ライフサイエンスコーパス: antianginal

1 , CAD, and stable angina treated with 1 to 2 antianginals.

2 systemic and coronary beds that subserve the antianginal action of GTN is not known.

3 reduce TDR suggest that, in addition to its antianginal actions, the drug may possess antiarrhythmic

4 Ranolazine is a novel antianginal agent capable of producing antiischemic effe

5 Ranolazine is a unique antianginal agent that has been effective in stable angi

6 Ranolazine is a novel antianginal agent that reduces ischemia in patients with

7 Ranolazine is an antianginal agent that targets a number of ion channels

8 Ranolazine (Ran), an antianginal agent, inhibits late Na(+) current.

9 Ranolazine, a new antianginal agent, reduces ischemic symptoms in patients

10 ssion of ambulatory myocardial ischemia with antianginal agents or revascularization therapy is super

11 78% statins, 89% beta-blockers, average 2.9 antianginal agents).

12 n symptomatic despite treatment with up to 2 antianginal agents.

13 of maximum recommended doses of conventional antianginal agents.

14 evidence of ischemia but no obstructive CAD, antianginal and anti-ischemic therapies can improve symp

15 Ranolazine is a Na(V)1.5 antagonist with antianginal and antiarrhythmic properties.

16 This study evaluated the antianginal and antiischemic effects of ivabradine, a ne

17 Antianginal and lipid-lowering medications may modify th

18 n shown to be an effective antihypertensive, antianginal, and anti-ischemic agent, and because of its

19 ing arrhythmias and include antiarrhythmics, antianginals, antiemetics, gastrointestinal stimulants,

20 it from intensive medical therapy, including antianginal, antiplatelet, antithrombotic, and statin ag

21 Adjunctive antianginal, antiplatelet, antithrombotic, beta blocker,

22 n during follow-up did not fully explain the antianginal benefit of CABG in the overall population.

23 We conducted a randomized trial to test the antianginal benefit of ranolazine in patients with diabe

24 Trimetazidine acts as an effective antianginal clinical agent by modulating cardiac energy

25 The three major classes of antianginal drug all inhibit platelet aggregation at hig

26 ic pathway was identified as a target of the antianginal drug molsidomine, which may explain its chol

27 DH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxi

28 DH2) catalyzes vascular bioactivation of the antianginal drug nitroglycerin (GTN), resulting in activ

29 We also show that the antianginal drug ranolazine can abolish CO-induced early

30 Ranolazine is a new and unique antianginal drug that has been approved for the treatmen

31 nd its alleviation by the most commonly used antianginal drug, nitroglycerin, are incompletely unders

32 to develop a method by which the effects of antianginal drugs could be evaluated invasively during p

33 Randomized or crossover studies comparing antianginal drugs from 2 or 3 different classes (beta-bl

34 od, to evaluate the effect of representative antianginal drugs on platelet function in vivo in health

35 an increase in angina-free walking time with antianginal drugs or revascularization procedures, the r

36 at ivabradine, representing a novel class of antianginal drugs, is effective and safe during 3 months

37 mia and the actions of novel and established antianginal drugs.

38 This study sought to examine ranolazine's antianginal effect in relation to glucose control.

39 We investigated the antianginal effects of ranolazine in the subgroup of pat

40 In addition to its antianginal effects, ranolazine has been shown to reduce

41 vivo and thus at least partly underlies the antianginal mechanism of drug action.

42 The three main classes of antianginal medication have different and possible clini

43 We also examined the rates of antianginal medication prescriptions at discharge.

44 efractory angina and reduction in the use of antianginal medication with early intervention.

45 Use of antianginal medications (beta-adrenergic blockers, nitra

46 ence interval [CI], -15.22 to -0.41), use of antianginal medications (standardized MD, -0.59; 95% CI,

47 hospital referral regions in providing >/= 2 antianginal medications and in rates of PCI from the Dar

48 pital referral region and the rates of >/= 2 antianginal medications before PCI (Spearman rho, 0.0277

49 The median rate of providing >/= 2 antianginal medications before PCI was 18.9%.

50 007 on the regions' rates of providing >/= 2 antianginal medications before PCI.

51 to determine whether greater regional use of antianginal medications in PCI patients is associated wi

52 ble if they were unweanable from intravenous antianginal medications or were too unstable for a persa

53 na, 15.8% in 2010 and 38.4% in 2014), use of antianginal medications prior to PCI (at least 2 antiang

54 Symptoms of angina were improved and use of antianginal medications significantly reduced with the i

55 ociety angina class, exercise tolerance, and antianginal medications), myocardial perfusion, and clin

56 anginal medications prior to PCI (at least 2 antianginal medications, 22.3% in 2010 and 35.1% in 2014

57 d 2.8% of patients were on 0, 1, 2, or >/= 3 antianginal medications, respectively.

58 on did not substantially supplant the use of antianginal medications, which were commonly used despit

59 ginal episodes despite revascularization and antianginal medications.

60 c heart disease and may obviate the need for antianginal medications.

61 011, and calculated rates of providing >/= 2 antianginal medicines before PCI.

62 efits were not due to higher rates of use of antianginal medicines or aspirin and were not a conseque

63 In a previous trial, antianginal monotherapy with ranolazine, a drug believed

64 ast as high as those without DM despite more antianginal prescriptions at discharge.

65 fect on the ET(A) receptor may relate to the antianginal properties of estrogens.

66 using agents with both antihypertensive and antianginal properties.

67 protective hormones and are reported to have antianginal properties.

68 pure Na(+) channel blocker lidocaine and the antianginal ranolazine were additionally tested and also

69 ed exercise capacity and provided additional antianginal relief to symptomatic patients with severe c

70 Ranolazine is a novel antianginal shown in an exploratory analysis in patients

71 Ranolazine is an antianginal shown to reduce angina and improve exercise

72 Designing antianginal therapies that exploit these mechanisms may

73 ing (71.6%), or suboptimal (</=1 medication) antianginal therapy (95.8%).

74 9 to 1.00; p = 0.048) and intensification of antianginal therapy (HR: 0.77; 95% CI: 0.64 to 0.92, p =

75 dysfunction improves survival compared with antianginal therapy alone.

76 in blood pressure, heart rate, or background antianginal therapy and persisted throughout 12 weeks.

77 ound no association between the intensity of antianginal therapy and the use of PCI across hospital r

78 exist in many regions to increase the use of antianginal therapy before proceeding to elective PCI, a

79 The efficacy of conventional antianginal therapy in preventing myocardial ischemia in

80 The effects of antianginal therapy on blood pressure changes during isc

81 for the safety and efficacy of ranolazine as antianginal therapy.

82 ischemia and their management plan (i.e., no antianginal treatment, medical therapy or an invasive in

83 data have been published comparing these two antianginal treatments in this setting.