PMID- 12598068
OWN - NLM
STAT- MEDLINE
DCOM- 20030312
LR  - 20190708
IS  - 0735-1097 (Print)
IS  - 0735-1097 (Linking)
VI  - 41
IP  - 4
DP  - 2003 Feb 19
TI  - Effect of spironolactone on cardiac sympathetic nerve activity and left 
      ventricular remodeling in patients with dilated cardiomyopathy.
PG  - 574-81
AB  - OBJECTIVES: We sought to evaluate the effects of spironolactone on cardiac 
      sympathetic nerve activity and left ventricular (LV) remodeling in patients with 
      dilated cardiomyopathy (DCM). BACKGROUND: Aldosterone prevents the uptake of 
      norepinephrine and promotes structural remodeling of the heart. Spironolactone, 
      an aldosterone receptor blocker, improves LV remodeling in patients with DCM, but 
      its influence on cardiac sympathetic nerve activity has not been determined. 
      METHODS: We selected 30 patients with DCM who were treated with an 
      angiotensin-converting enzyme inhibitor and a loop diuretic. Fifteen patients 
      were assigned to receive spironolactone additionally, whereas the remaining 15 
      patients continued their current regimen. The delayed heart/mediastinum (H/M) 
      count ratio, delayed total defect score (TDS), and washout rate (WR) were 
      determined from iodine-123 ((123)I)-meta-iodobenzylguanidine (MIBG) images before 
      and six months after treatment. The left ventricular end-diastolic volume (LVEDV) 
      and left ventricular ejection fraction (LVEF) were determined by 
      echocardiography, and New York Heart Association (NYHA) functional class was 
      estimated. RESULTS: In the spironolactone group, the TDS decreased from 36 +/- 9 
      to 24 +/- 13 (p < 0.0001), the H/M ratio increased from 1.64 +/- 0.20 to 1.86 +/- 
      0.27 (p < 0.0001), and WR decreased from 55 +/- 12% to 41 +/- 15% (p < 0.0005). 
      In addition, the LVEDV decreased from 187 +/- 26 to 154 +/- 41 ml (p < 0.005), 
      and LVEF increased from 33 +/- 6% to 39 +/- 6% (p < 0.005). However, there were 
      no significant changes in these parameters in the control group. There was a 
      significant correlation between changes in the (123)I-MIBG findings and changes 
      in LVEDV with spironolactone treatment (TDS: r = 0.684, p = 0.0038; H/M ratio: r 
      = -0.878, p < 0.0001; and WR: r = 0.737, p = 0.0011). The NYHA functional class 
      improved in both groups but showed a greater improvement in the spironolactone 
      group than in the control group (p < 0.01). CONCLUSIONS: Spironolactone improves 
      cardiac sympathetic nerve activity and LV remodeling in patients with DCM.
FAU - Kasama, Shu
AU  - Kasama S
AD  - Second Department of Internal Medicine, Gunma University School of Medicine, 
      3-39-15 Showa-machi, Maebashi, Gunma 371-0034, Japan. s-kasama@bay.wind.ne.jp
FAU - Toyama, Takuji
AU  - Toyama T
FAU - Kumakura, Hisao
AU  - Kumakura H
FAU - Takayama, Yoshiaki
AU  - Takayama Y
FAU - Ichikawa, Shuichi
AU  - Ichikawa S
FAU - Suzuki, Tadashi
AU  - Suzuki T
FAU - Kurabayashi, Masahiko
AU  - Kurabayashi M
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Randomized Controlled Trial
PL  - United States
TA  - J Am Coll Cardiol
JT  - Journal of the American College of Cardiology
JID - 8301365
RN  - 0 (Mineralocorticoid Receptor Antagonists)
RN  - 27O7W4T232 (Spironolactone)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Cardiomyopathy, Dilated/diagnosis/*drug therapy/*physiopathology
MH  - Echocardiography
MH  - Female
MH  - Follow-Up Studies
MH  - Heart/*drug effects/*innervation/physiopathology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Mineralocorticoid Receptor Antagonists/*pharmacology/*therapeutic use
MH  - Radionuclide Imaging
MH  - Spironolactone/*pharmacology/*therapeutic use
MH  - Sympathetic Nervous System/*drug effects/*physiopathology
MH  - Time Factors
MH  - Ventricular Remodeling/*drug effects/*physiology
EDAT- 2003/02/25 04:00
MHDA- 2003/03/13 04:00
CRDT- 2003/02/25 04:00
PHST- 2003/02/25 04:00 [pubmed]
PHST- 2003/03/13 04:00 [medline]
PHST- 2003/02/25 04:00 [entrez]
AID - S0735109702028553 [pii]
AID - 10.1016/s0735-1097(02)02855-3 [doi]
PST - ppublish
SO  - J Am Coll Cardiol. 2003 Feb 19;41(4):574-81. doi: 10.1016/s0735-1097(02)02855-3.