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
CONCLUSION: Damaging variants in FOXI3 are the second most frequent genetic cause of CFM, causing 1% of all cases, including 13% of familial cases in our cohort.
Journal article
Microtia is a congenital malformation that encompasses mild hypoplasia to complete loss of the external ear, or pinna. Although the contribution of genetic variation and environmental factors to microtia remains elusive, Amerindigenous populations have the highest reported incidence. Here, using both transmission disequilibrium tests and association studies in microtia trios (parents and affected child) and microtia cohorts enrolled in Latin America, we map an ∼10-kb microtia locus (odds ratio =...
