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1 lic velocity was inversely related to portal systolic velocity.
2 qual to 3:1, and intrastent doubling of peak-systolic velocity.
3 versus 65.7+/-8.0%; P<0.0001; mitral annular systolic velocity, 11.7+/-2.6 versus 10.9+/-2.3 cm/s; P=
9 a values of the relationship between MA peak systolic velocity and LV end-diastolic volume and mass w
10 left ventricular function, assessed by peak systolic velocity and strain rate in 12 paired, nonapica
13 dneys and between regions was found for peak systolic velocity, but the magnitude of this variation w
17 iagnostic US criteria for stenosis were peak-systolic velocity greater than 1.25 m/sec, internal caro
18 riteria for stenosis were also applied: peak-systolic velocity greater than 1.7 m/sec, ICA end-diasto
20 ents with isolated, asymptomatic AS and peak systolic velocity > or =4 m/s by Doppler echocardiograph
21 long-axis ratio <0.6, tricuspid annulus peak systolic velocity >/= 8 cm/s, and peak systolic longitud
23 r imaging, viable segments show increases in systolic velocities in contrast to infarcted segments.
25 ptal-posterior delay, and SD in time to peak systolic velocity in the 12 left ventricular segments) a
26 g-axis ratio >/= 0.6, tricuspid annulus peak systolic velocity <8 cm/s, and peak systolic longitudina
28 id annular plane systolic excursion and peak systolic velocity, myocardial performance (expressed as
30 n TDI indices occurred with dobutamine: peak systolic velocity of 4.41 +/- 1.07 to 6.67 +/- 1.07 cm/s
31 ficant decreases occurred with esmolol: peak systolic velocity of 4.46 +/- 0.94 to 2.31 +/- 0.81 cm/s
34 7 mm; p < 0.05) and correlated with the peak systolic velocity of the second palmar digital artery (P
40 a focal twofold or higher elevation of peak systolic velocity (PSV) compared with the PSV immediatel
42 rvus tardus waveforms) with and without peak systolic velocity (PSV) thresholds (determined with rece
44 lly significant changes observed in the peak systolic velocity (PSV), end diastolic velocity (EDV), o
47 city (bAPV), hyperemic APV (hAPV), diastolic/systolic velocity ratio (DSVR), and coronary flow reserv
49 elocity greater than 0.4 m/sec, ICA/CCA peak-systolic velocity ratio greater than 2.0, and ICA/CCA en
50 ry (ICA) to common carotid artery (CCA) peak-systolic velocity ratio of greater than or equal to 3:1,
52 s/length-area ratios, tricuspid annulus peak systolic velocity, RV peak longitudinal global systolic
53 .5 cm/s, P=0.02), with a significantly lower systolic velocity S' septal (7.6+/-1.2 versus 8.5+/-1.2
54 sed by measuring differences in time-to-peak systolic velocity (T(SV)) between the RV free wall, vent
55 Reduced coronary forward wave energy and systolic velocity time integral imply a compromised syst
57 m/s (p = .002), right ventricular myocardial systolic velocities to 15.0 (11.8-23) cm/s, (p = .003),
58 al admission to discharge; septal myocardial systolic velocities to 8.8 (7-11) cm/s (p = .002), right
60 s myocardial function was quantified by peak systolic velocity (Vs) and strain rate (SR) responses.
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