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Egypt J Pediatr Allergy Immunol, (October 2006), Volume No. 4, Issue 02  
 
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Egypt J Pediatr Allergy Immunol 2006 ; 4 ( 02 ) : 61-69 -
, ESP - 114  
Assessment of left ventricular diastolic function in bronchial asthma: can we rely on transmitral inflow velocity patterns?
Ola Abd Elaziz Elmasry   Hebatallah M. Attia   Neveen M. AbdelFattah        
Background: Left ventricular (LV) diastolic dysfunction has been reported in bronchial asthma (BA), based on the finding of abnormal transmitral inflow velocities on Doppler echocardiography, and attributed to the use of long-term ?2-adrenoceptor agonists. However, these indices of LV filling may be affected by other factors. Objectives: We aimed to assess the effect of acute severe asthma in children on Doppler-derived transmitral inflow velocities and determine the factors influencing them. Methods: 23 asthmatic children [14 males, 9 females; age 8.4±4.2 years] and 15 age- and sex-matched, healthy children [10 males, 5 females; age 9.8±4.3 years] were studied clinically, by spirometry and by echocardiography both during and after resolution of acute severe asthma. Pulsed Doppler-derived right ventricular (RV) systolic time intervals [RV pre-ejection period corrected for heart rate (RVEPc), RV ejection time corrected for heart rate (RVETc), acceleration time (AT)], transmitral inflow velocities [peak E velocity, peak A velocity, E/A ratio], and isvolumic relaxation time (IVRT) were measured. Results: During acute exacerbations of BA, patients had significantly shorter RVETc (p<0.05) and AT (p<0.05), significantly higher peak A velocity (p<0.01), significantly lower E/A ratio (p<0.01), and significantly higher IVRT (<0.05). A highly significant inverse correlation existed between AT and peak A velocity [r= -0.634 (p<0.01)] during acute asthma exacerbation but disappeared after its resolution. Conclusion: Transmitral inflow velocity patterns during acute severe asthma in children are suggestive of altered LV preload due to an acute transient elevation in pulmonary artery pressure secondary to the altered lung mechanics, and are not reflective of intrinsic LV diastolic dysfunction.