Efficacy of very low-dose prostaglandin E1 in duct-dependent congenital heart disease

Yücel, İlker Kemal; Çevik, Ayhan; Bulut, Mustafa; Dedeoğlu, Reyhan; Demir, İbrahim; Erdem, Abdullah; Çelebi, Ahmet

doi:10.1017/s1047951113001522

Cited by 14 publications

(11 citation statements)

References 18 publications

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“…Previous studies of the pharmacological activities of PGE1 mainly focused on its effect on vasodilation. These studies showed that PGE1 can increase peripheral blood flow in heart, kidney, liver, and eyes in patients with peripheral vascular disease (Shin et al, 2012; Zhao et al, 2013; Yucel et al, 2015; Steigerwalt et al, 2016; Li et al, 2018). Emerging evidence has also shown that PGE1 activates angiogenesis and fibrinolysis, inhibits platelet aggregation, fibrinogenesis, inflammatory cell activity and proliferation (Schror and Hohlfeld, 2004; Huang et al, 2008; Gao et al, 2010).…”

Section: Introductionmentioning

confidence: 97%

Prostaglandin E1 Alleviates Cognitive Dysfunction in Chronic Cerebral Hypoperfusion Rats by Improving Hemodynamics

Xie

Chen

et al. 2019

Front. Neurosci.

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Compensatory vascular mechanisms can restore cerebral blood flow (CBF) but fail to protect against chronic cerebral hypoperfusion (CCH)-mediated neuronal damage and cognitive impairment. Prostaglandin E1 (PGE1) is known as a vasodilator to protect against ischemic injury in animal models, but its protective role in CCH remains unclear. To determine the effect of PGE1 on cerebral hemodynamics and cognitive functions in CCH, bilateral common carotid artery occlusion (BCCAO) was used to mimic CCH in rats, which were subsequently intravenously injected with PGE1 daily for 2 weeks. Magnetic resonance imaging, immunofluorescence staining and Morris water maze (MWM) were used to evaluate CBF, angiogenesis, and cognitive functions, respectively. We found that PGE1 treatment significantly restored CBF by enhancing vertebral artery dilation. In addition, PGE1 treatment increased the number of microvascular endothelial cells and neuronal cells in the hippocampus, and decreased the numbers of astrocyte and apoptotic cells. In the MWM test, we further showed that the escape latency of CCH rats was significantly reduced after PGE1 treatment. Our results suggest that PGE1 ameliorates cognitive dysfunction in CCH rats by enhancing CBF recovery, sustaining angiogenesis, and reducing astrocyte activation and neuronal loss.

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Section: Introductionmentioning

confidence: 97%

Prostaglandin E1 Alleviates Cognitive Dysfunction in Chronic Cerebral Hypoperfusion Rats by Improving Hemodynamics

Xie

Chen

et al. 2019

Front. Neurosci.

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“…This is in contrast with other studies that have suggested that patients with systemic obstruction require higher doses. 12,18 One possible explanation for this discrepancy is that our systemic obstruction cohort had a high level of prenatal diagnosis (74%) compared with other studies, where this patient population was typically older at diagnosis, and thus we were able to start prostaglandin E1 earlier in patients with systemic obstruction. Within our study, higher doses were required for those with systemic obstruction who were diagnosed postnatally (5/23, 22%) than for those diagnosed prenatally (4/65, 6%, p = 0.049).…”

Section: Efficacy Of Low-dose Prostaglandin E1mentioning

confidence: 82%

“…The authors also concluded that lesions with systemic obstruction may require higher doses. 18 Despite these investigations into the efficacy of lower dose prostaglandin E1, many dosage guidelines continue to recommend high starting doses. [6][7][8] Our current study is the largest retrospective study in the current era and is unique in describing infants who were uniformly started on low-dose prostaglandin E1, even prior to transport, and utilised the same low-dose infusion for maintenance.…”

Section: Efficacy Of Low-dose Prostaglandin E1mentioning

confidence: 99%

“…22 Other studies that have investigated lower dose prostaglandin E1 have found a lower incidence of respiratory depression. 17,18 There is evidence that prostaglandin E1-induced respiratory depression is dosedependent, 11,12 although one study does not support this. 13 In a 1994 study, Singh et al investigated lower doses (<0.01 μg/kg/ minute) in 34 patients.…”

Section: Adverse Effectsmentioning

confidence: 99%

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Low-dose prostaglandin E1 is safe and effective for critical congenital heart disease: is it time to revisit the dosing guidelines?

et al. 2020

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Introduction: Prostaglandin E1 is used to maintain ductal patency in critical congenital heart disease (CHD). The standard starting dose of prostaglandin E1 is 0.05 µg/kg/minute. Lower doses are frequently used, but the efficacy and safety of a low-dose regimen of prostaglandin E1 has not been established. Methods: We investigated neonates with critical CHD who were started on prostaglandin E1 at 0.01 µg/kg/minute. We reviewed 154 consecutive patients who were separated into three anatomical groups: obstruction to systemic circulation, obstruction to pulmonary circulation, and inadequate mixing (d-transposition of the great arteries). Treatment failure rates and two commonly reported side effects, respiratory depression and seizure, were studied. Results: A total of 26 patients (17%) required a dose increase in prostaglandin E1. Patients with pulmonary obstruction were more likely to require higher doses than patients with systemic obstruction (15/49, 31% versus 9/88, 10%, p = 0.003). Twenty-eight per cent of patients developed respiratory depression and 8% of patients needed mechanical ventilation. Prematurity (<37 week gestation) was the primary risk factor for respiratory depression. No patient required dose escalation or tracheal intubation while on transport. No patient had a seizure attributed to prostaglandin E1. Conclusions: Prostaglandin E1 at an initial and maintenance dose of 0.01 µg/kg/minute was sufficient to maintain ductal patency in 83% of our cohort. The incidence of respiratory depression requiring mechanical ventilation was low and was mostly seen in premature infants. Starting low-dose prostaglandin E1 at 0.01 µg/kg/minute is a safe and effective therapy for critical CHD.

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“…Prostaglandin E1 (PGE 1 ) kann eingesetzt werden, wenn sich der Ductus arteriosus schließt, um ein Rechtsherzversagen bei schwer betroffenen NG zu verhindern. PGE 1 verhindert den Verschluss des Ductus arteriosus und schafft so ein "Überdruckventil" und druckentlastet so das rechte Herz auf Kosten einer verstärkten Hypoxämie (18). Dieser Therapieansatz ist bislang nicht evidenzbasiert und daher als individueller Heilversuch zu betrachten.…”

Section: Prostaglandin E1unclassified

Persistierende pulmonale Hypertonie des Neugeborenen und chronisch progressive pulmonale Hypertonie im ersten Lebensjahr

Giagnorio

Deindl

Brinkmann

et al. 2015

Kinder- und Jugendmedizin

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ZusammenfassungDie persistierende pulmonale Hypertonie des Neugeborenen (PPHN) ist eine seltene, heterogene Erkrankung mit hoher Mortalität. Die PPHN ist gekennzeichnet durch einen hohen pulmonalen Gefäßwiderstand (PVR, Rp) und einen erhöhten pulmonalarteriellen Druck (PAP) sowie extra- und intrapulmonale Rechts-Links-Shunts. Entstehen kann sie auf dem Boden von Lungenentwicklungsstörungen, intrauterinen Ereignissen oder bei der Anpassung an das extrauterine Leben. Die PPHN tritt häufig in Assoziation mit einer primären oder sekundären Lungen -erkrankung auf, die entweder das Broncho-Alveolar system, die Lungengefäße oder die pulmonalen Lymphgefäße betrifft. Betroffen sind meist reife oder fast reife Neugeborene (NG) innerhalb der ersten 30 Lebenstage. Auslöser können Erkrankungen sein, die zu einem respiratorischen Versagen mit alveolärer Hypoxie führen (Mekonium -aspirationssyndrom (MAS), angeborene Pneumonie, Sepsis, Geburtsasphyxie, Atemnotsyndrom (RDS), Lungenhypoplasie, Zwerchfellhernie (CDH), alveoläre kapilläre Dysplasie (ACD), pulmonale Lymphangiektasie). Ferner kommen als Ursachen Noxen wie die Einnahme von Medikamenten und Drogen während der Schwangerschaft infrage. Die PPHN kann ebenfalls idiopathisch auftreten. Postnatal kommt es durch die zunehmende Belüftung der Lunge zu einem physiologischen Abfall des Widerstandes in den Lungenarteriolen. Bleibt diese extrauterine Adaptation aus oder besteht eine vorbestehende anatomische oder funktionelle Beeinträchtigung der pulmonalen Arteriolen, kann sich eine PPHN entwickeln. Über den Ductus arteriosus, das Foramen ovale und intrapulmonale Kurzschlüsse wird nicht oxygeniertes Blut im Sinne eines Recht-Links-Shunts an den ventilierten Arealen der Lunge vorbeigeleitet. Klinisch resultiert eine Zyanose. Der erhöhte pulmonale Gefäßwiderstand führt des Weiteren zu einer Nachlasterhöhung und einer Druckbelastung des rechten Ventrikels (RV), die über Tage bis Wochen in ein Rechtsherz versagen münden kann.Eine Sonderform der pulmonalen Hypertonie im ersten Lebensjahr stellt die chronisch progressive pulmonale Hypertonie (PH) dar, die sich im Laufe der ersten Lebenswochen bis -monate entwickeln kann. Im Vergleich zur neonatalen PPHN liegen hier wahrscheinlich andere Ursa-chen und Pathomechanismen zugrunde. Eine PPHN ist per se akut, kann aber auch in eine chronisch progressive PH übergehen.

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Efficacy of very low-dose prostaglandin E1 in duct-dependent congenital heart disease

Abstract: Our findings indicate that the infusion of prostaglandin at a very low dose (0.003-0.005 mcg/kg/minute) is sufficient to maintain the patency of the ductus arteriosus. A higher dose of prostaglandin E1 may be necessary in patients with inadequate systemic blood flow.

Cited by 14 publications

References 18 publications

Prostaglandin E1 Alleviates Cognitive Dysfunction in Chronic Cerebral Hypoperfusion Rats by Improving Hemodynamics

Prostaglandin E1 Alleviates Cognitive Dysfunction in Chronic Cerebral Hypoperfusion Rats by Improving Hemodynamics

Low-dose prostaglandin E1 is safe and effective for critical congenital heart disease: is it time to revisit the dosing guidelines?

Persistierende pulmonale Hypertonie des Neugeborenen und chronisch progressive pulmonale Hypertonie im ersten Lebensjahr

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