title: Recovery of the cardiac adrenergic nervous system after long-term beta-blocker therapy in idiopathic dilated cardiomyopathy: assessment by increase in myocardial 123I-metaiodobenzylguanidine uptake.
abstract: In chronic heart failure, elevated plasma norepinephrine (NE) levels and a disparity between the neuronal release and the effective reuptake of NE lead to an increased concentration of NE in the presynaptic cleft, causing a downregulation of the myocardial beta-adrenoceptors. The clinical and prognostic effectiveness of beta-blocker therapy has been shown in patients with chronic heart failure in several large trials. The purpose of this study was to investigate the effect of long-term beta-blocker therapy on the cardiac adrenergic nervous system as assessed by the myocardial uptake of 123I-metaiodobenzylguanidine (MIBG), an analog of NE, in idiopathic dilated cardiomyopathy (IDC).
  
  
  METHODS
  In 10 patients with IDC and stable chronic heart failure the myocardial MIBG uptake was measured at baseline and at 1 y (median, 11.5 mo) after treatment with beta-blockers (metoprolol, n = 5; bisoprolol, n = 1; and carvedilol, n = 4) in addition to standard medication. In parallel with the changes in MIBG uptake, the New York Heart Association functional class, the left ventricular ejection fraction (LVEF), and the left ventricular end-diastolic diameter (LVEDD) were documented before and after 1 y of therapy with beta-blockers.
  
  
  RESULTS
  During the 1-y follow-up, a significant increase in myocardial 123I-MIBG uptake (P = 0.005) in parallel with an improved LVEF (P = 0.005) and a reduced LVEDD (P = 0.019) was found. A trend toward an improvement of the New York Heart Association functional class under the beta-blocker therapy (P = 0.139) was also found.
  
  
  CONCLUSIONS
  Assessment of the myocardial 123I-MIBG uptake is a useful noninvasive tool for evaluating changes in cardiac sympathetic nerve activity under medical therapy. Long-term treatment with beta-blockers in IDC causes a recovery of the cardiac adrenergic nervous system concomitantly with a clinical and hemodynamic improvement.
authors.affiliation: Department of Internal Medicine III, Friedrich-Schiller-University, Jena, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Lotze
authors.forename: S
authors.initials: S
authors.lastname: Kaepplinger
authors.forename: A
authors.initials: A
authors.lastname: Kober
authors.forename: B M
authors.initials: BM
authors.lastname: Richartz
authors.forename: D
authors.initials: D
authors.lastname: Gottschild
authors.forename: H R
authors.initials: HR
authors.lastname: Figulla
mesh_terms: D019797:3-Iodobenzylguanidine; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging* / Q000188:drug therapy*; D005260:Female; D005500:Follow-Up Studies; D006321:Heart / Q000000981:diagnostic imaging / Q000294:innervation*; D006801:Humans; D007457:Iodine Radioisotopes; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D011446:Prospective Studies; D019275:Radiopharmaceuticals; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D017256:Technetium Tc 99m Sestamibi; D013997:Time Factors; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D000319:Adrenergic beta-Antagonists; D007457:Iodine Radioisotopes; D019275:Radiopharmaceuticals; D019797:3-Iodobenzylguanidine; D017256:Technetium Tc 99m Sestamibi