogenic cardiomyopathy as desmosome, cell junctio
53 Cardiomyocyte ILK deletion produces a lethal arrhythmogenic cardiomyopathy associated with important
54 rdium has revealed mechanistic insights into arrhythmogenic cardiomyopathy but cardiac samples are di
57 ALVC) is an under-characterized phenotype of arrhythmogenic cardiomyopathy involving the LV ab initio
61 nderstanding of the pathogenic mechanisms of arrhythmogenic cardiomyopathy over the past decade have
63 kedly diminished in buccal mucosa cells from arrhythmogenic cardiomyopathy patients with known desmos
64 re responsible for a subset of patients with arrhythmogenic cardiomyopathy who exhibit cardiac arrhyt
65 of titin's spring region is associated with arrhythmogenic cardiomyopathy, a disease characterized b
66 y of long-QT syndrome, Brugada syndrome, and arrhythmogenic cardiomyopathy, and in the study of funct
67 human PKP2 associate with a life-threatening arrhythmogenic cardiomyopathy, often of right ventricula
77 anish family with inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia and a high incid
78 nts presented data consistent with inherited arrhythmogenic cardiomyopathy/dysplasia phenotype with v
79 auses predominant inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia with a high inci
80 histochemistry was compatible with inherited arrhythmogenic cardiomyopathy/dysplasia, and the functio
85 onarrhythmogenic can suppress the ability of arrhythmogenic cells to generate delayed and early after
86 y sustained high atrial activation rates and arrhythmogenic cellular Ca2+ signaling instability; howe
87 rhythmias in vitro by preventing potentially arrhythmogenic changes in action potential characteristi
91 KCNE1 association protects KCNQ1 from an arrhythmogenic (constitutive current-inducing) effect of
96 Congenital Long QT syndrome (LQTS) is an arrhythmogenic disorder that causes syncope and sudden d
98 ersen-Tawil Syndrome type 1 (ATS1) is a rare arrhythmogenic disorder, caused by loss-of-function muta
99 ern of NaV1.5 subunits associated with these arrhythmogenic disorders and the associated channel regu
103 cal problem worldwide, but it is unclear how arrhythmogenic early afterdepolarizations (EADs) are tri
104 explore the potential antiarrhythmic and/or arrhythmogenic effect of modulation of the autonomic ner
105 n or pharmacological inhibition prevents the arrhythmogenic effects of a high saturated fat diet, in
106 iological models of hMSCs, predicts possible arrhythmogenic effects of hMSCs when directly coupled to
108 lore the potential role of Wnt signalling in arrhythmogenic electrical remodelling, we examined volta
109 aps before and after ajmaline determined the arrhythmogenic electrophysiological substrate (AES) as c
110 ociated cardiovascular death but not serious arrhythmogenic endpoints like sudden cardiac arrest (SCA
112 system development and the observation that arrhythmogenic foci can originate in areas near the atri
113 tissue correspond to a region enriched with arrhythmogenic foci, which may reflect a common developm
114 mosomes and intermediate filaments, cause an arrhythmogenic form of cardiomyopathy that has been vari
116 tivity to isoproterenol-induced induction of arrhythmogenic I(Na,L), and reduced CaMKII-dependent pho
118 cium affinity to the myofilament may promote arrhythmogenic intracellular calcium waves, we modified
120 diac hypertrophy and Epac2 activation can be arrhythmogenic, it is unknown whether distinct subcellul
121 did not bind to the main binding site of the arrhythmogenic KV11.1 blockers (the Phe656 pore residue)
125 ions such as carbon-12 ((12)C), delivered to arrhythmogenic locations of the heart could be a promisi
129 d of familial and genetic screening, and the arrhythmogenic mechanisms in the largest cohort of short
130 extracardiac pathogenesis when investigating arrhythmogenic mechanisms, even in inherited, monogenic
132 ls have proven challenging to use, targeting arrhythmogenic metabolic changes and redox imbalance may
133 rategy can be designed to correct a specific arrhythmogenic mutation, as in the catecholaminergic pol
135 mechanisms by which autonomic activation is arrhythmogenic or antiarrhythmic are complex and differe
140 (+)-selective transport in hERG1, leading to arrhythmogenic phenotypes associated with long-QT syndro
142 us diastolic Ca(2+) release (DCR) can induce arrhythmogenic plasma membrane depolarizations, although
144 ular myocyte to interrogate this potentially arrhythmogenic positive feedback in both control conditi
149 1-active hMSCs supports the claim of reduced arrhythmogenic potential of this cell type with low hMSC
150 ients with heart failure, causes potentially arrhythmogenic reductions in slow delayed-rectifier K(+)
151 ram fractionation may be helpful to identify arrhythmogenic regions in the postinfarction heart.
152 ustained VT can distinguish exercise-induced arrhythmogenic remodeling from ARVC and post-inflammator
153 rn may allow distinguishing exercise-induced arrhythmogenic remodeling from ARVC and post-inflammator
154 Novel cardiomyopathies have been discovered (arrhythmogenic, restrictive, and noncompacted) and added
155 Data characterizing structural changes of arrhythmogenic right ventricular (RV) cardiomyopathy are
156 elates of left ventricular (LV) substrate in arrhythmogenic right ventricular (RV) cardiomyopathy are
157 etic resonance (MR) imaging in patients with arrhythmogenic right ventricular (RV) dysplasia/cardiomy
158 pholamban R14del mutation causes dilated and arrhythmogenic right ventricular cardiomyopathies and is
159 viduals), dilated cardiomyopathy (1/250) and arrhythmogenic right ventricular cardiomyopathy (1/5,000
160 ic polymorphic ventricular tachycardia (4%), arrhythmogenic right ventricular cardiomyopathy (4%), an
161 rtrophy (LVH) and/or fibrosis (n = 59, 16%); arrhythmogenic right ventricular cardiomyopathy (ARVC) (
162 ventricular tachycardia (CPVT) (n = 9 [8%]), arrhythmogenic right ventricular cardiomyopathy (ARVC) (
177 d others such as strain imaging, to identify arrhythmogenic right ventricular cardiomyopathy (ARVC) i
178 Exercise has been proposed as a trigger for arrhythmogenic right ventricular cardiomyopathy (ARVC) p
180 possibility of cardiomyopathy, specifically arrhythmogenic right ventricular cardiomyopathy (ARVC).
181 malities precede overt structural disease in arrhythmogenic right ventricular cardiomyopathy (ARVC).
182 k Force Criteria (rTFC) for the diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC).
183 on (TWI), may create diagnostic overlap with arrhythmogenic right ventricular cardiomyopathy (ARVC).
185 ssess tissue and functional abnormalities in arrhythmogenic right ventricular cardiomyopathy (ARVC).
186 Our aim was to screen 315 patients with arrhythmogenic right ventricular cardiomyopathy (n = 111
187 onischemic dilated cardiomyopathy [NICM], 15 arrhythmogenic right ventricular cardiomyopathy [ARVC])
188 onance plus genetic variants associated with arrhythmogenic right ventricular cardiomyopathy and of a
189 rdioverter defibrillator (ICD) in males with arrhythmogenic right ventricular cardiomyopathy caused b
190 e 2010 International Task Force Criteria for arrhythmogenic right ventricular cardiomyopathy diagnosi
191 rline 2010 International Task Force Criteria arrhythmogenic right ventricular cardiomyopathy diagnosi
193 Thus, the hypothesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to b
194 ablation of ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy improves
196 and adjuvant EPI substrate ablation of VT in arrhythmogenic right ventricular cardiomyopathy is good.
197 xed cardiomyopathies occur infrequently; and arrhythmogenic right ventricular cardiomyopathy is rare.
198 nd the desmosomal variants that cause either arrhythmogenic right ventricular cardiomyopathy or dilat
201 cutive patients with Task Force criteria for arrhythmogenic right ventricular cardiomyopathy referred
202 enes (PKP2, DSP, DSG2, DSC2, and JUP) from 3 arrhythmogenic right ventricular cardiomyopathy registri
203 was higher in nonischemic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy than in
204 for a possible primary electric syndrome or arrhythmogenic right ventricular cardiomyopathy were ana
205 pathy, 15 nonischemic cardiomyopathy, and 14 arrhythmogenic right ventricular cardiomyopathy) with a
206 ar tachycardia, 3; short QT syndrome, 1; and arrhythmogenic right ventricular cardiomyopathy, 23).
208 se each (3%) of hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, long QT
210 that a mutation in alphaT-catenin linked to arrhythmogenic right ventricular cardiomyopathy, V94D, p
215 dress the current challenges associated with arrhythmogenic right ventricular cardiomyopathy/dilated
217 cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy/dysplasi
218 ers for risk stratification in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasi
219 ns were described in patients with inherited arrhythmogenic right ventricular cardiomyopathy/dysplasi
220 sisted of dilated cardiomyopathy (DCM, 49%), arrhythmogenic right ventricular dysplasia (ARVD, 17%),
222 earch has described the arrhythmic course of arrhythmogenic right ventricular dysplasia/cardiomyopath
224 M and they were diagnostic or suggestive for arrhythmogenic right ventricular dysplasia/cardiomyopath
225 ow overlap in the clinical presentation with arrhythmogenic right ventricular dysplasia/cardiomyopath
226 lete penetrance and variable expressivity of arrhythmogenic right ventricular dysplasia/cardiomyopath
227 can in turn facilitate ablation of the VT in arrhythmogenic right ventricular dysplasia/cardiomyopath
228 yopathy, left ventricular noncompaction, and arrhythmogenic right ventricular dysplasia; and delineat
235 cardiac magnetic resonance (CMR) imaging in arrhythmogenic RV cardiomyopathy (ARVC) may be inadequat
237 As, the potential for erroneous diagnosis of arrhythmogenic RV cardiomyopathy is considerably greater
239 ation is frequently present in patients with arrhythmogenic RV cardiomyopathy who have progressive RV
240 ck ventricular tachycardia in the setting of arrhythmogenic RV cardiomyopathy with procedures separat
247 mmonly used clinical procedure that destroys arrhythmogenic sources in patients suffering from atrial
248 the propensity and reduced the threshold for arrhythmogenic spontaneous Ca(2+) release in HEK293 cell
249 CPVT myocytes also evidenced characteristic arrhythmogenic spontaneous Ca(2+) waves under cholinergi
253 T isthmus may increase sensitivity to detect arrhythmogenic substrate and critical sites for reentry.
254 front may increase the sensitivity to detect arrhythmogenic substrate and critical sites for ventricu
255 l fibrillation are important elements of the arrhythmogenic substrate and result from endo-epicardial
256 d its possible value in the detection of the arrhythmogenic substrate associated with atrial fibrilla
258 to identify the RVOT as the location of the arrhythmogenic substrate by the noninvasive CineECG, bas
259 of cardiac activation before ablation of the arrhythmogenic substrate can reduce electrophysiological
262 ardiomyopathy (ARVC) has been suggested, the arrhythmogenic substrate for VTs in athletes is unknown.
263 adin, and/or junctin and RyR2 may produce an arrhythmogenic substrate in anthracycline-induced cardio
264 al fibrosis is an important component of the arrhythmogenic substrate in patients with atrial fibrill
265 e enabled characterization of the structural arrhythmogenic substrate in patients with VT with increa
266 ardial wall thinning (WT) imaged by MDCT and arrhythmogenic substrate in postinfarction ventricular t
269 hrone forces in the RVOT, congruent with the arrhythmogenic substrate location detected by epicardial
271 assess whether prophylactic ablation of the arrhythmogenic substrate reduces or prevents the recurre
273 ial function is thought to contribute to the arrhythmogenic substrate, but how mitochondria contribut
274 potential of CMR for characterization of the arrhythmogenic substrate, there is currently no standard
281 Most studies of arrhythmia mechanisms and arrhythmogenic substrates have been conducted in animal
282 suggesting that VT and VF share overlapping arrhythmogenic substrates in patients with structural he
283 l redox state during cardiac diseases foment arrhythmogenic substrates through direct or indirect mod
284 age heart failure, beta2-stimulation creates arrhythmogenic substrates via conduction velocity regula
287 ndrome (SQTS) is a rare and life-threatening arrhythmogenic syndrome characterized by abbreviated rep
288 The short QT syndrome (SQTS) is an inherited arrhythmogenic syndrome characterized by abnormal ion ch
290 new genes associated with monogenic familial arrhythmogenic syndromes, giving the opportunity to deli
291 have been associated with various inherited arrhythmogenic syndromes, including Brugada syndrome and
292 have been associated with various inherited arrhythmogenic syndromes, including cases of Brugada syn
295 patially discordant alternans, which is more arrhythmogenic than concordant alternans, may occur in t
296 exposed hearts showed increased incidence of arrhythmogenic-triggered activities in female ventricula
299 nalling silencing) and Ca(2+) destabilizing (arrhythmogenic unstable Ca(2+) signalling) factors.
300 Ca(2+)-sensing protein calmodulin (CaM) are arrhythmogenic, yet their underlying mechanisms are not