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Patients with pulmonary regurgitation after tetralogy of Fallot repair have impaired aerobic capacity; one of the reasons is the decreasing global ventricular performance at exercise, reflected by decreasing peak oxygen pulse. The aims of our study were to evaluate the impact of pulmonary valve replacement on peak oxygen pulse in a population with pure pulmonary regurgitation and with different degrees of right ventricular dilatation and to determine the predictors of peak oxygen pulse after pulmonary valve replacement.
The mean and median age at pulmonary valve replacement was 27 years. Mean pre-procedural right ventricular end-diastolic volume was 182 ml/m2. Out of 24 patients, 15 had abnormal peak oxygen pulse before pulmonary valve replacement. We did not observe a significant increase in peak oxygen pulse after pulmonary valve replacement (p=0.76). Among cardiopulmonary test/MRI/historical pre-procedural parameters, peak oxygen pulse appeared to be the best predictor of peak oxygen pulse after pulmonary valve replacement (positive and negative predictive values, respectively, 0.94 and 1). After pulmonary valve replacement, peak oxygen pulse was well correlated with left ventricular stroke and end-diastolic volumes (r=0.67 and 0.68, respectively).
Our study confirms the absence of an effect of pulmonary valve replacement on peak oxygen pulse whatever the initial right ventricular volume, reflecting possible irreversible right and/or left ventricle lesions. Pre-procedural peak oxygen pulse seemed to well predict post-procedural peak oxygen pulse. These results encourage discussions on pulmonary valve replacement in patients showing any decrease in peak oxygen pulse during their follow-up.
Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene–nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient–genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.
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