title: Right ventricular morphology and function in chronic obstructive pulmonary disease patients living at high altitude.
abstract: BACKGROUND
  Pulmonary vasculature is affected in patients with chronic pulmonary obstructive disease (COPD). As a result of increased pulmonary resistance, right ventricular morphology and function are altered in COPD patients. High altitude and related hypoxia causes pulmonary vasoconstriction, thereby affecting the right ventricle. We aimed to investigate the combined effects of COPD and altitude-related chronic hypoxia on right ventricular morphology and function.
  
  
  METHODS
  Forty COPD patients living at high altitude (1768 m) and 41 COPD patients living at sea level were enrolled in the study. All participants were diagnosed as COPD by a pulmonary diseases specialist depending on symptoms, radiologic findings and pulmonary function test results. Detailed two-dimensional echocardiography was performed by a cardiologist at both study locations.
  
  
  RESULTS
  Oxygen saturation and mean pulmonary artery pressure were higher in the high altitude group. Right ventricular end diastolic diameter, end systolic diameter, height and end systolic area were significantly higher in the high altitude group compared to the sea level group. Parameters of systolic function, including tricuspid annular systolic excursion, systolic velocity of tricuspid annulus and right ventricular isovolumic acceleration were similar between groups, while fractional area change was significantly higher in the sea level groups compared to the high altitude group. Indices of diastolic function and myocardial performance index were similar between groups.
  
  
  CONCLUSIONS
  An increase in mean pulmonary artery pressure and right ventricular dimensions are observed in COPD patients living at high altitude. Despite this increase, systolic and diastolic functions of the right ventricle, as well as global right ventricular performance are similar in COPD patients living at high altitude and sea level. Altitude-related adaptation to chronic hypoxia could explain these findings.
authors.affiliation: Kafkas University School of Medicine, Kars, Turkey. TSGuvenc@gmail.com
authors.forename: Tolga Sinan
authors.initials: TS
authors.lastname: Güvenç
authors.forename: Hatice Betül
authors.initials: HB
authors.lastname: Erer
authors.forename: Seref
authors.initials: S
authors.lastname: Kul
authors.forename: Gökhan
authors.initials: G
authors.lastname: Perinçek
authors.forename: Sami
authors.initials: S
authors.lastname: Ilhan
authors.forename: Nurten
authors.initials: N
authors.lastname: Sayar
authors.forename: Binnaz Zeynep
authors.initials: BZ
authors.lastname: Yıldırım
authors.forename: Coşkun
authors.initials: C
authors.lastname: Doğan
authors.forename: Yavuz
authors.initials: Y
authors.lastname: Karabağ
authors.forename: Bahattin
authors.initials: B
authors.lastname: Balcı
authors.forename: Mehmet
authors.initials: M
authors.lastname: Eren
mesh_terms: D000368:Aged; D062186:Arterial Pressure; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D000860:Hypoxia / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000473:pathology* / Q000503:physiopathology*; D012129:Respiratory Function Tests; D016278:Ventricular Function, Right