HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH RSS TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lotze, U. Articles by Figulla, H. R. Search for Related Content PubMed PubMed Citation Articles by Lotze, U. Articles by Figulla, H. R.

Recovery of the Cardiac Adrenergic Nervous System After Long-Term ß-Blocker Therapy in Idiopathic Dilated Cardiomyopathy: Assessment by Increase in Myocardial ¹²³I-Metaiodobenzylguanidine Uptake

Department of Internal Medicine III (Cardiology, Angiology, and Intensive Care Medicine) and Department of Nuclear Medicine, Friedrich-Schiller-University, Jena, Germany

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 ß-adrenoceptors. The clinical and prognostic effectiveness of ß-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 ß-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 ß-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 ß-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 ß-blocker therapy (P = 0.139) was also found. Conclusion: 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 ß-blockers in IDC causes a recovery of the cardiac adrenergic nervous system concomitantly with a clinical and hemodynamic improvement.

Key Words: cardiac adrenergic activity • ¹²³I-MIBG • idiopathic dilated cardiomyopathy • ß-blocker therapy

This article has been cited by other articles:

				S. G. Drakos, T. Athanasoulis, K. G. Malliaras, J. V. Terrovitis, N. Diakos, D. Koudoumas, A. S. Ntalianis, S. P. Theodoropoulos, M. H. Yacoub, and J. N. Nanas Myocardial Sympathetic Innervation and Long-Term Left Ventricular Mechanical Unloading J. Am. Coll. Cardiol. Img., January 1, 2010; 3(1): 64 - 70. [Abstract] [Full Text] [PDF]

				J. S. Floras Sympathetic nervous system activation in human heart failure: clinical implications of an updated model. J. Am. Coll. Cardiol., July 28, 2009; 54(5): 375 - 385. [Abstract] [Full Text] [PDF]

				M. Kobayashi, H. Izawa, X. W. Cheng, H. Asano, A. Hirashiki, K. Unno, S. Ohshima, T. Yamada, Y. Murase, T. S. Kato, et al. Dobutamine stress testing as a diagnostic tool for evaluation of myocardial contractile reserve in asymptomatic or mildly symptomatic patients with dilated cardiomyopathy. J. Am. Coll. Cardiol. Img., November 1, 2008; 1(6): 718 - 726. [Abstract] [Full Text] [PDF]

				S. Klotz, A. Barbone, S. Reiken, J. W. Holmes, Y. Naka, M. C. Oz, A. R. Marks, and D. Burkhoff Left ventricular assist device support normalizes left and right ventricular beta-adrenergic pathway properties J. Am. Coll. Cardiol., March 1, 2005; 45(5): 668 - 676. [Abstract] [Full Text] [PDF]

				C. Kurata, A. Uehara, and A. Ishikawa Improvement of Cardiac Sympathetic Innervation by Renal Transplantation J. Nucl. Med., July 1, 2004; 45(7): 1114 - 1120. [Abstract] [Full Text] [PDF]

				C.-s. Liang Sympatholysis and cardiac sympathetic nerve function in the treatment of congestive heart failure J. Am. Coll. Cardiol., August 6, 2003; 42(3): 549 - 551. [Full Text] [PDF]

				C.-S. Liang, Y. Himura, M. Kashiki, and S. Y. Stevens Differential pre- and postsynaptic effects of desipramine on cardiac sympathetic nerve terminals in RHF Am J Physiol Heart Circ Physiol, November 1, 2002; 283(5): H1863 - H1872. [Abstract] [Full Text] [PDF]

				K. Watanabe, T. Takahashi, M. Nakazawa, M. I. I. Wahed, K. Fuse, N. Tanabe, M. Kodama, Y. Aizawa, H. Ashino, and S. Tazawa Effects of Carvedilol on Cardiac Function and Cardiac Adrenergic Neuronal Damage in Rats with Dilated Cardiomyopathy J. Nucl. Med., April 1, 2002; 43(4): 531 - 535. [Abstract] [Full Text] [PDF]