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1 ion of extracellular space by calculation of extracellular volume fraction.
2 n to calculate global myocardial T1, T2, and extracellular volume fraction.
3 enhancement, native T1 relaxation times, and extracellular volume fraction.
4 portion to the square root of enlarged total extracellular volume fraction.
5 adolinium enhancement, 0.90; T2 ratio, 0.79; extracellular volume fraction, 0.71; early gadolinium en
6 versus 1152+/-46 milliseconds; P<0.001) and extracellular volume fraction (26+/-5% versus 30+/-6%; P
7 ly; P<0.001) and increased diffuse fibrosis (extracellular volume fraction, 27.4+/-2.2% versus 27.2+/
8 tauic), a cell size-dependent parameter, and extracellular volume fraction, a marker of interstitial
9 lar sodium concentration (C1, in mM) and the extracellular volume fraction (alpha) in grey and white
12 n the cellular compartment, while changes in extracellular volume fraction and tortuosity, which are
14 l size, vascular volume fraction, intra- and extracellular volume fractions, and pseudo-diffusivity a
15 fraction, thus confirming the suitability of extracellular volume fraction as an in vivo measure of d
16 resonance measures of interstitial fibrosis (extracellular volume fraction), as well as serum biomark
18 Both post-contrast myocardial T1 time and extracellular volume fraction correlated with beta, the
19 ise CMR parameters, global myocardial T1 nor extracellular volume fraction differed significantly bet
20 c resonance (CMR) measurements of myocardial extracellular volume fraction (ECV) and late gadolinium
23 d cardiac magnetic resonance measurements of extracellular volume fraction (ECV) to discover and quan
26 arditis as well as native T1, calculation of extracellular volume fraction (ECV), and T2 mapping (onl
28 T2>52 ms, 78% for native T1>981 ms, 74% for extracellular volume fraction >0.24, and 100% for T2 rat
30 tricular dysfunction and prevented increased extracellular volume fraction, indicating that T1 mappin
31 s not affect either the TMA diffusion or the extracellular volume fraction, indicating that the enzym
32 between HCM and hypertension, over and above extracellular volume fraction, LV wall thickness and ind
33 nterstitium and quantify ECM expansion using extracellular volume fraction measures and other derange
35 BNP was associated with a 0.62% increment in extracellular volume fraction (p < 0.001), 0.011 increme
36 stant (P = .0007) and 14.3% in extravascular-extracellular volume fraction (P = .002) were seen after
37 lation results indicate that even for larger extracellular volume fractions than what is reported for
38 For two different geometries with the same extracellular volume fraction the geometry with the most
39 olume transfer coefficient K(trans), and the extracellular volume fraction v(e) were calculated for t
40 rd CMR parameters, global myocardial T1, and extracellular volume fraction values for assessing the a
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