Victor G. Davila-Roman, MD, FACC, FASE

Victor G. Davila-Roman, MD, FACC, FASE

Professor of Medicine, Anesthesiology, and Radiology
Medical Director, Cardiovascular Imaging and Clinical Research Core Laboratory
Director, Global Health Center, Institute for Public Health

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Education

  • BS in Biology: University of Puerto Rico, Mayaguez, Puerto Rico, USA (1977)
  • Medical Doctor: University of Puerto Rico School of Medicine, San Juan, Puerto Rico, USA (1981)
  • Internal Medicine Internship: Brooke Army Medical Center, Fort Sam Houston, San Antonio, TX (1982)
  • Internal Medicine Residency: The Jewish Hospital of St. Louis, St. Louis, MO (1988)
  • Cardiology Fellowship: The Jewish Hospital of St. Louis, St. Louis, MO (1990)
  • Advanced Echocardiographic Fellowship: Barnes Hospital, Washington University School of Medicine, St. Louis, MO (1991)
  • Nuclear Cardiology Residency, Mallinckrodt Institue of Radiology, Division of Nuclear Medicine: Washington University School of Medicine, St. Louis, MO (1995)

Board Certifications

  • Cardiovascular Disease
  • Echocardiography
  • Nuclear Medicine

Recognition

  • American College Cardiology / European Society Cardiology International Academic Exchange Program, 1998
  • Jewish Hospital Biomedical Research Support Grant (BSRG), 1990
  • U.S. Army Commendation Medical, 1986

Clinical Interests

Cardiomyopathy; magnetic resonance imaging; myocardiology; hypertension; vascular surgery; coronary artery disease; supervising and interpreting diagnostic tests, such as echocardiograms, stress echocardiograms, treadmill stress test, Holter, event and loop monitors.

Research Interests

Research interests include the study of hypertension (HTN), a disease that affects over 65 million Americans and one of the most common chronic diseases in the world. Hypertensive heart disease (HHD)-endophenotypes, including left ventricular hypertrophy, LV diastolic dysfunction, LV systolic dysfunction, and vascular hypertrophy are common and inter-related. Furthermore, HHD-endophenotypes are worsened by co-morbid conditions such as diabetes, obesity, metabolic syndrome, and dyslipidemia, thus suggesting that common underlying pathologic processes control/modulate these phenotypes through gene-gene and/or gene-environment interactions. Genes involved in myocardial metabolism and inflammation have been postulated as modulators of these highly complex endophenotypes. Through our large cardiovascular disease phenotype-genotype repository, we are conducting a genome-wide association study where important genes will be associated with quantitative HHD-endophenotypes.