Standard pharmacologic closure of the patent ductus arteriosus currently involves the administration of 1 of 2 cyclooxygenase inhibitors: either indomethacin or ibuprofen. However, both of these drugs can be associated with potentially significant adverse effects. We present here the cases of 5 preterm infants (gestational age: 26-32 weeks; postnatal age: 3-35 days) with large, hemodynamically significant patent ductus arteriosus who had either failed or had contraindications to ibuprofen therapy. Each of these infants was treated with off-label oral paracetamol (15 mg/kg per dose every 6 hours). Ductal closure was achieved within 48 hours in all the treated infants. No toxicity was observed.

(PACE 2009; 32:7-12) permanent pacemaker, cardiac surgery IntroductionThe incidence of conduction disturbance requiring pacing after open heart operations is between 10% and 15%. [1][2][3][4] Most of these will recover, however, 1-3% of patients will require permanent pacemaker implantation. [5][6][7] We reviewed our experience with permanent pacemaker (PPM) implantation following cardiac surgery. Our aim was to identify predictors for PPM requirement and identify patients who will remain pacemaker dependent over long term.

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Numerous studies have found that depression is a strong independent risk factor for incident coronary heart disease (CHD), with increasing risk among those with higher levels of depressive symptoms. We examined the association between measures of inflammation (C-reactive protein, interleukin-6, soluble intracellular adhesion molecule-1), depressive symptoms, and CHD incidence among 1,794 participants of the population-based Canadian Nova Scotia Health Survey. There were 152 (8.5%) incident CHD events (141 nonfatal, 11 fatal) during the 15,514 person-years of observation (incidence rate=9.8 events/1000 person-years). Depression and inflammation were correlated at baseline and each significantly predicted CHD in separate models. When both risk factors were in the same model, each remained significant. The association between depressed group by the Center for Epidemiological Studies-Depression scale (score of 10+ vs. 0-9) and CHD incidence (HR=1.60, 95% CI = 1.12-2.27) was not reduced by the addition of inflammatory markers to the model (HR=1.59, 95% CI = 1.12-2.26). Findings were similar after adjustment for aspirin, lipid-lowering medication or anti-depressant use, and the association did not vary by sex, smoking status, age, obesity, cardiovascular medication use or antidepressant use. In conclusion, increased inflammation explains only a very small proportion of the association between depression and incident CHD.