Preeclampsia and risk of maternal pulmonary hypertension at high altitude in Bolivia.

Women with a history of preeclampsia (PE) have a greater risk of pulmonary arterial hypertension (PAH). In turn, pregnancy at high altitude is a risk factor for PE. However, whether women who develop PE during highland pregnancy are at risk of PAH before and after birth has not been investigated. We tested the hypothesis that during highland pregnancy, women who develop PE are at greater risk of PAH compared to women undergoing healthy highland pregnancies. The study was on 140 women in La Paz, Bolivia (3640m). Women undergoing healthy highland pregnancy were controls (C, n = 70; 29 ± 3.3 years old, mean±SD). Women diagnosed with PE were the experimental group (PE, n = 70, 31 ± 2 years old). Conventional (B- and M-mode, PW Doppler) and modern (pulsed wave tissue Doppler imaging) ultrasound were applied for cardiovascular íííassessment. Spirometry determined maternal lung function. Assessments occurred at 35 ± 4 weeks of pregnancy and 6 ± 0.3 weeks after birth. Relative to highland controls, highland PE women had enlarged right ventricular (RV) and right atrial chamber sizes, greater pulmonary artery dimensions and increased estimated RV contractility, pulmonary artery pressure and pulmonary vascular resistance. Highland PE women had lower values for peripheral oxygen saturation, forced expiratory flow and the bronchial permeability index. Differences remained 6 weeks after birth. Therefore, women who develop PE at high altitude are at greater risk of PAH before and long after birth. Hence, women with a history of PE at high altitude have an increased cardiovascular risk that transcends the systemic circulation to include the pulmonary vascular bed.

[Neonatal infectious endocarditis. Apropos of 5 cases]. / Endocardites infectieuses néonatales. A propos de cinq observations.

Five cases of neonatal infective endocarditis are reported. The mitral, tricuspid and pulmonary valves were involved either alone or in association. The predisposing factors were multiple: umbilical catheter, respiratory distress with assisted ventilation, septicemia, osteoarthritis or gastroenteritis. Only one child had a minor cardiac malformation. The causal organism was a staphylococcus aureus in all cases. All children had disseminated intravascular coagulation and a cardiac murmur. The diagnosis was confirmed by echocardiographic demonstration of bacterial vegetations. Three of the 5 children died despite long-term antibiotic therapy. In one case, a vegetation embolised to the pulmonary artery. In the two cured neonates the vegetations disappeared. These cases illustrate the value of echocardiography which should be performed in all neonates with septicemia or disseminated intravascular coagulation, especially when there is an associated cardiac murmur.