ライフサイエンスコーパス: CAD

1 with multivessel coronary artery disease (MV-CAD).

2 ry, and cognition in carotid artery disease (CAD).

3 atients with stable coronary artery disease (CAD).

4 without history of coronary artery disease (CAD).

5 r Disease (PVD) and Coronary Artery Disease (CAD).

6 ndicate obstructive coronary artery disease (CAD).

7 in the detection of coronary artery disease (CAD).

8 heimer's disease, but a lesser role than for CAD.

9 t guidance for the group without obstructive CAD.

10 e chronic inflammatory process that underpin CAD.

11 ical therapy for prevention and treatment of CAD.

12 lated 68 common targets shared by stroke and CAD.

13 ic model view on the genetic architecture of CAD.

14 with darker and lighter skin types who have CAD.

15 tized, many without an obvious connection to CAD.

16 eficiency is associated with protection from CAD.

17 stents) in diabetic patients with ACS and MV-CAD.

18 cular targets of coxibs for association with CAD.

19 igher serum calcium may increase the risk of CAD.

20 CTA in detecting hemodynamically significant CAD.

21 understanding of the genetic architecture of CAD.

22 ng women than men with severe multivessel/LM CAD.

23 was associated with lower mortality than MI-CAD.

24 to 13.9% of all gene sets to be involved in CAD.

25 l target for the prevention and treatment of CAD.

26 osis and suggest new therapeutic targets for CAD.

27 ver fat but decreased risks for both T2D and CAD.

28 of perfusion MR imaging in the detection of CAD.

29 and the presence as well as the severity of CAD.

30 ied 41% fewer patients as having significant CAD.

31 ile the effect of obesity appears to act via CAD.

32 in LT recipients, irrespective of underlying CAD.

33 score to predict the presence of significant CAD.

34 ted recently identified loci associated with CAD.

35 ncreasingly utilized in patients with milder CAD.

36 s likely to have higher grade or multivessel CAD.

37 on to men was restricted to patients with MI-CAD.

38 (CAD) may help reduce the societal burden of CAD.

39 CABG for patients with 3-vessel or left main CAD.

40 ing the presence of anatomically significant CAD.

41 fication of causative variants and genes for CAD.

42 deficiency is associated with lower risk for CAD.

43 37) occurred in patients with nonobstructive CAD (1%-69% stenosis).

44 tal mortality was lower after MINOCA than MI-CAD (1.1% versus 2.9%; P<0.0001).

45 ional assessment of coronary artery disease (CAD) ( 1 , 2 ).

46 In particular, an increased expression of Cad-11 can be detected on the plasma membrane of activat

47 pancreatitis and pancreatic cancer tissues, Cad-11 expression was significantly increased in PSCs an

48 Moreover, knockdown of Cad-11 in cancer cells reduced pancreatic cancer cell mi

49 er, our data underline the potential role of Cad-11 in PSC activation and pancreatic cancer metastasi

50 Cadherin-11 (Cad-11, also known as OB cadherin or CDH11) is a cell-to

51 atients being reported as having significant CAD (14%, 595 of 4347 vs 23%, 1000 of 4347; P < .001).

52 10.4%; severe CAD left untreated: 15.4%; no-CAD: 14.8%; P=0.765).

53 rty-six (84%) of 55 patients had significant CAD, 35 (64%) of 55 had acute thrombotic lesions, and 46

54 After excluding those with obstructive LM CAD, 5166 patients were categorized as having normal LM

55 Among patients with severe CAD, 53 patients (8.8%) underwent uncomplicated PCI.

56 cohort occurred in women without obstructive CAD, a condition often considered benign and without gui

57 endothelium-independent vasodilation in non-CAD adipose arterioles, which was reduced by paxilline,

58 k for events than men with nonobstructive LM CAD (adjusted hazard ratio, 1.78; P=0.017); sex-specific

59 ent predictors of mortality were obstructive CAD, age, baseline systolic blood pressure, history of d

60 The prevalence of coronary artery disease (CAD) among patients with refractory out-of-hospital (OH)

61 oci associated with coronary artery disease (CAD) among predominantly Europeans.

62 were 1.25 (95% CI, 1.08-1.45; P = .003) for CAD and 1.24 (95% CI, 1.05-1.46; P = .009) for myocardia

63 were ascertained in up to 21,980 people with CAD and 158,200 control subjects.

64 spine density was decreased significantly in CAD and AD compared to controls.

65 bly by enhancing the interactions between DE-Cad and alpha-Catenin.

66 positive association between the severity of CAD and CACS (P<0.001,r=0.781).

67 locus, and variants associated with risk of CAD and cholesterol levels.

68 as their quantities were determined by using CAD and DAD detectors.

69 ize the care of patients suspected of having CAD and improve outcomes while reducing overall health c

70 The association of each SNP with CAD and myocardial infarction was weighted by its associ

71 duals) that included cases (individuals with CAD and myocardial infarction) and noncases, with baseli

72 Co-primary outcomes were the odds of CAD and myocardial infarction.

73 levels was associated with increased risk of CAD and myocardial infarction.

74 Prevalence of obstructive CAD and myocardial ischemia was low (11.9% versus 12.7%,

75 ntegrated measure of large- and small-vessel CAD and myocardial ischemia, identifies patients at risk

76 We identified 64 novel genetic risk loci for CAD and performed fine mapping of all 161 risk loci to o

77 noninvasive method for direct assessment of CAD and plaque characterization with high diagnostic acc

78 to describe the prevalence and complexity of CAD and report survival to hospital discharge in patient

79 Multivessel CAD and residual uncontrolled risk factors are strongly

80 mputed tomographic angiography for suspected CAD and were followed for 5 years.

81 ally, we demonstrate that MAPPIN outperforms CADD and Eigen in predicting disease inheritance modes f

82 data, FATHMM-indel significantly outperforms CADD and GAVIN, state of the art models in assessing the

83 utagenesis allows full comparison with dicot CADs and elucidates the potential signature sequence for

84 etween the intake of calcium with vitamin D (CaD) and fracture risk.Data from 5823 white postmenopaus

85 on in patients with coronary artery disease (CAD) and investigate the effects of human L5 on the elec

86 levels and risk of coronary artery disease (CAD) and myocardial infarction using mendelian randomiza

87 free controls, 8 controls with AD pathology (CAD), and 21 AD cases.

88 lerotic CVD (ACVD), coronary artery disease (CAD), and stroke.

89 rable to angiogram group without obstructive CAD, and both control group I and control group II (P =

90 ients based on presence, severity, extent of CAD, and cardiac events within 90 days of LT.

91 farction when compared with patients without CAD, and patients with severe CAD left untreated (TAVR+P

92 sis) left main (LM) coronary artery disease (CAD) are at high risk for adverse events; prior studies

93 n isolated vascular smooth muscle cells from CAD arterioles, although mRNA or total cellular protein

94 licative interaction between the BMD-GRS and CaD assignment (P-interaction = 0.01).

95 Whether the risk of CAD associated with lifelong genetic exposure to increas

96 We identified 25 new SNP-CAD associations (P < 5 x 10(-8), in fixed-effects meta-

97 nse SNP, rs2075291, in APOA5 associated with CAD at a genome-wide significance level and provided new

98 a negative association of CXCL5 levels with CAD at an odds ratio (OR) of 0.46 (95% CI, 0.27-0.75).

99 1-2, > 2 segments, P = 0.304) and extent of CAD based on Reardon score (0, 1-9, >10, P = 0.224), com

100 17), we studied angiographic progression of CAD between baseline (pretransplant) and follow-up at 7

101 rol levels, risk of coronary artery disease (CAD), body mass index, as well as risk of asthma.

102 were reduced significantly in AD compared to CAD brains, whereas stubby spine density was decreased s

103 Photocontact allergy occurs in CAD but is less studied than contact allergy in this exq

104 One hundred eight patients with symptomatic CAD but no dementia were included, and a score less than

105 ls in subjects with coronary artery disease (CAD), but its mechanisms of action in subjects without C

106 commonly because of a finding of significant CAD by site but not by core laboratory interpretation (8

107 e level of vascular endothelial cadherin (VE-Cad) by inhibiting VE-Cad endocytosis.

108 In diabetic patients with MV-CAD, CABG was associated with a lower rate of long-term

109 rt period of time, due to physical strength, CAD/CAM fabrication, and low cost.

110 By CAD/CAM technique, it can correct jaw deformities simult

111 utments veneered with pressed ceramics or on CAD/CAM zirconia abutments veneered with hand buildup te

112 The computer-aided design and manufacture (CAD/CAM) technique was used to guide bony mass removal a

113 ion in substrate specificity and activity of CAD can result in significant changes in overall composi

114 er, the association remains significant in a CAD case control population matched for age and sex.

115 analytic sample of 184305 individuals (60801 CAD cases [approximately 70% with myocardial infarction]

116 < 5 x 10(-8)) were further evaluated in 291 CAD cases and 1,848 controls of Asian Indians.

117 ipants previously genotyped, totaling 88,192 CAD cases and 162,544 controls.

118 kb regions surrounding these genes in 84,813 CAD cases and 202,543 controls.

119 ed a genome-wide association study in 34 541 CAD cases and 261 984 controls of UK Biobank resource fo

120 studies and one Malay study (Total N = 2,169 CAD cases and 7,376 controls).

121 Spine density was similar among control and CAD cases but was reduced significantly in AD.

122 Increased spine extent distinguished CAD cases from controls and AD.

123 Cinnamyl alcohol dehydrogenase (CAD) catalyzes the final step in monolignol biosynthesis

124 e susceptibility to coronary artery disease (CAD), cigarettes smoked per day, lung cancer, insulin re

125 DNN-CAD classified polyps with perfect intra-observer agreem

126 This first crystal structure of a monocot CAD combined with enzyme kinetic data and a catalytic mo

127 her and correlated with QTc in patients with CAD compared to controls.

128 xed restorations from computer-aided design (CAD)/computer-aided manufacturing (CAM)-fabricated high-

129 nd December 2012 in patients with history of CAD defined as having previous myocardial infarction, pe

130 density lipoprotein cholesterol, multivessel CAD, diabetes with glycosylated hemoglobin >7%, and pers

131 Severity or extent of CAD does not impact post-LT survival, if appropriately r

132 ad mutant or an endocytic-defective Y658F-VE-Cad double mutant were both able to rescue TEER independ

133 reduced the biosynthetic turnover rate of DE-Cad during apical-basal polarization, and such biosynthe

134 dothelial cadherin (VE-Cad) by inhibiting VE-Cad endocytosis.

135 extensive array of Drosophila E-Cadherin (DE-Cad) endogenous knock-in alleles that carry mutations ta

136 based on reactions with TMMS and one or two CAD experiments.

137 k score in analysis of risks and benefits of CaD for bone.

138 ocytosis mediated by p120 is required for VE-Cad formation of a restrictive barrier, we restored VE-C

139 e, 58 [9] years), 92 (44.2%) had significant CAD (fractional flow reserve </=0.80).

140 The collision-activated dissociation (CAD) fragmentation patterns (obtained in MS(2) and MS(3)

141 for photosensitivity who were diagnosed with CAD from November 1, 2000, through August 31, 2015, at t

142 Among the 60 CAD genes, the strongest association was with NBEAL1 tha

143 In analysis limited to 60 CAD genes, we detected strong associations with COL4A2/C

144 This study aims to identify new CAD genetic loci through a large-scale linkage analysis

145 rall, patient survival in the revascularized CAD group was comparable to angiogram group without obst

146 rformed in 1126 patients, showed obstructive CAD (>/=50% stenosis) in 814 patients and severe CAD (>/

147 han 50% stenosis, 29 (33.3%) had obstructive CAD (>/=50% stenosis), 7 (8%) with single-vessel disease

148 (>/=50% stenosis) in 814 patients and severe CAD (>/=70% stenosis) in 708 patients.

149 The proportion of severe CAD (>/=70% stenosis) was lower in patients who had hype

150 group analysis, women with nonobstructive LM CAD had a nearly 80% higher risk for events than men wit

151 n studies (GWAS) in coronary artery disease (CAD) had identified 66 loci at 'genome-wide significance

152 vessel or left main coronary artery disease (CAD) had improved long-term outcomes with coronary arter

153 s of SPECT studies among patients with known CAD have not been evaluated previously.

154 lithia-based glass-ceramics (e.g., IPS e.max CAD HT).

155 led 4,184 unselected outpatients with stable CAD (i.e., MI or coronary revascularization >1 year prev

156 In the test set, the DNN-CAD identified neoplastic or hyperplastic polyps with 96

157 were protected from coronary artery disease (CAD); (ii) excluding the CETP locus, there was not a pre

158 a significantly lower burden of obstructive CAD in comparison with men but were not protected from C

159 ammation associated with atherosclerosis and CAD in men.

160 among patients with diabetes mellitus and MV-CAD in residents of British Columbia, Canada.

161 thways contributing to the susceptibility to CAD in the multi-ethnic populations from Southeast Asia.

162 f rs3811047 is significantly associated with CAD in two independent populations under a recessive mod

163 n association analysis between rs3811047 and CAD in two independent populations with 2,501 patients a

164 hances the recruitment of beta-Catenin by DE-Cad in vivo Moreover, phosphorylation potential of the s

165 Clinicians should thus be cognizant of CAD in younger women with darker skin types.

166 nce and severity of coronary artery disease (CAD) in patients with sign and symptoms of the disease.

167 1; 95% CI: 1.25, 1.61) and greatly increased CAD incidence (sub-HR: 1.64; 95% CI: 1.39, 1.93) compare

168 cance of nonobstructive (1%-49% stenosis) LM CAD, including sex-specific differences, has not been pr

169 SPECT utilization in patients with previous CAD increased between 1992 and 2003, but then decreased

170 r BMD-GRS.We observed significant effects of CaD intake on fracture risk only in women with the lowes

171 , the seventh member of the IL-1 family, and CAD is unknown.

172 Coronary artery disease (CAD) is a chronic inflammatory disease.

173 Coronary artery disease (CAD) is a leading cause of morbidity and mortality world

174 Coronary artery disease (CAD) is a significant problem during evaluation for live

175 osis of significant coronary artery disease (CAD) is ambiguous, but nuclear myocardial perfusion imag

176 Chronic actinic dermatitis (CAD) is classically described in older, white men, altho

177 en, yet obstructive coronary artery disease (CAD) is less prevalent in women.

178 Coronary artery disease (CAD) is the number one cause of death worldwide and invo

179 ncy reduces risk of coronary artery disease (CAD) is unknown.

180 As SbCAD4 is the only major CAD isoform in bmr6 mutants, replacing SbCAD4 with L119W

181 Our in-depth characterization of two major CAD isoforms, SbCAD2 (Brown midrib 6 [bmr6]) and SbCAD4,

182 for both stroke and coronary artery disease (CAD), its underlying common molecular mechanisms remain

183 tients without CAD, and patients with severe CAD left untreated (TAVR+PCI: 10.4%; severe CAD left unt

184 CAD left untreated (TAVR+PCI: 10.4%; severe CAD left untreated: 15.4%; no-CAD: 14.8%; P=0.765).

185 whereas overexpression of p120 increases VE-Cad levels and promotes a more restrictive monolayer.

186 ion of a restrictive barrier, we restored VE-Cad levels using an endocytic-defective VE-Cad mutant.

187 Loss of p120 results in a decrease in VE-Cad levels, leading to the formation of monolayers with

188 idual families confirmed the six significant CAD loci and identified seven new highly significant lin

189 Fine mapping of the 161 CAD loci generated lists of credible sets of single caus

190 Two highly significant CAD loci were identified on chromosome 17q21.2 (NPL scor

191 e, SPK recipients had similar progression of CAD long-term compared with LDK recipients.

192 deaths occurred in women without obstructive CAD (<50% stenosis).

193 The high mortality associated with CAD makes the development of medical interventions that

194 ict the presence of coronary artery disease (CAD) may help reduce the societal burden of CAD.

195 FR, particularly absent severely obstructive CAD, may represent a novel target for CVD risk reduction

196 ive approaches such as Condel, CoVEC, CAROL, CADD, MetaSVM and MetaLR using an independent validation

197 ed to large extensively genotyped studies of CAD, MI, diabetes, lipids, glycaemic traits and adiposit

198 ality decline was observed in either ACVD or CAD mortality rates after 2002.

199 In addition, expression of a Y658F-VE-Cad mutant or an endocytic-defective Y658F-VE-Cad double

200 E-Cad levels using an endocytic-defective VE-Cad mutant.

201 ization, and such biosynthetically stable DE-Cad mutants specifically rescued the polarity defects in

202 ad a higher risk of coronary artery disease (CAD), myocardial infarction (MI) and their risk factors.

203 its mechanisms of action in subjects without CAD (non-CAD) when compared with those with CAD remain u

204 artile range [IQR], 9.1-11.5) progression of CAD occurred at similar rates (10 of 21 cases in the SPK

205 se in calcium was positively associated with CAD (odds ratio (OR) 1.49, 95% confidence interval (CI)

206 s associated with a 34% reduction in odds of CAD (odds ratio: 0.66; 95% confidence interval: 0.44 to

207 CAD of latter products (MS(4) experiments) resulted in e

208 Collisionally activated dissociation (CAD) of these methanol-eliminated adduct ions (MS(3) exp

209 tratified analysis, the protective effect of CaD on fracture risk was observed in women in the lowest

210 served no interaction between the Fx-GRS and CaD on fracture risk; however, we observed a significant

211 ents were compared by sex and CAD status (MI-CAD or MINOCA).

212 portant role in microvascular dysfunction in CAD or other vascular diseases.

213 lysis using 13 SNPs showed a higher risk for CAD (OR 1.87, 95% CI 1.14-3.08).

214 24.8; p < 0.001), and those with no previous CAD (OR: 8.67; p < 0.001).

215 In stable CAD outpatients, incident MI occurs at a stable rate of

216 ted factors, and related mortality in stable CAD outpatients.

217 spective of prerevascularization severity of CAD (P = 0.357), number of segments involved (0, 1-2, >

218 rdial infarction, and burden of angiographic CAD (P<0.001), they demonstrated greater risk of CVD eve

219 d a higher frequency of severely obstructive CAD (P=0.002).

220 erapy on circulating inflammation markers in CAD patients.

221 nd other circulating inflammation markers in CAD patients.

222 ovascular events in coronary artery disease (CAD) patients and reducing the hs-CRP level may further

223 loss of p120 binding results in increased VE-Cad phosphorylation.

224 Firstly, four methods (CADD, PolyPhen-2, SIFT, and SNAP2) agreed within 10 perc

225 imal cutoff point for discriminating between CAD (presence of stenosis) and the non-stenosis conditio

226 re identified that, when combined with their CAD products (MS(3) experiments), can be used to sequenc

227 angiographic CAD were estimated by using the CAD prognostic index, and CFR was quantified by using po

228 The accuracy of CAD quantification was most significantly improved for h

229 sal women from the Women's Health Initiative CaD randomized trial were included.

230 lative to 1990-2001, atherosclerotic CVD and CAD rates began to decline more rapidly during the 2002-

231 CAD (non-CAD) when compared with those with CAD remain unknown.

232 es different K(+) channels in non-CAD versus CAD, resulting in an altered capacity for vasodilation d

233 genes affected by coxibs and those mediating CAD risk and points to further mechanisms, which are pot

234 was to narrow potential mechanisms affecting CAD risk as we hypothesized that the affected genes may

235 The association between CACS and different CAD risk factors was determined as well.

236 potentially responsible for coxib-associated CAD risk.

237 fects and increased coronary artery disease (CAD) risk.

238 ct via coronary angiography by calculating a CAD score.

239 Three of the four tumors harbored genes with CADD scores >/=20, indicative of mutations associated wi

240 A total of 604 patients undergoing CAD screening at the time of TAVR procedure were prospec

241 timized approach to coronary artery disease (CAD) screening and management in patients undergoing tra

242 r discriminating between different levels of CAD severity (<70%).

243 ive trait loci of genes correlated with both CAD severity and circulating CXCL5 levels.

244 Coronary artery disease (CAD) severity was quantified in each subject via coronar

245 uggest that among patients with a history of CAD, SPECT was being increasingly utilized in patients w

246 hospital treatments were compared by sex and CAD status (MI-CAD or MINOCA).

247 lationship between age, sex, and obstructive CAD status and outcomes post-MI has not been established

248 ular outcomes were analyzed by age, sex, and CAD status.

249 In arterioles from CAD subjects, H2O2-induced dilation was significantly re

250 e SNP (rs2075291, G > T, G185C) in APOA5 for CAD that reached robust genome-wide significance (Meta P

251 (13.8%), coronary angiography showed severe CAD that was left untreated.

252 and diagnostic time were compared among DNN-CAD, the novice endoscopists, and the expert endoscopist

253 ND When invasive coronary angiography showed CAD, the treatment strategy and completeness of revascul

254 SERMs, even the cationic amphiphilic drugs (CADs), this mechanism led to the endolysosomal calcium a

255 tality and incident coronary artery disease (CAD).This study followed 130,473 UK Biobank participants

256 harmacological efficacies on both stroke and CAD through multi-ingredient, multi-target, multi-functi

257 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, i

258 ed 1,800 patients with 3-vessel or left main CAD to either CABG or DES-PCI.

259 We developed a system called DNN-CAD to identify neoplastic or hyperplastic colorectal po

260 20 also allows the phosphorylated form of VE-Cad to participate in the formation of a restrictive mon

261 g mechanism linking DHI's role in stroke and CAD treatment was inflammatory response in the process o

262 rmacological mechanisms of DHI on stroke and CAD treatment.

263 wn, HDPDL1 exhibited no antitumor effect and CAd-VECPDL1 alone reduced tumors only to volumes compara

264 ty of local production of PD-L1 mini-body by CAd-VECPDL1 combined with administration of tumor-direct

265 efits of locally produced PD-L1 mini-body by CAd-VECPDL1 could not be replicated by infusion of anti-

266 However, combining CAd-VECPDL1 with HER2.CAR T cells enhanced antitumor act

267 Coadministration of these agents (CAd-VECPDL1) exhibited oncolytic effects with production

268 tion involves different K(+) channels in non-CAD versus CAD, resulting in an altered capacity for vas

269 investigations for coronary artery disease (CAD) (viewed as a positive control) and Alzheimer's dise

270 D printing translates computer-aided design (CAD) virtual 3D models into physical objects.

271 ed to test the diagnostic ability of the DNN-CAD vs endoscopists (2 expert and 4 novice), who were as

272 Results The prevalence of CAD was 39% (36 of 92) according to QCA and SPECT and 64

273 CAD was assessed by (1) vessel score (>/=50% reduction i

274 Significant CAD was defined as stenosis greater than or equal to 50%

275 Severe CAD was found in 136 patients (22.5%).

276 Nonobstructive LM CAD was frequently detected on coronary computed tomogra

277 er risk of post-MI death among women with MI-CAD was most pronounced at younger ages.

278 Complex but treatable CAD was prevalent in patients with refractory OH VF/VT c

279 e involvement of known canonical pathways in CAD was tested by Ingenuity Pathway Analysis.

280 ODS AND Obstructive coronary artery disease (CAD) was defined as >/=50% stenosis on angiography by co

281 raphy (HPLC) with charged aerosol detection (CAD) was investigated for 50 compounds with a wide range

282 Comorbid coronary artery disease (CAD) was present in 24.3% of visits.

283 The extent and severity of angiographic CAD were estimated by using the CAD prognostic index, an

284 Genetic risk variants of CAD were linked to development of atrial fibrillation, h

285 or patients with PAD alone, comorbid PAD and CAD were more likely to be prescribed antiplatelet thera

286 Patients with darker skin types and CAD were younger at diagnosis (mean [SD] age, 40.7 [3.5]

287 ity for obstructive coronary artery disease (CAD) were randomly assigned to functional testing (exerc

288 nisms of action in subjects without CAD (non-CAD) when compared with those with CAD remain unknown.

289 fect progression of coronary artery disease (CAD) when compared with transplantation of a kidney-alon

290 showed a higher frequency of nonobstructive CAD, whereas men showed a higher frequency of severely o

291 fat, higher risk for T2D, and lower risk for CAD, whereas TG-lowering alleles involved in peripheral

292 rioles, H2O2-induced dilation is impaired in CAD, which is associated with a transition from a combin

293 t that IL37 is a new susceptibility gene for CAD, which provides a potential target for the preventio

294 ibute to cognitive impairment in symptomatic CAD, which suggests that subcortical disconnection withi

295 study involving 208 patients with suspected CAD who underwent CCTA, technetium 99m/tetrofosmin-label

296 There were 19 373 patients with a history of CAD who underwent SPECT between 1991 and 2012 (mean age,

297 levels allowed for identifying or excluding CAD with >90% predictive value in 42% of subjects.

298 In patients undergoing TAVR, screening of CAD with invasive coronary angiography and ad hoc PCI du

299 esting should be considered in patients with CAD, with coexistent photocontact allergy occurring in a

300 Among patients with MI-CAD, women had higher mortality than men (3.9% versus 2.