ライフサイエンスコーパス: forced vital capacity

1 ssociated also with airway obstruction (FEV1/forced vital capacity).

2 ced expiratory volume in 1 second (FEV1) and forced vital capacity.

3 sustained improvement in skin thickness and forced vital capacity.

4 ung dysfunction based on predicted values of forced vital capacity.

5 fy long-term associations of pollutants with forced vital capacity.

6 ree-quarters of these abnormalities were low forced vital capacity.

7 nctional rating scale and measurement of the forced vital capacity.

8 ization of strength and a slight increase in forced vital capacity.

9 A similar pattern emerged for forced vital capacity.

10 Similar results were obtained for forced vital capacity.

11 ed with lung injury score and inversely with forced vital capacity.

12 ator forced expiratory flow at 25% to 75% of forced vital capacity.

13 nd we found some evidence of less decline in forced vital capacity.

14 - 19 mL; P = 1.1 x 10(-5), respectively) and forced vital capacity (-100 +/- 21 mL; P = 2.7 x 10(-6)

15 7%, 95% confidence interval: -5.2, -0.1) and forced vital capacity (-2.4%, 95% confidence interval: -

16 with low magnesium intake showed deficits in forced vital capacity (-2.8%, 95% confidence interval: -

17 patients up to 48 weeks post-ART initiation (forced vital capacity, 206 mL higher; 95% confidence int

18 piratory volume in 1 second (FEV1) (388 mL), forced vital capacity (298 mL), and the FEV1/forced vita

19 S had significantly lower percent predicted: forced vital capacity (61.5+/-16 versus 80.5+/-14; P<0.0

20 4 [52%] women; mean age 66.1 years [SD 9.3]; forced vital capacity 83.7% [SD 14.2]; diffusing capacit

21 5.2 +/- 4.6 vs. 88.4 +/- 5.6%; P = 0.03) and forced vital capacity (83.2 +/- 4.7 vs. 109.2 +/- 6.0%;

22 centage of predicted values and were 92% for forced vital capacity, 93% for forced expiratory volume

23 ls) were associated with a 2.4% decrement in forced vital capacity (95% confidence interval (CI): -4.

24 forced vital capacity, and 6-month change in forced vital capacity, a decrease in forced vital capaci

25 o phenotypes used to assess asthma severity: forced vital capacity, a sensitive measure of airway obs

26 5% to 75% of forced vital capacity, and FEV1/forced vital capacity (all P < .0001).

27 mediated 13% to 20% of the association with forced vital capacity and 29% to 42% of the association

28 0% of children were able to produce a second forced vital capacity and a second forced expired volume

29 ts negatively and positively correlated with forced vital capacity and age, respectively.

30 disease extent, and the percentage predicted forced vital capacity and carbon monoxide diffusing capa

31 ulmonary fibrosis as determined by change in forced vital capacity and death.

32 Forced vital capacity and diffusing capacity for carbon

33 vitamin C, were associated with deficits in forced vital capacity and FEV1 in boys.

34 OH)D was associated with lower mean residual forced vital capacity and forced expiratory volume in 1

35 We observed a modest reduction in forced vital capacity and forced expiratory volume in on

36 t respiratory-related events, lung function (forced vital capacity and gas transfer), and patient-rep

37 Forced vital capacity and mid-expiratory flow did not si

38 The rate of progression of the forced vital capacity and of the ALS Functional Rating S

39 ated with increased airflow limitation (FEV1/forced vital capacity and residual volume/total lung cap

40 ation was associated with a decrease in FVC (forced vital capacity) and FEV1 (forced expiratory volum

41 diagnosis, gender, smoking history, baseline forced vital capacity, and 6-month change in forced vita

42 ciated with a decreased total lung capacity, forced vital capacity, and diffusing capacity for carbon

43 Spirometric outcomes (FEV(1), forced vital capacity, and FEV(1)/forced vital capacity

44 EV1, forced expiratory flow at 25% to 75% of forced vital capacity, and FEV1/forced vital capacity (a

45 t predicted FEV1 [ppFEV1], percent predicted forced vital capacity, and FEV1/forced vital capacity ra

46 is inadequate and functional rating scales, forced vital capacity, and patient survival have been th

47 ced expiratory volume in 1 second (FEV1) and forced vital capacity, and the 10-year incidence of coro

48 forced expiratory volume in 1 second (FEV1), forced vital capacity, and total lung capacity were cate

49 The primary endpoint, change in forced vital capacity as a percentage of the predicted n

50 ith forced expiratory volume in 1 second and forced vital capacity as the percentage of the predicted

51 of forced expiratory volume in 1 second and forced vital capacity as the percentage of the predicted

52 For example, the decrease in forced vital capacity associated with a 70-ppb/month gre

53 in forced expiratory volume in 1 second and forced vital capacity associated with a decrease of 1 st

54 01), and 3 years (27 patients; p<0.0001) and forced vital capacity at 1 year (58 patients; p=0.009),

55 ebo group had a decline in percent predicted forced vital capacity at 48 weeks (p=0.0373).

56 ratio of forced expiratory volume at 1 s to forced vital capacity at age 22 years.

57 %, A/C 5.2%, and C/C 9.5%; p = 0.003), lower forced vital capacity at diagnosis (median percentage A/

58 Forced vital capacity at F-FDG PET/CT inversely correlat

59 either signal associated with FEV(1), FEV(1)/forced vital capacity, atopy, and age of asthma onset.

60 ced expiratory volume in 1 second (FEV1) and forced vital capacity below 0.7.

61 ciated with reduced prebronchodilator FEV(1)/forced vital capacity (beta coefficient, -0.10; 95% CI,

62 ose with initial mRSS >14) or an increase in forced vital capacity by more than 10%.

63 related myopathies by analysing longitudinal forced vital capacity data in a large international coho

64 a statistically significant increase in ALS-forced vital capacity decline in SOD1(A4V) compared with

65 lity were similar in all 3 groups, while the forced vital capacity decreased significantly in the rel

66 >25% increase in mRSS or decrease of >10% in forced vital capacity) despite treatment with cyclophosp

67 ate pregnancy was negatively associated with forced vital capacity (difference in standard deviation

68 disease activity, pulmonary function tests (forced vital capacity, diffusing capacity for carbon mon

69 and lung involvement in SSc, as well as the forced vital capacity, diffusing capacity for carbon mon

70 ere examined together with 6-month change in forced vital capacity, diffusing capacity for carbon mon

71 B with survival was independent of age, sex, forced vital capacity, diffusing capacity of carbon mono

72 rkers of disease severity, including a lower forced vital capacity, diffusion capacity for carbon mon

73 s the change in longitudinal measurements of forced vital capacity during a 60-week treatment period.

74 d expiratory flow between 25% and 75% of the forced vital capacity (FEF(25-75)) (-16.2%, 95% confiden

75 orced expiratory flow between 25% and 75% of forced vital capacity (FEF(25-75)), -5.5%, 95% CI: -10.5

76 ed midexpiratory flow between 25% and 75% of forced vital capacity (FEF(25-75)), 48%; total airway re

77 d lower forced expiratory flow at 75% of the forced vital capacity (FEF(75)) (-8.3%, 95% confidence i

78 ed midexpiratory flow between 25% and 75% of forced vital capacity (FEF25-75) was associated with the

79 Forced expiratory volume in 1 s/forced vital capacity (FEV(1)/FVC) but not FVC was relat

80 of forced expiratory volume in 1 second over forced vital capacity (FEV(1)/FVC) was measured in 4,267

81 n the first second (FEV(1)) and its ratio to forced vital capacity (FEV(1)/FVC), an indicator of airf

82 e second (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FEV(1)/FVC).

83 p = 2.3 x 10(-8)) and the ratio of FEV(1) to forced vital capacity (FEV(1)/FVC: r(g) = 0.137, p = 2.0

84 o of forced expiratory volume in 1 second to forced vital capacity (FEV(1):FVC ratio; pulmonary), hem

85 olume in 1 s (FEV1) and the ratio of FEV1 to forced vital capacity (FEV1/FVC) in the general populati

86 teria, based on the forced expiratory volume/forced vital capacity (FEV1/FVC) ratio and then using th

87 expiratory volume in the first second to the forced vital capacity (FEV1:FVC) of less than 0.70, yet

88 s at V2 was negatively correlated with FEV1, forced vital capacity, FEV1/forced vital capacity ratio,

89 percentile) was associated with deficits in forced vital capacity for both boys and girls and with d

90 Pulmonary parameters of response included forced vital capacity, forced expiratory volume in 1 sec

91 nt from baseline to 12 months in measures of forced vital capacity, functional residual capacity, ser

92 one-second forced expiratory volume (FEV1%), forced vital capacity (FVC%), and the FEV1/FVC ratio.

93 mild restrictive spirometric pattern [60 <= forced vital capacity (FVC) < 80% predicted] vs. 21.2% w

94 d for 10 pack-years or more, and had an FEV1/forced vital capacity (FVC) <0.7.

95 that correlated with the absolute change in forced vital capacity (FVC) (% predicted values) and the

96 concentrations were associated with maximum forced vital capacity (FVC) (P </= 0.01) and forced expi

97 EV(1)) (p for trend < 0.001), 55.2-ml higher forced vital capacity (FVC) (p = 0.001), 0.4% higher FEV

98 point required 12% or greater improvement in forced vital capacity (FVC) and 1 point or greater decre

99 me measures were change in percent predicted forced vital capacity (FVC) and change in single-breath

100 ed Expiratory Volume in one second (FEV(1)), Forced Vital Capacity (FVC) and FEV(1)/FVC).

101 gain between 3 and 7 years of age and higher forced vital capacity (FVC) and FEV1 values at age 15 ye

102 n of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC with 1000 Genom

103 We assessed lung function by measuring forced vital capacity (FVC) and forced expiratory volume

104 as characterized by the spirometric measures forced vital capacity (FVC) and forced expiratory volume

105 ns had significantly lower percent predicted forced vital capacity (FVC) and forced expiratory volume

106 y reduced decline in percentage of predicted forced vital capacity (FVC) and stabilised 6-min walking

107 is performing forced respiratory cycles, the Forced Vital Capacity (FVC) and the Forced Expiratory Vo

108 Forced vital capacity (FVC) and total lung capacity (TLC

109 y volume in 1 second (FEV1) and its ratio to forced vital capacity (FVC) are used in the diagnosis an

110 The primary outcome was estimated change in forced vital capacity (FVC) at 30 weeks (mean follow-up)

111 endpoint was change in percentage predicted forced vital capacity (FVC) at week 72.

112 Similar associations were seen for forced vital capacity (FVC) but not for the FEV(1):FVC r

113 year, was defined as a decrease in predicted forced vital capacity (FVC) by 10% or more, a decrease i

114 CNV association (discovery P = 0.0007) with Forced Vital Capacity (FVC) downstream of BANP on chromo

115 ced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) during that period (referred

116 g forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) have been reported.

117 ance was negatively associated with FEV1 and forced vital capacity (FVC) in adolescents with and with

118 This resulted from a lower forced vital capacity (FVC) in HIV-infected participants

119 riants associated with FEV1 and its ratio to forced vital capacity (FVC) in never-smokers.

120 ancestry is associated with lower FEV(1) and forced vital capacity (FVC) in Puerto Rican children ind

121 e in 1 s (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FVC) in the SpiroMeta consortium

122 SAMS scores were associated with changes in forced vital capacity (FVC) in two cohorts.

123 EV1) increased by 118+/-330 ml (P=0.06), the forced vital capacity (FVC) increased by 390+/-570 ml (P

124 Change in forced vital capacity (FVC) is widely accepted as a surr

125 We recruited 20 SSc patients with a forced vital capacity (FVC) of <85% predicted, dyspnea o

126 alue, a ratio of post-bronchodilator FEV1 to forced vital capacity (FVC) of 0.70 or less, a smoking h

127 xacerbation, lung transplant, or decrease in forced vital capacity (FVC) of 10% or greater or decreas

128 sing unclassifiable ILD, a percent predicted forced vital capacity (FVC) of 45% or higher and percent

129 lmonary fibrosis and percentage of predicted forced vital capacity (FVC) of 55% or greater were enrol

130 ter bronchodilation and a ratio of FEV(1) to forced vital capacity (FVC) of 70% or less.

131 lmonary fibrosis within the past 3 years and forced vital capacity (FVC) of 80% predicted or higher w

132 n American Thoracic Association guidelines), forced vital capacity (FVC) of at least 45%, 6MWD of 150

133 rced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) of less than 0.70 as assesse

134 COPD was defined as FEV1/forced vital capacity (FVC) of less than 70% and less th

135 iltrate or FF scores and greater declines in forced vital capacity (FVC) or DL(CO) at 6 months.

136 e progression, as measured by the decline in forced vital capacity (FVC) or vital capacity, in patien

137 The primary outcome was the change in forced vital capacity (FVC) over a 60-week period.

138 ed with PEA showed a lower decrease in their forced vital capacity (FVC) over time as compared with u

139 bject pollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted, FEV1/FVC

140 ssociation of alpha-T levels with FEV(1) and forced vital capacity (FVC) percent predicted.

141 forced expiratory volume in 1-second (FEV1)/forced vital capacity (FVC) ratio <0.7.

142 ume in 1 second (FEV(1)) (r = -0.68), FEV(1)/forced vital capacity (FVC) ratio (r = -0.74) (P < .001)

143 ), although the correlation between the FEV1/forced vital capacity (FVC) ratio and 129Xe VDP (r=-0.95

144 The degree of FEV(1)/forced vital capacity (FVC) ratio impairment was the lar

145 The FEV1/forced vital capacity (FVC) ratio is used as a criterion

146 orced expiratory volume in 1 second (FEV(1))/forced vital capacity (FVC) ratio with increasing age wa

147 unger gestational age had a lower FEV1, FEV1/forced vital capacity (FVC) ratio, and forced expiratory

148 ed expiratory volume in 1 second (FEV(1)) to forced vital capacity (FVC) ratio, those with chronic ob

149 -related decrease in FEV(1) and its ratio to forced vital capacity (FVC) stratified a priori by asthm

150 I < 22.5) and obese (BMI > or = 30) men, but forced vital capacity (FVC) tended to decrease with incr

151 expiratory volume in 1 second (FEV(1)) and a forced vital capacity (FVC) that were significantly high

152 n forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) under the lower limit of nor

153 Forced vital capacity (FVC) was associated with moderate

154 , 398.4; p < 0.001) and the average adjusted forced vital capacity (FVC) was reduced by 287.8 ml (95%

155 ced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) were lower in the HIV+ compa

156 truction phenotype (A Trpg) was defined as a forced vital capacity (FVC) z score of less than -1.64 o

157 Forced vital capacity (FVC), a spirometric measure of pu

158 forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and 6-minute walk distance.

159 enome-wide association study (GWAS) of FEV1, forced vital capacity (FVC), and FEV1/FVC in 1144 Hutter

160 de polymorphisms in 15 genes with TEW, FEV1, forced vital capacity (FVC), and FEV1/FVC ratio was stud

161 rced expiratory volume in 1 second (FEV(1)), forced vital capacity (FVC), and forced expiratory flow

162 were forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and forced expiratory flow

163 icantly correlated with vital capacity (VC), forced vital capacity (FVC), and forced expiratory volum

164 Forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and physical activity were

165 rced expiratory volume in 1 second (FEV(1)), forced vital capacity (FVC), and ratio of FEV(1) to FVC.

166 ory volume in 1 s (FEV(1), primary outcome), forced vital capacity (FVC), and respiratory or allergic

167 forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and their ratio (FEV1:FVC).

168 end point was the annual rate of decline in forced vital capacity (FVC), assessed over a 52-week per

169 Exploratory efficacy measurements included forced vital capacity (FVC), carbon monoxide diffusing c

170 ditional associations with percent predicted forced vital capacity (FVC), FEV(1)/FVC ratio, and PC(20

171 with forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), FEV1/FVC, and diffusing cap

172 We measured forced vital capacity (FVC), forced expiratory volume in

173 Secondary outcome measures were forced vital capacity (FVC), manual muscle testing (MMT)

174 ced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC), obtained by spirometry, wer

175 orced expiratory volume in 1 sec (FEV(1)) or forced vital capacity (FVC), or both, after administrati

176 Lung function parameters (forced vital capacity (FVC), pre- and postbronchodilator

177 Eligible patients, stratified by baseline forced vital capacity (FVC), serum LOXL2 (sLOXL2) concen

178 Forced vital capacity (FVC), the forced expiratory flow

179 tion, measured using percentage of predicted forced vital capacity (FVC).

180 end point was the annual rate of decline in forced vital capacity (FVC).

181 th older age, being HIV+, and having reduced forced vital capacity (FVC).

182 d expiratory volume in one-second (FEV1) and forced vital capacity (FVC).

183 expiratory volume in one second (FEV1 ) and forced vital capacity (FVC)] (n = 414).

184 [forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC)] was measured at 2 and up to

185 y volume in the first second (FEV(1), %) and forced vital capacity (FVC, %) values.

186 irst year, and the primary end point was the forced vital capacity (FVC, expressed as a percentage of

187 of forced expiratory volume in 1 s [FEV1] to forced vital capacity [FVC] <70%, bronchodilator reversi

188 Spirometry (forced vital capacity [FVC] and forced expiratory volume

189 es, and physiologic parameters of breathing (forced vital capacity [FVC] and single-breath diffusing

190 or forced expiratory volume in 1 s [FEV1] to forced vital capacity [FVC] ratio <0.7 in patients with

191 ion (defined as a post-bronchodilator FEV(1)/forced vital capacity [FVC] ratio <=0.70) and a speciali

192 have the greatest decline in lung function (forced vital capacity [FVC]% predicted) in the early yea

193 ratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wav

194 n 1 second [FEV(1)], percentage of predicted forced vital capacity [FVC]) results were compared by us

195 Measures of lung function (FEV1, forced vital capacity [FVC], and forced expiratory flow

196 forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], and peak expiratory flow ra

197 t data on expiratory flow variables (FEV(1), forced vital capacity [FVC], FEV(1)/FVC ratio, and force

198 (forced expiratory volume in 1 second [FEV1]/forced vital capacity [FVC], Pearson r = -0.69, P < .001

199 We conclude that a 6-month change in forced vital capacity gives additional prognostic inform

200 forced expiratory volume in 1 second to the forced vital capacity greater than or equal to 70% (HR,

201 ary fibrosis (defined as death or decline in forced vital capacity >10% at 12 months after study enro

202 ither ALS Functional Rating Scale-Revised or forced vital capacity, having at least 25% improvement a

203 ssociated with mortality after adjusting for forced vital capacity (HR 2.47, 95% CI 1.48-4.15; p=0.00

204 of DM, including rash, alopecia, and reduced forced vital capacity, improved markedly in patients wit

205 o of forced expiratory volume in 1 second to forced vital capacity in 48,201 individuals of European

206 01) whereas the relationship between age and forced vital capacity in patients with Bethlem myopathy

207 d expiratory volume in 1 second (FEV(1)) and forced vital capacity in the CARDIA cohort.

208 A reduced forced vital capacity is prevalent in patients with adul

209 ren with asthma and airway obstruction (FEV1/forced vital capacity < 0.85 and FEV1 < 100% predicted)

210 Moderate/severe airflow obstruction (FEV1/forced vital capacity <0.70 and FEV1 < 80% of predicted

211 mortality: age > or =65 years at enrollment, forced vital capacity <50% predicted, clinically signifi

212 orced expiratory volume in 1 second (FEV(1))/forced vital capacity <70% and FEV(1 )<80% predicted.

213 scale score >1), and impaired lung function (forced vital capacity <=75% predicted) conducted in 39 U

214 P=.36) and forced expiratory flow at 50% of forced vital capacity (mean z score for cases vs control

215 A total of 486 forced vital capacity measurements obtained in 145 patie

216 RI: r = -0.70, P < .001), ratio of FEV(1) to forced vital capacity (model: r = -0.73, P < .001; MRI:

217 levels below 85% of those predicted for both forced vital capacity (odds ratio (OR) = 3.10, 95% CI: 1

218 forced expiratory volume in 1 s (FEV(1)) to forced vital capacity of 0.70 or less after bronchodilat

219 mediate patients had a cumulative decline in forced vital capacity of 2.3% per year (P < 0.0001) wher

220 on, and demonstrated a cumulative decline in forced vital capacity of 2.6% per year (P < 0.0001).

221 been diagnosed in the past 48 months, had a forced vital capacity of 55-90% of the predicted value,

222 ume of back extrapolation as a proportion of forced vital capacity of less than 5%, whereas all but 4

223 EV1] of less than 80% and a ratio of FEV1 to forced vital capacity of less than 70%), and had a smoki

224 monary fibrosis was independent of age, sex, forced vital capacity, or diffusing capacity of carbon m

225 -0.797, P <.001) and the ratio of FEV(1) to forced vital capacity, or FVC, (r = -0.930, P <.001).

226 ty for forced expiratory volume in 1 second, forced vital capacity, or the forced expiratory volume i

227 as <5% and >/=10% decline, respectively, in forced vital capacity over the preceding 6-month period.

228 roup was characterized by considerably lower forced vital capacity (P < .001) and higher S(cond) (P =

229 oved patients' HRCT scan scores (P < .0001), forced vital capacity (P = .0017), FEV(1) (P = .037), an

230 (P < .001) and C3 (P < .001), and decreased forced vital capacity (P = .013).

231 onths (P = .001) whereas mean ADC (P = .17), forced vital capacity (P = .12), and diffusing capacity

232 n the ratio of maximal midexpiratory flow to forced vital capacity (p = 0.02), whereas exposure to oz

233 with a lower value for the percent predicted forced vital capacity (P<0.0001).

234 ted that improvements in mRSS (p<0.0001) and forced vital capacity (p<0.03) persisted.

235 of dysphagia (OR=10.67; p=0.03) and reduced forced vital capacity (p=0.005).

236 l volume (P=0.007), a lower ratio of FEV1 to forced vital capacity (P=0.03), and a reduced carbon mon

237 rectly proportional to weight (P < .001) and forced vital-capacity (P = .001) and inversely proportio

238 om -5.1% to -1.2%/month percentage predicted forced vital capacity, P < .04 and from -1.2 to 0.6 ALS

239 Pseudomonas aeruginosa infection, FEV1/FVC (forced vital capacity), PA:A greater than 1, and previou

240 luding forced expiratory volume in 1 second, forced vital capacity, peak expiratory flow, diffusing c

241 1) [percent predicted], 38.1 [13.9]%; FEV(1)/forced vital capacity [percent predicted], 40.9 [11.8]%;

242 er, measures of pulmonary dysfunction (PaO2, forced vital capacity percentage predicted, total lung c

243 iated with acute care visits, decreased FEV1/forced vital capacity percentage values, fraction of exh

244 Mean peak VO2 and forced vital capacity (% Pred) were significantly reduce

245 t contributors to AQLQ(S) score were R20 and forced vital capacity (% pred.).

246 r layer thickness positively correlated with forced vital capacity % predicted and forced expiratory

247 Jacobian values correlated with changes in forced vital capacity (R = -0.38; 95% CI: -0.25, -0.49;

248 rced expiratory volume in 1 second (FEV1) to forced vital capacity (r = 0.63, r = 0.67, and r = -0.60

249 V values of patients with CF correlated with forced vital capacity (r = 0.7; 95% confidence interval

250 ed expiratory volume in 1 second (r = 0.70), forced vital capacity (r = 0.84), and %VV (r = 0.56).

251 forced vital capacity (298 mL), and the FEV1/forced vital capacity ratio (3.7%) over the follow-up, c

252 een the C-C and C-UC groups, except for FEV1/forced vital capacity ratio (86% vs 82%, respectively; P

253 el was associated with a 5% decrease in FEV1/forced vital capacity ratio (beta = -0.05; 95% CI, -0.08

254 , and IL4R were associated with reduced FEV1/forced vital capacity ratio (beta = -0.11, -0.08, and -0

255 12-4.01; P = 0.021), as did a decreased FEV1/forced vital capacity ratio (FEV1 response increased 0.3

256 ion to asthma (P = .03) and decreased FEV(1)/forced vital capacity ratio (P = .03).

257 l Test score, FEV1 (percent predicted), FEV1/forced vital capacity ratio (percent predicted), and for

258 with FEV(1) (r = -0.35; P = .04) and FEV(1)/forced vital capacity ratio (r = -0.41; P = .01).

259 kers forced expiratory volume in 1 second-to-forced vital capacity ratio (r = -0.70; 95% confidence i

260 (FEV(1)) (r = 0.65, P < .001), the FEV(1)-to-forced vital capacity ratio (r = 0.81, P < .001), and di

261 or the forced expiratory volume in 1 second/forced vital capacity ratio among white, African-America

262 A lower postbronchodilator FEV1/forced vital capacity ratio and a higher number of cigar

263 Subjects with preserved FEV(1)-to-forced vital capacity ratio and reduced FEV(1) percentag

264 ed FEV(1) percent predicted and an FEV(1)-to-forced vital capacity ratio at age 50 years (-3.36% [95%

265 We defined COPD as postbronchodilator FEV(1)/forced vital capacity ratio below the lower limit of nor

266 ry forced expiratory volume in 1 s (FEV1) to forced vital capacity ratio of less than 0.7, without an

267 , and the mean (SD) prebronchodilator FEV(1)/forced vital capacity ratio was 80.2% (9.0%).

268 s (FEV(1), forced vital capacity, and FEV(1)/forced vital capacity ratio) are proposed as core outcom

269 nt predicted forced vital capacity, and FEV1/forced vital capacity ratio) were performed in 4 white p

270 9% of baseline for every 1% decrease in FEV1/forced vital capacity ratio).

271 lated with FEV1, forced vital capacity, FEV1/forced vital capacity ratio, transfer lung capacity of c

272 er prevalence of asthma and decreased FEV(1)/forced vital capacity ratio.

273 associated with the forced expiratory volume/forced vital capacity ratio.

274 ange in forced vital capacity, a decrease in forced vital capacity remained an independent risk facto

275 Forced expiratory volume in 1 second and forced vital capacity remained unchanged after BEP but i

276 None of the SNPs identified for FEV1/forced vital capacity replicated in the independent coho

277 ices for assessment of physical fitness were forced vital capacity, resting heart rate, hand grip str

278 or carbon monoxide, total lung capacity, and forced vital capacity (rho = -0.76, -0.70, and -0.62, re

279 o of forced expiratory volume in 1 second to forced vital capacity (rs=-0.72; 95% CI: -0.92, -0.52; P

280 s who could be reviewed after 4 weeks, FEV1, forced vital capacity, S(acin), and S(cond) values showe

281 rately), but assisted ventilation rating and forced vital capacity showed moderate correlations with

282 iratory volume in 1 second normalized to the forced vital capacity (standardized coefficients [betaS]

283 atory volume in 1 s and percentage predicted forced vital capacity than did those consuming the high-

284 Pulmonary function tests (PFTs) included forced vital capacity, total lung capacity, forced expir

285 ntedanib prevent about 50% of the decline in forced vital capacity typically seen in this disease; fu

286 ith forced expiratory volume in 1 second and forced vital capacity using data collected from 1996 to

287 significant improvement from baseline, while forced vital capacity values declined from baseline.

288 ator forced expiratory volume in 0.5 seconds/forced vital capacity values than did boys (mean differe

289 uced forced expiratory volume in 0.5 seconds/forced vital capacity values than did girls of equivalen

290 o of forced expiratory volume in 1 second to forced vital capacity was -0.75 (95% confidence interval

291 an 1 serving weekly, the mean difference for forced vital capacity was -102 (95% confidence interval

292 flow between the 25th and 75th percentile of forced vital capacity was also inversely associated with

293 lationship between maximal motor ability and forced vital capacity was highly significant (P < 0.0001

294 with usual interstitial pneumonia, change in forced vital capacity was the best physiologic predictor

295 (>/=200 mL and >/=12% increase in FEV(1) or forced vital capacity) was present in 20 (9.0%) particip

296 ), forced expiratory volume in 1 second, and forced vital capacity were performed systematically befo

297 or carbon monoxide, total lung capacity, and forced vital capacity were rho = -0.65, -0.70, and -0.57

298 Age at diagnosis and most recent forced vital capacity were significant predictors of mor

299 apacity of the lungs for carbon monoxide and forced vital capacity, were performed at each examinatio

300 tional hazards models were used for FEV1 and forced vital capacity, with gender-specific lung functio