Iodine-123 metaiodobenzylguanidine scintigraphic assessment of pulmonary vascular status in patients with chronic obstructive pulmonary disease.

BACKGROUND AND OBJECTIVE: Lung uptake of iodine-123 metaiodobenzylguanidine (¹²³I-MIBG) is used as an indicator of pulmonary endothelial function. Decreased lung uptake of ¹²³I-MIBG has been demonstrated in patients with COPD as compared with normal subjects. The present study was performed to examine the relationship between lung uptake of ¹²³I-MIBG and pulmonary artery pressure (Ppa) at rest and during exercise, in patients with COPD. METHODS: ¹²³I-MIBG scintigraphy was performed in 19 patients with COPD. Anterior planar images were acquired 15 min after the injection of ¹²³I-MIBG, and the total lung to upper mediastinum ratio (LMR) was calculated for both lungs. Right heart catheters were used to monitor Ppa continuously at rest and during exercise. Exercise was performed on an electrically braked bicycle ergometer at a constant workload of 25 W for 3 min. RESULTS: In COPD patients the LMR were not correlated with the pulmonary function parameters measured before exercise, including FEV1, PaO2, DL(CO), or Ppa at rest. However, the percentage increase in Ppa during exercise was significantly correlated with LMR. CONCLUSIONS: Evaluation of the kinetics of lung uptake of ¹²³I-MIBG may be a novel scintigraphic tool for the assessment of exercise-induced pulmonary hypertension in patients with COPD.

Reduced lung uptake of iodine-123 metaiodobenzylguanidine in high-altitude pulmonary oedema.

BACKGROUND AND OBJECTIVE: Iodine-123 metaiodobenzylguanidine ((123)I-MIBG) uptake in the lungs is a potentially suitable marker of pulmonary endothelial function because MIBG behaviour in the pulmonary circulation is quantitatively similar to that of norepinephrine. In addition, hypoxia reduces (123)I-MIBG transport in pulmonary endothelial cells in vitro. The present study was undertaken to evaluate (123)I-MIBG uptake in the lungs of patients with high-altitude pulmonary oedema (HAPE). METHODS: (123)I-MIBG scintigraphy was performed in eight patients with HAPE. The findings were compared with those in 24 patients with congestive heart failure due to idiopathic dilated cardiomyopathy (DCM) and in 13 normal control subjects. In patients with HAPE, the (123)I-MIBG examination was performed 7-14 days after admission. Anterior planar images were acquired 15 min after injection of (123)I-MIBG and the total lung to upper mediastinum ratio (L/M ratio) was calculated for both lungs. RESULTS: The L/M ratio in patients with HAPE (1.39 +/- 0.15, mean +/- SD) was significantly lower than in those with congestive heart failure/DCM (1.66 +/- 0.16) or in normal controls (1.53 +/- 0.14). There were no significant differences among the groups in (123)I-MIBG accumulation in the heart. CONCLUSIONS: Although the mechanism of altered (123)I-MIBG kinetics in HAPE remains obscure, decreased (123)I-MIBG uptake in the lungs may potentially be a suitable technique for the assessment of pathological conditions associated with the pulmonary endothelium.

Iodine-123 metaiodobenzylguanidine scintigraphic analysis of myocardial sympathetic innervation in patients with AL (primary) amyloidosis.

BACKGROUND: Although a high incidence of myocardial adrenergic denervation has been reported in patients with familial amyloid polyneuropathy, assessment of cardiac sympathetic nerve function has not been available in patients with AL (primary) amyloidosis. METHODS: To test the hypothesis that myocardial sympathetic nerve innervation might be impaired and variable according to the presence or absence of clinical autonomic abnormalities and congestive heart failure in AL amyloidosis, we examined 25 patients by use of iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy. RESULTS: Ten of the 16 patients without autonomic symptoms and 5 of the 9 patients with autonomic neuropathy showed congestive heart failure. The heart/mediastinal activity (H/M) ratio (1.53 +/- 0.06 vs 1.29 +/- 0.05 at 3 hours, P <.001) and myocardial washout ratio (41.5% +/- 4.8% vs 30.8% +/- 4.0%, P <.001) of MIBG were significantly increased in patients without autonomic symptoms compared with patients showing autonomic neuropathy. In patient groups with and without autonomic dysfunction, patients demonstrating congestive heart failure exhibited a significantly decreased H/M ratio and increased washout compared with patients with no heart failure, and left ventricular fractional shortening was positively correlated with the H/M ratio and inversely correlated with the washout ratio. There were significant correlations between the low-frequency component of the heart rate variability and the H/M ratio and washout ratio in the entire patient population. CONCLUSIONS: Patients with AL amyloidosis and no autonomic dysfunction showed variable degrees of enhanced cardiac adrenergic neuronal activity with presynaptic sympathetic dysfunction. In contrast, patients with AL amyloidosis and autonomic neuropathy exhibited prominent myocardial adrenergic denervation with normal or impaired sympathetic neural function of the heart. This study demonstrates that myocardial uptake and turnover of MIBG in patients with AL amyloidosis are heterogeneous and dependent on the presence or absence of congestive heart failure and cardiac autonomic dysfunction.