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Abstract
Summary and Conclusion
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 RV diastolic filling should be unchanged immediately after successful relief of pulmonary stenosis by PBV (Vermillion et al, 1992 and Pac et al, 2000).
This work aimed at assessment of right ventricular diastolic functions in congenital severe PS before and after PBV as well as evaluation of the effect of PBV 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 PBV, clinical as well as radiological and ECG evidences of PS and RVH were clearly demonstrated in our patients. Six months thereafter, chest x-ray films and ECG showed significant regression of RVH with improvement of pulmonary blood flow, yet when compared with control subjects, RVW thickness was still significantly increased in patients with PS.
One day before PBV, 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<0.001), decreased E/A velocity ratio (0.84 vs 1.6, P<0.001), decreased acceleration time of peak E (66.4412.21 vs 74.5414.06 ms, P<0.05), and decreased deceleration time of peak E (61.7612.32 vs 85.9513.83 ms, P<0.001) in patients versus control subjects respectively.
The LV myocardial performance index performed one day before PBV was found to be higher in patients than in control subjects (0.52 vs 0.34 respectively) indicating both systolic and diastolic LV dysfunction in cases of PS.
One day after PBV, right ventricular diastolic filling indices were nearly unchanged in patients compared to their values one day before PBV; peak E velocity was found to be 60.8110.45 vs 60.2811.41 cm /sec. Peak A velocity was found to be 78.0316.81 vs 78.8317.47 cm/sec, E/A velocity ratio was found to be 0.80.21 vs 0.80.21 acceleration time of peak E was found to be 67.5211.99 vs 66.4412.21 ms, and deceleration time of peak E was found to be 619.99 vs 61.7612.32 ms.
The LV Tei index absolute values were minimally reduced form 0.570.12 pre-PBV to 0.550.12 post-PBV but this reduction was consistently present in every patient giving rise to a highly significant statistical difference (P<0.001) denoting that LV dysfunction in cases of PS is partially due to increased RV afterload.
Six months following PBV, right ventricular diastolic functions were markedly improved which was evidenced by increased peak E velocity (64.668.44 vs 60.2811.41 cm/sec, P<0.05, decreased peak A velocity (58.5515.24 vs 78.8317.47 cm/sec. P<0.001), increased peak E/peak A velocity ratio (1.180.37 vs 0.80.21, P<0.001), prolongation of acceleration & deceleration times of peak E (69.7711.33 and 78.6211.55 vs 66.4412.21 and 61.7612.32ms, P<0.001) in patients 6 months after PBV vs one day before PBV respectively. The LV Tei index showed a greater decline to 0.440.08 six months following PBV suggesting that LV dysfunction in PS not only due to increased RV afterload but also due to RVH.
Conclusion:
Patients with severe to critical PS have right ventricular as well as left ventricular function impairment. The RV functional abnormalities were nearly unchanged immediately after balloon dilation of the pulmonary valve and were significantly improved 6 months thereafter suggesting that they are not due to increased right ventricular afterload but are due to right ventricular hypertrophy. The LV myocardial performance index showed an early improvement one day following PBV followed by a greater extent of improvement 6 months later suggesting that LV MPI impairment in cases of PS is due to both increased RV afterload and RVH.