One option for improving the welfare of purebred dog breeds is to implement health breeding programmes, which allow selection to be directed against known diseases while controlling the rate of inbreeding to a minimal level in order to maintain the long-term health of the breed. The aim of this study is to evaluate the predicted impact of selection against disease in two breeds: the Cavalier King Charles spaniel (CKCS) and the Labrador Retriever. Heritabilities for mitral valve disease, syringomyelia in the CKCS and hip dysplasia in the Labrador were estimated to be 0.64 (± 0.07), 0.32 (± 0.125) and 0.35 (± 0.016), respectively, which suggest encouraging selection responses are feasible based upon the estimation of breeding values (EBVs) if monitoring schemes are maintained for these breeds. Although using data from disease databases can introduce problems due to bias, as a result of individuals and families with disease usually being over-represented, the data presented is a step forward in providing information on risk. EBVs will allow breeders to distinguish between potential parents of high and low risk, after removing the influence of life history events. Analysis of current population structure, including numbers of dogs used for breeding, average kinship and average inbreeding provides a basis from which to compare breeding strategies. Predictions can then be made about the number of generations it will take to eradicate disease, the number of affected individuals that will be born during the course of selective breeding and the benefits that can be obtained by using optimisation to constrain inbreeding to a pre-defined sustainable rate.

A 15-month-old child underwent percutaneous expansion of a Melody transcatheter pulmonary valve in the mitral position to accommodate growth after initial surgical implantation during infancy, but transiently decompensated after valvuloplasty owing to stent malformation. The Melody valve in the mitral position of small patients can be further expanded by percutaneous dilation, but there are a number of potential complications and technical improvements to consider.

Differentiation between a cleft of the mitral valve and the cleft of the left side of an atrioventricular septal defect – a lesion commonly found in patients with Down's syndrome – is surgically important since the distribution of the conduction tissue varies between the 2 lesions. We sought to determine if cleft of the mitral valve occurs also in patients with Down's syndrome. We studied 5 patients with Down's syndrome and cleft of the mitral valve followed in our institution. Echocardiography showed in all 5 patients a cleft dividing the anterior (aortic) leaflet of mitral valve with normal papillary muscle position, mural leaflet size, and ratio of the inlet/outlet dimension of the left ventricle. Associated cardiac lesions were present in all 5 patients: perimembranous ventricular septal defect in 3, ostium secundum atrial septal defect in 2 and patent ductus arteriosus in 2 patients. During the 5.6 years (0.2–11) of the follow-up period, surgical repair of the cleft was never indicated since the mitral regurgitation through the cleft remained mild or absent in all the patients. Two patients underwent closure of a ventricular septal defect, with atrial septal defect closure in one and ductal ligation in 2. One patient died suddenly at home, without evidence of a cardiac cause. In conclusion, a cleft of the mitral valve has important developmental and morphologic differences with atrioventricular septal defect and may occur in patients with Down's syndrome. If surgical repair of the cleft or of associated cardiac lesion is indicated, it is necessary to distinguish it from atrioventricular septal defect where the conduction axis is displaced posteriorly and may be exposed during surgery.