Patent arterial duct

Abstract

Patent arterial duct (PAD) is a congenital heart abnormality defined as persistent patency in term infants older than three months. Isolated PAD is found in around 1 in 2000 full term infants. A higher prevalence is found in preterm infants, especially those with low birth weight. The female to male ratio is 2:1. Most patients are asymptomatic when the duct is small. With a moderate-to-large duct, a characteristic continuous heart murmur (loudest in the left upper chest or infraclavicular area) is typical. The precordium may be hyperactive and peripheral pulses are bounding with a wide pulse pressure. Tachycardia, exertional dyspnoea, laboured breathing, fatigue or poor growth are common. Large shunts may lead to failure to thrive, recurrent infection of the upper respiratory tract and congestive heart failure. In the majority of cases of PAD there is no identifiable cause. Persistence of the duct is associated with chromosomal aberrations, asphyxia at birth, birth at high altitude and congenital rubella. Occasional cases are associated with specific genetic defects (trisomy 21 and 18, and the Rubinstein-Taybi and CHARGE syndromes). Familial occurrence of PAD is uncommon and the usual mechanism of inheritance is considered to be polygenic with a recurrence risk of 3%. Rare families with isolated PAD have been described in which the mode of inheritance appears to be dominant or recessive. Familial incidence of PAD has also been linked to Char syndrome, familial thoracic aortic aneurysm/dissection associated with patent arterial duct, and familial patent arterial duct and bicuspid aortic valve associated with hand abnormalities. Diagnosis is based on clinical examination and confirmed with transthoracic echocardiography. Assessment of ductal blood flow can be made using colour flow mapping and pulsed wave Doppler. Antenatal diagnosis is not possible, as PAD is a normal structure during antenatal life. Conditions with signs and symptoms of pulmonary overcirculation secondary to a left-to-right shunt must be excluded. Coronary, systemic and pulmonary arteriovenous fistula, peripheral pulmonary stenosis and ventricular septal defect with aortic regurgitation and collateral vessels must be differentiated from PAD on echocardiogram. In preterm infants with symptomatic heart failure secondary to PAD, treatment may be achieved by surgical ligation or with medical therapy blocking prostaglandin synthesis (indomethacin or ibuprofen). Transcatheter closure of the duct is usually indicated in older children. PAD in preterm and low birth weight infants is associated with significant comorbidity and mortality due to haemodynamic instability. Asymptomatic patients with a small duct have a normal vital prognosis but have a lifetime risk of endocarditis. Patients with moderate-tolarge ducts with significant haemodynamic alterations may develop irreversible changes to pulmonary vascularity and pulmonary hypertension.

Controversies in the definition and management of insignificant left-to-right shunts

“…PDAs account for 10% of all CHDs with an incidence of 1 per 2000 term births 44 45. Small PDAs represent 3% of these cases.…”

Patent ductus arteriosus in mice with smooth muscle-specific Jag1 deletion

“…One of the primary physiological signals regulating patency of the ductus arteriosus is the level of circulating prostaglandins (Clyman, 2006;Forsey et al, 2009;Schneider and Moore, 2006). The most important of these is prostaglandin E2 (PGE 2 ), which signals through the G protein-coupled receptor EP4 (also known as PTGER4).…”

“…Failure of the ductus arteriosus to close after birth is termed PDA and is one of the most common human congenital heart defects. PDA patients are at increased risk of pulmonary and cardiac problems such as pulmonary hemorrhage, congestive heart failure, chronic lung disease, sepsis and necrotizing enterocolitis (Clyman, 2006;Forsey et al, 2009;Schneider and Moore, 2006). Mice with smooth muscle-specific deletion of Jag1 exhibit defects in contractile smooth muscle cell differentiation in the vascular wall of the ductus arteriosus and adjacent descending aorta.…”

Paracetamol (acetaminofeno) intravenoso para cierre de conducto arterioso permeable en prematuros ≤ 32 semanas de gestación

“…Por otro lado, el cierre espontáneo ocurre solo en el 30-35% de los RNPT con peso < 1000 g 5 . El PCA se asocia fuertemente con las trisomías 21, 18 y 13, y con otras condiciones como los síndromes de CHARGE, Noonan y Holt-Oram, y la rubéola congénita 6 . El tratamiento puede incluir medidas generales de control de la ventilación y líquidos, el uso de fármacos inhibidores de la ciclooxigenasa o el cierre quirúrgico 7 .…”