Background-Plasma levels of atrial natriuretic peptide (ANP) are elevated in patients with chronic obstructive pulmonary disease (COPD) and may have a role in preventing oedema formation in these patients. Methods-Plasma ANP levels were measured in 60 patients with COPD and these measurements were related to pulmonary haemodynamics, response to treatment during exacerbations, and clinical patterns of the stable disease. Results-Plasma ANP levels did not correlate significantly with right atrial or pulmonary arterial pressures but did correlate significantly with both the right ventricular end diastolic volume and right ventricular wall volume measured by magnetic resonance imaging. Oxygen (2 1/min by nasal prongs for 30 minutes) did not change the mean pulmonary arterial pressure or the level of plasma ANP. In 20 patients with an acute exacerbation of COPD plasma ANP levels were higher in those with oedema (302 (185) pg/ml) than in those without oedema (87 (43) pg/ml). Oxygen given for one hour had no effect on plasma levels of ANP. However, plasma ANP levels fell over the first three days during treatment in those with oedema, the fall correlating with the change in body weight. In a further 20 stable patients with hypoxic COPD, those with hypercapnia and previous episodes of oedema had higher levels of plasma ANP (120 (50) pglml) than normocapnic patients with no previous oedema (54 (15) pg/ml). Conclusions-The level of ANP is high in the plasma of patients with COPD, particularly during exacerbations in those with oedema. The association of a high plasma ANP level and volume overload is shown by the fall in ANP levels with treatment of the oedema, and the correlation between levels of ANP and right ventricular end diastolic or wall volumes. (Thorax 1993;48:730-735) The traditional view of the development of peripheral oedema in patients with chronic obstructive pulmonary disease (COPD) suggests that chronic hypoxia is responsible for pulmonary vasoconstriction which eventually leads to irreversible pulmonary hypertension, increased right ventricular work, and right ventricular failure.' 2 This sequence of events has been challenged recently.3 The right ventricular performance is relatively well preserved in patients with COPD, even in the face of pulmonary hypertension.45 Moreover, the decline in right ventricular function in patients with COPD presenting with oedema may not be as a direct result of an augmented right ventricular afterload.5 6 Furthermore, not all patients with COPD and pulmonary hypertension develop oedema, suggesting decompensated cor pulmonale during exacerbations of their condition.

Background and aims Neurodevelopmental disorders are common in children with congenital heart disease (CHD) and largely ascribed to prenatal factors such as impaired cerebral growth. It remains to be established whether this is due to impaired intrauterine cerebral blood flow or genuine genetic causes. Down syndrome (DS) is a known cause of CHD, neurodevelopmental disorders and microcephaly. Hence, studies on DS may provide insight into the causes of impaired cerebral growth in CHD. We aimed to assess the risk of microcephaly in children with DS and CHD compared to children with DS and no CHD. Methods Children with DS (n = 389) and specific birth characteristics were identified in national registries. Head circumference and the risk of microcephaly (head circumference <-2SD) was compared between children with CHD (n = 168) and children without CHD (n = 221) by linear and logistic regression analyses (unadjusted and adjusted for gender and gestational age). Results There was no difference in head circumference between the groups, 0.0 cm (95% CI -0.4-0.4). Adjustment did not significantly alter the results. The risk of microcephaly was slightly higher in newborns with CHD, OR 1.4 (95% CI 0.8-2.6). Adjustment did not significantly alter the results. Conclusions We did not find indications of impaired head growth in children with DS and concomitant CHD. There might be a slight increase in the risk of microcephaly. We suggest that the most common types of CHD in DS i.e. atrioventricular septal defects, ventricular septal defects and atrial septal defects do not impair prenatal cerebral growth in children with DS.