ライフサイエンスコーパス: extrasystole

1 picardial extrasystole versus an endocardial extrasystole).

2 lated to treatment (grade 2 supraventricular extrasystoles).

3 dverse events (lethargy and supraventricular extrasystoles).

4 l conduction block and reentry than a single extrasystole.

5 ional conduction block by a single premature extrasystole.

6 leading to conduction block of a subsequent extrasystole.

7 and the development of late phase 3 EADs and extrasystoles.

8 iveness in animals with multiple ventricular extrasystoles.

9 These changes may promote ventricular extrasystoles and increase the incidence of wavebreaks d

10 icity the requirements for the generation of extrasystoles and the factors causing ectopies to be arr

11 A number of case reports of R-on-T extrasystoles and ventricular tachyarrhythmia induction

12 hich it was lost, generating closely coupled extrasystoles and ventricular tachycardia and fibrillati

13 n=9), and abolished phase 2 reentry-induced extrasystoles and ventricular tachycardia and fibrillati

14 ling in adult cardiomyocytes that results in extrasystoles, and provides a rationale for the arrhythm

15 (minimal cell number) for the generation of extrasystoles, and the properties leading ectopies to be

16 on of refractoriness in response to multiple extrasystoles, and thus enhance vulnerability to conduct

17 Multiple extrasystoles are often more effective at inducing unidi

18 occurred in 5 of 11 monolayers, initiated by extrasystoles arising from the border zone or unidirecti

19 With multiple extrasystoles at random coupling intervals, vulnerabilit

20 show that in homogeneous tissue, a premature extrasystole can create a large dispersion of refractori

21 n heterogeneous tissue, however, a premature extrasystole can either reduce or enhance the dispersion

22 Unidirectional conduction block of premature extrasystoles can lead to initiation of cardiac reentry,

23 hase 2 reentry can in turn produce an R-on-T extrasystole capable of initiating VF.

24 ted in phase 2 reentry and associated R-on-T extrasystoles capable of initiating VF in 7 of 15 prepar

25 nd Ca2+-sparks, PUFAs can reduce spontaneous extrasystoles in the heart.

26 These extrasystoles initiated AF in 15 cases (involving 9 righ

27 Extrasystoles lead to several consequences, ranging from

28 P) dome can produce a closely coupled R-on-T extrasystole leading to ventricular fibrillation (VF) un

29 , in this study we investigate how the first extrasystole modulates this dispersion to influence the

30 d 23.2+/-1.0 pA/pF) in the group without the extrasystoles (n=8, P<0.01).

31 In addition to extrasystoles of pulmonary vein (PV) origin, those arisi

32 is required for the initiation of reentry by extrasystoles or rapid pacing.

33 on abnormalities at CMRI; >1,000 ventricular extrasystoles (or >500 non-RV outflow tract) per 24 h; a

34 The R-on-T phenomenon (an extrasystole originating on the T-wave of a preceding ve

35 e window" for conduction block by subsequent extrasystoles, particularly in relation to action potent

36 The mechanism(s) responsible for the extrasystole that reinduces AF is largely unknown.

37 se in phasic tension, late phase 3 EADs, and extrasystoles that initiate AF.

38 adient for conduction block is higher for an extrasystole traveling in the opposite direction from th

39 g in the same direction (e.g., an epicardial extrasystole versus an endocardial extrasystole).

40 he group with phase 2 reentry-related R-on-T extrasystoles were 32.2+/-1.3 mV and 30.3+/-0.5 pA/pF (n

41 Multiple extrasystoles were induced by right ventricular pacing (

42 rally, thus giving rise to phase 2 reentrant extrasystole, which precipitated ventricular tachycardia

43 to develop early afterdepolarization-induced extrasystoles, which are thought to trigger episodes of

44 n the PVs and difficulties in mapping atrial extrasystoles, which may be rare or repeatedly induce AF

45 rphic VT events were invariably triggered by extrasystoles with short (364+/-36 ms) coupling interval