title: Evidence of diminished coronary flow in pulmonary hypertension: explaining angina pectoris in this patient group?
abstract: BACKGROUND
  Many patients with pulmonary hypertension (PH) have symptoms of angina without evidence of occlusive coronary artery disease. For the first time, this study addresses the influence of progressively increasing pulmonary artery pressure (PAP) on left anterior descending artery flow in a rat model of PH. The role of pulmonary artery dilatation, septal wall motion abnormality, cardiac output or diastolic blood pressure in determining coronary blood flow (CBF) during PH was determined.
  
  
  METHODS
  Pulmonary hypertension was induced in 6-week-old female nude rats (n = 44) using monocrotaline. Animals underwent right heart catheterization and echocardiography, and blood pressure measurement was taken at baseline, 21 and 35 days.
  
  
  RESULTS
  A total of 103 echocardiographic studies were carried out at three fixed time points in rats with variable PAP. CBF decreased from 46·6 ± 14·3 to 24·7 ± 12·3 cm s(-1) (P<0·001) over time. Pulmonary artery diameter increased from 2·30 ± 0·19 to 2·83 ± 0·30 mm (P<0·001), and left ventricular (LV) cardiac output decreased from 143 ± 23 to 78 ± 30 ml min(-1) (P<0·001). Using observed solution estimates of 0·00170 (P = 0·0005) and -1·75 (P = 0·006) for these variables, we calculated that CBF increased by 5·90 cm s(-1) (15·6%, CI: 14·5-17·1%) or decreased by -4·86 cm s(-1) (-12·9%, CI: -14·1-11·9%) for every standard deviation increase in LV cardiac output or pulmonary artery diameter, respectively. CBF decreased significantly with increasing PAP. Pulmonary artery diameter and LV cardiac output appear to be independent determinants of coronary flow in PH.
  
  
  CONCLUSIONS
  Coronary flow reduction in murine PH has potential to be clinically meaningful and should therefore further studied in a clinical trial.
authors: Division of Cardiology, Department of Medicine, University of California, San Francisco, USA. juhkos@utu.fi
authors: Juha W
authors: JW
authors: Koskenvuo
authors: Rachel
authors: R
authors: Mirsky
authors: Yan
authors: Y
authors: Zhang
authors: Hans
authors: H
authors: Helenius
authors: Franca S
authors: FS
authors: Angeli
authors: Teresa
authors: T
authors: De Marco
authors: Andrew J
authors: AJ
authors: Boyle
authors: Yerem
authors: Y
authors: Yeghiazarians
mesh_terms: D000787:Angina Pectoris / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D006328:Cardiac Catheterization; D002302:Cardiac Output; D003326:Coronary Circulation; D004108:Dilatation, Pathologic; D004195:Disease Models, Animal; D015150:Echocardiography, Doppler; D005260:Female; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D016686:Monocrotaline; D011651:Pulmonary Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D011652:Pulmonary Circulation; D051381:Rats; D011923:Rats, Nude; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: D016686:Monocrotaline