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1 in TRACE (Transitions, Risks and Actions in Coronary Events).
2 (median follow-up 17.2 years; 1070 incident coronary events).
3 d sudden cardiac death (SCD) during an acute coronary event.
4 y medicolegal autopsy to be because of acute coronary event.
5 r high-risk individual prior to a subsequent coronary event.
6 ACS grew larger in the 16 weeks following a coronary event.
7 e independent predictors of risk of an acute coronary event.
8 h type 2 diabetes who had had a recent acute coronary event.
9 , 130 subjects developed a fatal or nonfatal coronary event.
10 genetic effects on loge(CAC+1) and incident coronary events.
11 patients at a high risk of sustaining acute coronary events.
12 helial function are recognized predictors of coronary events.
13 ar events, 162 heart failure events, and 142 coronary events.
14 89; 95% CI: 0.74 to 0.90) although not major coronary events.
15 lop coronary arterial lesions and subsequent coronary events.
16 ut was associated with a lower risk of major coronary events.
17 ociated with each end point (P<0.001) except coronary events.
18 cation, that underlies the majority of acute coronary events.
19 erms and when compared with the reduction in coronary events.
20 cted by CT and has been suggested to predict coronary events.
21 Findings were similar for coronary events.
22 s, but was not found for patients with acute coronary events.
23 r therapeutic potential for reducing adverse coronary events.
24 urden and with the development of subsequent coronary events.
25 pattern reduced risks of diabetes and major coronary events.
26 h heart failure and outcomes associated with coronary events.
27 719Arg (rs20455) in KIF6 was associated with coronary events.
28 savings, while avoiding a negative impact on coronary events.
29 y of the Framingham equations for predicting coronary events.
30 el window on gene expression preceding acute coronary events.
31 /- 1.4 y were followed over 5 more years for coronary events.
32 ation is the major determinant of most acute coronary events.
33 ntral in risk-stratifying patients for acute coronary events.
34 in treatment for the secondary prevention of coronary events.
35 rganism have been linked to a higher risk of coronary events.
36 also lead to occlusive thrombosis and acute coronary events.
37 do not have a correspondingly higher rate of coronary events.
38 There have been no late coronary events.
39 fected patients may be at increased risk for coronary events.
40 RP) levels are independently associated with coronary events.
41 ive intervention strategies to avoid adverse coronary events.
42 risk factor and has an inverse relation with coronary events.
43 and thrombosis and is associated with acute coronary events.
44 hould clearly separate chronic CAD and acute coronary events.
45 lar health and dysfunction is a predictor of coronary events.
46 thogenic sequelae of atherogenesis and acute coronary events.
47 ls were associated with lower rates of major coronary events.
48 atients for decades, hoping to prevent acute coronary events.
49 spontaneous fibrinolytic activity with acute coronary events.
50 y studies have been associated with clinical coronary events.
51 italization did not reduce the risk of major coronary events.
52 y identify patients with high risk of future coronary events.
53 yme are associated with an increased risk of coronary events.
54 iation of AKI with long-term risk of adverse coronary events.
55 lular adhesion molecule-1 (ICAM-1) and acute coronary events.
56 94) for strokes, 0.91 (CI, 0.74 to 1.12) for coronary events, 0.80 (CI, 0.57 to 1.12) for heart failu
58 y associated with the absolute rate of major coronary events (11301 events, including coronary death
59 90; 95% CI, 0.82 to 1.00; P=0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95
60 486, 0.79 [0.69-0.90], p=0.0005), and total coronary events (178 vs 247, 0.71 [0.59-0.86], p=0.0005)
61 There were significant excess risks of major coronary event (2.44, 95% CI 2.18-2.73), ischaemic strok
62 sociated with an increase in the risk of any coronary event (2091 events; hazard ratio, 1.04; 95% con
66 no significant effect on the risk of primary coronary events (533 vs. 553 events; hazard ratio, 0.95;
67 ared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95%
69 vy drinkers had a 74% higher risk of a major coronary event, a 133% higher risk of stroke, and a 127%
70 any cardiovascular event (a composite of any coronary event, a cerebrovascular event, peripheral vasc
72 ship between mean heart dose (MHD) and acute coronary event (ACE) rate was reported in a study of pat
74 verse associations were found for HDL-C with coronary events across a range of LDL-C values, includin
75 OR 0.64, 95% CI 0.37-1.11; p=0.11) or acute coronary events (adjusted hazard ratio [HR] 0.76, 95% CI
76 CAC and hsCRP independently predicted 91 coronary events (adjusted hazard ratios [HRs]: log(2)(CA
77 have an excellent prognosis for survival and coronary events after 3 years compared with patients wit
81 olytic function are associated with incident coronary events among several, but not all, prospective
82 ociations were found for HDL-C with incident coronary events among women with a range of LDL-C values
83 consecutive victims of SCD because of acute coronary event and 532 survivors of such an event, in wh
85 mg/l) were 5.92 (95% CI: 3.14 to 11.16) for coronary events and 3.02 (95% CI: 1.82 to 5.01) for all-
86 es discrimination and stratification of hard coronary events and all-cause mortality in the general p
88 stic curves for the prediction of both major coronary events and any coronary event were higher when
89 ry associated with higher long-term risks of coronary events and death in this cohort, suggesting tha
90 the assessment of plaque burden and risk of coronary events and evaluation of therapeutic interventi
91 counted for about half of the differences in coronary events and for about 40% of the differences in
92 rotein 6, is associated with greater risk of coronary events and greater benefit from pravastatin ver
93 meta-analysis has confirmed benefit on major coronary events and ischaemic stroke in many diabetic pa
94 f postprandial hypotension on a high risk of coronary events and mortality in aging, we hypothesized
96 6 to 2.89; p = 0.029), the composite of hard coronary events and stroke (HR: 1.72; 95% CI: 1.16 to 2.
99 the assessment of plaque burden and risk of coronary events and the evaluation of therapeutic interv
101 patients at increased risk of posttransplant coronary events and was also useful to define a low-risk
102 carotid stenosis, and 10-year risk of acute coronary events) and of cardioembolism (ie, risk of card
104 tion is associated with an increased odds of coronary events, and inflammation, as assessed by higher
106 KIF6 719Arg allele had an increased risk of coronary events, and pravastatin treatment substantially
108 ues is responsible for the majority of acute coronary events, and the culprit lesions demonstrate dis
109 now inclusive of stroke in addition to hard coronary events, and there are now separate equations to
110 who experience major bleeding after an acute coronary event are at higher risk of death in the months
113 in the cardiology community that most acute coronary events arise from ruptures of mildly stenotic p
115 However, it is unclear whether the risk of coronary events associated with decreased kidney functio
116 endently predicted the risk of major adverse coronary events at 30 days (unadjusted 2nd, 3rd, and 4th
117 whether troponin concentration could predict coronary events, be modified by statins, and reflect res
119 disease (defined as 12 months from an acute coronary event) between 2002 and 2011 were identified.
120 als have shown that fibrates reduce nonfatal coronary events but do not confer any benefit on mortali
123 s have been used for determining the risk of coronary events, but the exact role of this marker for c
124 Psychosocial factors have been linked to coronary events, but the mechanisms underlying these ass
125 ular calcification are at increased risk for coronary events, but the relationship between calcium co
126 RP) are associated with an increased risk of coronary events, but whether inflammation is associated
127 calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary
128 riability (by ASV) increased the risk of any coronary event by 16% (hazard ratio [HR]: 1.16; 95% conf
132 ollow-up, there were 434 deaths overall, 472 coronary events (CE), 213 myocardial infarctions (MI), a
134 lprit lesion had a higher mortality and more coronary events compared with those without (p < 0.0005,
135 management of coronary artery disease, acute coronary events continue to occur in many patients.
136 duction in LDL-C level; 5-year rate of major coronary events (coronary death or MI) associated with a
137 nts with coronary artery disease but without coronary event), coronary artery disease was evaluated u
138 ole of vulnerable plaque in the causation of coronary events, coupled with novel diagnostic and thera
139 ts of the primary end point as well as major coronary events (death from coronary heart disease, myoc
140 arization for myocardial ischemia) and total coronary events (death from coronary heart disease, myoc
142 to assess the 1-year risk of first recurrent coronary events defined as coronary death or myocardial
143 disease received a diagnosis of an incident coronary event (defined as nonfatal myocardial infarctio
144 The effect of raloxifene on the incidence of coronary events differed significantly by age (interacti
145 status, and GRACE (Global Registry of Acute Coronary Events) discharge risk scores (hazard ratio: 1.
146 iovascular risk factors and age at the first coronary event displayed significant heritable component
148 nt was also a strong predictor of stroke and coronary events (eg, top-decile HR for stroke: 3.25, 2.3
149 m particulate exposures contributed to acute coronary events, especially among patients with underlyi
150 a substantial reduction in the incidence of coronary events, even in populations with a high prevale
151 ion in the standardized 10-year incidence of coronary events from 10.7% for an unfavorable lifestyle
152 fied post-discharge Global Registry of Acute Coronary Events (GRACE) score was used to calculate an i
153 iuretic peptide and Global Registry of Acute Coronary Events (GRACE) scores as comparators and to ide
154 nd PATIENTS: In the Global Registry of Acute Coronary Events (GRACE), a multinational cohort study, 4
155 risk measures (eg, Global Registry of Acute Coronary Events [GRACE] score) for death, death/myocardi
157 lerotic plaques that are precursors of acute coronary events harbor abundant macrophage infiltration,
158 ve demonstrated that plaques which result in coronary events have larger plaque volume and necrotic c
159 AKI recovery associated with higher risk of coronary events (hazard ratio [HR], 1.67; 95% confidence
160 and additional risk allele) and for incident coronary events (hazard ratiogxincome=0.69 [95% confiden
161 adjustment gave HRs of 0.94 (0.81-1.08) for coronary events (HDL cholesterol being the largest contr
163 population-based case-control study of major coronary events (i.e., myocardial infarction, coronary r
164 disease (CAD) could be at increased risk for coronary events if diastolic pressure falls below critic
165 ure (IH-CHF) and interim hospitalization for coronary events (IH-CE), were examined with proportional
166 ivariate analyses, the odds ratio (OR) for a coronary event in women with an estimated CrCl <60 ml/mi
171 Raloxifene had no effect on the incidence of coronary events in any subgroup except in the case of a
172 educe myocardial perfusion abnormalities and coronary events in comparison to usual-care cholesterol-
173 PIbalpha subunit predicts risk for recurrent coronary events in diabetic postinfarction patients, but
175 d paraoxon is an independent risk factor for coronary events in men at high risk because of preexisti
177 not reduce mortality but may reduce nonfatal coronary events in patients at risk for cardiovascular d
178 t fluctuation is a risk factor for death and coronary events in patients without cardiovascular disea
180 the usefulness of Lp PLA2 as a predictor of coronary events in the general population and in those w
181 al fat is associated with fatal and nonfatal coronary events in the general population independent of
183 Sixty-two percent (95% CI: 49%, 74%) of coronary events in this cohort may have been prevented w
185 between treatment groups in the incidence of coronary events in women > or =60 and <70 or > or =70 ye
187 icantly associated with an increased odds of coronary events in women with an estimated CrCl < or =74
188 r, had no overall effect on the incidence of coronary events in women with established coronary heart
189 does provide benefit in reducing the risk of coronary events in women; however, women remain undertre
190 er in patients with CP for all major adverse coronary events, including stroke, bleeding, and mortali
192 h coronary artery calcification, the risk of coronary events increased incrementally across tertiles
195 enoses, that patients who experience a fatal coronary event invariably had antecedent exposure to one
196 d coronary inflammation for predicting acute coronary events is a currently a source of considerable
197 e use of aspirin for secondary prevention of coronary events is controversial in patients with HF.
198 ociation between inflammatory biomarkers and coronary events is influenced by level of kidney functio
200 points included patient-oriented major acute coronary events (MACE) (death, myocardial infarction [MI
202 ntifying patients who have a high risk for a coronary event may decrease morbidity and mortality.
203 olesterolemia, 57% (95% CI: 32%, 79%) of all coronary events may have been prevented with a low-risk
204 n (CRP), in addition to being a predictor of coronary events, may have direct actions on the vessel w
205 or major vascular events (MVEs) (i.e., major coronary events [MCE] [nonfatal myocardial infarction or
206 on was higher with versus without subsequent coronary events (median, 115 [Q1-Q3, 23-360] versus 8 [0
208 ndently conferred an increased risk for hard coronary events (myocardial infarction or death from cor
210 ) and 3 registries (Global Registry of Acute Coronary Events, National Registry of Myocardial Infarct
214 some pediatric disease states, with clinical coronary events occurring in childhood and very early ad
218 I and II, were significantly associated with coronary events only in women with reduced kidney functi
220 ing to heart failure cases without preceding coronary events or developed diabetes during follow-up.
223 ciated with a reduction in risk of recurrent coronary events or thromboembolism, whereas risk of blee
224 ary end point of cardiovascular death, major coronary event, or nonfatal stroke, the relative risk re
225 neither target (cardiovascular death, major coronary event, or stroke; 38.9% versus 28.0%; adjusted
226 acy composite of cardiovascular death, major coronary events, or stroke was significantly lower in pa
227 er in the statin-treated arm: by 18% for any coronary event (P=0.002), by 24% for myocardial infarcti
229 ntion cohort resulted in an 11% reduction in coronary events (P = 0.16), a similar but significant re
230 nts) at baseline were not at higher risk for coronary events (P=0.91 for interaction) or stroke (P=0.
231 umber, the hazard ratios for major occlusive coronary event per 1-SD-higher level were 0.91 (95% CI,
233 e proportional increase in the rate of major coronary events per gray was similar in women with and w
237 s that statins substantially reduce not only coronary event rates but also total stroke rates in pati
238 ngle years revealed increasing major adverse coronary event rates from 0.30 to 0.54 (P=0.001) for y-2
239 onary angiography was associated with higher coronary event rates than was undergoing the procedure.
240 s and test-positive angina, age-standardized coronary event rates were 9.9 per 100 person-years in wo
241 mpared with patients without FH, the risk of coronary event recurrence after ACS was similar in patie
242 h FH and ACS have a >2-fold adjusted risk of coronary event recurrence within the first year after di
243 ons (or deaths) for all 4 diagnostic groups: coronary events (relative risk, 0.848; 95% confidence in
245 r lack of interaction was observed for major coronary events, revascularizations, and strokes conside
247 plore altered platelet function in recurrent coronary event risk among diabetic postinfarction patien
249 elationship between plaque rupture and acute coronary event risk suggested by pathology studies and c
251 sus 72), had higher Global Registry of Acute Coronary Events risk score (129 versus 127), and were wi
252 association between Global Registry of Acute Coronary Events risk score variables and optimal in-hosp
253 o assessed were the Global Registry of Acute Coronary Events risk score, Charlson comorbidity index,
255 (RR=0.86; 95% CI, 0.75-0.99; P=0.03) but not coronary events (RR=0.86; 95% CI, 0.67-1.11; P=0.24).
256 (NSTEMI) and GRACE (Global Registry of Acute Coronary Events) score >140, coronary angiography (CAG)
258 ith strategies proved to reduce the risk for coronary events, such as statins or dietary changes in t
260 victims of SCD than in survivors of an acute coronary event suggests that the presence of ER increase
261 ssociated with a substantially lower risk of coronary events than an unfavorable lifestyle (defined a
262 associated with a 46% lower relative risk of coronary events than an unfavorable lifestyle (hazard ra
265 th 70% or greater narrowing experienced more coronary events than patients with less significant lesi
267 pass) and may more effectively prevent acute coronary events than these more invasive approaches.
268 In postmenopausal women at increased risk of coronary events, the overall lack of benefit of raloxife
270 ciated with increased risk of acute ischemic coronary events (unstable angina and myocardial infarcti
271 ll validated GRACE (Global Registry of Acute Coronary Events) variables together with troponin I and
272 hest variation in body weight, the risk of a coronary event was 64% higher, the risk of a cardiovascu
273 no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among p
275 ence of cerebrovascular events compared with coronary events was 1.19 (95% CI 1.06-1.33) overall; 1.4
278 rs, coronary artery calcification (CAC), and coronary events was assessed using regression analysis.
279 relationship between diastolic pressure and coronary events was documented in treated patients with
280 e relation between BMI and the risk of acute coronary events was evident for even mildly elevated BMI
282 clopidogrel), no increased risk of recurrent coronary events was seen for OAC plus clopidogrel (hazar
285 tes that has a known association with future coronary events, we divided individuals from the Malmo D
286 iction of both major coronary events and any coronary event were higher when the calcium score was ad
292 parable negative predictive values for major coronary events were obtained in studies considering the
294 f EAT was associated with a 1.5-fold risk of coronary events when adjusting for cardiovascular risk f
295 There was a 5-fold greater reduction in coronary events when troponin concentrations decreased b
296 the entire coronary vascular tree predicted coronary events, whereas changes in the worst flow-limit
297 (respiratory failure, myositis, and an acute coronary event), which could have been precipitated by t
300 dard glycaemic control significantly reduces coronary events without an increased risk of death.
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