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1 ritance is based on pedigree observation and M-mode echocardiography.
2 eter and simultaneous two-dimensional guided M-mode echocardiography.
3 t model as well as in vivo, by transthoracic M-mode echocardiography.
4 Heart function was assessed using serial M-mode echocardiography.
5 group, as reflected by RV/left ventricle on M-mode echocardiography (0.66 +/- 0.22 versus 0.81 +/- 0
6 sing LV remodeling, LV diameters measured by M-mode echocardiography allow acceptable estimation of L
7 ined the association between MAC assessed by M-mode echocardiography and the incidence of CVD, CVD de
8 was then quantitated by two-dimensional and M-mode echocardiography as well as by molecular and path
9 cause of LV outflow tract obstruction in the M-mode echocardiography era, in the 1990s structural abn
10 of their initial two-dimensionally directed M-mode echocardiography exam (year 5); half the cohort h
11 n the 1960s standardized the clinical use of M-mode echocardiography for quantitative assessment of l
12 intervals, tissue Doppler imaging, and color M-mode echocardiography have enhanced the means to asses
13 echanisms were evaluated by prenatal Doppler/M-mode echocardiography, immediate neonatal surface elec
16 ased left atrial dimension (LAD) measured by M-mode echocardiography is a risk factor for atrial fibr
17 iography), less diastolic dysfunction (color M-mode echocardiography), less lactate production, and l
18 ction, assessed using 2-dimensionally guided M-mode echocardiography, showed significantly depressed
20 systolic internal dimensions, as measured by M-mode echocardiography, to the risk of congestive heart
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