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 ((123)I-MIBG) is used as an indicator of pulmonary endothelial function. Decreased lung uptake of (123)I-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 (123)I-MIBG and pulmonary artery pressure (Ppa) at rest and during exercise, in patients with COPD. Methods: (123)I-MIBG scintigraphy was performed in 19 patients with COPD. Anterior planar images were acquired 15 min after the injection of (123)I-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 FEV(1), PaO(2), 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 (123)I-MIBG may be a novel scintigraphic tool for the assessment of exercise-induced pulmonary hypertension in patients with COPD.ArticleRESPIROLOGY. 15(8):1215-1219 (2010)journal articl

Iodine-123 Metaiodobenzylguanidine Scintigraphic Assessment of Myocardial Sympathetic Innervation in Patients With Familial Amyloid Polyneuropathy

AbstractObjectives. This study attempted to assess myocardial sympathetic innervation using iodine-123 (I-123) metaiodobenzylguanidine (MIBG) imaging in patients with familial amyloid polyneuropathy.Background. Signs and symptoms of cardiac autonomic dysfunction are commonly seen in patients with cardiac amyloidosis. However, the incidence and magnitude of abnormalities in myocardial sympathetic nerve function by means of I-123 MIBG imaging and their relation to clinical findings, cardiac function and the results of thallium-201 (Tl-201) and technetium-99m pyrophosphate (Tc-99m PYP) myocardial scanning have not yet been clarified.Methods. We performed M-mode, two-dimensional and Doppler echocardiography and I-123 MIBG, Tl-201 and Tc-99m PYP imaging of the heart in 12 patients with familial amyloid polyneuropathy and biopsy-proved cardiac amyloidosis.Results. Ten of 12 patients had no clinical evidence of overt heart disease, but left ventricular (LV) wall thickening was observed in 4 of these 10. Left ventricular percent fractional shortening and Doppler transmitral flow velocity patterns were found to be normal in all 12 patients. Eight of 12 patients showed no myocardial MIBG accumulation, with limited uptake in the remaining 4 demonstrated only in the LV anterior wall. Diffuse but mild myocardial uptake of Tc-99m PYP occurred in only 4 of 12 patients, and all 12 had normal results on Tl-201 myocardial scanning. Complete defects on myocardial MIBG scans were found in five of eight patients with negative findings on Tc-99m PYP myocardial scanning. The incidence and magnitude of myocardial uptake of MIBG were independent of clinical findings, extent of endomyocardial amyloid deposition, electrocardiographic QRS voltage and ventricular wall thickness.Conclusions. Patients with familial amyloid polyneuropathy show a high incidence of myocardial adrenergic denervation with viable myocardium that can be identified very early in cardiac amyloidosis, before the development of clinically apparent heart disease, ventricular wall thickening, significant LV systolic and diastolic dysfunction and positive findings on Tc-99m PYP myocardial scanning.(J Am Coll Cardiol 1997;29:168–74)

Radionuclide angiographic assessment of left ventricular diastolic filling in amyloid heart disease: A study of patients with familial amyloid polyneuropathy

AbstractTo assess left ventricular diastolic filling in amyloid heart disease, 17 patients with familial amyloid polyneuropathy and 20 normal subjects were examined by radionuclide angiography. None of the patients showed clinical evidence of restrictive cardiomyopathy. All but two patients had normal left ventricular ejection fraction. Peak filling rate was significantly lower and time to peak filling rate was significantly greater in patients than in normal subjects (2.60 ± 0.52 versus 3.10 ± 0.44 EDV/s, p < 0.001, and 215 ± 53 versus 147 ± 18 ms, p < 0.001, respectively). The mean left ventricular filling volume during rapid diastolic filling and atrial systole in patients was 54.5 ± 19.5% and 44.2 ± 21.6% of the stroke volume, respectively, compared with 83.8 ± 6.6% (p < 0.001) and 20.0 ± 6.0% (p < 0.001), respectively, in normal subjects.Although 10 of the 14 patients without clinical evidence of overt heart disease had normal ventricular wall thickness as well as normal ejection fraction, 8 of the 10 showed abnormal diastolic filling. In patients with familial amyloid polyneuropathy, indexes of diastolic filling were significantly related to ventricular wall thickness alone. The incidence and magnitude of abnormalities in time to peak filling rate and contribution of rapid filling as well as atrial systole to ventricular filling increased with age and duration of illness.Thus, abnormal diastolic filling can be seen even in the early stage of familial amyloid polyneuropathy and may be related to myocardial amyloid deposition as well as to fibrosis. Careful consideration should be given to age and duration of illness when diastolic filling is assessed in this disorder