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1 ightened risk for ischemic events related to atherothrombosis.
2 and monocytes, to the vessel wall modulating atherothrombosis.
3 which causes plaque necrosis, a precursor to atherothrombosis.
4 fluid shear is an important step regulating atherothrombosis.
5 e or treatment intensity of individuals with atherothrombosis.
6 , thereby contributing to the development of atherothrombosis.
7 future understanding of the pathogenesis of atherothrombosis.
8 lving HDL regulatory genes and their role in atherothrombosis.
9 Inflammation is causally related to atherothrombosis.
10 ition of fibrinolysis, it could also promote atherothrombosis.
11 ications for both the metabolic syndrome and atherothrombosis.
12 r of generalized endothelial dysfunction and atherothrombosis.
13 s in the treatment of patients with coronary atherothrombosis.
14 pendent risk factor for vascular disease and atherothrombosis.
15 mplicated by plaque rupture and subsequently atherothrombosis.
16 etween sVCAM-1 and sICAM-1 in the genesis of atherothrombosis.
17 niae has been hypothesized to play a role in atherothrombosis.
18 atheroma versus later stenotic or occlusive atherothrombosis.
19 ased risk or apparent protective effects for atherothrombosis.
20 identify persons who are prone to premature atherothrombosis.
21 ammation is important in the pathogenesis of atherothrombosis.
22 tion may be important in the pathogenesis of atherothrombosis.
23 r noninvasive imaging of atherosclerosis and atherothrombosis.
24 ied as index MI, of which 68% were caused by atherothrombosis.
25 t JCAD as a potential therapeutic target for atherothrombosis.
26 IL-6 has emerged as a pivotal factor in atherothrombosis.
27 reactive, leading to pathophysiology such as atherothrombosis.
28 the involvement of platelet TXA2 in diabetic atherothrombosis.
29 ivated platelets, plays an important role in atherothrombosis.
30 cess, possibly preventing the development of atherothrombosis.
31 wall, inducing local changes predisposing to atherothrombosis.
32 t harbor potential therapeutic value against atherothrombosis.
33 lly favorable effects on pathways related to atherothrombosis.
34 hil extracellular traps in atherogenesis and atherothrombosis.
35 de may differentially affect dysglycemia and atherothrombosis.
36 lerotic lesions of primary APS patients with atherothrombosis.
37 nt plaque instability that eventually favors atherothrombosis.
38 endothelial barrier function in experimental atherothrombosis.
39 a therapeutic potential for CD31 agonists in atherothrombosis.
40 y likely contributing to the pathogenesis of atherothrombosis.
41 telet activity effective in the treatment of atherothrombosis.
42 f vorapaxar in 26,449 patients with previous atherothrombosis.
43 that could lead to vascular dysfunction and atherothrombosis.
44 l oxygen supply and demand in the absence of atherothrombosis.
45 l of discontinuity in the natural history of atherothrombosis.
46 isruption using a rabbit model of controlled atherothrombosis.
47 nogen facilitate fibrinolysis and may reduce atherothrombosis.
48 ve and prothrombotic phenotype that promotes atherothrombosis.
49 venues in the treatment of atherogenesis and atherothrombosis.
50 is a proximate event in the pathogenesis of atherothrombosis.
51 e pathophysiological implications in AMI and atherothrombosis.
52 the broad range of risk for outpatients with atherothrombosis.
53 thrombotic disease or >/= 3 risk factors for atherothrombosis.
54 in the treatment and prevention of vascular atherothrombosis.
55 n human clinical trials for the treatment of atherothrombosis.
56 impair insulin signaling and contributes to atherothrombosis.
57 ncreased platelet aggregation, a hallmark of atherothrombosis.
58 nction, weight homeostasis, and/or premature atherothrombosis.
61 auses comprised the majority of MI in women (atherothrombosis 47% vs 75%, secondary myocardial infarc
62 lower in women, particularly in MI caused by atherothrombosis (48 vs 137 per 100,000 person years and
63 mortality was highest after SSDM (SSDM 33%, atherothrombosis 8%, embolism 8%, SCAD 0%) with low card
64 test formally the inflammatory hypothesis of atherothrombosis, an agent is needed that reduces inflam
65 ogrel treatment in patients with symptomatic atherothrombosis and a suggestion of harm in patients wi
67 uggesting a causal role for IL-6 in systemic atherothrombosis and aneurysm formation; and then detail
68 etabolism, summarize the effects of Abeta on atherothrombosis and cardiac dysfunction, discuss the cl
70 otentially implicated in the acceleration of atherothrombosis and CV risk in SLE and RA, as well as i
72 ) has been implicated in the pathogenesis of atherothrombosis and is expressed by the major cell type
73 s has been implicated in the pathogenesis of atherothrombosis and other vascular disorders accompanie
75 at platelets and coagulation factors play in atherothrombosis and review the rationale and clinical e
77 infarction (MI) to identify type 1 MI due to atherothrombosis and type 2 MI due to myocardial oxygen
78 ents with prior MI, 7804 patients with known atherothrombosis, and 2101 patients with risk factors al
82 involved in the transition from atheroma to atherothrombosis, and that control of this pattern may b
83 nly a moderate relative risk reduction after atherothrombosis, and their inhibitory effects are compr
84 hanisms by which homocysteine contributes to atherothrombosis are complex and their in vivo relevance
87 OX-1 inhibitors) effectiveness in preventing atherothrombosis, as well as its shared (with other anti
88 ng platelet functions in atherosclerosis and atherothrombosis at different stages of disease will be
90 sis for Continued Health (REACH) registry of atherothrombosis, baseline characteristics and 4-year fo
91 t only effective for secondary prevention of atherothrombosis but also for prevention of venous throm
92 .4%-12.9%); and patients without established atherothrombosis but with risk factors only (n = 8073) h
93 the essential platelet collagen receptor in atherothrombosis, but its inhibition causes only a mild
97 ype 1 myocardial infarction (T1MI) caused by atherothrombosis, characteristics and outcomes of type 2
100 iate regression models evaluating markers of atherothrombosis (fibrin, antithrombin and tissue plasmi
101 stroke results in plaque destabilization and atherothrombosis, finally leading to arterioarterial emb
102 ronary artery disease index and Reduction of Atherothrombosis for Continued Health (REACH) and Second
103 sis were enrolled in the global Reduction of Atherothrombosis for Continued Health (REACH) Registry a
104 SETTING, AND PARTICIPANTS: The Reduction of Atherothrombosis for Continued Health (REACH) Registry c
108 tional study of patients in the Reduction of Atherothrombosis for Continued Health (REACH) registry w
109 , SWEDEHEART, the international REduction of Atherothrombosis for Continued Health (REACH) Registry,
110 ied using 2 methods: the REACH (REduction of Atherothrombosis for Continued Health) atherothrombosis
111 on (n = 16,875) from the REACH (REduction of Atherothrombosis for Continued Health) Registry of stabl
112 s from the international REACH (Reduction of Atherothrombosis for Continued Health) registry, which e
113 hown in other inflammatory processes such as atherothrombosis, genes initially characterized in early
115 rks of cardiovascular disease (CVD), such as atherothrombosis, heart failure, dysrhythmias, vessel ca
117 ia and increased platelet production promote atherothrombosis; however, a potential link between alte
119 rect link between eosinophilia, EETosis, and atherothrombosis in hematopoietic Lnk deficiency and an
122 l dysfunction, aberrant vascular repair, and atherothrombosis in murine models of lupus and atheroscl
123 pirin or rivaroxaban alone for prevention of atherothrombosis in patients with coronary or peripheral
127 s fibrinolysis, endothelial dysfunction, and atherothrombosis in the coronary circulation and may exp
129 ifferent clinical manifestations of coronary atherothrombosis, in light of comorbidities and/or inter
130 rythematosus (SLE) are at risk for premature atherothrombosis independent of Framingham risk factors.
133 in this secondary analysis of the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With
134 cardiovascular (CV) events in the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with
135 uce the Incidence of Vascular Events and The Atherothrombosis Intervention in Metabolic Syndrome with
136 g data from the recently published AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with
143 n activator inhibitor-1 (PAI-1), a marker of atherothrombosis, is also elevated in the metabolic synd
144 endent and may be integrated under the term "atherothrombosis." It is now clear that plaque compositi
145 slipoproteinemia is associated with arterial atherothrombosis, little is known about plasma lipoprote
146 oxidized phospholipids (OxPLs), part of its atherothrombosis might be mediated through this pathway.
147 rction, cardiac dysfunction and remodelling, atherothrombosis, myocarditis and pericarditis, cardioto
148 ase, n = 8273) or 3 or more risk factors for atherothrombosis (n = 12,389) between 2003 and 2004.
150 rtery disease (CAD) may result from coronary atherothrombosis not evident using standard angiography
151 provide a possible explanation for increased atherothrombosis observed in CBS-deficient patients.
153 C-reactive protein as a causative factor in atherothrombosis or to enable the recommendation of C-re
157 Their role in the primary prevention of atherothrombosis remains controversial because of the un
159 laques, which have the propensity to develop atherothrombosis, remains an elusive goal in clinical me
160 volved in the development and progression of atherothrombosis responsible for coronary, cerebral, and
161 on of Atherothrombosis for Continued Health) atherothrombosis risk score and CART (Classification and
163 f 6 adjudicated pathophysiologic mechanisms: atherothrombosis, spontaneous coronary artery dissection
165 In the subgroup with clinically evident atherothrombosis, the rate was 6.9 percent with clopidog
166 plaque inflammation is also associated with atherothrombosis, the relationship between inflammation
167 arette smoke (CS) increases the incidence of atherothrombosis, the release of prostaglandin (PG) E2,
169 thelial dysfunction may increase the risk of atherothrombosis through a reduction in the acute fibrin
171 Lipoprotein(a) (Lp(a)) is associated with atherothrombosis through several mechanisms, including p
172 viously developed in a large population with atherothrombosis to predict CV death, myocardial infarct
173 randomly assigned patients with a history of atherothrombosis to receive vorapaxar (2.5 mg daily) or
174 ardial injury, whether attributable to acute atherothrombosis (type 1 MI) or supply/demand mismatch w
176 et need in myocardial oxygen demand, without atherothrombosis, usually in the context of another acut
177 induced ruptures of coronary plaques trigger atherothrombosis, vessel occlusions, myocardial infarcti
178 al disease or with multiple risk factors for atherothrombosis were enrolled in the global Reduction o
180 iovascular disease is prevalently due to the atherothrombosis, where a pivotal role is played by plat
181 c1 gene display prominent medial erosion and atherothrombosis, whereas their macrophages accumulate f
182 platelet therapy would improve biomarkers of atherothrombosis without causing unacceptable bleeding i
183 l antiplatelet therapy reduces biomarkers of atherothrombosis without causing unacceptable bleeding.