title: Myocardial beta-adrenoceptor density one month after acute myocardial infarction predicts left ventricular volumes at six months.
abstract: OBJECTIVE
  To investigate whether myocardial beta-adrenoceptor (beta-AR) downregulation precedes and predicts left ventricular (LV) dilation after acute myocardial infarction (AMI), we measured beta-AR density within four weeks of AMI and correlated it with serial measurements of LV volumes.
  
  
  BACKGROUND
  Patients who develop heart failure following AMI have an increased sympathetic drive to the heart within the first four weeks after infarction.
  
  
  METHODS
  We prospectively studied 61 patients in whom AMI was the first presentation of coronary artery disease (CAD) and with no signs of heart failure. The LV volumes were measured one, three, and six months after AMI by echocardiography. Beta-AR density was measured using positron emission tomography with S-[(11)C]CGP 12177. Seventeen matched healthy volunteers served as controls.
  
  
  RESULTS
  Whole heart beta-AR density was lower in patients than in controls (6.25 +/- 0.98 pmol/g vs. 8.32 +/- 2.14 pmol/g, p < 0.0001). In patients, beta-AR density was inversely correlated with end-systolic and end-diastolic volumes six months after AMI. Patients whose LV was dilated at six months had a lower beta-AR density in noninfarcted myocardium than patients without dilation (6.15 pmol/g vs. 6.98 pmol/g, p = 0.008). In addition, beta-AR density in noninfarcted myocardium was higher when the infarct-related artery was patent (6.87 +/- 1.14 pmol/g vs. 5.76 +/- 0.86 pmol/g occluded, p < 0.01).
  
  
  CONCLUSIONS
  Myocardial beta-AR density is reduced after AMI in the absence of heart failure, and the reduction predicts later LV dilation. These data are suggestive of an enhanced sympathetic drive to the heart, having an important etiologic role in LV remodeling after AMI.
authors.affiliation: Medical Research Council Clinical Sciences Centre and National Heart and Lung Institute, Faculty of Medicine, Imperial College, London, United Kingdom.
authors.forename: Nicos
authors.initials: N
authors.lastname: Spyrou
authors.forename: Stuart D
authors.initials: SD
authors.lastname: Rosen
authors.forename: Farzin
authors.initials: F
authors.lastname: Fath-Ordoubadi
authors.forename: Rohan
authors.initials: R
authors.lastname: Jagathesan
authors.forename: Rodney
authors.initials: R
authors.lastname: Foale
authors.forename: Jaspal S
authors.initials: JS
authors.lastname: Kooner
authors.forename: Paolo G
authors.initials: PG
authors.lastname: Camici
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D002395:Catecholamines / Q000097:blood; D018450:Disease Progression; D015536:Down-Regulation; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications* / Q000473:pathology* / Q000628:therapy; D011237:Predictive Value of Tests; D011446:Prospective Studies; D011943:Receptors, Adrenergic, beta / Q000032:analysis* / Q000235:genetics; D012720:Severity of Illness Index; D013318:Stroke Volume; D013997:Time Factors; D014055:Tomography, Emission-Computed; D016896:Treatment Outcome; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D002395:Catecholamines; D011943:Receptors, Adrenergic, beta