The Journal of Thoracic and Cardiovascular Surgery
Volume 140, Issue 1 , Pages 150-157, July 2010

Patent ductus arteriosus ligation is associated with impaired left ventricular systolic performance in premature infants weighing less than 1000 g

  • Patrick J. McNamara, MB Bch MRCPCH

      Affiliations

    • Physiology and Experimental Medicine, the Hospital for Sick Children Research Institute, University of Toronto, Toronto, Ontario, Canada
    • Division of Neonatology, University of Toronto, Toronto, Ontario, Canada
    • Department of Paediatrics, University of Toronto, Toronto, Ontario, Canada
    • Corresponding Author InformationAddress for reprints: Patrick J. McNamara, MB Bch MRCPCH, the Hospital for Sick Children, 555 University Ave, Toronto, Ontario M5G 1X8, Canada.
  • ,
  • Lilian Stewart, MD

      Affiliations

    • Division of Neonatology, University of Toronto, Toronto, Ontario, Canada
  • ,
  • Sandesh P. Shivananda, MD

      Affiliations

    • Division of Neonatology, University of Toronto, Toronto, Ontario, Canada
  • ,
  • Derek Stephens, MSc

      Affiliations

    • Department of Paediatrics, University of Toronto, Toronto, Ontario, Canada
  • ,
  • Arvind Sehgal, MD

      Affiliations

    • Division of Neonatology, University of Toronto, Toronto, Ontario, Canada

Received 21 July 2009; received in revised form 4 December 2009; accepted 2 January 2010. published online 05 April 2010.

Objective

Patent ductus arteriosus ligation is often complicated by systemic hypotension and oxygenation failure. The ability of the immature myocardium to compensate for altered afterload is poorly understood. The aim of this study was to characterize the effects of patent ductus arteriosus ligation on myocardial performance in preterm infants.

Methods

Serial echocardiographic analysis was performed before and after patent ductus arteriosus ligation. Characteristics of the patent ductus arteriosus, myocardial performance (fractional shortening, mean velocity of circumferential fiber shortening, and left ventricular output) and left ventricular afterload (end-systolic wall stress) were assessed. The stress–velocity relationship was measured as a preload-independent, afterload-adjusted measure of myocardial contractility.

Results

Forty-six preterm infants were assessed at 28.5 ± 11.3 days and a weight of 1058 ± 272 g. Patent ductus arteriosus ligation was followed by increased left ventricular exposed vascular resistance temporally coinciding with reduced left ventricular preload, decreased left ventricular contractility, and low left ventricular output. Neonates weighing 1000 g or less had a higher rate of low fractional shortening (<25%) or low left ventricular output (<170 mL · kg−1 · h−1) and increased need for cardiotropes and demonstrated a trend toward an impaired stress–velocity relationship. Neonates with impaired left ventricular systolic performance were more likely to require cardiotropes and have low systolic arterial pressure, increased heart rate, and abnormal base deficit.

Conclusion

Patent ductus arteriosus ligation is sometimes associated with impaired left ventricular systolic performance, which is most likely attributable to altered loading conditions. Neonates weighing 1000 g or less are at increased risk of impaired left ventricular systolic performance, which might relate to maturational differences and decreased tolerance to altered loading conditions.

CTSNet classification: 17, 22

Abbreviations and Acronyms: ANOVA, analysis of variance, ESWS, end-systolic wall stress, FS, fractional shortening, HSDA, hemodynamically significant ductus arteriosus, IQR, interquartile range, LA/Ao, ratio of left atrium to aortic root dimension, LV, left ventricular, LVEDD, left ventricular end-diastolic dimension, LVESD, left ventricular end-systolic dimension, LVET, left ventricular ejection time, LVE-VR, left ventricular exposed vascular resistance, LVO, left ventricular output, MAP, mean arterial pressure, mVCFc, mean velocity of circumferential fiber shortening, PDA, patent ductus arteriosus, SAP, systolic arterial pressure, SVC, superior vena cava, SVR, systemic vascular resistance

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 Disclosures: None.

 Dr Stewart is a coprincipal author.

PII: S0022-5223(10)00040-1

doi:10.1016/j.jtcvs.2010.01.011

Refers to erratum:

  • Notice of Correction

    The Journal of Thoracic and Cardiovascular Surgery October 2010 (Vol. 140, Issue 4, Page 944)

The Journal of Thoracic and Cardiovascular Surgery
Volume 140, Issue 1 , Pages 150-157, July 2010