ライフサイエンスコーパス: atherothrombotic

1 Of 11 atherothrombotic biomarkers assessed at baseline, the to

2 dent clinical strokes (450 [44%] in men, 629 atherothrombotic brain infarctions [61%]) in 9152 person

3 Diabetic patients have a larger atherothrombotic burden and may be more prone to have PP

4 ythematosus (SLE) have a notable increase in atherothrombotic cardiovascular disease (CVD) which is n

5 rhomocysteinemia, a putative risk factor for atherothrombotic cardiovascular disease morbidity and mo

6 The most effective therapy against atherothrombotic cardiovascular disease to date--low den

7 l target for therapeutic intervention in the atherothrombotic complications associated with COX-2 inh

8 ction has been linked to the pathogenesis of atherothrombotic complications in cardiovascular disease

9 these abnormalities as risk factors for the atherothrombotic complications of transplantation.

10 promote atherosclerotic lesion formation and atherothrombotic complications of vascular disease.

11 dition known to be associated with premature atherothrombotic complications.

12 vides a safe, long-term mechanism to prevent atherothrombotic complications.

13 may be an exposure more relevant to systemic atherothrombotic coronary events than clinical measures.

14 y of 67 888 subjects with either established atherothrombotic (coronary, cerebrovascular, and/or peri

15 Distal protection devices can retrieve atherothrombotic debris and prevent its embolization int

16 nd impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell

17 associated with the presence of subclinical atherothrombotic disease (e.g. carotid wall thickness) a

18 In the known atherothrombotic disease and the risk factors alone coho

19 ronary syndromes and other manifestations of atherothrombotic disease are primarily caused by atheros

20 uantitative assessment of atherosclerotic or atherothrombotic disease during its natural history and

21 echanism for accelerated plaque necrosis and atherothrombotic disease in patients with sitosterolemia

22 ease, but the link between hyperglycemia and atherothrombotic disease is not completely understood.

23 rkers that reflect the clinical potential of atherothrombotic disease may allow more precise risk str

24 the Executive Committee of the Prevention of Atherothrombotic Disease Network to issue a "call to act

25 atients >/= 45 years of age with established atherothrombotic disease or >/= 3 risk factors for ather

26 stry, which evaluates subjects with clinical atherothrombotic disease or risk factors for its develop

27 f recurrent ischemic events in patients with atherothrombotic disease processes.

28 d TF may contribute to the increased risk of atherothrombotic disease that accompanies these conditio

29 ay a critical role in the pathophysiology of atherothrombotic disease, and aspirin is the most common

30 Given that the prevalence of atherothrombotic disease, as well as diseases with throm

31 AR1 signaling with MMP inhibitors, including atherothrombotic disease, in-stent restenosis, heart fai

32 pathological remodeling processes including atherothrombotic disease, inflammation, angiogenesis, an

33 Hypercholesterolemia is a risk factor for atherothrombotic disease, largely attributed to its impa

34 possible etiologic role for C. pneumoniae in atherothrombotic disease, raising questions about the co

35 Stroke, mainly attributable to atherothrombotic disease, represents a leading cause of

36 In this paper, we review atherothrombotic disease, venous thrombotic disease, and

37 concluded that CRP is probably a mediator of atherothrombotic disease.

38 n prothrombotic genes with atherogenesis and atherothrombotic disease.

39 ent vascular abnormality in the evolution of atherothrombotic disease.

40 ombin generation in normal hemostasis and in atherothrombotic disease.

41 enetics of platelet reactivity pertaining to atherothrombotic disease.

42 rs of platelet and endothelial function, and atherothrombotic disease.

43 rotein's function and has been implicated in atherothrombotic disease.

44 gen are associated with an increased risk of atherothrombotic diseases although a causative correlati

45 ed circulating pool of tissue factor (TF) in atherothrombotic diseases.

46 ry markers has been examined in a variety of atherothrombotic diseases.

47 omising approaches to the treatment of human atherothrombotic diseases.

48 targeting MRP-14 has potential for treating atherothrombotic disorders, including MI and stroke.

49 tion of proteins involved in haemostasis and atherothrombotic disorders, including myocardial infarct

50 of a link between inflammation and arterial atherothrombotic disorders.

51 may have clinical relevance given the early atherothrombotic effects of HRT in postmenopausal women.

52 periprocedural complications resulting from atherothrombotic embolization after percutaneous interve

53 d aspiration system has been shown to reduce atherothrombotic embolization and peri-procedural myocar

54 ischemia secondary to cholesterol crystal or atherothrombotic embolization leading to occlusion of sm

55 ; 95% CI: 1.52 to 1.88), and was weakest for atherothrombotic events (HR: 1.24; 95% CI: 1.10 to 1.40)

56 This reflected fewer atherothrombotic events and sudden deaths with rosuvasta

57 fusions may offer a new approach to reducing atherothrombotic events associated with increased platel

58 Atherothrombotic events in coronary arteries are most of

59 he treatment of choice for the prevention of atherothrombotic events in patients with acute coronary

60 tial therapy to reduce the risk of recurrent atherothrombotic events in patients with acute coronary

61 ess the positive predictive value of WBV for atherothrombotic events in SLE.

62 a novel mechanism for the increased risk of atherothrombotic events in smokers.

63 may contribute to the increased incidence of atherothrombotic events in these patients.

64 the primary outcome plus hospitalization for atherothrombotic events or a revascularization procedure

65 Bextra), but the mechanisms underlying these atherothrombotic events remain unclear.

66 hesion, activation, and aggregation in acute atherothrombotic events such as myocardial infarction an

67 heral artery disease are at risk of systemic atherothrombotic events, as well as acute and chronic li

68 ia pneumoniae infection to atherogenesis and atherothrombotic events, but the underlying mechanisms a

69 betes mellitus (DM) are at increased risk of atherothrombotic events, underscoring the importance of

70 y increased risk of both first and recurrent atherothrombotic events, which makes aspirin therapy of

71 ociation between (18)F-NaF uptake and future atherothrombotic events.

72 Smoking increases the risk of atherothrombotic events.

73 s represent potential mechanisms for reduced atherothrombotic events.

74 th diabetes appear to be at elevated risk of atherothrombotic events.

75 ting aspirin use for secondary prevention of atherothrombotic events.

76 g biomarkers that predict near-term (3-year) atherothrombotic events.

77 ection is associated with fatal and nonfatal atherothrombotic events.

78 uch as clopidogrel results in a reduction of atherothrombotic events.

79 SLE patients with a history of thrombotic or atherothrombotic events.

80 road population of patients at high risk for atherothrombotic events.

81 ceptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2 degrees P)-TIMI

82 ceptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events-Thrombolysis in Myocard

83 ceptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events-Thrombolysis in Myocard

84 ceptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events-TIMI 50 trial was a ran

85 ceptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events-TIMI 50].

86 apy is the cornerstone of treatment of acute atherothrombotic ischemic stroke but is associated with

87 ed CD4(+) T cells that recognize beta2GPI in atherothrombotic lesions.

88 iet-induced coronary plaque ruptures trigger atherothrombotic occlusions, resulting in myocardial inf

89 y, may contribute to the excess incidence of atherothrombotic outcomes in the dialysis-dependent end-

90 Atherothrombotic patients throughout the world had simil

91 ent mutants, such as the R212C, the enhanced atherothrombotic phenotype is likely dependent on the pr

92 RI permit depiction of various components of atherothrombotic plaque, including lipid, fibrous tissue

93 rkers may represent different aspects of the atherothrombotic process at different points in the natu

94 dence supports the position that the chronic atherothrombotic process is intimately associated with w

95 V) might have the capacity to accelerate the atherothrombotic process.

96 egulate thrombin formation, a contributor to atherothrombotic processes, was assessed.

97 intima of arteries, thereby contributing to atherothrombotic processes.

98 dentified independent clinical indicators of atherothrombotic risk among 8598 stable, placebo-treated

99 t hoc analysis from the Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Manage

100 atients enrolled in the Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Manage

101 n Trial], and CHARISMA [Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Manage

102 ants from the CHARISMA (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Manage

103 luated in the CHARISMA (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Manage

104 completed fourth trial (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Manage

105 Atherothrombotic risk assessment may be useful to identi

106 Stratification of baseline atherothrombotic risk can assist with therapeutic decisi

107 ve a more advanced disease status and higher atherothrombotic risk compared with non-ITDM (NITDM).

108 Outcomes included the baseline prevalence of atherothrombotic risk factors and the rate of incident c

109 /or peripheral arterial) disease or multiple atherothrombotic risk factors enrolled from 5587 physici

110 ed endothelial PAR-1 action to the increased atherothrombotic risk of cigarette smokers.

111 Residual atherothrombotic risk remains higher in patients with ve

112 This study tested the hypothesis that atherothrombotic risk stratification may be useful to id

113 Atherothrombotic risk stratification using the TRS 2 deg

114 mmatory marker levels and their influence on atherothrombotic risk, and the role of specific hormones

115 en and factor XIII genes are associated with atherothrombotic risk, but clinical studies have produce

116 vel in the bloodstream of patients with high atherothrombotic risk, such as smokers, diabetics, and s

117 ficiency states may have variable effects on atherothrombotic risk.

118 roepidemiologic studies of C. pneumoniae and atherothrombotic risk.

119 V do not appear to be a marker for increased atherothrombotic risk.

120 atible with insulin resistance and increased atherothrombotic risk.

121 cal conditions, is associated with increased atherothrombotic risk.

122 ntribution of hemostasis and inflammation to atherothrombotic risk.

123 activation phenotype, contributing to a pro-atherothrombotic state that may drive cardiovascular ris

124 APS and SLE patients, is associated to their atherothrombotic status, further modulated by specific a

125 directly related to an inflammatory and pro-atherothrombotic status, relies on alterations in mitoch

126 tio of Treg/Th17 between patients in MMD and atherothrombotic stroke group or control subjects (P = 0

127 26 MMD, 21 atherothrombotic stroke, and 32 healthy controls were en

128 primary end point of myocardial infarction, atherothrombotic stroke, and coronary heart disease deat

129 ed for age, sex, and decennium of inclusion, atherothrombotic stroke, cardioembolic stroke, and lacun

130 Lp(a) may be atherothrombotic through its low-density lipoprotein moi

131 ong insulin resistance, plaque necrosis, and atherothrombotic vascular disease and suggest novel ther

132 weaker association between homocysteine and atherothrombotic vascular disease compared to retrospect

133 ility of homocysteine in predicting risk for atherothrombotic vascular disease has been evaluated in

134 Atherothrombotic vascular disease is often triggered by

135 Atherothrombotic vascular disease is the major cause of

136 th, and stroke) are common manifestations of atherothrombotic vascular disease, and accurate identifi

137 sterol and other plant sterols and premature atherothrombotic vascular disease.

138 ith folic acid and other vitamins to prevent atherothrombotic vascular disease.

139 in clinical development for the treatment of atherothrombotic vascular events.

140 as a therapeutic approach for prevention of atherothrombotic vascular events.

141 herosclerotic plaques that precipitate acute atherothrombotic vascular occlusion ("vulnerable plaques