ACE inhibition reduces cardiac iodine-123-MIBG release in heart failure

Radioiodinated metaiodobenzylguanidine (123I-MIBG), an analog of norepinephrine, has been used to assess cardiac sympathetic nerve activity. Decreased myocardial accumulation and enhanced washout of 123I-MIBG have been reported in patients with congestive heart failure (CHF). The purpose of this study was to determine whether angiotensin converting enzyme (ACE) inhibition reduced 123I-MIBG release and improved cardiac 123I-MIBG accumulation in patients with CHF.

Twenty-nine patients receiving conventional treatment for CHF, New York Heart Association (NYHA) functional class 2-3, were studied. Nineteen patients received additional treatment with enalapril, an ACE inhibitor, and 10 patients who were treated with conventional therapy alone were defined as a control group. Iodine-123-MIBG imaging and echocardiography were performed on all patients before treatment and repeated after 9.1 +/- 3.0 mo of treatment. Images were obtained 30 min and 4 hr after injection of 123I-MIBG, and a heart to mediastinum (H/M) ratio was defined to quantify cardiac 123I-MIBG uptake as a fraction of the mean counts per pixel in the heart divided by those in the mediastinum. The washout rate of 123I-MIBG from the heart was calculated as follows: (early counts - delayed counts)/early counts x 100(%).

In patients with enalapril group, the H/M ratio of 123I-MIBG was increased after treatment (early image: 1.60 +/- 0.22 vs. 1.73 +/- 0.28, p < 0.05, delayed image: 1.63 +/- 0.28 vs. 1.82 +/- 0.33, p < 0.01). The washout rate of 123I-MIBG was reduced from 38% +/- 11% to 30% +/- 12% after treatment (p < 0.01). However in the conventional therapy group, the H/M ratios in the early and delayed images (early image: 1.58 +/- 0.31 vs. 1.52 +/- 0.23, delayed image: 1.49 +/- 0.27 vs. 1.49 +/- 0.25) and the washout rate (34% +/- 8% vs. 33% +/- 7%) remained unchanged after treatment. In patients with an increased H/M ratio of enalapril group (n = 13), a left ventricular ejection fraction increased from 48% +/- 12% to 55% +/- 9% (p < 0.01) after treatment.

ACE inhibition reduces cardiac 123I-MIBG release and thus lowers cardiac sympathetic nerve activity. Iodine-123-MIBG may be helpful in evaluating the therapeutic effects of ACE inhibition on the cardiac sympathetic nervous system in patients with CHF.