Objectives: To assess survival and long term arch patency rates in a consecutive group of children after extended arch repair for coarctation of the aorta. Methods: Review of 191 consecutive children (154 (81%) under 1 year of age) operated on between 1990 and 2002 by a single surgeon using extended arch reconstructive techniques. For assessment of survival patients were divided into three groups: 1, coarctation alone, n = 104; 2, coarctation and ventricular septal defect, n = 38; and 3, coarctation in association with complex intracardiac anomalies, n = 49. A prospective and systematic clinical and echocardiographic evaluation of the aortic arch was undertaken. Results: Median time to follow up was 4.2 years (range 1-10.6 years). Overall actuarial survival was 92%, 88%, and 88% at two, five, and 10 years. Mortality was significantly higher in those patients with complex intracardiac anatomy. Arch obstruction recurred in seven of 165 (4.2%) patients: four of 139 (2.9%) term and three of 10 (30%) premature infants (p , 0.001). Conclusions: Survival after extended arch reconstruction for coarctation is excellent. At long follow up recurrent arch obstruction is rare, with prematurity the only risk factor.
A 20-year old woman presented with prolonged refractory ventricular fibrillation and pulmonary oedema following hypothermia while she was under self-administered heroin in an attempt to commit suicide. She was successfully resuscitated with cardiopulmonary bypass for core rewarming and internal defibrillation.
Ficolins are pattern recognition molecules that are involved in innate immune defense. Ficonin-2 (FCN2) has a specific affinity for lipoteichoic acid present in the cell wall of Streptococcus pyogenes, an etiological agent for rheumatic heart disease (RHD). We have estimated FCN2 serum levels and analyzed the functional variants of FCN2 in 400 RHD patients, 617 healthy controls, and 581 individuals belonged to various ethnic populations, who are inhabited in various geographical regions of India. Our study revealed that the FCN2 -986A and +6359T alleles were the risk factors for RHD susceptibility ( p = 0.0007 for -986G>A; p = 0.0004 for +6359C>T). The haplotype AGGT ( p = 0.0024) was observed to be a risk factor for RHD susceptibility, and the haplotype GGAC ( p = 0.002) was found to confer protection against RHD. The level of serum FCN2 was significantly higher in controls ( p < 0.0001) and in controls with GGAC haplotypes ( p < 0.0001). The frequency of the risk alleles -986A and +6359T was found to be more prevalent in Northern and North-Western (Indo-European) India. The protective GGAC haplotype was found more prevalent in Eastern (Tibeto-Burman) and South-Western (Dravidian) India. Alleles -986A and +6359T were in positive correlation with the prevalence of RHD (regression coefficient = 1.84 and 1.94, respectively), whereas GGAC haplotype was in negative correlation with prevalence of RHD (regression coefficient = -1.71). In conclusion, we found that low level of serum ficolin-2 is significantly associated with RHD. Further, FCN2 -986A and +6359T alleles and AGGT haplotype are associated with increased susceptibility to RHD, while GGAC haplotype is associated with moderate protection against RHD.
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