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16840

Does Significant PDA Increase Myocardial Oxygen Demand In Premature Infants

Friday, October 19, 2012
Room 275-277 (Morial Convention Center)
Pooja H. Desai1, Ashraf M. Aly2, Amyn K. Jiwani2, Michael H. Malloy3 and Sunil K. Jain3, (1)Pediatrics, University of Texas Medical Branch, Galveston, TX, (2)Pediatrics Cardiology, University of Texas Medical Branch, Galveston, TX, (3)Pediatric Neonatology, University of Texas Medical Branch, Galveston, TX

Purpose: The stroke volume of the heart increases in response to increase in volume of blood filling the heart, which stretches myocardium & increases contractility. The contractile force generated by myocardium is proportionate to the initial myocardial length called preload. However, increased preload beyond optimum decreases myocardial contraction and increases workload.  A significant patent ductus arteriosus (SPDA) causes volume overload (i.e. preload) on the heart leading to myocardial muscle overstretching. This overstretch of myocardium may be more than optimum which may lead to increased workload & increased O2 requirement of the myocardium

The purpose of this study is to evaluate if a significant PDA increases O2 demand of myocardium as measured by serum BNP and CKMB.

Methods: We obtained consent from the parents of 37 infants weighing <1500 gms & performed an echocardiogram at 3-7 days of life. SPDA was defined as PDA diameter >1.5 mm on echocardiography. BNP, CKMB & Troponin I were measured in both infants with SPDA (Study group, n=7) and those without (Control group, n=30). Infants with SPDA were treated with 3 doses of indomethacin. We compared BNP, CKMB & Troponin I in SPDA & control groups prior to treatment. ANOVA and student t test were used for the statistical analysis (p <0.05, significant).

Results: The SPDA group had significantly lower gestation (25.8 vs 27.9 weeks), there was a higher prevalence of females in the SPDA group (85% vs 43%), and only 57% of SPDA infants were exposed to antenatal MgSO4 vs 100% of controls. Antenatal Indomethacin use, antenatal steroids exposure, and method of postnatal respiratory support were not significantly different between groups. Serum BNP levels in the SPDA group were significantly elevated (1195 ng/ml) compared to levels in the control group (29.8 ng/ml) as were CKMB levels (3.27 ng/ml vs 1.27 ng/ml). There were no significant differences between the groups in Troponin I levels.  Multivariate ANOVA controlling for race, sex, Indomethacin exposure, MgSO4 exposure, and antenatal steroid exposure, continued to demonstrate a significant elevation in both BNP and CKMB levels in the SPDA group.

Conclusion: These data demonstrate significant elevations in BNP and CKMB among infants with SPDA and suggest by proxy an increased oxygen demand of the infant’s mycocardium.