ライフサイエンスコーパス: CCB

1 CCB did not alter PAP or PVR/SVR from baseline values.

2 CCBs should be avoided among patients taking cyclosporin

3 r (eight groups) 0.67 (0.56-0.80, p<0.0001); CCB (nine groups): 0.75 (0.62-0.90, p=0.002); placebo (n

4 09), beta blockers (1.97%; 0.97, 0.88-1.07), CCBs (2.11%; 1.05, 0.96-1.13), diuretics (2.02%; 1.00, 0

5 10), beta blockers (1.23%; 0.93, 0.80-1.08), CCBs (1.27%; 0.96, 0.82-1.11), diuretics (1.30%; 0.98, 0

6 ent: a Mg2+-supplemented diet; amlodipine, a CCB; and N-acetylcysteine, an antioxidant.

7 d the lowest among tacrolimus users not on a CCB (15%).

8 ded low dosage and not in combination with a CCB may not be associated with a significant risk for GE

9 dropyridine calcium channel blocking agents (CCBs) appears to reduce reinfarction in patients with is

10 esolution of mebudipine revealed that MR and CCB activity reside in opposite enantiomers.

11 iteria used to identify acute responders and CCB use are insufficiently studied.

12 nteraction between clopidogrel treatment and CCB (HR for patients not on CCBs, 0.87; 95% CI, 0.62-1.2

13 revalence among those taking cyclosporin and CCBs (76%) and the lowest among tacrolimus users not on

14 of ARBs, ACEi, beta blockers, diuretics, and CCBs.

15 yme inhibitors (ACEIs), calcium antagonists (CCBs) and alpha-blockers in preventing one or more major

16 onocarboxylate transport and cytochalasin B (CCB) to inhibit glucose transport, we examined the role

17 d analysis, there was no association between CCB use for 2-<12 years and breast cancer: All 95% confi

18 oncern about a potential causal link between CCB use and an increased risk for cancer development.

19 children includes calcium channel blockade (CCB) for acute responders with vasodilator testing and c

20 a T-type and L-type calcium channel blocker (CCB) released in the United States in 1997 for managemen

21 ble prognosis using calcium-channel blocker (CCB) therapy.

22 22,941, or 7.05%), calcium-channel blocker (CCB, 2791 of 38,607, or 7.23%), placebo (1686 of 24,767,

23 itro potency and no calcium channel-blocker (CCB) activity.

24 Calcium channel blockers (CCB) are considered the agents of choice to treat hypert

25 Calcium channel blockers (CCB) are widely prescribed anti-hypertensive agents.

26 c oxide (iNO), and calcium channel blockers (CCB) in 10 patients with BPD who underwent cardiac cathe

27 Treatment with calcium channel blockers (CCB), proven to be beneficial in a subset of patients wi

28 ut respond well to calcium channel blockers (CCB).

29 r the past decade, calcium channel blockers (CCBs) and ACE inhibitors have been used increasingly in

30 for the effect of calcium channel blockers (CCBs) and supragingival plaque.

31 Calcium channel blockers (CCBs) are prescribed to patients with Marfan syndrome fo

32 h long-term use of calcium channel blockers (CCBs) or angiotensin-converting enzyme inhibitors (ACEis

33 Calcium channel blockers (CCBs) represent a chemically and pharmacologically diver

34 The potential of calcium channel blockers (CCBs) to induce gingival enlargement (GE) as well as the

35 ut associations of calcium channel blockers (CCBs) with outcomes in patients with heart failure and p

36 (ACE) inhibitors, calcium channel blockers (CCBs), alpha-blockers, and angiotensin receptor blockers

37 h also metabolizes calcium channel blockers (CCBs).

38 i], beta blockers, calcium-channel blockers [CCBs], or diuretics) with follow-up of at least 1 year.

39 owest for ARB and ACE inhibitors followed by CCB and placebo, beta blockers and diuretics in rank ord

40 rogression is not known, but dihydropyridine CCB should be used cautiously in African Americans with

41 A number of known 1,4-dihydropyridine CCBs were identified as having comparable potency to the

42 ta-blockers who began taking dihydropyridine CCBs.

43 Propensity scores for CCB initiation, calculated for each of the 7514 patients

44 Advertising for CCBs increased from 4.6% of advertising pages in 1985 to

45 art failure, new discharge prescriptions for CCBs had no associations with composite or individual en

46 nts received new discharge prescriptions for CCBs.

47 ing and not receiving CCBs (hazard ratio for CCBs, 1.03; 95% confidence interval, 0.92-1.14).

48 Exposures included CCB or ACEi use of 1-12 years' duration, determined from

49 rted EPSPs after administration of 50 microM CCB, whereas CCB failed to alter the slow decay of pyruv

50 The effect of a new CCB, amlodipine, has not been established.

51 those receiving amlodipine and nonamlodipine CCBs.

52 Two percent (n = 397) of CCB users and 1.9% (n = 1,733) of ACEi users developed b

53 ly evaluate associations between duration of CCB or ACEi use and breast cancer in hypertensive women

54 mber 31, 2008), 7514 had no prior history of CCB use.

55 hospitalization, regardless of the class of CCBs.

56 As) and veins (MVs) to the dilator effect of CCBs.

57 this review demonstrated that the effects of CCBs on apoptosis are complex as both increases and decr

58 Long-acting formulas of CCBs appear to decrease congestive heart failure in pati

59 t an effect (either positive or negative) of CCBs on apoptosis requires doses in the supra-pharmacolo

60 Increasing promotion of CCBs has mirrored trends in physician prescribing.

61 relationship between the therapeutic use of CCBs and an increased incidence of cancer development as

62 nificant risk factors for GE were the use of CCBs and the widespread presence of abundant supragingiv

63 univariate analysis stratified by the use of CCBs, but multivariate analysis revealed that the only s

64 r differences between patients on and not on CCB, there was still no evidence of an interaction betwe

65 Treatment success on CCB decreased significantly when acute responders became

66 Among the 580 patients (27%) on CCBs at enrollment, at 28 days, the combined end point w

67 f clopidogrel was similar in patients not on CCBs at 1 year (HR, 0.78; 95% CI, 0.56-1.09).

68 el treatment and CCB (HR for patients not on CCBs, 0.87; 95% CI, 0.62-1.23; HR for patients on CCBs,

69 lopidogrel in patients on CCBs versus not on CCBs.

70 eatment effect of clopidogrel in patients on CCBs versus not on CCBs.

71 0.87; 95% CI, 0.62-1.23; HR for patients on CCBs, 0.74; 95% CI, 0.45-1.21).

72 ificant damage during glucose deprivation or CCB administration.

73 switching patients to amlodipine from other CCB for reasons of cost.

74 81% of patients receiving and not receiving CCBs (hazard ratio for CCBs, 1.03; 95% confidence interv

75 omen; 10% black) receiving and not receiving CCBs, balanced on 114 baseline characteristics.

76 of inherited thoracic aortic aneurysm taking CCBs display increased risk of aortic dissection and nee

77 ong older women with hypertension, long-term CCB use does not increase breast cancer risk and long-te

78 l to provide support for the hypothesis that CCB use is associated with an increased susceptibility f

79 In CREDO, there was no evidence that CCBs decrease the efficacy of clopidogrel.

80 There is little evidence at present that CCBs offer a major advantage over other antihypertensive

81 eclinical studies, it has been proposed that CCBs may work differently in humans by interfering with

82 Several studies have reported that CCBs reduce the ability of clopidogrel to inhibit platel

83 t platelet aggregability; one suggested that CCBs reduce the efficacy of clopidogrel.

84 herapeutic concentrations (nanomolar) of the CCB nifedipine while higher than therapeutic concentrati

85 n venous SMCs to confer venous resistance to CCB-induced dilation, a fundamental drug property that w

86 esolve the mechanism of venous resistance to CCBs.

87 ter administration of 50 microM CCB, whereas CCB failed to alter the slow decay of pyruvate-supported

88 Whether CCB treatment is detrimental to human lymphatic vessel f

89 g and prescribing patterns could explain why CCBs have supplanted better-substantiated therapies for

90 hypertension has significantly improved with CCB and epoprostenol.

91 For acute responders treated with CCB (n=31), survival at 1, 5, and 10 years was 97%, 97%,

92 ts with excellent survival when treated with CCB therapy.

93 acute responders, only 23% were treated with CCB without additional PAH-targeted therapy.

94 who had excellent outcome when treated with CCB.

95 en who are acute responders are treated with CCB; they are treated with epoprostenol if they become n

96 ponders to AVT and subsequent treatment with CCB therapy demonstrated large discrepancies with curren

97 OR 1.14, 95% CI 1.04-1.24; p=0.004) and with CCBs (1.06, 1.01-1.12; p=0.02).

98 Compared with CCBs, low-dose diuretics were associated with reduced ri

99 Unexpectedly, Marfan mice treated with CCBs show accelerated aneurysm expansion, rupture, and p