ライフサイエンスコーパス: heart attack

1 eral inflammation (e.g., infection, surgery, heart attack).

2 de protection against myocardial infarction (heart attacks).

3 rrent smoking; and no history of diabetes or heart attack.

4 e significant declines in community rates of heart attack.

5 to the brain or heart, leading to stroke or heart attack.

6 rticipants, and participants with a previous heart attack.

7 se fields, including treatment of stroke and heart attack.

8 tes mellitus, glucose, and family history of heart attack.

9 ed as genes implicated in predisposition for heart attack.

10 value reached in the first few minutes of a heart attack.

11 when heart muscle cells die en masse after a heart attack.

12 the prognosis and mortality in patients with heart attack.

13 processes involved in wound healing after a heart attack.

14 iminates regeneration after injury including heart attack.

15 ndividuals are prone to higher incidences of heart attack.

16 tions, smoking status, and family history of heart attack.

17 on the causes, treatment, and prevention of heart attack.

18 therapeutics to improve the response after a heart attack.

19 asal Cell Carcinoma, Malignant Melanoma, and Heart Attack.

20 creased cardiac damage in an animal model of heart attack.

21 % of respondents; of these, 67.8% reported a heart attack.

22 life-threatening events, such as strokes and heart attacks.

23 reducing the tissue damage that is caused by heart attacks.

24 ew therapeutic interventions for strokes and heart attacks.

25 farction, one of the most prevalent forms of heart attacks.

26 risk for development of premature, familial heart attacks.

27 etus IQ decrements and 194 deaths from fatal heart attacks.

28 lar disease (CVD) epidemiology would prevent heart attacks.

29 ss strenuous PA had little effect on risk of heart attacks.

30 ffer new hope for patients suffering massive heart attacks.

31 ovascular disease epidemiology would prevent heart attacks.

32 ons that raise LDLRs reduce LDL and diminish heart attacks.

33 Our results demonstrated higher rates of heart attack (14% vs 11.8%) and stroke (19.8% vs 10%) in

34 ation (36%) rather than heart disease (17%), heart attack (14%), or stroke (5%).

35 g the 3.1% of respondents with self-reported heart attack, 32.8% had claims-identified AMI, 16.5% had

36 no-claim control to report that it prevents heart attacks (370 of 592 [62.5%] vs 306 of 568 [53.9%];

37 sm (54%) and deep-vein thrombosis (44%) than heart attack (88%) and stroke (85%).

38 ate matter and ozone (95CI: 25 000-120 000), heart attacks (900-9400), and lost work days (3.6M-4.9M)

39 detect myocyte death are used to diagnose a heart attack (acute myocardial infarction, AMI), there i

40 and PM(2.5)) and to the type of outcome (MI, heart attack, acute coronary syndrome).

41 king group has been convened by the National Heart Attack Alert Program (which is coordinated by the

42 The odds for heart attack among those with diabetes, increased by 20

43 The associations with heart attack and alcohol consumption are new findings.

44 mong participants without self-reported CHD (heart attack and angina pectoris), stroke, peripheral va

45 f incident coronary heart disease (including heart attack and angina) or stroke (including ischaemic

46 1.5-5.1) and among those with self-reported heart attack and claims-identified AMI (odds ratio, 2.5;

47 ascular disease and the predominant cause of heart attack and ischemic stroke.

48 ypertension is a significant risk factor for heart attack and stroke and represents a major public he

49 .g., rofecoxib [Vioxx]) increase the risk of heart attack and stroke and should be avoided in patient

50 drome have a significantly increased risk of heart attack and stroke compared with people with normal

51 Although reports of parental premature heart attack and stroke had high likelihood ratios, thei

52 tion and atherosclerosis, the major cause of heart attack and stroke in humans.

53 s could be associated with the prevention of heart attack and stroke in humans.

54 orapaxar [SCH 530348; MK-5348] in Preventing Heart Attack and Stroke in Participants With Acute Coron

55 orapaxar [SCH 530348; MK-5348] in Preventing Heart Attack and Stroke in Participants With Acute Coron

56 sess the Effects of SCH 530348 in Preventing Heart Attack and Stroke in Patients With Acute Coronary

57 ssess the Effects of Vorapaxar in Preventing Heart Attack and Stroke in Patients With Atherosclerosis

58 sess the Effects of SCH 530348 in Preventing Heart Attack and Stroke in Patients With Atherosclerosis

59 ssess the Effects of Vorapaxar in Preventing Heart Attack and Stroke in Patients With Atherosclerosis

60 Given the recent declines in heart attack and stroke incidence, it is unclear how wom

61 sterone levels are associated with increased heart attack and stroke risk.

62 Unwanted clots lead to heart attack and stroke that result in a large number of

63 on, leaving people with SCI at daily risk of heart attack and stroke(2-5).

64 gen is a primary step in the pathogenesis of heart attack and stroke, and drugs to block platelet act

65 ases and morbidities varied by more than 2% (heart attack and stroke, diabetes, kidney disease, osteo

66 es, including ischemia/reperfusion injury in heart attack and stroke, neurodegenerative conditions, a

67 sclerosis, a disease of arteries that causes heart attack and stroke, through poorly defined mechanis

68 tored, and underlies many disorders, notably heart attack and stroke.

69 aemia-reperfusion injury in murine models of heart attack and stroke.

70 rd most common cause of vascular death after heart attack and stroke.

71 e of death from cardiovascular disease after heart attack and stroke.

72 ises blood pressure, increasing the risk for heart attack and stroke.

73 r safer antiplatelet therapeutics to prevent heart attack and stroke.

74 therosclerosis is the process that underlies heart attack and stroke.

75 premature vascular disease and death due to heart attack and stroke.

76 of adults and is the leading risk factor for heart attack and stroke.

77 and volume are independent risk factors for heart attack and stroke.

78 the small intestine, thus protecting against heart attack and stroke.

79 ting in acute cardiovascular events, such as heart attack and stroke.

80 Atherosclerosis is the process underlying heart attack and stroke.

81 hat PAD is associated with increased risk of heart attack and stroke; and only 14% were aware that PA

82 n the coronary arteries, which can result in heart attack and sudden death, is a common disease and p

83 d that more strenuous PA reduced the risk of heart attack and that it was necessary to continue PA af

84 c pain--examples include the chest pain of a heart attack and the leg pain of a 30 s sprint--occurs w

85 35 cases indicated that two-thirds had had a heart attack and the remainder had other coronary heart

86 timates, a twofold higher incidence of fatal heart attacks and a 10% higher incidence of cancer than

87 or the importance of PA in the prevention of heart attacks and as a public health recommendation and

88 sis and in arterial thrombosis, which causes heart attacks and other events triggered by abnormal clo

89 vated inappropriately and causes thrombosis, heart attacks and stroke.

90 ature arteriosclerotic disease that leads to heart attacks and strokes at a mean age of 13 years.

91 nner intimal layer of arteries and can cause heart attacks and strokes(1).

92 y disease, cardiovascular disease (including heart attacks and strokes), and neurodegeneration, while

93 Plaque disruption, a major cause of heart attacks and strokes, cannot generally be predicted

94 Heart attacks and strokes, leading causes of deaths glob

95 s the tissue injury of ischaemic necrosis in heart attacks and strokes, the most common causes of dea

96 therosclerotic cardiovascular disease causes heart attacks and strokes, which are the leading causes

97 nitiative has a goal of preventing 1 million heart attacks and strokes-the leading causes of mortalit

98 ues plays a critical role in pathogenesis of heart attacks and strokes.

99 t clots can obstruct blood vessels and cause heart attacks and strokes.

100 -dependent arterial thrombosis triggers most heart attacks and strokes.

101 n, is responsible for considerable damage in heart attacks and strokes.

102 epatobiliary diseases; and the likelihood of heart attacks and strokes.

103 nting its downstream sequelae, which include heart attacks and strokes.

104 spectively, a daily medication that prevents heart attacks and strokes.

105 s about statin therapy for the prevention of heart attacks and strokes.

106 diseases (such as coronary heart disease and heart attack) and many beta-adrenoceptor acting drugs ar

107 ause of most cases of myocardial infarction (heart attack) and of about 80% of strokes, collectively

108 talization, new diagnosis of cancer, stroke, heart attack), and interaction (multiplicative and addit

109 so causes severe tissue damage after stroke, heart attack, and other ischemia reperfusion injuries.

110 ge, hypertension, smoking, family history of heart attack, and periodontitis, the significant associa

111 with increased risk of cerebral infarction, heart attack, and reduced cardiac ejection fraction.

112 sease/heart failure, angina/angina pectoris, heart attack, and stroke, who provided complete data for

113 resent a major risk factor for hypertension, heart attack, and stroke.

114 tant contributor to the onset of thrombosis, heart attack, and stroke.

115 sed risk of hypertension, diabetes, obesity, heart attack, and stroke.

116 s may have increased cardiovascular disease, heart attack, and stroke.

117 blood pressure, serum cholesterol, previous heart attack, and treatment for diabetes.

118 For pneumonia, heart attacks, and all-cause mortality, the effect size

119 osis is the immediate cause of some strokes, heart attacks, and peripheral artery disease.

120 n many disorders, including ischemic stroke, heart attacks, and reperfusion injury.

121 this study was defined as prior diagnosis of heart attack, angina and stroke, while diabetes was defi

122 Self-reported CVD (history of heart attack, angina, or congestive heart failure) and C

123 s for treating damaged heart tissues after a heart attack are normally produced by seeding heart cell

124 (IQ) decrements and 7,360 deaths from fatal heart attacks are related to the intake of methylmercury

125 per mm Hg; 95% CI, 1.07-1.48) and history of heart attack at baseline (OR, 13.49; 95% CI, 2.85-63.87)

126 line PEX, higher IOP at baseline, history of heart attack at baseline, and no alcohol consumption wer

127 s effective at saving lives in patients with heart attacks because it explosively generates plasmin i

128 e common in Fabry patients, with strokes and heart attacks being significant contributors to a shorte

129 sociations were limited to smokers who had a heart attack between the ages of 25 and 50 years, with o

130 cTnI detection, providing insights into post-heart attack biomarker levels.

131 to limit the damage that can occur during a heart attack by stress-induced hyperglycaemia.

132 Restoration of coronary blood flow after a heart attack can cause reperfusion injury potentially le

133 s such as cardiovascular disease (stroke and heart attack), cancer, chronic respiratory disease, and

134 The 352 women who reported having had a heart attack (cases) were frequency matched 5:1 on age w

135 eir use is associated with increased risk of heart attacks caused by blocking COX-2 in the vasculatur

136 Heart attacks caused by occlusion of coronary arteries a

137 or triaging patients directly to specialized heart-attack centers.

138 h common (eg, viral illness) and severe (eg, heart attack) conditions were used.

139 order to prevent CVD manifestations such as heart attack, congestive heart failure, or stroke.

140 including blood clots in formation, ongoing heart attack, coronary artery blockage, etc.

141 etes, and previous admission to hospital for heart attack decreased the relative risk to 1.40 (1.35-1

142 disease conditions, including Breast Cancer, Heart Attack, Diabetes, etc.

143 I (cTnI) is a critical protein biomarker for heart attack diagnosis.

144 Prior research in heart attacks has suggested a paradoxical role of the so

145 ardiovascular effects and increased risk for heart attacks have been associated with this drug.

146 tive heart failure, coronary artery disease, heart attack, heart valve disease, stroke, transient isc

147 mentia or improved memory (eg, lower risk of heart attack: "Heart Health" label, 209 of 525 [40.0%];

148 een periodontal loss of attachment (LOA) and heart attack history for smokers, with odds ratios and 9

149 relationship between periodontal disease and heart attack history.

150 y complications that can lead to strokes and heart attacks if left untreated.

151 f 829 patients (6.7 years +/- 3.5, including heart attack in 39 [5%] and death in 79 [10%]).

152 , elevated cholesterol level, and history of heart attack in a parent.

153 l damage during surgery, transplantation, or heart attack in humans.

154 h existing estimates of the relative risk of heart attack in individuals attributable to passive smok

155 Self-reported heart attack in the previous 2 years was compared with c

156 rhage in the recreational activity group and heart attack in the VRWii group).

157 ons that eliminate LDLRs raise LDL and cause heart attacks in childhood, whereas mutations that raise

158 rate physical activity reduces mortality and heart attacks in older men with and without diagnosed ca

159 After two heart attacks in three years, an associate professor dis

160 s in mediating the fibrotic response after a heart attack include extracellular matrix turnover and a

161 e to the 0% category, the unadjusted odds of heart attack increased with each higher category of atta

162 is then validated for the measurement of the heart attack indicator cardiac troponin I and is shown t

163 , including cardiovascular diseases (such as heart attacks), injuries, mental and behavioral disorder

164 patient appears worse: yield of testing for heart attack is 19% lower with each standard deviation i

165 ar risk including stroke, heart failure, and heart attack is present even after normalization of bloo

166 ction of cardiac biomarkers for diagnosis of heart attack is the key to saving lives.

167 x proportional hazards models for predicting heart attack, ischemic stroke, heart failure hospitaliza

168 Primary outcomes were mortality, stroke, heart attack, major adverse cardiovascular events (MACE)

169 This serum heart attack marker was used as an example of analytes o

170 y and Efficacy Study of MGuard Stent After a Heart Attack [MASTER]; NCT01368471).

171 Although self-reported heart attack may be inaccurate, it indicates increased r

172 ity of life/HRQoL/QoL, myocardial infarction/heart attack/MI and predict*/factor.

173 e and blood pressure surges, that stroke and heart attack most frequently happen.

174 patient are needed to replace losses during heart attack, multiple sclerosis and diabetes.

175 Cardiac immunosensor for early detection of heart attack (myocardial infarction) was developed using

176 the heart muscle contributes to millions of heart attacks (myocardial infarction, MI) around the wor

177 Reports of angina, heart attack, myocardial infarction, and arrhythmia attr

178 ate the Effects of ACT-246475 in Adults With Heart Attack; NCT03487445, 2018-000765-36 [EudraCT]).

179 ve predictive values for reports of paternal heart attack occurring before 55 years of age and for st

180 inite further reductions in the incidence of heart attack, of revascularisation, and of ischaemic str

181 aving Had a Recent Coronary Event, Such as a Heart Attack or a Procedure to Open the Vessels of the H

182 ypertension (for females), diabetes, asthma, heart attack or angina (for females), and stroke (for fe

183 For males, heart attack or angina is higher in the United States on

184 ore likely to report the supplement prevents heart attack or heart failure, while those shown a label

185 vascular disease was defined as a history of heart attack or heart surgery.

186 t's root cause of illness, such as missing a heart attack or infection or assigning the wrong diagnos

187 vate CHD risk among individuals with a prior heart attack or self-reported pre-existing cardiovascula

188 Arriving rapidly to the hospital after a heart attack or stroke is critical for patients to be wi

189 during ischemia-reperfusion injury (IRI), in heart attack or stroke settings, but also as an unavoida

190 aging disease resulting in early death from heart attack or stroke.

191 curs at a mean age of 13 years, usually from heart attack or stroke.

192 of immediate help in responding to an acute heart attack or stroke.

193 major adverse cardiovascular events such as heart attacks or strokes has been established.

194 solve rapidly when treatment is stopped, the heart attacks or strokes that may occur if statin therap

195 ellular to cellular to whole vessel scale of heart attacks or strokes.

196 alcohol consumption and having a history of heart attacks (OR = 2.04, 95% CI 1.44-2.89), and physica

197 tion (EPIC) study, free of cancer, diabetes, heart attack, or stroke at baseline.

198 reported history of receiving heart disease, heart attack, or stroke diagnosis.

199 art failure, coronary heart disease, angina, heart attack, or stroke.

200 hospitalization, bariatric surgery, cancer, heart attack, or stroke.

201 [e.g., Death From Heart or Vascular Disease, Heart Attack, or Stroke] in Patients With Prior Heart At

202 isodes of care (e.g., treatment of diabetes, heart attack, or urinary tract infection), assigned each

203 gnificantly higher odds of CAD (P </= 0.04), heart attack (P </= 0.01), and congestive heart failure

204 ds of CAD (P </= 0.02), angina (P </= 0.02), heart attack (P </= 0.047), other heart disease (P < 0.0

205 static prediction problems for mortality in heart attack patients and can offer clinical insight fro

206 al value of technological change for elderly heart attack patients in 1984-1990.

207 ed to individuals with a self-reported prior heart attack, periodontitis was associated with a 34% de

208 tery disease (POR, 2.92; 95% CI, 1.95-4.29), heart attack (POR, 1.79; 95% CI, 1.23-2.54), and stroke

209 nt medical tasks, such as auto diagnosis and heart-attack prediction.

210 due to diabetes, hypertension, and previous heart attack.Published under a CC BY 4.0 license.

211 articipants of the Sertraline Antidepressant Heart Attack Randomized Trial (SADHART) to establish fea

212 vs placebo in the Sertraline AntiDepressant Heart Attack Randomized Trial (SADHART).

213 The Sertraline Antidepressant Heart Attack Randomized Trial assessed HRV from 24-hour

214 katchewan Health database, and the Worcester Heart Attack Registry.

215 although catastrophic events such as stroke, heart attack, renal failure, and dementia usually happen

216 option for several diseases such as stroke, heart attack, reperfusion injuries, and rheumatoid arthr

217 stimates of reductions in community rates of heart attacks resulting from smoking restriction laws wi

218 ministration for patients with chest pain or heart attacks (rho = 0.24; p < 0.001) and shorter median

219 water Horizon oil spill (Gulf of Mexico) and heart attack risk among 24,375 oil spill workers enrolle

220 he article "Physical Activity as an Index of Heart Attack Risk in College Alumni", established that m

221 parts per million (ppm) were associated with heart attack risk, with a 1.8-fold risk for exposure of

222 r removal, hospital admission with suspected heart attack, ruptured gut, and ruptured Achilles tendon

223 There were 312 first heart attacks (self-reported physician-diagnosed myocard

224 Regional heart attack services have improved clinical outcomes fo

225 d pressure correlates with increased risk of heart attack, stroke and progression to heart and kidney

226 tly predicted incident (3 years) thrombosis (heart attack, stroke) risk.

227 e that PAD imposes a high short-term risk of heart attack, stroke, and death.

228 Incident cardiometabolic conditions (e.g., heart attack, stroke, and diabetes) were self-reported a

229 a key role in the pathophysiology of cancer, heart attack, stroke, and other major causes of mortalit

230 ry of coronary artery disease (CAD), angina, heart attack, stroke, and peripheral vascular disease (P

231 ndex, and histories of hypertension, angina, heart attack, stroke, diabetes, rheumatoid arthritis, an

232 ed, professionally diagnosed, heart disease, heart attack, stroke, high blood pressure, diabetes, and

233 ime to the first major cardiovascular event (heart attack, stroke, new or worsening congestive heart

234 rimary composite outcome of all-cause death, heart attack, stroke, or hospitalization for heart failu

235 ich only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death.

236 a number of life threatening diseases, e.g., heart attack, stroke, pulmonary embolism.

237 enation injury, ischemia reperfusion injury (heart attack, stroke, trauma hemorrhage), and sepsis.

238 to life-threatening diseases (e.g., cancer, heart attack, stroke, wound healing).

239 a major cause of blindness, kidney failure, heart attacks, stroke and amputation of lower limbs.

240 Spikes in deaths due to heart attacks, strokes and other diseases occurred durin

241 clot and, thus, have a critical influence on heart attacks, strokes, and embolisms.

242 e the risk of cardiovascular disease events (heart attacks, strokes, and the need for arterial revasc

243 To prevent heart attacks, strokes, death, and other complications o

244 nzymes so as not to form a thrombus, causing heart attacks, strokes, or pulmonary emboli, but the ori

245 As part of the Worcester Heart Attack Study, a community-wide study examining cha

246 Building on the Worcester Heart Attack Study, an ongoing community-wide investigat

247 Awareness of heart attack symptoms also declined.

248 The Morgan Incongruence of Heart Attack Symptoms Index was used to quantify symptom

249 ancer, and ever congestive heart failure and heart attack, the associations were attenuated, but all

250 fied by smoking status and tertile of age at heart attack, the statistically significant associations

251 abetes, congestive heart failure, or a prior heart attack, the utilization patterns closely followed

252 e a vital part of the diagnostic pathway for heart attack treatment, ultimately reducing healthcare c

253 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) have generated worldwide rea

254 sive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) have shown the risk of CHF t

255 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) is re-evaluated considering

256 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) showed that the primary end

257 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) stipulated assessment of the

258 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), 42 418 high-risk hypertensi

259 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), a multicenter randomized, d

260 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), a randomized, double-blind,

261 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), but it is unknown whether t

262 sive and Lipid-Lowering Treatment To Prevent Heart Attack Trial (ALLHAT), low-dose chlorthalidone as

263 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).

264 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT; pravastatin 40 mg versus

265 The Sertraline Antidepressant Heart Attack Trial (SADHART) tested the safety and effic

266 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]; NCT00000542).

267 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial and the Anglo-Scandinavian Cardiac Ou

268 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial failed to achieve similar success due

269 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial failed to find a significant reductio

270 sive and Lipid-Lowering treatment to prevent Heart Attack Trial reported that treatment initiated wit

271 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) data, which randomized adults to chl

272 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) determined that treatment with amlod

273 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) with baseline diabetes, incident dia

274 sive and Lipid-Lowering Treatment to Prevent Heart Attack Trial), a randomized, double-blind, active-

275 Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

276 Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

277 Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

278 Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

279 Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

280 Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

281 rt Attack, or Stroke] in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

282 Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

283 Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

284 Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

285 Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

286 Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a B

287 The odds of having a heart attack were eight times higher in the presence of

288 e periodontal assessments and information on heart attack were evaluated.

289 dden cardiac death, and his father died of a heart attack when he was 57 years old.

290 Acute hyperglycaemia at the time of a heart attack worsens the outcome for the patient.

291 The outcome was the self-reported history of heart attack (yes vs. no).