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
Trisomy 21 (T21), a recurrent aneuploidy occurring in 1:800 births, predisposes to congenital heart disease (CHD) and multiple extracardiac phenotypes. Despite a definitive genetic etiology, the mechanisms by which T21 perturbs development and homeostasis remain poorly understood. We compared the transcriptome of CHD tissues from 49 patients with T21 and 226 with euploid CHD (eCHD). We resolved cell lineages that misexpressed T21 transcripts by cardiac single-nucleus RNA sequencing and RNA in...
Journal article
CONCLUSIONS: Pathogenic variants and viral myocarditis were identified in 45.9% of patients with unexplained end-stage cardiomyopathy. Damaging gene variants are significantly more frequent among transplant compared with patients with ambulatory cardiomyopathy. Genetic analyses can help define cause of end-stage cardiomyopathy to guide management and risk stratification of patients and family members.
