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Daniel Quiat

M.D., Ph.D.

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.

Daniel Quiat

M.D., Ph.D.

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.

Recent Publications

Damaging variants in FOXI3 cause microtia and craniofacial microsomia

Published On 2022 Oct 19

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.


An ancient founder mutation located between ROBO1 and ROBO2 is responsible for increased microtia risk in Amerindigenous populations

Published On 2022 May 18

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 =...