ライフサイエンスコーパス: atherothrombotic

1 The association between atherothrombotic biomarkers and 877 ASCVD events with an

2 dy sought to examine the association between atherothrombotic biomarkers and ASCVD events.

3 Of 11 atherothrombotic biomarkers assessed at baseline, the to

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

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

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

7 hematopoiesis (CH) has been associated with atherothrombotic cardiovascular disease (CVD).

8 n(a) (Lp[a]) is an important risk factor for atherothrombotic cardiovascular disease and aortic steno

9 ophic factors and hemostatic risk factors of atherothrombotic cardiovascular disease at baseline and

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

11 The implications for atherothrombotic cardiovascular disease need further exp

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

13 cipants had no previous history of diagnosed atherothrombotic cardiovascular events, dementia, or per

14 e coronary syndromes, heart failure, and the atherothrombotic complications associated with chronic k

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

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

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

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

19 dition known to be associated with premature atherothrombotic complications.

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

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

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

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

24 he benefit of protection devices to retrieve atherothrombotic debris during percutaneous coronary int

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

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

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

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

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

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

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

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

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

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

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

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

37 ommonly used sugar substitute erythritol and atherothrombotic disease risk.

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

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

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

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

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

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

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

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

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

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

48 n prothrombotic genes with atherogenesis and atherothrombotic disease.

49 ent vascular abnormality in the evolution of atherothrombotic disease.

50 ombin generation in normal hemostasis and in atherothrombotic disease.

51 sis and reducing the likelihood of ischaemic atherothrombotic disease.

52 on and hyperlipidaemia jointly contribute to atherothrombotic disease.

53 domains) for reducing cardiovascular risk in atherothrombotic disease.

54 in patients with chronic - but not stable - atherothrombotic disease.

55 enetics of platelet reactivity pertaining to atherothrombotic disease.

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

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

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

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

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

61 omising approaches to the treatment of human atherothrombotic diseases.

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

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

64 of a link between inflammation and arterial atherothrombotic disorders.

65 iant (R262W, T allele) with eosinophilia and atherothrombotic disorders.

66 against cardiovascular disease exert an anti-atherothrombotic effect via inhibition of platelet activ

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

68 rs whether a causal mechanism exists through atherothrombotic effects on the vasculature which can in

69 periprocedural complications resulting from atherothrombotic embolization after percutaneous interve

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

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

72 ned phenotype increases the risk of post-PCI atherothrombotic event only in AMI patients.

73 re and laboratory confirmed in hospital, and atherothrombotic events (acute myocardial infarction and

74 s arterio-venous (AV)-access bleeding, major atherothrombotic events (composite of fatal or non-fatal

75 ; 95% CI: 1.52 to 1.88), and was weakest for atherothrombotic events (HR: 1.24; 95% CI: 1.10 to 1.40)

76 The primary outcome was major atherothrombotic events (MAE) within 1 year after PCI.

77 modialysis (KF-HD) are at high risk for both atherothrombotic events and bleeding.

78 capacity might lead to reduced frequency of atherothrombotic events and improved outcome in patients

79 associated with increased risk of subsequent atherothrombotic events and mortality in high-risk parti

80 This reflected fewer atherothrombotic events and sudden deaths with rosuvasta

81 Atherothrombotic events are influenced by systemic hyper

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

83 ithrombotic therapies can reduce the risk of atherothrombotic events but increase bleeding.

84 mbotic therapy reduces de novo (spontaneous) atherothrombotic events in addition to preventing compli

85 Atherothrombotic events in coronary arteries are most of

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

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

88 xaban has been shown to reduce mortality and atherothrombotic events in patients with coronary artery

89 inhibition strategies for the prevention of atherothrombotic events in patients with different manif

90 r V Leiden may be a stronger risk factor for atherothrombotic events in patients with established CHD

91 aspirin in reducing lipoprotein(a)-mediated atherothrombotic events in primary prevention is not est

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

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

94 The risk of atherothrombotic events in subjects >=50 years old incre

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

96 Risk of atherothrombotic events is not uniform in patients with

97 Major atherothrombotic events occurred in 1 patient (1.3%) in

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

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

100 actor V Leiden status is unlikely to improve atherothrombotic events risk stratification in this popu

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

102 py in patients with kidney failure to reduce atherothrombotic events, (ii) highlight the limitations

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

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

105 We developed and validated a risk score for atherothrombotic events, leveraging 16 routinely assesse

106 strated a robust and consistent reduction in atherothrombotic events, particularly in patients with e

107 or V Leiden among patients at higher risk of atherothrombotic events, such as those with established

108 of stable vascular patients at high risk of atherothrombotic events, the subset with multiple enrich

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

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

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

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

113 Smoking increases the risk of atherothrombotic events.

114 to advanced atherosclerosis, culminating in atherothrombotic events.

115 as initially linked to a twofold increase in atherothrombotic events.

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

117 to account the diversity and future risks of atherothrombotic events.

118 s represent potential mechanisms for reduced atherothrombotic events.

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

120 ting aspirin use for secondary prevention of atherothrombotic events.

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

122 ection is associated with fatal and nonfatal atherothrombotic events.

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

124 stimated ASCVD free survival highest for low atherothrombotic Factor 1 and high atherothrombotic Fact

125 t for low atherothrombotic Factor 1 and high atherothrombotic Factor 2.

126 the complex interplay of atherosclerotic and atherothrombotic factors integral to ASCVD events.

127 Two atherothrombotic factors, one representative of thrombot

128 etylgutamine (PAGln) is both associated with atherothrombotic heart disease in humans, and mechanisti

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

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

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

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

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

134 t therapy driven largely by reducing de novo atherothrombotic ischemic events.

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

136 surface of leukocytes infiltrating unhealed atherothrombotic lesions and that the physiological immu

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

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

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

140 Atherothrombotic patients throughout the world had simil

141 sis for Continued Health) Registry of stable atherothrombotic patients.

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

143 nd/or reduced supply in the absence of acute atherothrombotic plaque disruption; a condition called t

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

145 sease (CAD) patients, who exhibit a distinct atherothrombotic platelet lipidome.

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

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

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

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

150 intima of arteries, thereby contributing to atherothrombotic processes.

151 h ASCVD event risk specifically due to their atherothrombotic profile.

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

153 6 months before enrollment) and were at high atherothrombotic risk and currently receiving long-term

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

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

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

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

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

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

160 th chronic coronary syndrome who are at high atherothrombotic risk and receiving long-term oral antic

161 Atherothrombotic risk assessment may be useful to identi

162 of inflammation, atherosclerosis burden, or atherothrombotic risk associated with CHIP.

163 te inflammation, atherosclerosis burden, and atherothrombotic risk associated with CHIP.

164 Stratification of baseline atherothrombotic risk can assist with therapeutic decisi

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

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

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

168 tory of cardiovascular disease or at least 2 atherothrombotic risk factors were randomized; follow-up

169 tailoring therapy according to the variable atherothrombotic risk in different individuals are empha

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

171 Residual atherothrombotic risk remains higher in patients with ve

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

173 Atherothrombotic risk stratification using the TRS 2 deg

174 ients with chronic coronary syndrome at high atherothrombotic risk who were receiving an oral anticoa

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

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

177 levels of CRP, a population at high residual atherothrombotic risk, high residual inflammatory risk,

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

179 n demonstrated to modulate vessel repair and atherothrombotic risk, this study aimed to determine the

180 ficiency states may have variable effects on atherothrombotic risk.

181 roepidemiologic studies of C. pneumoniae and atherothrombotic risk.

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

183 atible with insulin resistance and increased atherothrombotic risk.

184 cal conditions, is associated with increased atherothrombotic risk.

185 ntribution of hemostasis and inflammation to atherothrombotic risk.

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

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

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

189 umulative risk was highest for patients with atherothrombotic stroke (22.7%; 95% CI, 10.6%-34.7%) and

190 ing ASCVD (coronary artery disease (CAD) and atherothrombotic stroke (ATS)) with 9-month all-cause an

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

192 26 MMD, 21 atherothrombotic stroke, and 32 healthy controls were en

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

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

195 iated with a recurrent short-term event were atherothrombotic stroke, rare causes of stroke, and hype

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

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

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

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

200 Atherothrombotic vascular disease is often triggered by

201 Atherothrombotic vascular disease is the major cause of

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

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

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

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

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

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