title: Cardiac sympathetic dysfunction correlates with abnormal myocardial contractile reserve in dilated cardiomyopathy patients.
abstract: OBJECTIVE
  We investigated the relationship between iodine-123-metaiodobenzylguanidine (123I-MIBG) findings and myocardial contractile reserve in patients with mild to moderate dilated cardiomyopathy (DCM).
  
  
  BACKGROUND
  Little is known regarding the relationship between cardiac sympathetic nervous function and myocardial contractile reserve in DCM.
  
  
  METHODS
  Twenty-four DCM patients who showed sinus rhythm underwent echocardiography, biventricular catheterization, and myocardial 123I-MIBG scintigraphy. Left ventricular (LV) pressures were measured using a micromanometer-tipped catheter. The myocardial contractile function (LV dP/dt(max)) was determined at rest and during atrial pacing. The messenger ribonucleic acid (mRNA) expressions of intracellular Ca2+-regulatory proteins were analyzed by real-time quantitative reverse transcription-polymerase chain reaction. Myocardial 123I-MIBG accumulation was quantified as a heart-mediastinum ratio (HMR).
  
  
  RESULTS
  A significant correlation was observed between the delayed 123I-MIBG HMR and the percentage change in LV dP/dt(max) from the baseline to the peak or critical heart rate (r = 0.64; p < 0.001). The delayed 123I-MIBG HMR was significantly lower in patients showing a worsening change in LV dP/dt(max) than in those showing a favorable change (p < 0.005). The maximum LV dP/dt(max) during pacing and the sarcoplasmic reticulum Ca2+-ATPase (SERCA2) mRNA levels were significantly more reduced in patients with a delayed HMR < or =1.8 than in those with a delayed HMR >1.8 (p < 0.05, respectively).
  
  
  CONCLUSIONS
  Abnormal myocardial 123I-MIBG accumulation is related to an impaired myocardial contractile reserve and down-regulation of SERCA2 mRNA in DCM. Myocardial 123I-MIBG scintigraphy can be useful in noninvasively evaluating myocardial contractile reserve in patients with mild to moderate DCM.
authors.affiliation: Department of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.
authors.forename: Satoru
authors.initials: S
authors.lastname: Ohshima
authors.forename: Satoshi
authors.initials: S
authors.lastname: Isobe
authors.forename: Hideo
authors.initials: H
authors.lastname: Izawa
authors.forename: Mamoru
authors.initials: M
authors.lastname: Nanasato
authors.forename: Akitada
authors.initials: A
authors.lastname: Ando
authors.forename: Akira
authors.initials: A
authors.lastname: Yamada
authors.forename: Kiyoyasu
authors.initials: K
authors.lastname: Yamada
authors.forename: Tomoko S
authors.initials: TS
authors.lastname: Kato
authors.forename: Koji
authors.initials: K
authors.lastname: Obata
authors.forename: Akiko
authors.initials: A
authors.lastname: Noda
authors.forename: Takao
authors.initials: T
authors.lastname: Nishizawa
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Kato
authors.forename: Kohzo
authors.initials: K
authors.lastname: Nagata
authors.forename: Kenji
authors.initials: K
authors.lastname: Okumura
authors.forename: Toyoaki
authors.initials: T
authors.lastname: Murohara
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yokota
mesh_terms: D019797:3-Iodobenzylguanidine; D000368:Aged; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging / Q000503:physiopathology*; D005260:Female; D006321:Heart / Q000294:innervation*; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D009638:Norepinephrine / Q000097:blood; D011877:Radionuclide Imaging; D019275:Radiopharmaceuticals; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013318:Stroke Volume; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D019275:Radiopharmaceuticals; D019797:3-Iodobenzylguanidine; D009638:Norepinephrine