Person: Colan, Steven
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Colan
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Colan, Steven
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Publication Report on the International Colloquium on Cardio-Oncology (Rome, 12–14 March 2014)(Cancer Intelligence, 2014) Ewer, Michael; Gianni, Luca; Pane, Fabrizio; Sandri, Maria Teresa; Steiner, Rudolf K; Wojnowski, Leszek; Yeh, Edward T; Carver, Joseph R; Lipshultz, Steven E; Minotti, Giorgio; Armstrong, Gregory T; Cardinale, Daniela; Colan, Steven; Darby, Sarah C; Force, Thomas L; Kremer, Leontien CM; Lenihan, Daniel J; Sallan, Stephen E; Sawyer, Douglas B; Suter, Thomas M; Swain, Sandra M; van Leeuwen, Flora ECardio-oncology is a relatively new discipline that focuses on the cardiovascular sequelae of anti-tumour drugs. As any other young adolescent discipline, cardio-oncology struggles to define its scientific boundaries and to identify best standards of care for cancer patients or survivors at risk of cardiovascular events. The International Colloquium on Cardio-Oncology was held in Rome, Italy, 12–14 March 2014, with the aim of illuminating controversial issues and unmet needs in modern cardio-oncology. This colloquium embraced contributions from different kind of disciplines (oncology and cardiology but also paediatrics, geriatrics, genetics, and translational research); in fact, cardio-oncology goes way beyond the merging of cardiology with oncology. Moreover, the colloquium programme did not review cardiovascular toxicity from one drug or the other, rather it looked at patients as we see them in their fight against cancer and eventually returning to everyday life. This represents the melting pot in which anti-cancer therapies, genetic backgrounds, and risk factors conspire in producing cardiovascular sequelae, and this calls for screening programmes and well-designed platforms of collaboration between one key professional figure and another. The International Colloquium on Cardio-Oncology was promoted by the Menarini International Foundation and co-chaired by Giorgio Minotti (Rome), Joseph R Carver (Philadelphia, Pennsylvania, United States), and Steven E Lipshultz (Detroit, Michigan, United States). The programme was split into five sessions of broad investigational and clinical relevance (what is cardiotoxicity?, cardiotoxicity in children, adolescents, and young adults, cardiotoxicity in adults, cardiotoxicity in special populations, and the future of cardio-oncology). Here, the colloquium chairs and all the session chairs briefly summarised what was said at the colloquium. Topics and controversies were reported on behalf of all members of the working group of the International Colloquium on Cardio-Oncology.Publication Longitudinal Assessment of Growth in Hypoplastic Left Heart Syndrome: Results From the Single Ventricle Reconstruction Trial(Blackwell Publishing Ltd, 2014) Burch, Phillip T.; Gerstenberger, Eric; Ravishankar, Chitra; Hehir, David A.; Davies, Ryan R.; Colan, Steven; Sleeper, Lynn A.; Newburger, Jane; Clabby, Martha L.; Williams, Ismee A.; Li, Jennifer S.; Uzark, Karen; Cooper, David S.; Lambert, Linda M.; Pemberton, Victoria L.; Pike, Nancy A.; Anderson, Jeffrey B.; Dunbar‐Masterson, Carolyn; Khaikin, Svetlana; Zyblewski, Sinai C.; Minich, L. LuAnnBackground: We sought to characterize growth between birth and age 3 years in infants with hypoplastic left heart syndrome who underwent the Norwood procedure. Methods and Results: We performed a secondary analysis using the Single Ventricle Reconstruction Trial database after excluding patients <37 weeks gestation (N=498). We determined length‐for‐age z score (LAZ) and weight‐for‐age z score (WAZ) at birth and age 3 years and change in WAZ over 4 clinically relevant time periods. We identified correlates of change in WAZ and LAZ using multivariable linear regression with bootstrapping. Mean WAZ and LAZ were below average relative to the general population at birth (P<0.001, P=0.05, respectively) and age 3 years (P<0.001 each). The largest decrease in WAZ occurred between birth and Norwood discharge; the greatest gain occurred between stage II and 14 months. At age 3 years, WAZ and LAZ were <−2 in 6% and 18%, respectively. Factors associated with change in WAZ differed among time periods. Shunt type was associated with change in WAZ only in the Norwood discharge to stage II period; subjects with a Blalock‐Taussig shunt had a greater decline in WAZ than those with a right ventricle‐pulmonary artery shunt (P=0.002). Conclusions: WAZ changed over time and the predictors of change in WAZ varied among time periods. By age 3 years, subjects remained small and three times as many children were short as were underweight (>2 SD below normal). Failure to find consistent risk factors supports the strategy of tailoring nutritional therapies to patient‐ and stage‐specific targets. Clinical Trial Registration URL: http://clinicaltrials.gov/. Unique identifier: NCT00115934.Publication Adrenergic receptor genotype influences heart failure severity and β-blocker response in children with dilated cardiomyopathy(Nature Publishing Group, 2015) Reddy, Sushma; Fung, Alan; Manlhiot, Cedric; Selamet Tierney, Elif Seda; Chung, Wendy K.; Blume, Elizabeth; Kaufman, Beth D.; Goldmuntz, Elizabeth; Colan, Steven; Mital, SeemaBackground: Adrenergic receptor (ADR) genotypes are associated with heart failure (HF) and β-blocker response in adults. We assessed the influence of ADR genotypes in children with dilated cardiomyopathy (DCM). Methods: Ninety-one children with advanced DCM and 44 with stable DCM were genotyped for three ADR genotypes associated with HF risk in adults: α2cdel322-325, β1Arg389, and β2Arg16. Data were analyzed by genotype and β-blocker use. Mean age at enrollment was 8.5 y. Results: One-year event-free survival was 51% in advanced and 80% in stable DCM. High-risk genotypes were associated with higher left ventricular (LV) filling pressures, higher systemic and pulmonary vascular resistance, greater decline in LV ejection fraction (P < 0.05), and a higher frequency of mechanical circulatory support while awaiting transplant (P = 0.05). While β-blockers did not reduce HF severity in the overall cohort, in the subset with multiple high-risk genotypes, those receiving β-blockers showed better preservation of cardiac function and hemodynamics compared with those not receiving β-blockers (interaction P < 0.05). Conclusion: Our study identifies genetic risk markers that may help in the identification of patients at risk for developing decompensated HF and who may benefit from early institution of β-blocker therapy before progression to decompensated HF.