cardiovascular-agents and Respiratory-Distress-Syndrome--Newborn

Botallo's duct connects the systemic and pulmonary circulation. It can play a crucial hemodynamic role in some cardiac and respiratory diseases of the newborn, and strongly influences the outcome if it remains patent after birth or if it closes rapidly. The recently acquired in-depth knowledge on the genesis of these events have advanced the so called ''pharmacological manipulation of Botallo's duct'', i.e. pharmacological treatment to regulate the opening or closure of the ductus depending on clinical requirements and that, as will be described, is a key issue in managing newborns with severe cardiac and/or respiratory distress. This study illustrates the main underlying mechanisms of duct patency during intrauterine life and its closure after birth, and then describes the clinical conditions of the newborn where Botallo's duct must be kept patent after birth (duct-dependent cardiac malformations) and where its closure must be accelerated (patent duct associated idiopathic respiratory syndrome). It also reports the recent findings on the use of prostaglandins (PGE1) and prostaglandin synthesis inhibitors (indomethacin, ibuprofen) and the potential use of drugs capable of favouring or inhibiting nitric oxide in the duct endothelium.

Topics: Alprostadil; Anti-Inflammatory Agents, Non-Steroidal; Cardiovascular Agents; Cerebral Angiography; Cyanosis; Cyclooxygenase Inhibitors; Ductus Arteriosus; Ductus Arteriosus, Patent; Heart Defects, Congenital; Heart Failure; Hemodynamics; Humans; Ibuprofen; Indomethacin; Infant, Newborn; Infant, Premature, Diseases; Respiratory Distress Syndrome, Newborn; Vasodilator Agents

Respiratory distress and patent ductus arteriosus (PDA) in neonates are mutually perpetuating. Contrary to the situation in premature infants, the recognition, clinical relevance and optimal management of PDA in full-term neonates are unclear. The present study aimed to identify PDA as a possible cause of respiratory distress in term and near-term neonates, and to examine the clinical responsiveness of PDA to different treatment modalities in mature-gestational-age neonates.. Patients with gestational ages of over 34 weeks were included in this retrospective chart review; they had PDA as the sole recognizable cause of respiratory distress and were free of all other diseases. Clinical responsiveness to different regimens, including conservative treatment, drug therapy with preload reduction and inotropic agent with or without the addition of indomethacin, and surgical intervention were analyzed.. Forty-four neonates qualified for this study. Six received no treatment and their cardiorespiratory symptoms resolved within 1 week (regimen A). Symptoms in 11 neonates were relieved after use of diuretic and inotropic agents (regimen B). Twelve neonates became asymptomatic without further intervention after indomethacin treatment in addition to preload reduction and inotropes (regimen C). A total of 15 of the 44 infants underwent PDA ligation (regimen D) due to persistent heart failure following regimens B or C, but had speedy resolution of respiratory symptoms following surgery. There were significant differences in birth body weight and hemodynamic variation based on left atrium to aortic root dimensional ratio between the treatment (regimens B, C and D) and non-treatment (regimen A) groups (p < 0.05).. PDA plays an important role in prolonging respiratory distress in term or near-term neonates. Although most infants respond to noninvasive medical treatment, surgical ligation during the neonatal period is warranted in certain mature infants. Surgical treatment should be considered in patients with smaller birth body weights and those with increased left atrium to aortic root dimensional ratios.

Topics: Analysis of Variance; Cardiac Surgical Procedures; Cardiotonic Agents; Cardiovascular Agents; Diuretics; Ductus Arteriosus, Patent; Female; Gestational Age; Humans; Indomethacin; Infant, Newborn; Male; Respiratory Distress Syndrome, Newborn; Retrospective Studies; Treatment Outcome

Wide pulse pressure is considered to be a sign of patent ductus arteriosus (PDA). We tested the hypothesis that, following indomethacin therapy, PDA closure is associated with a significant decrease in pulse pressure. Thirty-two ventilated preterm infants were echocardiographically diagnosed within the first 24 hours of life with PDA. Systolic, diastolic, and mean arterial blood pressures were measured prior to indomethacin treatment and after echocardiographically confirmed PDA closure. Following PDA closure, systolic and diastolic blood pressures and mean arterial pressure increased significantly without a significant change of pulse pressure (17 +/- 7 to 20 +/- 12 torr). We conclude that in preterm infants with PDA, systolic, diastolic, and mean arterial blood pressures increase significantly within first few days of life. Pulse pressure does not appear to be affected by early PDA closure. We speculate that high pulmonary resistance in the first days of life prevents significant diastolic aortic runoff and leaves pulse pressure unaffected by PDA, as well as by its closure.

Topics: Blood Pressure; Cardiovascular Agents; Ductus Arteriosus, Patent; Humans; Indomethacin; Infant, Low Birth Weight; Infant, Newborn; Intensive Care Units, Neonatal; Predictive Value of Tests; Respiratory Distress Syndrome, Newborn; Retrospective Studies; Time Factors

The aim of this study was to determine if it was possible to decrease the number of boluses of indomethacin for the treatment of patent ductus arteriosus. This retrospective study included 46 preterm neonates (<34 weeks' GA) who had had an ultrasound diagnosis predictive of subsequent symptomatic patent ductus arteriosus. All patients had received a daily intravenous doses of indomethacin, 0.1 mg/kg. Mean age at initiation of treatment was 4.5 +/- 3.1 days. Patency of the ductus arteriosus was controlled echocardiographically each day and treatment was discontinued as soon as the ductus arteriosus was closed. The initial success rate was 84.7%, of which 6.5% reopened. The mean cumulative dose of indomethacin was 0.35 mg/kg. There was no correlation between gestational age or birth weight and total cumulative dose. Overall tolerance was satisfactory with only one case of transient acute renal failure. A weak correlation between the cumulative dose of indomethacin and natremia (r = -0.43) or weight gain (r = 0.35) was noted, and none with serum creatinine or blood urea nitrogen levels. We confirm that lower indomethacin treatment of patent ductus arteriosus in premature neonates are as effective as standard protocols.

Topics: Cardiovascular Agents; Dose-Response Relationship, Drug; Ductus Arteriosus, Patent; Echocardiography; Female; Humans; Indomethacin; Infant, Newborn; Infant, Premature; Male; Respiratory Distress Syndrome, Newborn; Retrospective Studies

Cardiac troponin T (cTnT) represents a sensitive and specific marker of ischemic myocardial damage in adult and neonatal populations. The aim of this study was to detect the potential ischemic effect of persistent patent ductus arteriosus (PDA) and indomethacin treatment on the coronary vascular bed by measuring cTnT concentrations. cTnT levels were measured in 23 preterm infants (<32 weeks of gestational age) with respiratory distress syndrome (RDS), 11 with PDA and 12 without, at 2, 4, and 7 days after birth. cTnT concentrations (mean +/- SEM) significantly decreased (P<0.05) from the 2nd (0.63+/-0.09 microg/l) and the 4th (0.77+/-0.13 microg/l) to the 7th postnatal day (0.28+/-0.04 microg/l). At day 2 after birth, cTnT levels in preterm infants with RDS were significantly higher (P<0.05) than our reference values for healthy preterm neonates (0.63+/-0.09 microg/l vs. 0.18+/-0.04 microg/l). No differences were found between RDS infants with and without PDA at 2 (0.65+/-0.13 vs. 0.61+/-0.14 microg/l), 4 (0.71+/-0.21 vs. 0.87+/-0.16 microg/l), and 7 (0.26+/-0.05 vs. 0.29+/-0.07 microg/l) days of life. In infants with PDA, cTnT levels did not differ before the first dose of indomethacin was given (0.65+/-0.14 microg/l) or 2 h (0.65+/-0.15 microg/l) and 48 h (0.71+/-0.21 microg/l) afterwards.. In preterm infants with RDS the occurrence of PDA and indomethacin treatment are not associated with ischemic cardiac damage as detected by cTnT measurements.

Topics: Cardiovascular Agents; Ductus Arteriosus, Patent; Humans; Indomethacin; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Myocardial Ischemia; Respiratory Distress Syndrome, Newborn; Troponin T