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العنوان
Right Ventricular Diastolic Functions In Congenital Severe Pulmonary Stenonsis Befor And After Pulmonary Ballon Valvulopllasty/
المؤلف
Abo-zeid, Heba mohamed hussein.
الموضوع
heart diseases in children.
تاريخ النشر
2005 .
عدد الصفحات
213 p . :
الفهرس
Only 14 pages are availabe for public view

from 260

from 260

Abstract

Children with valvular pulmonary stenosis have right ventricular
diastolic filling abnormalities, which may be due to either right
ventricular hypertrophy or right ventricular outflow tract obstruction. It is
postulated that children with right ventricular hypertrophy caused by
valvular pulmonary stenosis have abnormalities of right ventricular
diastolic filling. Furthermore, if these abnormalities are caused by
hypertrophy alone then RY diastolic filling should be unchanged
immediately after successful relief of pulmonary stenosis by PBV
(Vermillion et al, 1992 and Pac eta), 2000).
This work aimed at assessment of right ventricular diastolic
functions in congenital severe PS before and after PBY as well as
evaluation of the effectofPBY on right ventricular diastolic functions.
To achieve these aims, this study was conducted from October
2003 to April 2005 and it included 38 patients from whom 26 patients
were included and 12 patients were excluded; only patients with isolated
valvular PS with a transvalvular systolic gradient > 70 mmHg were
included.
Before PBY, clinical as well as radiological and BCG evidences
of PS and RYH were clearly demonstrated in our patients. Six months
ihereafter, chest x-ray films and EeG showed significant regression of
RVH with improvement of pulmonary blood flow, yet when compared
with control subjects, RYW thickness was still significantly increased in
patients with PS.
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One day before PBY, our patients showed diastolic filling
abnormalities when compared to control subjects. This diastolic
dysfunction was evidenced by increased peak A velocity (72.5 vs
41.5cm/sec, P<O.OOI), decreased EtA velocity ratio (0.84 vs 1.6,
P<O.OO 1), decreased acceleration time of peak E (66A4± 12.21 vs
74.S4± 14.06 ms, P<O.OS), and decreased deceleration time of peak E
(61.76±12.32 vs 85.9S±13.83 ms, P<O.OOl) in patients versus control
subjects respectively.