Maternal tobacco use and extremely premature birth - a population-based cohort study.

OBJECTIVE: To study the associations of maternal tobacco use (smoking or use of snuff) and risk of extremely preterm birth, and if tobacco cessation before antenatal booking influences this risk. To study the association between tobacco use and spontaneous or medically indicated onset of delivery. DESIGN: Population-based cohort study. SETTING: Sweden. POPULATION: All live singleton births, registered in the Swedish Medical Birth Register, 1999-2012. METHODS: Odds ratios (OR) with 95% confidence intervals (CI) were calculated using multiple logistic regression analysis. MAIN OUTCOME MEASURES: Extremely preterm birth (<28 weeks of gestation), very preterm birth (28-31 weeks), moderately preterm birth (32-36 weeks). RESULTS: Maternal snuff use (OR 1.58; 95% CI: 1.14-2.21) and smoking (OR 1.61; 95% CI: 1.39-1.87 and OR 1.91; 95% CI: 1.53-2.39 for moderate and heavy smoking, respectively) were associated with an increased risk of extremely preterm birth. When cessation of tobacco use was obtained there was no increased risk of preterm birth. Snuff use was associated with a twofold risk increase of medically indicated extremely preterm birth, whereas smoking was associated with increased risks of both medically indicated and spontaneous extremely preterm birth. CONCLUSIONS: Snuff use and smoking in pregnancy were associated with increased risks of extremely preterm birth. Women who stopped using tobacco before the antenatal booking had no increased risk. These findings indicate that nicotine, the common substance in cigarettes and snuff, is involved in the mechanisms behind preterm birth. The use of nicotine should be minimized in pregnancy. TWEETABLE ABSTRACT: Tobacco use increases risk of extremely preterm birth. Cessation is preventive. Avoid nicotine in pregnancy.

Obese children without comorbidities have impaired microvascular endothelial function.

AIM: The aim was to test acetylcholine-induced endothelium-dependent vasodilatation in obese children without comorbidities, compared with normal weight controls, and to analyse associations between vasodilatation and other potential risk factors. METHODS: Endothelium-dependent vasodilatation was induced by transdermal iontophoresis of acetylcholine in 54 obese children (8.3-18.2 years old, 41% girls) and 44 normal weight controls (7.5-20.2 years old, 82% girls), and the subsequent change in perfusion was measured with laser Doppler flowmetry. In a subgroup of the obese children, associations between acetylcholine-induced vasodilatation and blood lipids, glucose/insulin metabolism, inflammation, 24-h ambulatory blood pressure (ABP), cardiovascular fitness and duration of obesity were evaluated. RESULTS: We found a lower endothelium-dependent vasodilatory response to acetylcholine in the obese children than the controls (p < 0.001). The peak perfusion response was 33% lower in obese children (p = 0.001). There was a trend towards lower vasodilatation in obese children with higher levels of triglycerides (p = 0.07). Children with the shortest duration of obesity exhibited the lowest vasodilatation (p = 0.03). No associations were found between 24-h ABP, cardiovascular fitness, inflammation and glucose/insulin metabolism. CONCLUSION: Obese children without comorbidities have significantly impaired microvascular endothelial function. The children who had been obese for a longer time seemed less affected.

[Patent ductus arteriosus. A common clinical problem in extremely premature infants]. / Oppetstående ductus arteriosus. Ett vanligt kliniskt problem för extremt underburna barn.

An analysis was made of the incidence and treatment regimen of symptomatic patent ductus arteriosus (PDA) in 95 preterm infants treated 1997-1999 in a level three intensive care unit in Stockholm. 47 infants (49 percent) had PDA. Of these 17 infants were managed conservatively (fluid restriction and diuretics), 13 were treated with indomethacin, 10 underwent primary surgical ligation and 7 were treated with indomethacin first and surgery later on. The proportion of infants given "active" therapy (surgery and/or indomethacin) rose from 50 percent in 1997 to 85 percent in 1999. In a stepwise multiple regression analysis low birthweight, septicaemia and need for mechanical ventilation were all independently associated with PDA.

Aortic growth arrest after preterm birth: a lasting structural change of the vascular tree.

Young people who are born very preterm exhibit a narrower arterial tree as compared with people born at term. We hypothesized that such arterial narrowing occurs as a direct result of premature birth. The aim of this study was to compare aortic and carotid artery growth in infants born preterm and at term. Observational and longitudinal cohort study of 50 infants (21 born very preterm, all appropriate for gestational age, 29 controls born at term) was conducted. Diameters of the upper abdominal aorta and common carotid artery were measured with ultrasonography at three months before term, at term and three months after term-equivalent age. At the first assessment, the aortic end-diastolic diameter (aEDD) was slightly larger in very preterm infants as compared with fetal dimensions. Fetal aortic EDD increased by 2.6 mm during the third trimester, whereas very preterm infants exhibited 0.9 mm increase in aEDD during the same developmental period (P < 0.001 for group difference). During the following 3-month period, aortic growth continued unchanged (+0.9 mm) in very preterm infants, whereas postnatal growth in term controls slowed down to +1.3 mm (P < 0.001 v. fetal aortic growth). At the final examination, aEDD was 22% and carotid artery EDD was 14% narrower in infants born preterm compared with controls, also after adjusting for current weight (P < 0.01). Aortic and carotid artery growth is impaired after very preterm birth, resulting in arterial narrowing. Arterial growth failure may be a generalized vascular phenomenon after preterm birth, with implications for cardiovascular morbidity in later life.