Attending, Department of Cardiology, Boston Children’s Hospital
Instructor in Pediatrics, Harvard Medical School
Dr. Daniel Quiat is a pediatric
cardiologist at Boston Children’s Hospital and an Instructor of Pediatrics at
Harvard Medical School. Dr. Quiat earned his MD and PhD in 2014 from the
Medical Science Training Program (MSTP) at University of Texas Southwestern
Medical Center. Dr. Quiat then completed both his residency and fellowship at
Boston Children’s Hospital, where he is board certified in pediatrics and
pediatric cardiology with specialties in pediatric cardiomyopathies and
congenital heart defects. In addition to his clinical responsibilities, Dr.
Quiat pursues biomedical research in cardiovascular development and genetics in
collaboration with the Seidman Lab at Harvard Medical School
Department of Genetics, with a goal of identifying genetic causes of single
ventricle heart disease and illuminating the role of those genetic factors in
the development of heart failure and other clinical outcomes.
Attending, Department of Cardiology, Boston Children’s Hospital
Instructor in Pediatrics, Harvard Medical School
Dr. Daniel Quiat is a pediatric
cardiologist at Boston Children’s Hospital and an Instructor of Pediatrics at
Harvard Medical School. Dr. Quiat earned his MD and PhD in 2014 from the
Medical Science Training Program (MSTP) at University of Texas Southwestern
Medical Center. Dr. Quiat then completed both his residency and fellowship at
Boston Children’s Hospital, where he is board certified in pediatrics and
pediatric cardiology with specialties in pediatric cardiomyopathies and
congenital heart defects. In addition to his clinical responsibilities, Dr.
Quiat pursues biomedical research in cardiovascular development and genetics in
collaboration with the Seidman Lab at Harvard Medical School
Department of Genetics, with a goal of identifying genetic causes of single
ventricle heart disease and illuminating the role of those genetic factors in
the development of heart failure and other clinical outcomes.
Journal article
remains challenging. To test the hypothesis that SVs from people with congenital heart disease (CHD) disrupt developmental chromatin interactions, we developed CardioAkita, a machine-learning model that predicts how variants alter 3D chromatin structure. Analyzing previously genotyped de novo SVs (dnSVs), we observed a positive association between CHD severity and CardioAkita scores across dozens of families. From whole-genome sequencing of three individuals with CHD we predicted disruptive...
Journal article
CONCLUSION: A small MAD distance can be measured in healthy children and young adults. Children and young adults with CTD have a longer MAD distance than healthy control subjects, and a longer MAD distance is associated with adverse outcomes.