Chronic Low Dose Prostaglandin and Neonatal Heart Block

Safwat A Aly1, Sawsan M Awad2, Ra-Id Abdulla2

  • 1Department of Pediatrics, Division of Cardiology, Rush University Medical College, 1653 W. Congress Pkwy., Pavilion 654, Chicago, IL, 60612, USA. safwat_aly@rush.edu.

Insights

Prostaglandin E1 (PGE1) infusion in neonates with critical coarctation of the aorta can cause atrioventricular blocks, even at low doses. These heart rhythm disturbances resolved after discontinuing PGE1 and surgical repair.

Area of Science:

  • Neonatal Cardiology
  • Pediatric Pharmacology
  • Congenital Heart Disease

Background:

  • Prostaglandin E1 (PGE1) is crucial for maintaining ductus arteriosus patency in neonates with congenital heart defects like coarctation of the aorta.
  • Commonly reported side effects of long-term prostaglandin use include bone and soft tissue abnormalities.

Observation:

  • A neonate with critical coarctation of the aorta experienced second and third-degree atrioventricular blocks during a prolonged Prostaglandin E1 (PGE1) infusion.
  • These cardiac conduction abnormalities were observed specifically at low doses of PGE1.

Findings:

  • The study identified a novel association between low-dose Prostaglandin E1 (PGE1) infusion and severe atrioventricular blocks in a neonate with critical aortic coarctation.
  • Resolution of atrioventricular blocks occurred promptly upon cessation of PGE1 infusion.

Implications:

  • This case highlights a potential risk of cardiac conduction disturbances with PGE1 use in neonates, even at low therapeutic doses.
  • Careful cardiac monitoring is warranted during PGE1 therapy, particularly in neonates with complex congenital heart disease.
  • The findings suggest a need for further investigation into the dose-dependent effects of PGE1 on cardiac electrophysiology in neonates.

Related Concept Videos

Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is...
1.3K
Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in...
1.8K
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
1.3K
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
555
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
1.0K
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
1.4K