TY - JOUR
T1 - Regional myocardial velocities and isovolumic contraction acceleration before and after device closure of atrial septal defects
T2 - A color tissue Doppler study
AU - Pauliks, Linda B.
AU - Chan, Kak Chen
AU - Chang, Dennis
AU - Kirby, Scott K.
AU - Logan, Loralee
AU - DeGroff, Curt G.
AU - Boucek, Mark M.
AU - Valdes-Cruz, Lilliam M.
PY - 2005/8
Y1 - 2005/8
N2 - Background: The study analyzed the effect of atrial septal defect (ASD) device closure on regional wall motion in the right (RV) and left ventricles (LV) using color tissue Doppler imaging (TDI). Atrial septal defect closure results in acute volume unloading of the RV. For unknown reasons, some patients develop acute left-sided heart failure postintervention. Methods: Color TDI was performed in 39 pediatric ASD and 75 age-matched controls. Regional wall motion in 5 LV and 1 RV segment were analyzed before, immediately after, and 24 hours after interventional ASD closure. Off-line postprocessing of echocardiographic data was used to determine myocardial velocities and acceleration during isovolumic contraction (IVA). Isovolumic contraction acceleration is the slope of the upstroke of the isovolumic contraction wave (IVA = peak velocity/acceleration time). Results: At baseline, patients with ASD had significantly higher RV systolic velocities than controls. Isovolumic contraction acceleration was similar in patients with ASD and controls. In the catheterization laboratory postintervention, conventional function parameters remained stable but systolic myocardial velocities decreased significantly in all segments. Diastolic velocities fell in LV segments but not in the RV. In contrast to velocities, IVA was stable during ASD device closure. On follow-up at 24 hours, myocardial velocities had normalized. Conclusions: Device closure of ASD results to an acute transient decrease of regional myocardial velocities in the LV and RV, whereas the load-insensitive marker isovolumic acceleration remained stable. Therefore, the velocity changes may represent a response to altered left and right ventricular loading conditions. Color TDI is a sensitive tool to analyze ventricular mechanics.
AB - Background: The study analyzed the effect of atrial septal defect (ASD) device closure on regional wall motion in the right (RV) and left ventricles (LV) using color tissue Doppler imaging (TDI). Atrial septal defect closure results in acute volume unloading of the RV. For unknown reasons, some patients develop acute left-sided heart failure postintervention. Methods: Color TDI was performed in 39 pediatric ASD and 75 age-matched controls. Regional wall motion in 5 LV and 1 RV segment were analyzed before, immediately after, and 24 hours after interventional ASD closure. Off-line postprocessing of echocardiographic data was used to determine myocardial velocities and acceleration during isovolumic contraction (IVA). Isovolumic contraction acceleration is the slope of the upstroke of the isovolumic contraction wave (IVA = peak velocity/acceleration time). Results: At baseline, patients with ASD had significantly higher RV systolic velocities than controls. Isovolumic contraction acceleration was similar in patients with ASD and controls. In the catheterization laboratory postintervention, conventional function parameters remained stable but systolic myocardial velocities decreased significantly in all segments. Diastolic velocities fell in LV segments but not in the RV. In contrast to velocities, IVA was stable during ASD device closure. On follow-up at 24 hours, myocardial velocities had normalized. Conclusions: Device closure of ASD results to an acute transient decrease of regional myocardial velocities in the LV and RV, whereas the load-insensitive marker isovolumic acceleration remained stable. Therefore, the velocity changes may represent a response to altered left and right ventricular loading conditions. Color TDI is a sensitive tool to analyze ventricular mechanics.
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U2 - 10.1016/j.ahj.2004.09.052
DO - 10.1016/j.ahj.2004.09.052
M3 - Article
C2 - 16086934
AN - SCOPUS:23644433036
SN - 0002-8703
VL - 150
SP - 294
EP - 301
JO - American Heart Journal
JF - American Heart Journal
IS - 2
ER -