ライフサイエンスコーパス: stable angina

1 th Optimal Medical Therapy of Angioplasty in Stable Angina).

2 tion (60.8% patients with ACS and 39.2% with stable angina).

3 mmon in patients with ACS than in those with stable angina.

4 se microvascular resistance in patients with stable angina.

5 cardial infarctions compared with those with stable angina.

6 exercise capability in patients with chronic stable angina.

7 DES for AMI and compared with patients with stable angina.

8 dical therapy is a proven option for chronic stable angina.

9 ith an acute myocardial infarction than with stable angina.

10 ations and evidence-based medical therapy in stable angina.

11 in 14 patients with ACS and 9 patients with stable angina.

12 nd in stable lesions in patients with ACS or stable angina.

13 ith an acute myocardial infarction than with stable angina.

14 lable rho kinase inhibitor, in patients with stable angina.

15 s on the management of patients with chronic stable angina.

16 e on the management of patients with chronic stable angina.

17 e on the management of patients with chronic stable angina.

18 c plaque complexity in patients with chronic stable angina.

19 er design, we enrolled 336 CAD patients with stable angina.

20 aspects of quality of life in patients with stable angina.

21 m-derived nitric oxide (NO) in patients with stable angina.

22 oncentrations than did patients with chronic stable angina.

23 new clinical domains beyond the confines of stable angina.

24 rate (ISMN) or glyceryl trinitrate (GTN) for stable angina.

25 ts in randomized trials of patients who have stable angina.

26 y aspirin treatment in patients with chronic stable angina.

27 anatomic extent of disease in patients with stable angina.

28 d toward an ad hoc approach in patients with stable angina.

29 7 for management of hypertension and chronic stable angina.

30 coronary arterial stenoses in patients with stable angina.

31 ary artery stenoses in patients with chronic stable angina.

32 , respectively, p = 0.03) than patients with stable angina.

33 (CFR), is a common finding in patients with stable angina.

34 fractional flow reserve on the management of stable angina.

35 -elevation myocardial infarction and 31 with stable angina.

36 it the greatest morbidity and mortality from stable angina.

37 equently performed to reduce the symptoms of stable angina.

38 ient is important for effective treatment of stable angina.

39 r acute coronary syndromes and the remainder stable angina.

40 lex treatment decisions in older adults with stable angina.

41 ebo-controlled trial of PCI in patients with stable angina.

42 in patients with a new diagnosis of chronic stable angina.

43 bout its importance in patients with chronic stable angina.

44 th intravascular ultrasound in patients with stable angina.

45 ain across a broad spectrum of patients with stable angina.

46 Fewer patients underwent PCI for stable angina.

47 ith best medical therapy among patients with stable angina.

48 of ranolazine in patients with diabetes and stable angina.

49 f patients in both cohorts underwent PCI for stable angina.

50 sites in patients with ACS versus those with stable angina.

51 ther non-ST segment elevation MI (NSTEMI) or stable angina.

52 nts; and 15 (3.0%) patients hospitalized for stable angina.

53 rachnoid haemorrhage (1.43 [1.25-1.63]), and stable angina (1.41 [1.36-1.46]), and weakest for abdomi

54 3.22]), ischaemic stroke (1.72 [1.52-1.95]), stable angina (1.62 [1.49-1.77]), heart failure (1.56 [1

55 6-3.22), ischaemic stroke (1.72, 1.52-1.95), stable angina (1.62, 1.49-1.77), heart failure (1.56, 1.

56 or myocardial infarction (MI, 33%), but also stable angina (11%) or no symptoms (11%).

57 % CI: 0.53 to 2.10; p = 0.88) and those with stable angina (11.6% vs. 15.8%; HR: 0.82; 95% CI: 0.50 t

58 arger in unstable angina (42 +/- 3%) than in stable angina (18 +/- 4%) (P = .0001).

59 cost differences of $1,300 for patients with stable angina, $2,100 for patients with unstable angina

60 th Optimal Medical Therapy of Angioplasty in Stable Angina-2) found that percutaneous coronary interv

61 percent had unstable angina), 6 percent had stable angina, 21 percent had other cardiac problems, an

62 patients compared with those who had chronic stable angina (28.4 versus 14.0 pg/mL; 95% CI, 9.8 to 19

63 (n = 401) or DES (n = 399) for treatment of stable angina (32%) or acute coronary syndrome (68%).

64 7 +/- 8%) than in samples from patients with stable angina (40 +/- 5%) (P = .00007).

65 arger in unstable angina (16 +/- 2%) than in stable angina (5 +/- 2%) (P = .002).

66 eous coronary intervention were included: 50 stable angina, 50 NSTEMI, and 40 STEMI.

67 The remaining 83 were being evaluated for stable angina (53), valvular heart disease (8), atypical

68 ) prospectively randomized 350 patients with stable angina (55% women; aged 55+/-10 years), mostly wi

69 (CD66b) was similar in patients with ACS and stable angina (6.61 [4.91-7.72] versus 6.62 [5.27-8.73],

70 was greatest in PCI procedures performed for stable angina (66%), followed by non-ST-segment-elevatio

71 ts with ACS and less common in patients with stable angina (73.3% versus 17.6%, P=0.002).

72 rwent percutaneous coronary intervention for stable angina (77.9% versus 46.2%).

73 omposed of LCP than targets in patients with stable angina (84.4% versus 52.8%, P=0.004), approximate

74 undergoing cardiac catheterization (65 with stable angina, 84 with unstable angina or a myocardial i

75 Conclusion In individuals with stable angina, a normal coronary CTA-derived FFR test re

76 ndex age 30 years, whereas heart failure and stable angina accounted for the largest proportion (19%

77 The coronary arteries of patients with stable angina also contain many nonobstructive plaques,

78 ripheral blood T cells from 34 patients with stable angina and 34 patients with UA were compared for

79 were compared with those of 40 patients with stable angina and 40 healthy controls.

80 nts undergoing coronary angiography, 37 with stable angina and 50 with unstable angina or a myocardia

81 Within stable angina and ACS cohorts, 7% of patients were black

82 ol/10(8) platelets in coronary patients with stable angina and acute coronary syndromes, respectively

83 Fifteen patients with chronic stable angina and angiographically proven CAD (>70% sten

84 ronary revascularization among patients with stable angina and at least 1 coronary lesion with a frac

85 uation) trial enrolled patients with chronic stable angina and at least 1 significant (> or =70%) ang

86 adverse prognosis observed among women with stable angina and confirmed coronary disease.

87 myocardial infarction than in patients with stable angina and controls (P<0.001).

88 mmarizes the current evidence for its use in stable angina and heart failure and its future direction

89 epression is common in patients with chronic stable angina and is associated with increased morbidity

90 percutaneous coronary intervention (PCI) in stable angina and is commonly observed clinically.

91 Twenty-eight patients with stable angina and ischemia documented by a stress test w

92 ion, and more chronic disease states such as stable angina and ischemic cardiomyopathy.

93 g hemorrhagic complications in patients with stable angina and non-ST-segment elevation acute coronar

94 Twenty-four men with chronic stable angina and normal left ventricular function under

95 nary intervention (PCI) reduces only chronic stable angina and not myocardial infarction (MI) or asso

96 The resistive reserve ratio was similar in stable angina and NSTEMI patients (P=0.6).

97 ications for the evaluation of patients with stable angina and public policy.

98 Fifty-two patients with stable angina and reversible ischemia comprising >9% of

99 Among patients with stable angina and risk factors for coronary artery disea

100 n all patient subgroups those with including stable angina and single-vessel disease.

101 e investigation and subsequent management of stable angina and to assess gender differences in clinic

102 non-ST-elevation acute coronary syndromes or stable angina and to evaluate long-term outcomes of none

103 unstable angina compared with patients with stable angina and to investigate the effect of percutane

104 t problems, including myocardial infarction, stable angina and unstable angina, were confirmed.

105 th Optimal Medical Therapy of Angioplasty in Stable Angina) and ISCHEMIA (Initial Invasive or Conserv

106 ndary prevention strategies and treatment of stable angina), and in the selection of revascularizatio

107 infarction, 20 with unstable angina, 19 with stable angina, and 13 controls without atherosclerosis.

108 theterization with asymptomatic/mild angina, stable angina, and unstable angina/non-ST-elevation myoc

109 to consider in younger women presenting with stable angina-anginal symptom characterization may align

110 th Optimal Medical Therapy of Angioplasty in Stable Angina] app) for 14 days before undergoing invasi

111 dual aims of treating patients with chronic stable angina are 1) to reduce morbidity and mortality a

112 of lipid core plaque (LCP), lesions causing stable angina are believed to be composed of fibrocalcif

113 rs after PCI, and type IVa MI was defined in stable angina as a rise of at least 3x upper reference l

114 ting with acute myocardial infarction versus stable angina as the initial manifestation of CHD.

115 ts before and after coronary angioplasty for stable angina at three sampling sites: the femoral arter

116 ecutive patients with symptoms suggestive of stable angina attending for outpatient coronary angiogra

117 t included patients in Ontario, Canada, with stable angina based on obstructive coronary artery disea

118 Among patients with stable angina, both those treated with PCI and those tre

119 antianginal agent that has been effective in stable angina, but it has not been studied in the settin

120 duction should benefit patients with chronic stable angina by improving myocardial perfusion and redu

121 Patients with suspected chronic stable angina can be evaluated in three stages.

122 Seventy-nine patients with chronic stable angina Canadian Cardiovascular Society class 2 or

123 the Combination Assessment of Ranolazine In Stable Angina (CARISA) trial from July 1999 to August 20

124 Women have a similarly high incidence of stable angina compared with men.

125 Forty-six men with stable angina completed a 2-week, single-blind placebo r

126 lesions in ACS and stable lesions in ACS or stable angina, consistent with previous intravascular ul

127 one half of target lesions in patients with stable angina contained LCP.

128 me (ACS) compared with patients with chronic stable angina (CSA).

129 usion percutaneous coronary intervention for stable angina (CTO-PCI) is a rare but serious event.

130 ial clinical experience in six patients with stable angina demonstrates that high-quality NIR spectra

131 re performed in individuals free from CAD or stable angina diagnosis.

132 f CTCA with selective FFRCT in patients with stable angina did not differ significantly from standard

133 men, mean age 60.1+/-2.3 years) with chronic stable angina due to angiographically documented coronar

134 aged 18-75 years with symptoms of suspected stable angina due to coronary heart disease.

135 stic test in the evaluation of patients with stable angina due to higher sensitivity and comparable s

136 For patients with stable angina, emphasis should be placed on optimizing l

137 e culprit site in patients receiving DES for stable angina, emphasizing the importance of underlying

138 Randomized trials in patients with chronic stable angina enroll few patients who are over age 65 ye

139 The Euro Heart Survey of Stable Angina enrolled patients with a clinical diagnosi

140 ion to current traditional drugs for chronic stable angina, especially in aggressive multidrug regime

141 eous Coronary Intervention for the Relief of Stable Angina) found that percutaneous coronary interven

142 betes mellitus, coronary artery disease, and stable angina from the multinational Type 2 Diabetes Eva

143 ing diagnostic angiography for assessment of stable angina had angiographically normal or near normal

144 18 (45%) patients with stable angina had plaques with focal (18)F-NaF uptake (m

145 Diagnostic tests and medical therapies for stable angina have evolved over the last decade with a b

146 alternative therapies for many patients with stable angina; however, patients may have misconceptions

147 Clinical indications included stable angina in 22.5% of cases, unstable angina in 31.9

148 angina was present in 95 patients (78%) and stable angina in 27 (22%).

149 lacebo were administered to 15 subjects with stable angina in a double-blind crossover trial.

150 Ultimately, the management of stable angina in older adults will need to be informed b

151 Furthermore, stable angina in women is associated with increased coro

152 In this review, we will explore stable angina in young women, consider possible pathophy

153 Among patients with stable angina, in hospitals with high-capacity CCUs, use

154 ography for acute coronary syndrome (ACS) or stable angina, in whom there is angiographic evidence fo

155 Stable angina is associated with an average annual risk

156 most effective as a first-line treatment for stable angina is not known.

157 , through modest (hazard ratio, 1.5-2.0) for stable angina, ischemic stroke, peripheral arterial dise

158 n in Patients With Normal Blood Pressure and Stable Angina?; ISRCTN73579730).

159 the Monotherapy Assessment of Ranolazine In Stable Angina (MARISA) trial was to determine the dose-r

160 ents with UA and infrequent in patients with stable angina (median frequencies: 10.8% versus 1.5%, P<

161 tients with myocardial infarction (n = 7) or stable angina (n = 10) underwent (18)F-NaF PET and prosp

162 ients with ACS (n = 13) and in patients with stable angina (n = 13) (17.5 +/- 5.9 mm2 vs. 9.1 +/- 4.8

163 ents referred for angiographic evaluation of stable angina (n=375,886) or acute coronary syndromes (A

164 tients with myocardial infarction (n=40) and stable angina (n=40) underwent (18)F-NaF and (18)F-FDG P

165 he US and approximately 400,000 new cases of stable angina occur each year.

166 rolled patients with a clinical diagnosis of stable angina on initial assessment by a cardiologist.

167 acute coronary syndrome and 369 [27.2%] for stable angina) on patients admitted to nonintensive care

168 among patients who underwent PCI for either stable angina or a positive stress test.

169 of patients developing stroke after PCI for stable angina or acute coronary syndrome (ACS) in daily

170 (Evaluation of iFR vs FFR in Stable Angina or Acute Coronary Syndrome [iFR SWEDEHEART

171 Patients diagnosed with stable angina or acute coronary syndrome and those who u

172 ase activity increases in men and women with stable angina or acute coronary syndromes, supporting pr

173 A total of 2037 participants with stable angina or an acute coronary syndrome who had an i

174 Among patients with stable angina or an acute coronary syndrome, an iFR-guid

175 nstable angina) and stable presentation (51% stable angina or atypical symptoms).

176 % CI: 1.17 to 1.57), but no association with stable angina or intracerebral hemorrhage.

177 vention (PCI), particularly in patients with stable angina or ischemia, in whom event rates are low i

178 Patients undergoing PCI for stable angina or non-ST-segment-elevation myocardial inf

179 oronary angiography for the investigation of stable angina or non-ST-segment-elevation myocardial inf

180 85 years and had had either elective PCI for stable angina or urgent PCI for unstable angina or non-S

181 entified: elevated troponin (OR, 3.9), prior stable angina (OR, 1.8), ST-segment deviation >or=0.5 mm

182 ngs where the intrinsic risks are low (e.g., stable angina) or in which the device used carries a red

183 1.2% in unstable rest angina versus 18.3% in stable angina (p = 0.05); alpha-actin area was greater i

184 compared with 4 of 25 arteries in those with stable angina (p less than 0.0001) in whom an "angina-pr

185 seen more frequently in the 47 patients with stable angina (p less than 0.05).

186 was reported for white women presenting with stable angina (P<0.00001).

187 odds ratio for mortality than white men with stable angina (P<0.0001), with higher rates noted for wh

188 In patients with stable angina, PAPP-A and PAPP-A/proMBP ratio are associ

189 c) were higher in ACS patients compared with stable angina patients (1.38 [1.16-1.52] versus 1.17 [1-

190 We studied 396 stable angina patients (age 63+/-10 years, 230 men) of w

191 mean plaque Lp(a) areas than specimens from stable angina patients (n = 26): 64.4% versus 47.7% (p =

192 plicated in an independent population of 482 stable angina patients (rSA) and of 675 ACS patients, re

193 ectoris had higher VEGF levels compared with stable angina patients and healthy control subjects (P<0

194 ower in the STEMI patients compared with the stable angina patients both culprit and nonculprit vesse

195 mples of 2,000 persons drawn from the 10,128 stable angina patients in the CALIBER database with comp

196 We prospectively enrolled 11,372 consecutive stable angina patients who were referred for stress myoc

197 on-based cohort study on 49 556 adult ACS or stable angina patients with angiographic evidence of obs

198 ute cardiac events in predominantly low-risk stable angina patients with confirmed coronary disease a

199 patients than in a control group of chronic stable angina patients with multivessel IVUS imaging.

200 cacy and safety of fasudil were evaluated in stable angina patients.

201 This was not observed in stable angina patients.

202 28(null) T cells from circulation of ACS and stable angina patients.

203 .87x10(-8)) risk for ACS in individuals with stable angina pectoris (hazard ratio, 1.163 [95% CI, 1.0

204 82-1.251]) compared with individuals without stable angina pectoris (hazard ratio, 1.531 [95% CI, 1.4

205 cardial infarction (n=5371, 901 deaths), and stable angina pectoris (n=6536, 965 deaths) in 4 age cat

206 dependent cohorts of patients with suspected stable angina pectoris (SAP) (3033 patients; median 10.7

207 elective coronary angiography for suspected stable angina pectoris (SAP) (n = 4131) and an independe

208 203 patients referred for angiography due to stable angina pectoris (SAP) or acute coronary syndrome

209 egment elevation AMI and unstable angina, or stable angina pectoris (SAP).

210 -segment-elevation myocardial infarction and stable angina pectoris , similar patterns were found alb

211 Male patients (n = 328) with stable angina pectoris and ischemia on treadmill testing

212 tations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes.

213 We identified 80 conventional (eg, stable angina pectoris and type 2 diabetes) and unconven

214 erformance than medical therapy for men with stable angina pectoris due to single-vessel disease.

215 The indication for PTCA was stable angina pectoris in 69 patients, unstable angina i

216 going PCI (with or without FFR guidance) for stable angina pectoris in Sweden between January 2005 an

217 Stable angina pectoris in women has often been considere

218 Rapid CAD progression in patients with stable angina pectoris is associated with increased C-re

219 We studied 124 chronic stable angina pectoris patients (84 men; mean age, 61+/-

220 analysis at rest in patients with suspected stable angina pectoris predicts the presence of coronary

221 emia during patch-off hours in patients with stable angina pectoris receiving a beta-adrenergic block

222 Patients (n=141) with stable angina pectoris undergoing PCI had serial venous

223 n Trial) undergoing coronary angiography for stable angina pectoris were studied.

224 However, a diagnosis of stable angina pectoris yielded a differential associatio

225 sion of ambulatory ischemia in patients with stable angina pectoris, but it remains to be established

226 In patients with suspected stable angina pectoris, global longitudinal peak systoli

227 nsecutive patients with clinically suspected stable angina pectoris, no previous cardiac history, and

228 e of atrial fibrillation, renal dysfunction, stable angina pectoris, or advanced New York Heart Assoc

229 Eligible patients had stable angina pectoris, unstable angina pectoris, or non

230 -culprit plaques in patients presenting with stable angina pectoris, unstable angina pectoris,and ST-

231 (CAD), including acute coronary syndrome and stable angina pectoris, were independent predictors of M

232 s of sGPVI were observed in 10 patients with stable angina pectoris, with well-defined single vessel

233 s been approved for the treatment of chronic stable angina pectoris.

234 infarction, in chronic heart failure, and in stable angina pectoris.

235 sent with either acute coronary syndromes or stable angina pectoris.

236 pid CAD progression in patients with chronic stable angina pectoris.

237 dipine on long-term outcome in patients with stable angina pectoris.

238 differed between patients with unstable and stable angina pectoris.

239 ia and angina pectoris in most patients with stable angina pectoris.

240 in patients with ischemic heart disease and stable angina pectoris.

241 rs) effect adverse outcomes in patients with stable angina pectoris.

242 erance, symptoms and myocardial perfusion in stable angina pectoris.

243 long-term clinical outcomes in patients with stable angina pectoris.

244 confers prognostic benefit in patients with stable angina pectoris.

245 nd restenosis in patients undergoing PCI for stable angina pectoris.

246 In total, 23,860 patients underwent PCI for stable angina pectoris; of these, FFR guidance was used

247 eous Coronary Intervention for the Relief of Stable Angina) provided evidence for the role of percuta

248 e, prior myocardial infarction, unstable and stable angina, recent coronary artery bypass graft, and

249 l testosterone treatment in men with chronic stable angina reduces exercise-induced myocardial ischem

250 oaches to diagnose ischemia in patients with stable angina referred for invasive coronary angiography

251 diagnosis of acute infarction (Al) (n = 20), stable angina (SA) (n = 20), and unstable angina (UA) (n

252 gamma driven, patients with unstable (UA) or stable angina (SA) were compared for nuclear translocati

253 tion myocardial infarction (NSTEMI), 20 with stable angina (SA), and 20 controls.

254 going percutaneous coronary intervention for stable angina (SA), unstable angina (UA), or acute myoca

255 ts with UA (Braunwald's class IIIB) and with stable angina (SA).

256 with a model of preserved microcirculation (stable angina [SA] cohort: culprit and nonculprit vessel

257 coronary angiography for suspected CAD (432 stable angina [SA], 572 acute coronary syndrome [ACS]) w

258 For patients with chronic stable angina, several randomized trials have been perfo

259 HODS AND Patients referred for evaluation of stable angina symptoms underwent adenosine-stress dynami

260 ation of Ranolazine in Subjects With Chronic Stable Angina (TERISA) trial.

261 ation of Ranolazine in Subjects With Chronic Stable Angina [TERISA]; NCT01425359).

262 Ranolazine is an approved drug for chronic stable angina that acts by suppressing a noninactivating

263 s in asymptomatic adults or in patients with stable angina, the effect of statins on the markedly hei

264 In stable angina, the risk-adjusted OR for significant CAD

265 In a multinational cohort of patients with stable angina, the SAQ angina frequency domain was signi

266 efficacy of bypass surgery in patients with stable angina, there are relatively few studies that hav

267 placebo in patients with diabetes, CAD, and stable angina treated with 1 to 2 antianginals.

268 In patients with stable angina, two strategies are often used to guide re

269 FFR and all-cause mortality in patients with stable angina undergoing PCI.

270 procedural outcome measures in patients with stable angina undergoing percutaneous coronary intervent

271 tients with acute coronary syndrome (ACS) or stable angina underwent coronary 16-slice MDCT and invas

272 we included 1,379 consecutive patients with stable angina, unobstructed coronaries and ACH test perf

273 cal strata based on the indication for PTCA (stable angina, unstable angina and after myocardial infa

274 in all three presenting clinical syndromes (stable angina, unstable angina, and MI).

275 free of CHD at baseline and in patients with stable angina, unstable angina, or a history of myocardi

276 However, their role in stable angina versus unstable angina is less well define

277 atients with recent-onset chest pain in whom stable angina was suspected.

278 ation of Ranolazine in Subjects With Chronic Stable Angina) was an international, randomized, double-

279 ergoing directional coronary atherectomy for stable angina were analyzed for immunoreactivity for ET-

280 e angina and 15 specimens from patients with stable angina were analyzed.

281 Patients with ACS and those with stable angina were compared for the frequency of LCP at

282 S and stable lesions in patients with ACS or stable angina were determined.

283 Eighty-two patients with stable angina were randomized in a ratio of 1:1 to lesio

284 ents with a > or =3-month history of chronic stable angina were randomly assigned to receive ivabradi

285 Forty patients with stable angina were studied before and following percutan

286 Nearly 10 million US adults experience stable angina, which occurs when myocardial oxygen suppl

287 , coronary artery disease (CAD), and chronic stable angina who remain symptomatic despite treatment w

288 Among patients with stable angina who were receiving little or no antiangina

289 Twenty-six patients who had stable angina with thick-cap fibroatheroma treated by DE

290 Of these, 50 patients had chronic stable angina (with stable symptoms over 3 months), and

291 ents with systolic heart failure and chronic stable angina without clinically significant adverse eff

292 omputed tomography registry of patients with stable angina without prior myocardial infarction or rev