title: Echocardiographic Pulmonary Artery Systolic Pressure in the Coronary Artery Risk Development in Young Adults (CARDIA) Study: Associations With Race and Metabolic Dysregulation.
abstract: BACKGROUND
  The determinants of pulmonary artery systolic pressure (PASP) are not fully understood. It is unknown whether racial differences in PASP exist or if other population characteristics are associated with pulmonary pressure in humans. We examined echocardiographically estimated PASP in the Coronary Artery Risk Development in Young Adults (CARDIA) study, a middle-aged, biracial community-based cohort.
  
  
  RESULTS
  At the CARDIA year-25 examination, 3469 participants underwent echocardiography, including measurement of tricuspid regurgitant jet velocity to estimate PASP. Clinical features, laboratory values, pulmonary function tests, and measurement of adipose depot volume were analyzed for association with PASP. PASP was estimated in 1311 individuals (61% female, 51% white). Older age, higher blood pressure, and higher body mass index were associated with higher PASP. Black race was associated with higher PASP after adjustment for demographics and left and right ventricular function (β 0.94, 95% CI 0.24-1.64;P=0.009), but this association was no longer significant after further adjustment for lung volume (β 0.42, 95% CI -0.68 to 0.96;P=0.74). Insulin resistance, inflammation (C-reactive protein and interleukin-6), and visceral adipose volume were independently associated with higher PASP after adjustment for relevant covariates. PASP rose with worsening diastolic function (ratio of early transmitral Doppler velocity to average mitral annular tissue Doppler velocity [E/e'] and left atrial volume index).
  
  
  CONCLUSIONS
  In a large biracial cohort of middle-aged adults, we identified associations among black race, insulin resistance, and diastolic dysfunction with higher echocardiographically estimated PASP. Further studies are needed to examine racial differences in PASP and whether insulin resistance directly contributes to pulmonary vascular disease in humans.
authors.affiliation: Vanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University Medical Center, Nashville, TN evan.brittain@vanderbilt.edu.|Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN.
authors.forename: Evan L
authors.initials: EL
authors.lastname: Brittain
authors.affiliation: Division of Cardiology, Johns Hopkins Hospital, Baltimore, MD.|Harvard Medical School, Mount Auburn Hospital, Cambridge, MA.
authors.forename: Chike
authors.initials: C
authors.lastname: Nwabuo
authors.affiliation: Department of Biostatistics, Vanderbilt University School of Medicine, Nashville, TN.
authors.forename: Meng
authors.initials: M
authors.lastname: Xu
authors.affiliation: Vanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University Medical Center, Nashville, TN.|Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN.
authors.forename: Deepak K
authors.initials: DK
authors.lastname: Gupta
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN.
authors.forename: Anna R
authors.initials: AR
authors.lastname: Hemnes
authors.affiliation: Division of Cardiology, Johns Hopkins Hospital, Baltimore, MD.|Division of Cardiology, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Henrique T
authors.initials: HT
authors.lastname: Moreira
authors.affiliation: Division of Cardiology, Johns Hopkins Hospital, Baltimore, MD.
authors.forename: Henrique Doria
authors.initials: HD
authors.lastname: De Vasconcellos
authors.affiliation: Vanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University Medical Center, Nashville, TN.
authors.forename: James G
authors.initials: JG
authors.lastname: Terry
authors.affiliation: Vanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University Medical Center, Nashville, TN.
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Carr
authors.affiliation: Division of Cardiology, Johns Hopkins Hospital, Baltimore, MD.
authors.forename: Joao A C
authors.initials: JA
authors.lastname: Lima
mesh_terms: D001741:Black or African American; D000367:Age Factors; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000276:immunology; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000453:epidemiology* / Q000208:ethnology; D004452:Echocardiography; D015150:Echocardiography, Doppler; D005006:Ethnicity; D005260:Female; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000208:ethnology; D006976:Hypertension, Pulmonary / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000208:ethnology; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000276:immunology; D050152:Intra-Abdominal Fat / Q000000981:diagnostic imaging / Q000473:pathology; D008297:Male; D024821:Metabolic Syndrome / Q000453:epidemiology* / Q000208:ethnology; D008875:Middle Aged; D050177:Overweight / Q000453:epidemiology / Q000208:ethnology; D011651:Pulmonary Artery; D013599:Systole; D014022:Tissue Survival; D014057:Tomography, X-Ray Computed; D044465:White People
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D002097:C-Reactive Protein
keywords: adipose tissue; echocardiography; inflammation; metabolic syndrome; pulmonary hypertension