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Biomedical subjects

R J Ascuitto

Publications and source records attributed to R J Ascuitto.

At least 19 recordsLinked to original sources
PubMed2004

Systematic-to-pulmonary collaterals: a source of flow energy loss in Fontan physiology.

Patients with Fontan-modified, single-ventricle heart frequently have systemic collaterals that increase pulmonary blood flow. Competitive flow from these auxiliary vessels can also elevate pulmonary artery pressure, a process leading to erosion of flow's mechanical energy. An analogous analytical description of mixing fluid streams was used to provide insight into flow energetics associated with systemic-to-pulmonary collaterals in Fontan-type circulation. We find that theoretical pressure increases and flow energy losses due to mixing vary quadratically as the velocity differences of the interacting fluid streams. Moreover, the predicted flow energy loss is shown to depend directly on the resultant pressure increase. Based on studies of aortopulmonary collaterals in patients with Fontan anatomy, we provide an estimate of pulmonary artery pressure elevation and flow energy loss, factors that are of considerable clinical importance.

Blood Flow Velocity↗
PubMed2003

Streamlining fluid pathways lessens flow energy dissipation: relevance to atriocavopulmonary connections.

Flow energy dissipation reduces cardiac efficiency, particularly in the Fontan-modified, single-ventricle heart. To provide insight into flow energetics relevant to Fontan-type anatomy, a simple, analytical description of fluid motion was employed. Mechanical energy balance and the force-momentum relationship were used to describe theoretical pressure changes and flow energy losses. When either flow's cross-sectional area or direction changes abruptly, fluid disturbances ensue that can lead to erosion of a stream's available energy. Conversely, passages anatomically streamlined to favor gradual alterations in these flow characteristics lessen such fluid dynamic effects. We show by analogy that flow energy dissipation becomes clinically important in Fontan circuits when the magnitude and/or direction of the average velocity of flow suddenly changes as fluid enters or leaves a large chamber or negotiates a sharp bend in its connection pathway.

Biophysical Phenomena↗
PubMed1999

Mechanical function and substrate oxidation in the neonatal pig heart subjected to pacing-induced tachycardia.

Isolated, paced, isovolumically beating, neonatal pig ( approximately 2 days) hearts were perfused with a crystalloid solution during four periods: (1) baseline, HR 150 bpm; (2) HR-response curves, HR 150-360 bpm; (3) tachycardia, HR 300 bpm; and (4) posttachycardia, HR 150 bpm. Group I was studied with glucose (5. 5 mM) as the sole substrate. During baseline, left ventricular peak systolic pressure (PSP) averaged 123 +/- 7 mm Hg; end diastolic pressure (EDP), 4.9 +/- 0.4 mm Hg; relaxation time constant (Tau), 29.5 +/- 3.9 ms; glucose oxidation (14CO2 from [14C]glucose), 1535 +/- 96 nmol/min/gdry; and myocardial oxygen consumption (MVO2), 17.4 +/- 0.4 micromol/min/gdry. During tachycardia, PSP was 83 +/- 4* mm Hg; EDP, 9.8 +/- 1.7* mm Hg; Tau, 29.9 +/- 5.4 ms; glucose oxidation, 1921 +/- 136* nmol/min/gdry; and MVO2, 21.1 +/- 0.7* micromol/min/gdry (*different from baseline, P < 0.05). Posttachycardia, all parameters returned to near baseline values, except EDP, which remained elevated. Group II was studied with glucose (5.5 mM) and palmitate (0.55 mM). When compared to those of Group I, the mechanical responses were similar. During baseline, glucose oxidation was 149 +/- 24 nmol/min/gdry; palmitate oxidation, 343 +/- 28 nmol/min/gdry; and MVO2, 18.4 +/- 0.7 micromol/min/gdry. Both oxidation rates increased significantly during tachycardia, indicating aerobic metabolic reserve. Posttachycardia, glucose oxidation returned to baseline, but palmitate oxidation remained elevated, suggesting enhanced beta oxidation. Group III was perfused with glucose (5.5 mM) and pyruvate (5.5 mM), along with iodoacetate (50 microM) to inhibit glycolysis. PSP was maintained, but Tau (HRs >/= 270 bpm) and EDP (HRs >/= 180 bpm) markedly increased. In conclusion, for the isovolumically beating, neonatal pig heart stressed with tachycardia: (1) PSP decreases, EDP increases, and Tau remains relatively constant; (2) substrate oxidation is enhanced; and (3) glycolysis, rather than glucose oxidation, appears to be important for supporting ventricular diastolic function.

Animals↗
PubMed1996

Analysis of cardiovascular responses to PACAP-27, PACAP-38, and vasoactive intestinal polypeptide.

Responses to pituitary adenylate cyclase polypeptide (PACAP)-27, PACAP-38, and vasoactive intestinal peptide (VIP) were compared in the peripheral and pulmonary vascular beds of the cat and in the isolated perfused neonatal pig heart. Intravenous injections of PACAP-27 and PACAP-38 produced biphasic changes in systemic arterial pressure whereas iv injections of VIP caused only decreases in arterial pressure. When blood flow to the hind limb and mesenteric vascular beds was maintained constant, PACAP-27 and PACAP-38 caused dose-related biphasic changes in perfusion pressure, whereas VIP only decreased perfusion pressure. PACAP-27 was approximately threefold more potent than PACAP-38, and the pressor component of the biphasic response was blocked by alpha-adrenergic antagonists and adrenalectomy. PACAP-27, PACAP-38, and VIP produced decreases in pulmonary vascular resistance, and all three peptides had significant vasodilator activity in the isolated perfused neonatal pig heart. Although all three peptides decreased coronary vascular resistance, only PACAP-27 and PACAP-38 increased left ventricular contractility, with PACAP-27 approaching isoproterenol in potency. The results of these experiments show that PACAP-27, PACAP-38, and VIP have significant effects on vasomotor tone that depend on the vascular bed studied and the contribution of adrenal catecholamines.

Amino Acid Sequence↗
PubMed1996

Substrate metabolism in the developing heart.

The developing heart undergoes a remarkable metabolic transformation as it adjusts to the higher-oxygen, extrauterine environment. During gestation, glycolysis and lactate oxidation constitute the major sources of adenosine triphosphate (ATP) for the fetal heart. After birth, however, there is a rapid shift from carbohydrate to fatty acid utilization. Despite the transition to primarily aerobic metabolism, the neonatal heart retains an enhanced capacity for anaerobic energy production. This unique metabolic adaptation is important when assessing the immature heart's responses to states of oxygen insufficiency, such as ischemia, hypoxia, and tachycardia. This article reviews the dramatic changes in enzyme activities, mitochondrial morphology and function, and substrate availability that underlie this change in metabolism in the maturing heart.

Adenosine Triphosphate↗
PubMed1996

Contractile and coronary vascular effects of pituitary adenylate cyclase activating polypeptide in neonatal pig hearts.

OBJECTIVE: The purpose was to investigate the influence of the 38-amino-acid neuropeptide, pituitary adenylate cyclase activating polypeptide (PACAP38), on contractile function and coronary vascular tone in neonatal hearts. METHODS: Isolated, paced (150 bpm), isovolumically-beating, piglet hearts (n = 19) underwent retrograde aortic perfusion at constant coronary flow (approximately 2.5 ml/min/gwet) with an erythrocyte-enriched (Hct 15-20%) solution (37 degrees C). Agonists were injected into the aortic root of hearts, and the changes in +dP/dtmax and -dP/dtmax (reflecting contractility), and coronary perfusion pressure (reflecting vascular tone) were determined. Responses to PAPCAP38 were compared to isoproterenol, and to the truncated peptide PACAP6-38. RESULTS: PACAP38 (0.1 and 0.5 nmol) increased +dP/dtmax from 1387.4 +/- 134.6 to 1619.0 +/- 118.7, and from 1296.2 +/- 93.4 to 1872.2 +/- 111.4 mmHg/s (P < 0.05); changed -dP/dtmax from -1087.6 +/- 107.5 to -1206.6 +/- 93.6, and from -1025.0 +/- 46.8 to -1375.4 +/- 80.9 mmHg/s (P < 0.05) and decreased coronary perfusion pressure from 61.8 +/- 2.5 to 51.0 +/- 3.8, and from 62.5 +/- 1.0 to 45.3 +/- 3.3 mmHg (P < 0.005), respectively. In comparison, isoproterenol (0.1 nmol) increased +dP/dtmax from 1313.6 +/- 62.8 to 1679.0 +/- 74.4 (P < 0.05), and -dP/dtmax from -1026.4 +/- 54.1 to -1222.6 +/- 57.4 mmHg/s (P < 0.05). PACAP6-38 reduced PACAP38's coronary vasodilatory, but not its contractile, effect. When compared to our previous studies of the 27-amino-acid neuropeptide PACAP27, PACAP38 had less potent contractile, but similar vasodilatory effects. CONCLUSIONS: PACAP38 enhanced contractility and produced coronary vasodilation in piglet hearts, which may make PACAP38 a promising cardiotonic agent for the treatment of neonates with heart failure.

1-Methyl-3-isobutylxanthine↗
PubMed1995

Mechanical and metabolic characterization of ischemic contracture in the neonatal pig heart.

Isolated, paced, isovolumetrically beating piglet hearts (n = 37) underwent retrograde aortic perfusion with a crystalloid solution during three periods: 1) baseline (coronary perfusion pressure 60 mm Hg), 2) ischemia (coronary flow 10% of baseline for approximately 80 min), and 3) reperfusion (perfusion pressure returned to baseline). In one group of hearts, glycolysis (using 3H2O formation from [3H]glucose) was assessed. During baseline, peak systolic pressure (PSP) was 101.1 +/- 5.0 mm Hg, end diastolic pressure (EDP) 4.4 +/- 0.5 mm Hg, glycolysis 970.5 +/- 65.3 nmol/min/gwet, and myocardial glycogen 234.8 +/- 12.0 mumol/gdry. During ischemia, PSP decreased to 23.3 +/- 2.7 mm Hg, EDP increased to 12.3 +/- 0.7 mm Hg, myocardial glycogen decreased to 181.5 +/- 30.3 mumol/gdry, and lactate (approximately 154 mumol/gwet) and glycerol (approximately 930 nmol/gwet) were released. Myocardial contracture correlated with a decrease in lactate release. Glycolysis decreased to approximately 400 nmol/min/gwet and remained stable, accounting for approximately 50% of the lactate produced. During reperfusion, PSP recovered to 79.8 +/- 3.5 mm Hg, EDP 6.6 +/- 1.7 mm Hg, and glycolysis 1103.9 +/- 81 nmol/min/gwet. In a second group of hearts, with similar mechanical responses, glucose oxidation (using 14CO2 formation from [14C]glucose) was evaluated. During baseline, glucose oxidation was 165.4 +/- 15.9 nmol/min/gwet and correlated closely (r = 0.957) with mechanical activity. With ischemia, glucose oxidation decreased to approximately 17 nmol/min/gwet, yet accounted for approximately 42% of the ATP produced. Upon reperfusion, glucose oxidation returned to baseline values, but now correlated poorly (r = 0.574) with mechanical activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Vasoactive intestinal peptide: electrophysiologic activity in the newborn heart.

We performed intracardiac electrophysiologic studies of the effects of vasoactive intestinal peptide (VIP, 0.125 micrograms/kg/min) on sinus and atrioventricular (AV) nodal function, intracardiac conduction, and myocardial refractoriness in two groups of neonatal dogs (aged 6-16 d). Group I consisted of eight neonates in whom VIP was administered after bilateral vagotomy and beta-blockade with propranolol. Group II consisted of five neonates studied after vagotomy and propranolol, plus total chemical sympathectomy (6-hydroxydopamine). In both groups, VIP resulted in a significant shortening of sinus cycle length. AV nodal conduction time, measured as the AH interval (the time from the onset of the atrial electrogram to the onset of the His bundle electrogram in the His electrode catheter) during atrial pacing, also shortened after VIP. His-Purkinje conduction time and atrial effective refractory periods were unchanged by VIP. In other experiments, the direct chronotropic effect of VIP was evaluated in five isolated neonatal canine hearts using a modified Langendorff technique. In these hearts, the spontaneous cycle length decreased from 403 +/- 88 to 293 +/- 69 ms, or -28 +/- 4% (mean +/- SD), after exposure to 0.1-0.5 nmol of VIP (p < 0.001). In nine other newborns (aged 4-16 days), the effect of selective alpha 1- and alpha 2-adrenergic receptor blockade on the positive chronotropic effect of VIP was evaluated. The effect of VIP on sinus cycle length was not altered by the alpha 1-adrenergic receptor blocker prazosin or by the alpha 2-adrenergic receptor blocker yohimbine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Pituitary adenylate cyclase activating polypeptide: a neuropeptide with potent inotropic and coronary vasodilatory effects in neonatal pig hearts.

Cardiac effects of the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) have not previously been reported. We investigated the influence of PACAP, vasoactive intestinal polypeptide (68% homology with PACAP) and the beta-adrenergic receptor agonist isoproterenol on contractile function and coronary vascular tone in isolated piglet hearts (1 to 5 d of age). Paced (180 beats/min) isovolumically beating hearts underwent retrograde aortic perfusion at constant coronary flow (approximately 3 mL.min-1.g-1) with an erythrocyte-enriched (hematocrit 15 to 20%) solution (37 degrees C). Agonists were injected into the aortic root of hearts, and the positive (+) and negative (-) changes in maximum rate of change of systolic pressure with respect to time (dP/dtmax) and in coronary perfusion pressure (that reflected alterations in vascular tone) were measured. PACAP (n = 8, 0.1 and 0.5 nmol) increased (+) dP/dtmax from 944 +/- 59 to 1519 +/- 206 mm Hg/s and from 867 +/- 40 to 2010 +/- 226 mm Hg/s (p < 0.05); increased (-) dP/dtmax from 1114 +/- 41 to 1439 +/- 95 mm Hg and from 999 +/- 37 to 1668 +/- 145 mm Hg/s (p < 0.05); and decreased perfusion pressure from 61.4 +/- 3.1 to 48.9 +/- 2.3 mm Hg and from 60.5 +/- 2.4 to 43.9 +/- 2.3 mm Hg (p < 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1992

Acetylcholine-induced coronary vasoconstriction and negative inotropy in the neonatal pig heart.

We investigated the influence of exogenously administered acetylcholine, nitric oxide, ADP, ATP, bradykinin, and substance P on coronary vascular tone in isolated, neonatal pig hearts (less than or equal to 4 d). Paced (180 bpm), isovolumically beating hearts underwent retrograde aortic perfusion, with an erythrocyte-enriched solution (hematocrit 0.15-0.20) at constant coronary flow (approximately 2.5 mL/min/g) corresponding to a perfusion pressure of approximately 60 mm Hg. Agonists were injected into the aortic root, and the peak change in coronary perfusion pressure from baseline and left ventricular pressure development were assessed. Nitric oxide (3 microL), ADP (30 nmol), ATP (30 nmol), bradykinin (125 ng), and substance P (50 ng) decreased the perfusion pressure (vasodilation) by 16.9 +/- 1.2, 25.3 +/- 4.4, 18.3 +/- 1.2, 18.9 +/- 1.4, and 7.1 +/- 1.6 mm Hg, respectively. Acetylcholine (0.5 and 1.0 nmol) produced a modest decrease in perfusion pressure (vasodilatation) of 4.2 +/- 0.8 and 3.8 +/- 0.5 mm Hg, respectively, whereas acetylcholine (5, 20, and 100 nmol) increased the perfusion pressure (vasoconstriction) by 16.7 +/- 2.7, 48.2 +/- 8.2, and 85.3 +/- 15.1 mm Hg, respectively. Acetylcholine also decreased left ventricular peak systolic pressure from 108.7 +/- 5.0 to 69.2 +/- 4.6, 56.3 +/- 6.1, and 48.2 +/- 6.4 mm Hg, for the 5, 20, and 100 nmol doses, respectively. Responses to acetylcholine were abolished by atropine (50 nmol). In a separate group of hearts, indomethacin (10(-6) M) reduced the peak change in perfusion pressure for the 5, 20, and 100 nmol doses of acetylcholine by 87%, 66%, and 48%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Intralobar pulmonary sequestration presenting as congestive heart failure in a neonate.

We recently evaluated a premature infant with intralobar pulmonary sequestration which presented with signs of CHF. The infant initially underwent ligation of a PDA but subsequently developed tachycardia, tachypnea, and a continuous murmur which radiated to the back. The diagnosis of a pulmonary sequestration was suggested by Doppler echocardiography and confirmed by aortography. The sequestration was successfully treated by surgical removal of the involved lobe.

Aortography↗
PubMed1991

The effects of milrinone in the neonatal pig heart.

Milrinone, a selective inhibitor of phosphodiesterase (PDE), was examined in neonatal hearts and in ventricular myocytes. Isolated, paced (180 beats/min), isovolumically beating hearts from pigs, less than 3 days of age, were perfused with an erythrocyte-enriched solution. In one group (control, n = 6), milrinone was studied at perfusate concentrations of 1, 10, and 100 micrograms/ml. In a second group (postischemia, n = 10), hearts were subjected to 30 minutes of no-flow ischemic arrest, prior to the addition of milrinone. Left ventricular peak systolic pressure (PSP) and end-diastolic pressure, coronary flow (CF), heart rate (HR), and myocardial oxygen consumption (MVO2) were measured. The PSP averaged approximately 100 mmHg during the baseline periods for both groups and decreased to approximately 85 mmHg in those hearts subjected to ischemic arrest. In both groups, PSP increased approximately 14% at the 1 micrograms/ml concentration of milrinone. No additional increases in PSP were observed in the control group at the higher concentrations. However, PSP increased 28% and 41% (p less than 0.05), in the postischemia group at the 10 and 100 micrograms/ml concentrations, respectively. The CF averaged approximately 3 ml/min/g during the baseline periods of both groups and increased significantly at each milrinone concentration. The HR in both groups increased to approximately 200 and approximately 250 beats/min at the 10 and 100 micrograms/ml concentrations, respectively. Additionally, milrinone's effects in intact hearts were found to be comparable to those of isobutylmethyl xanthine (IBMX), a nonspecific PDE inhibitor. In isolated myocytes, however, milrinone produced only modest increases in cAMP levels, compared to IBMX.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1990

Mechanical function and fatty acid oxidation in the neonatal pig heart with ischemia and reperfusion.

We investigated mechanical function and exogenous fatty acid oxidation in neonatal pig hearts subjected to ischemia, followed by reperfusion. Isolated, isovolumically-beating hearts, from pigs 12 h to 2 days of age, were perfused with an erythrocyte-enriched (hematocrit approximately 15%) solution (37 degrees C). All hearts were studied for 30 min. with a perfusion pressure of 60 mmHg (pre-ischemia). One group of hearts (low-flow ischemia, N = 12) was then perfused for 30 min. with a perfusion pressure of approximately 12 mmHg. In the other group (no-flow ischemic arrest, N = 9), the perfusion pressure was zero for 30 min. Following ischemia in both groups, the perfusion pressure was restored to 60 mmHg for 40 min. (reperfusion). Pre-ischemia parameters for all hearts averaged: left ventricular peak systolic pressure, 99.0 +/- 2.0 mmHg; end diastolic pressure, 1.9 +/- 0.2 mmHg; coronary flow, 3.4 +/- 0.1 ml/min per g; myocardial oxygen consumption, 56.6 +/- 1.6 microliter/min per g and fatty acid oxidation, 33.4 +/- 1.4 nmol/min per g. During low-flow ischemia, hearts released lactate, and the corresponding parameters decreased to: 30.7 +/- 0.9 mmHg; 1.2 +/- 0.3 mmHg; 0.8 +/- 0.1 ml/min per g; 26.6 +/- 2.3 microliters/min per g and 12.9 +/- 1.1 nmol/min per g, respectively. Early in reperfusion in both groups, all parameters, except for fatty acid oxidation, exceeded pre-ischemia values, before recovering to near pre-ischemia values. Late in reperfusion, however, rates of fatty acid oxidation exceeded pre-ischemia rates by approximately 60%. Thus, the neonatal pig heart demonstrated similar recovery following 30 min of low-flow ischemia or no-flow ischemic arrest.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Importance of fatty acid oxidation in the neonatal pig heart with hypoxia and reoxygenation.

We investigated mechanical and metabolic responses in isolated, isovolumically-beating, pig hearts (n = 7), 12 h to 2 days of age; subjected to hypoxia followed by reoxygenation. Hearts were perfused with an erythrocyte-enriched (hematocrit approximately 15%) solution during 3 consecutive 30-min periods: pre-hypoxia, arterial perfusate [O2] = 7.6 +/- 0.2 vol% (PO2 approximately 270 torr); hypoxia, [O2] = 0.6 +/- 0.1 vol% (approximately 10% hemoglobin saturation) and reoxygenation. Prehypoxia parameters averaged: left ventricular peak systolic pressure, 107.1 +/- 2.9 mmHg and end-diastolic pressure, 0.9 +/- 0.3 mmHg; coronary flow, 2.8 +/- 0.2 ml/min per g; myocardial O2 consumption, 59.4 +/- 1.6 microliters/min per g and fatty acid oxidation, 37.1 +/ 1.1 nmol/min per g. Fatty acid oxidation was determined using [14C]palmitate. Early in hypoxia, coronary flow increased 3-4 fold but then decreased. Throughout hypoxia, hearts released lactate yet continued to oxidize fatty acids (45-50% of myocardial O2 consumption). By the end of the hypoxia period, hearts exhibited mechanical failure (peak systolic pressure approximately 55 mmHg and end-diastolic pressure approximately 19 mmHg). After 30 min of reoxygenation, peak systolic pressure recovered to 80.6 +/- 2.6 mmHg and end-diastolic pressure remained elevated at 6.1 +/- 1.9 mmHg. However, fatty acid oxidation rates were 90-95% above pre-hypoxia values. Thus, during 30 min of severe hypoxia neonatal pig hearts exhibited mechanical dysfunction, yet continued to oxidize exogenously supplied fatty acids. Moreover, fatty acid oxidation was enhanced during reoxygenation.

Animals↗
PubMed1989

Ventricular function and fatty acid metabolism in neonatal piglet heart.

Studies in which subcellular systems were used suggest that neonatal myocardium has a sharply limited capacity to metabolize fatty acids. The relationship of these findings to the intact heart was tested on piglets, 8 h to 12 days of age. Left ventricular (LV) performance, O2 consumption (MVO2), and fatty acid (FA) uptake and oxidation were measured. Hearts were perfused at 70 cmH2O pressure with buffer containing 2% bovine serum albumin, insulin (100 microU/ml), 5 mM glucose, and 1.5 mM lactate. 14C-labeled palmitate was added (net FA, 0.5 mM). Washed erythrocytes were used to assure adequate O2 delivery. LV end-diastolic pressure (EDP) was controlled with a fluid-filled balloon. FA oxidation was estimated by measuring 14CO2 production. Hearts less than 24 h (group I, n = 6), those approximately 3 days (group II, n = 5), and those 6-12 days of age (group III, n = 10) were compared. Measurements at a low EDP (2-4 cmH2O) and at a higher EDP (7-9 cmH2O) were compared. At the low EDP, rates of FA oxidation for groups I-III averaged 30.0 +/- 3.0, 31.4 +/- 2.9, and 50.2 +/- 2.6 nmol.min-1.g-1, respectively. These values increased to 43.8 +/- 3.7, 42.6 +/- 2.5, and 63.8 +/- 4.0 nmol.min-1.g-1, respectively, at the higher EDP level (P less than 0.01 for each group). Thus within a few hours of birth, pig hearts are able to oxidize long-chain FA, and the rate of oxidation is linked to mechanical function. However, both the oxidation rate and the percentage of MVO2 accounted for by FA oxidation are greater in older hearts.

Algorithms↗
PubMed1988

Aneurysms of the right ventricular outflow tract after tetralogy of Fallot repair: role of radiology.

Eight patients with aneurysms of the right ventricular outflow tract patch following tetralogy of Fallot repair were found to have residual distal obstructions. The site of such an obstruction must be carefully documented preoperatively because failure to relieve significant distal obstruction may result in recurrent aneurysm formation. Chest radiography; echocardiography, including Doppler analysis; and cardiac catheterization, including angiocardiography, each have a role in the detection and evaluation of this complication.

Angiocardiography↗
PubMed1988

Late closure of the ductus arteriosus using indomethacin in the preterm infant.

Several studies have shown a lack of effect of indomethacin therapy for the closure of a patent ductus arteriosus (PDA) in premature infants over 14 days of postnatal age. In this report we describe two cases in which a hemodynamically significant PDA was closed with indomethacin in preterm infants over 20 days of age. The response to indomethacin may be more related to postconceptual age than to actual postnatal age. We suggest that intravenous indomethacin therapy should be attempted before surgical ligation is performed in those premature infants under 34 weeks postconceptual age who have a hemodynamically significant patent ductus arteriosus.

Ductus Arteriosus, Patent↗