title: Patent ductus arteriosus ligation is associated with impaired left ventricular systolic performance in premature infants weighing less than 1000 g.
abstract: 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 x kg(-1) x 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Physiology and Experimental Medicine, the Hospital for Sick Children Research Institute, Toronto, Ontario, Canada. patrick.mcnamara@sickkids.ca
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: McNamara
authors.forename: Lilian
authors.initials: L
authors.lastname: Stewart
authors.forename: Sandesh P
authors.initials: SP
authors.lastname: Shivananda
authors.forename: Derek
authors.initials: D
authors.lastname: Stephens
authors.forename: Arvind
authors.initials: A
authors.lastname: Sehgal
mesh_terms: D001724:Birth Weight; D001794:Blood Pressure; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002316:Cardiotonic Agents / Q000627:therapeutic use; D016009:Chi-Square Distribution; D004374:Ductus Arteriosus, Patent / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000601:surgery*; D005865:Gestational Age; D006339:Heart Rate; D006801:Humans; D052577:Infant, Extremely Low Birth Weight; D007231:Infant, Newborn; D007234:Infant, Premature; D008026:Ligation; D016014:Linear Models; D009864:Ontario; D011446:Prospective Studies; D012121:Respiration, Artificial; D018570:Risk Assessment; D012307:Risk Factors; D013318:Stroke Volume; D013599:Systole; D016896:Treatment Outcome; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents