Abstract

In the 16th century, Potosi (3976 m) was one of the most important cities in the world, because of its silver mountain. A Spaniard chronicle reported 100% mortality of newborns from Spaniard parents at that time, and women migrated to lower altitude cities to give birth. Several generations later, “the miracle of Saint Nicolas” occurred and a boy survived in Potosí after 6 dead siblings. Since that time, more and more children from sea level mothers (not high altitude natives) survive birth at high altitude, and the genes for postnatal adaptation to chronic hypobaric hypoxia are widespread in the 21st century. Some factors—such as birth weight, maternal anemia, pre-eclampsia, and existence of congenital diseases—have been clearly defined as prognostic for surviving birth. Pregnancy at high altitude is associated with a reduction in birth weight of approximately 100 g per 1000 m of ascent. Low birth weight affects mostly children from mothers without high altitude ancestry, but not native babies, and evidence of endoplasmatic reticulum stress and protein synthesis inhibition in the placenta of nonnative women at high altitude have been found. Children from natives may be protected by the augmented uterine artery flow described for this group. Also, there is the possibility that elevated enzymatic antioxidant activity contributes to the Andean protection against altitude-associated small for gestational age infants. Hemoglobin concentrations in mothers at high altitude are well studied. When appropriate adjustments were used, maternal anemia was associated with lower infant Apgar scores at both 1 minute and 5 minutes after birth, as well as complication of labor, lower gestational age at birth, and higher parity. Little is reported about congenital heart diseases, their natural history, especially regarding pulmonary hypertension, and the unique physiology of indigenous high altitude residents in this context. Our investigation team has been working on this last topic since 2003. We report the results of 4000 echocardiographic studies performed in 3500 patients born at 3600 m in La Paz, Bolivia, not older than 3 months. The patient group was selected by pediatricians and referred because of heart murmur, cyanosis, syndromal fenotype, heart failure, oxygen dependency, and enhanced cardiac size in the Rx. Of these, 20.1% of the children showed no abnormal finding, 18.1% showed pulmonary hypertension (defined as systolic pulmonary pressure of more than 40 mm Hg or more than two thirds from the systemic pressure) in the absence of congenital heart disease, 14.6% showed ventricular septal defect, 20% presented with patent ductus arteriosus, 14.2% atrial septal defect, 5.1% tricuspidal atresia, 2.6% complete atrioventricular channel, 2.5% tetralogy of Fallot, 2.5% Shone complex, and 0.4% others. We assume that the high incidence of pulmonary hypertension in this group, with oxygen dependency and right ventricle hypertrophy for weeks, is due to a prolonged postnatal adaptation period. The most important reason for this phenomenon is the late remodeling of the pulmonary artery branches, which implies the persistence of a thick musculary media. The persistent elevation of the pulmonary pressure and hypoxia are predisposing factors to patency of the ductus arteriosus. Right-sided congenital heart diseases like tricuspid atresia are 3 times more frequent in our patient cohort than at sea level; being left-sided significantly lowers their incidence. Environmental and genetic circumstances may both play a role in the pathogenesis of congenital heart disease at high altitude.

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