ライフサイエンスコーパス: sinus bradycardia

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1 n part may account for autoimmune-associated sinus bradycardia.

2 ), and not S1P(1), is directly implicated in sinus bradycardia.

3 3-day postnatal Postn-Cre H2CKO pups exhibit sinus bradycardia.

4 1D Ca channel in mice results in significant sinus bradycardia and atrioventricular block, a phenotyp

5 pproximately 50% of TG(N488I) mice displayed sinus bradycardia and features suggestive of pre-excitat

6 reover, Slc26a6(-/)(-) mice show evidence of sinus bradycardia and fragmented QRS complex, supporting

7 monstrated that Possum mice exhibited marked sinus bradycardia and R-R variability upon scruffing, ab

8 Later changes, such as intra-atrial block, sinus bradycardia, and atrial flutter, may be attributed

9 ied by ECG abnormalities including AV block, sinus bradycardia, and ventricular dysfunction.

10 on 2.0 grade 1 hypertension; two had grade 1 sinus bradycardia; and one had grade 1 palpitation.

11 atrial rhythm, A-V rhythm, A-V dissociation, sinus bradycardia, atrial flutter, escape-capture bigemi

12 able, progressive conduction-system disease (sinus bradycardia, atrioventricular conduction block, or

13 hibited both I(Ca.T) and I(Ca.L) and induced sinus bradycardia but did not affect I(f) and I(K).

14 we investigated the functional basis of this sinus bradycardia by characterizing the effects of antib

15 and/or 2 degrees atrioventricular block, but sinus bradycardia, defined as fetal heart rate<3% for ge

16 s atrioventricular block (group 2, n=4), and sinus bradycardia (group 3, n=32).

17 Sinus bradycardia has also been associated with fetal LQ

18 k of CHB is complete atrioventricular block, sinus bradycardia has been reported recently in animal m

19 Familial forms of primary sinus bradycardia have sometimes been attributed to muta

20 ent in isolated cardiac myocytes and induced sinus bradycardia in a murine model of CHB.

21 literature describe patients presenting with sinus bradycardia in association with left ventricular n

22 echanism by which maternal antibodies induce sinus bradycardia in CHB.

23 ent, If, underlies exercise training-induced sinus bradycardia in rodents.

24 One such disorder, familial sinus bradycardia, is caused by the S672R mutation in HC

25 rtant clinical significance and suggest that sinus bradycardia may be a potential marker in the detec

26 Before ablation, Cav3.1(-/-) mice showed sinus bradycardia (mean+/-SEM; RR intervals, 148+/-3 ver

27 sed by electrocardiographic demonstration of sinus bradycardia or sinus arrest.

28 nd reported, for the first time, significant sinus bradycardia preceding AV block.

29 T-type Ca current that could account for the sinus bradycardia remain unknown.

30 s could provide, in part, the ionic basis of sinus bradycardia reported in animal models of CHB and c

31 ge has functional consequences, as it causes sinus bradycardia, similar to mice lacking SEMA3A.

32 ion induces electrical changes, resulting in sinus bradycardia, sinus pauses, and a susceptibility to

33 Rare episodes of sinus bradycardia, spontaneous seizure, and sudden death

34 Endurance athletes exhibit sinus bradycardia, that is a slow resting heart rate, as

35 ex arrhythmias also had severe and sustained sinus bradycardia throughout gestation.

36 Sinus bradycardia was observed in 19% of relatives, wher

37 ng sofosbuvir and daclatasvir for 3 days and sinus bradycardia was recorded each day, 2 hrs after int

38 common in the family with D1595H, but rather sinus bradycardia was the predominant clinical finding.

39 mily and a cohort of unrelated probands with sinus bradycardia were examined by electrocardiography,

40 nel-deficient mice (Cav1.3(-/-)) demonstrate sinus bradycardia with a prolonged PR interval.

41 at the null mutant (Ca(v)1.3(-/-)) mice have sinus bradycardia with a prolonged PR interval.

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