Improvement of cardiac neuronal function after carvedilol treatment in dilated cardiomyopathy: a 123I-MIBG scintigraphic study.

Carvedilol can induce important clinical and hemodynamic improvements in patients with chronic heart failure resulting from severe left ventricular (LV) dysfunction. This study examines the impact of carvedilol on cardiac neuronal function using 123I-metaiodobenzylguanidine (MIBG) scintigraphy in dilated cardiomyopathy. METHODS: Twenty-two patients with chronic heart failure (19 men, 3 women; mean age, 54 y; age range, 34-64 y) assessed as New York Hospital Association (NYHA) class II or III and with initial resting radionuclide LV ejection fractions (LVEF) < 0.40 were enrolled in the study. Patients had long histories of symptomatic LV dysfunction despite optimal diuretics and angiotensin-converting enzyme inhibitor treatment. Over a 6-mo period, 50 mg/day carvedilol was administered to these patients. Planar 123I-MIBG scintigraphy provided measurements of cardiac neuronal uptake (as heart-to-mediastinum count activity ratio [HMR]), 4h after intravenous injection of 185 MBq MIBG. Hemodynamic, clinical, radionuclide LVEF and HMR data measured at the outset and after 6 mo of carvedilol were compared. RESULTS: Resting heart rate decreased from 81 +/- 13 to 71 +/- 9 bpm (P = 0.003). After carvedilol therapy NYHA functional classification for these patients improved from 2.6 +/- 0.5 to 2.3 +/-0.5 (P = 0.04), LVEF improved from 22% +/- 9% to 30% +/- 13% (P = 0.005), and HMR improved from 145% +/- 23% to 170% +/- 25% (P = 0.0001). CONCLUSION: Carvedilol induces improvements of clinical symptoms and cardiac neuronal and systolic functions in patients with dilated cardiomyopathy and chronic optimal treatment.     

Use of <Superscript>123</Superscript>I-MIBG scintigraphy to assess the impact of carvedilol on cardiac adrenergic neuronal function in childhood dilated cardiomyopathy

Iodine-123 metaiodobenzylguanidine (MIBG) cardiac scintigraphy is a useful tool for the assessment of cardiac adrenergic neuronal function, which is impaired in children with idiopathic dilated cardiomyopathy (DCM). In adults with DCM, long-term treatment with carvedilol improves both cardiac adrenergic neuronal function and left ventricular function. The aim of this prospective study was to evaluate the impact of carvedilol on cardiac adrenergic neuronal function using ¹²³I-MIBG scintigraphy and on left ventricular function using equilibrium radionuclide angiography in children with DCM. Seventeen patients (11 female, six male; mean age 39±57 months, range 1–168 months) with DCM and left ventricular dysfunction underwent ¹²³I-MIBG cardiac scintigraphy and equilibrium radionuclide angiography before and after a 6-month period of carvedilol therapy. A static anterior view of the chest was acquired 4 h after intravenous injection of 20–75 MBq of ¹²³I-MIBG. Cardiac neuronal uptake of ¹²³I-MIBG was measured using the heart to mediastinum count ratio (HMR). Radionuclide left ventricular ejection fraction (LVEF) was assessed following a standard protocol. MIBG cardiac uptake and left ventricular function respectively increased by 38% and 65% after 6 months of treatment with carvedilol (HMR=223%±49% vs 162%±26%, P<0.0001, and LVEF=43%±17% vs 26%±11%, P<0.0001). Carvedilol can improve cardiac adrenergic neuronal and left ventricular function in children with dilated cardiomyopathy. Further studies are needed to assess the relationship between improvement in MIBG cardiac uptake and the beneficial effects of carvedilol on morbidity and mortality.     

Comparison of parameters of 123I-MIBG scintigraphy for predicting prognosis in patients with dilated cardiomyopathy.

123I-metaiodobenzylguanidine (MIBG) scintigraphy has been used to predict prognosis of patients with dilated cardiomyopathy (DCM), although it is unknown which parameter of MIBG is the most useful clinically. We studied MIBG in 59 patients with DCM, and followed them up to evaluate the prognosis of DCM. Single photon emission tomography (SPET) and planar imaging were performed, both early (e) and 4 h (delayed, d) post-injection. 201Tl (TL) SPET and radionuclide-ventriculography were also investigated. The total defect score of early and delayed MIBG and 201 Tl (MIBGeDS, MIBGdDS, TLDS) was analysed visually for each SPET image. The heart to mediastinum ratio (H/M) for both the early and delayed MIBG planar images and myocardial washout rate at 4 h were analysed quantitatively. Sixteen patients died during follow-up. Cox Hazards univariate analysis selected washout rate (P < 0.0001), H/Me (P = 0.0012), H/Md (P = 0.0001) and left ventricular ejection fraction (P = 0.0004) as indices for the prediction of cardiac death. Multivariate analysis selected washout rate as the most powerful independent predictor of prognosis (P < 0.0001). Survival curves with a threshold value of 52% for washout rate were able to differentiate a negative outcome from survival (P < 0.0001). TLDS, MIBGeDS and MIBGdDS were not useful in the prediction of prognosis. The washout rate of MIBG is the most potent predictor of cardiac death and is considered clinically useful.     

Effects of carvedilol on cardiac function and cardiac adrenergic neuronal damage in rats with dilated cardiomyopathy.

Metaiodobenzylguanidine (MIBG) is a reliable marker for the detection of cardiac adrenergic neuronal damage in heart failure. The cardioprotective properties of carvedilol, a vasodilating beta-adrenoceptor-blocking agent, were studied in a rat model of dilated cardiomyopathy after autoimmune myocarditis. METHODS: Twenty-eight days after immunization, surviving rats (41/55, or 75%) were divided into 2 groups treated with carvedilol, 2 mg/kg/d (group C, n = 19), or vehicle alone (0.5% methylcellulose, group V, n = 22). After oral administration for 2 mo, heart weight, heart rate, left ventricular end-diastolic pressure (LVEDP), and myocardial fibrosis were measured and compared with those in untreated rats (group N, n = 19). Myocardial uptake of (125)I-MIBG (differential absorption ratio) in the left ventricle was measured by autoradiography at 10, 30, or 240 min after tracer injection. RESULTS: Four (18%) of 22 rats in group V died between days 28 and 84 after immunization. None of the rats in group C or N died. Heart weight, heart rate, LVEDP, and area of myocardial fibrosis in group C (1.14 +/- 0.04 g, 345 +/- 16 beats per minute, 7.6 +/- 1.5 mm Hg, and 12% +/- 1%) were significantly lower than those in group V (1.34 +/- 0.04 g, 389 +/- 10 beats per minute, 12.3 +/- 1.3 mm Hg, and 31% +/- 2%). Although the differential absorption ratio was lower at all time points in group V than in group N, uptake after treatment increased in group C, compared with group V, at 10 min (12.5 +/- 1.0 vs. 7.6 +/- 0.8, not significant), 30 min (10.1 +/- 1.1 vs. 6.3 +/- 0.9, not significant), and 240 min (6.5 +/- 0.5 vs. 2.5 +/- 0.2, P < 0.05). The late washout ratio from myocardial radioactivity between 30 and 240 min in group C was lower than that in group V (36% vs. 60%). CONCLUSION: These observations indicated that carvedilol has beneficial effects and protects cardiac adrenergic neurons in dilated cardiomyopathy.     

Uptake of 123I-MIBG in a hepatic hemangioma in the scintigraphic study of an adrenal gland lesion

A 60 year old symptom free female in whom a lesion in left adrenal gland was found by chance in a CT scan is presented. She also had increased serum and urine catecholamines levels. 123I-MIBG scintigraphy showed a non-physiological uptake in right adrenal gland that is still seen in the delayed image, with normal left gland. MRI confirmed the presence of a mass in the left adrenal gland suggestive of an adenoma and found a lesion in the right hepatic area at the level of the previously seen MIBG image. This lesion was labelled as a hemangioma and would explain the findings of the isotopic study with MIBG. It must be considered as a false positive for phaechromocytoma. The increased catecholamine serum and urine levels were due to drug interactions.     

Prediction of effect of beta-blocker therapy in patients with dilated cardiomyopathy by using 123I-BMIPP, 123I-MIBG scintigraphy

We investigated prediction of the efficacy of beta-blocker therapy in patients with dilated cardiomyopathy (DCM) by using myocardial scintigraphy with 123I-BMIPP (BMIPP) and 123I-MIBG (MIBG). Thirty-seven patients with DCM were examined by myocardial scintigraphy with BMIPP and MIBG before beta-blocker therapy. Patients were classified into two groups, based on whether they improved > 10% of the left ventricular ejection fraction (LVEF) (improved group, n = 21) or not (unimproved group, n = 16). The extent and severity score of BMIPP for the improved group was significantly lower (p < 0.001) than that for unimproved group. It has been suggested that BMIPP is useful in evaluating the prediction of efficacy of beta-blocker therapy in patients with DCM.     

Relation between myocardial response to dobutamine stress and sympathetic nerve activation in patients with idiopathic dilated cardiomyopathy: A comparison of123I-MIBG scintigraphic and echocardiographic data

It is likely that a close association exists between findings obtained by two methods: dobutamine stress echocardiography and 123I-MIBG scintigraphy. Both of these methods are associated with beta-adrenergic receptor mechanisms. This study was conducted to demonstrate the relation between myocardial response to dobutamine stress and sympathetic nerve release of norepinephrine in the failing heart. In 12 patients with heart failure due to idiopathic dilated cardiomyopathy, the myocardial effects of dobutamine stress were evaluated by low-dose dobutamine stress echocardiography: and sympathetic nerve function was evaluated by scintigraphic imaging with iodine-123 [123I] meta-iodobenzylguanidine (MIBG), an analogue of norepinephrine. Echocardiography provided quantitative assessment of wall motion and left ventricular dilation; radiotracer studies with 123I-MIBG provided quantitative assessment of the heart-to-mediastinum (H/M) uptake ratio and washout rate. Results showed that H/M correlated with baseline wall motion (r = 0.682, p = 0.0146), wall motion after dobutamine stress (r = 0.758, p = 0.0043), the change in wall motion (r = 0.667, p = 0.0178), and with left ventricular diastolic diameter (r = 0.837, p = 0.0007). In addition, the 123I-MIBG washout rate correlated with baseline wall motion (r = 0.608, p = 0.0360), wall motion after dobutamine stress (r = 0.703, p = 0.0107), and with the change in wall motion (r = 0.664, p = 0.0185). Wall motion, especially in the myocardial response to dobutamine stress, is related to sympathetic nerve activity in heart failure.     

Myocardial 123I-MIBG scintigraphy predicts an impairment in myocardial functional reserve during dobutamine stress in patients with idiopathic dilated cardiomyopathy

Purpose

We investigated whether myocardial ¹²³I-metaiodobenzylguanidine (¹²³I-MIBG) scintigraphy predicts impairment of myocardial functional reserve in response to dobutamine stress in patients with idiopathic dilated cardiomyopathy (DCM).

Methods

Forty DCM patients (LVEF 39?±?12 %) underwent myocardial ¹²³I-MIBG scintigraphy, echocardiography, and cardiac catheterization. Myocardial ¹²³I-MIBG uptake was quantified as the delayed heart to mediastinum (H/M) ratio and washout rate (WR). Local denervation was evaluated on polar map images. LV dP/dt _max and T_1/2 were determined from left ventricular pressure curves at baseline and during dobutamine infusion (15 μg/kg?/min). Patients were classified into two groups as follows: group A comprised 21 patients showing a delayed H/M ratio of <1.9 (median value); group B comprised 19 patients showing a delayed H/M ratio of ≥1.9.

Results

The percentage change in heart rate (%HR), LV dP/dt _max (%LV dP/dt _max), and T _1/2 (%T _1/2) from baseline to dobutamine stress were significantly more reduced in group A than in group B (39.3?±?20.2 %, 55.2?±?24.1 %, p?<?0.01; 102.3?±?46.3 %, 152.0?±?72.3 %, p?<?0.05; 38.7?±?15.3 %, 46.9?±?15.4 %, p?<?0.05, respectively). No significant differences between the two groups were observed in the echocardiographic parameters or baseline cardiac catheterization parameters. Significant correlations were found between delayed H/M ratio and %HR (r?=?0.35, p?<?0.05), %LV dP/dt _max (r?=?0.45, p?<?0.05) and %T _1/2 (r?=?0.34, p?<?0.05). Significant inverse correlations were also found between WR and %HR (r?=??0.37, p?<?0.05), %LV dP/dt _max (r?=??0.60, p?<?0.0001), and %T _1/2 (r?=??0.34, p?<?0.05). SPECT images revealed enhanced denervation from the inferoposterior to anterior wall in accordance with the advancement of global denervation.

Conclusion

Reduced ¹²³I-MIBG uptake and increased washout were related to impairment in adrenergic myocardial functional reserve in idiopathic DCM.     

Dynamic SPET parameters of 123I-MIBG cardiac imaging.

Early dynamic and late 123I-MIBG SPET studies were performed to investigate several parameters used to distinguish the characteristics of various cardiac disorders. Forty-six individuals (34 non-diabetic, 12 diabetic) with or without heart disease were included in the study. Early dynamic and late static SPET images were acquired using a triple-headed gamma camera. After selecting mid-sections from vertical (VLA) and horizontal (HLA) long-axis images, regions of interest were created over the apex, whole heart and anterior, inferior, septal and lateral walls of the heart. Various uptake ratios at 3, 11 and 19 min and 4 h after injection (HU3, HU11, HU19, DUP) and clearances (Kse: between HU3 and HU11; Ke: between HU11 and HU19; Kd: between HU19 and DUP) were calculated. There were significant differences among various cardiac pathologies on the delayed images. Cardiomyopathy patients showed the lowest uptake on the delayed images. When all segments in normal patients and all involved segments in myocardial infarcted patients were compared, there was significantly lower uptake of MIBG in infarcted segments at all time points. Kd showed the lowest value compared with Kse and Ke. In cardiomyopathy patients, Kse, Ke and Kd were significantly different from each other. Both Kse and Ke were significantly higher in cardiomyopathy patients than in normal patients. In conclusion, the results of this study are in line with published data and precise measurement of uptake and clearance was possible when excluding background and blood pool activity.     

Impact of exercise rehabilitation on cardiac neuronal function in heart failure: an iodine-123 metaiodobenzylguanidine scintigraphy study

Exercise training can induce important haemodynamic and metabolic adaptations in patients with chronic heart failure due to severe left ventricular dysfunction. This study examined the impact of exercise rehabilitation on cardiac neuronal function using iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy. Fourteen patients (11 men, 3 women; mean age 48 years; range: 36–66 years) with stable chronic heart failure of NYHA class II–III and an initial resting radionuclide left ventricular ejection fraction (LVEF) <50% were enrolled in the study. Patients underwent progressive, supervised endurance training (treadmill test, Bruce protocol) during a 6-month period (60 sessions, 3 sessions per week) at a cardiac rehabilitation referral centre in order to measure exercise parameters. Planar ¹²³I-MIBG scintigraphy provided measurements of cardiac neuronal uptake (heart-mediastinum ratio activity, 4 h after intravenous injection of 185 MBq of MIBG). Radionuclide LVEF was also assessed at the outset and after 6 months of exercise training. Workload (801±428 vs 1229±245 kpm·min^–1, P = 0.001), exercise duration (504±190 vs 649±125 s, P = 0.02), and myocardial MIBG uptake (135%±19% vs 156%±25%, P = 0.02) increased significantly after rehabilitation. However, LVEF did not change significantly (23%±9% vs 21%±10%, p = NS). It is concluded that exercise rehabilitation induces improvement of cardiac neuronal function without having negative effects on cardiac contractility in patients with stable chronic heart failure. Received 23 September and in revised form 24 November 1997     

123I-MIBG myocardial scintigraphy in patients with "takotsubo" cardiomyopathy.

The clinical characteristics of reversible left ventricular dysfunction due to "takotsubo" cardiomyopathy have been described, but the origin of this condition remains unclear. This study investigated (123)I-metaiodobenzlguanidine ((123)I-MIBG) myocardial scintigraphy in patients with takotsubo cardiomyopathy. METHODS: Eight consecutive patients with takotsubo cardiomyopathy were studied. Left ventricular wall motion was monitored by echocardiography until wall motion normalized. (123)I-MIBG myocardial scintigrams were performed within 3 d of admission (0 mo) and after the improvement of left ventricular dysfunction (3 mo). Early images were obtained at 30 min after radioisotope injection and delayed images were obtained after 4 h. The heart-to-mediastinum ratio (H/M ratio) and the washout rate were calculated. RESULTS: The mean left ventricular ejection fraction improved significantly (from 42.8% +/- 8.7% to 66.5% +/- 7.9%; P < 0.0001) and normalized after 19.4 +/- 5.4 hospital days. The early H/M ratio was significantly higher than the late ratio at 0 mo (2.16 +/- 0.25 vs. 1.89 +/- 0.24, respectively; P < 0.05), but not at 3 mo. The washout rate was significantly greater at 0 mo than at 3 mo (39.1% +/- 10.2% vs. 25.4% +/- 6.3%, respectively; P < 0.05). CONCLUSION: In patients with takotsubo cardiomyopathy, initial (123)I-MIBG myocardial scintigraphy depicted a unique pattern of ventricular asynergy and indicated the existence of cardiac sympathetic hyperactivity, although coronary blood flow was maintained. These findings strongly suggest that takotsubo cardiomyopathy could be caused by neurogenic myocardial stunning.     

No-carrier-added 123I-MIBG: an initial clinical study in patients with phaeochromocytoma

Radioiodinated meta-iodobenzylguanidine (MIBG) is used routinely for imaging and targeted radiotherapy of tumours derived from the neural crest. Since active uptake of MIBG by the noradrenaline transporter (NAT) makes a greater contribution to total drug accumulation than passive uptake when MIBG is present at low concentrations, tumour-specific uptake should be enhanced by the administration of lower molar amounts of MIBG. This could be achieved through the use of MIBG with a high specific activity. Commercially available preparations of 123I-MIBG have specific activities of approximately 200 MBq.mg-1. We have synthesized and used no-carrier-added (n.c.a.) 123I-MIBG produced by an iododesilylation reaction (specific activity 0.7 TBq.mg-1). We report here the first clinical studies comparing the commercially available and n.c.a. MIBG diagnostic preparations. Five patients with known phaeochromocytoma were studied. Unlike studies in animal models, no consistent improvement in tumour uptake was observed with the n.c.a. material. A larger patient group is required to determine whether there are significant differences between the two preparations, before proceeding to studies at therapeutic activity levels of n.c.a. 131I-MIBG. Even with no improvement in tumour uptake, n.c.a. MIBG may be the favoured formulation for therapeutic applications to reduce the molar amount of drug injected.     

Sympathetic reinnervation of cardiac allografts evaluated by 123I-MIBG imaging.

Some heart-transplant patients present with improved heart rate response to exercise and anginal pain suggesting reinnervation of allografts. Studies performed up to 5 y post-transplantation have suggested that reinnervation is a slow process that occurs only after 1 y post-transplantation. The purpose of this study was to evaluate the extent of sympathetic reinnervation in heart-transplant patients and its relation to cardiac function. METHODS: We performed 123I-metaiodobenzylguanidine (MIBG) studies and rest/exercise radionuclide ventriculography in 31 heart-transplant patients 6 mo to 12 y post-transplantation. Intensity of myocardial MIBG uptake was quantified by a heart-to-mediastinum ratio (HMR), and the regional distribution of MIBG was determined by tomographic studies. RESULTS: HMR correlated positively with time after transplantation (r = 0.607, P < 0.001). Patients studied from 2 to 12 y post-transplantation had an HMR significantly higher than patients studied before 2 y post-transplantation (1.62 +/- 0.2 versus 1.34 +/- 0.2, P < 0.05). Myocardial MIBG uptake was anterolateral in 16 patients, anterior in 3 and anterolateral and septal in 3. Myocardial MIBG uptake was absent in 9 patients. Vasculopathy developed in 8 patients, and 5 of them (63%) had decreased myocardial MIBG uptake. Peak filling rate was higher in patients studied from 2 to 12 y post-transplantation (2.7 +/- 0.8 end-diastolic volume (EDV)/s versus 2.16 +/- 0.5 EDV/s, P = 0.02). CONCLUSION: Sympathetic reinnervation increases with time after heart transplantation and is seen more frequently after 2 y post-transplantation. Complete reinnervation of the transplanted heart does not occur even up to 12 y post-transplantation. Early vasculopathy may delay the process of sympathetic reinnervation.     

Cardiac sympathetic activity estimated by 123I-MIBG myocardial imaging in patients with dilated cardiomyopathy after beta-blocker or angiotensin-converting enzyme inhibitor therapy.

Impaired cardiac sympathetic activity can be evaluated by 123I-metaiodobenzylguanidine (MIBG) imaging. METHODS: We studied the significance of MIBG imaging for 24 patients (age 58+/-12 y) with dilated cardiomyopathy (DCM). We compared 12 patients (group A) treated with metoprolol (dose from 30-60 mg/d) with 12 patients treated with angiotensin-converting enzyme (ACE) inhibitors. Patients were studied before treatment, after 5 mo of treatment (only in group A) and after 1 y of treatment. Cardiac MIBG uptake was assessed as the heart-to-mediastinum activity ratio (H/M) and total defect score (TDS) from anterior planar and SPECT MIBG images, which were acquired in 4 h after tracer injection. New York Heart Association (NYHA) class and left ventricular ejection fraction (LVEF) calculated by echocardiography were also assessed. RESULTS: TDS decreased in both groups (in group A, from 30+/-7 through 23+/-9 to 18+/-10; P < 0.01, in group B, from 30+/-6 to 24+/-8; P < 0.01) and H/M was increased in both groups (in group A, from 1.87+/-0.31 through 2.03+/-0.28 to 2.14+/-0.29; P < 0.01, in group B, from 1.82+/-0.28 to 1.94+/-0.26; P < 0.05). But TDS and H/M were more improved in group A than in group B (P < 0.05). LVEF was significantly increased in only group A (from 38+/-6 through 43+/-8 to 49%+/-9%; P < 0.01). NYHA improved in both groups (in group A, from mean 2.5 through 2.1 to 1.8; P < 0.01, in group B, from mean 2.6 to 2.1; P < 0.05) but was more improved in group A than in group B (P < 0.05). CONCLUSION: Cardiac function, symptom and cardiac sympathetic activity evaluated by MIBG images improved after the beta-blocker therapy more than with the treatment that used ACE inhibitors.     

123I-MIBG myocardial scintigraphy in diabetic patients: Relationship with201Tl uptake and cardiac autonomic function

Purpose

To investigate the influence of diabetic myocardial damage (suspected myocardial damage; SMD) diagnosed by²⁰¹T1-SPECT and diabetic cardiac autonomic neuropathy (AN) on myocardial MIBG uptake in patients with non-insulin-dependent diabetes mellitus (NIDDM).

Subjects and Methods

Eighty-seven diabetic patients divided into four subgroups: 23 with SMD (+) AN (+); 19 with SMD (+) AN (?); 27 with SMD (?) AN (+); 18 with SMD (?) AN (?), and 10 controls were studied. Both planar and SPECT images were taken at 30 minutes (early) and 3 hours (delayed) after¹²³I-MIBG injection. The heart to mediastinum uptake ratio (H/M) and washout ratio of¹²³I-MIBG (WR) were obtained from both planar images. On SPECT images, the total uptake score (TUS) was obtained by the 5 point score method by dividing the myocardium into 20 segments on visual analysis. Similarly, the difference between the²⁰¹Tl image and the¹²³I-MIBG image in TUS was taken as the difference in the total uptake score (ΔTUS) representing cardiac sympathetic denervation without SMD.

Results

On both early and delayed planar images, the mean H/M value in the subgroups of diabetic patients was significantly lower in the SMD (+) AN (+) group than in the control group, but among those subgroups, there was statistically significant difference between the SMD (+) AN (+) and SMD (?) AN (?) groups only on the delayed images. Regarding the WR value, there was no statistically significant difference among subjects. On SPECT image analysis, the diabetic sub-group with AN or SMD had statistically significant lower values for TUS than those of the control group. Among diabetics, there was a statistically significant differences between SMD [+] AN [+] and SMD [?] AN [?] on both early and delayed images. Similarly, the SMD [+] AN [?] group also had significantly lower values than those of SMD [?] AN [?] on early images. Regarding ΔTUS, there was a statistically significant differences between AN [+] subgroups and controls. Similarly, the mean value for ΔTUS was much higher in AN [+] subgroups than in AN [?] subgroups with or without SMD in diabetes mellitus.

Conclusion

¹²³I-MIBG myocardial uptake is affected by both SMD and cardiac autonomie neuropathy. Based on the finding that ΔTUS was much higher in AN [+] subgroups and there was no statistically significant difference between SMD [+] AN [+] and SMD [?] AN [+] subgroups, a decrease in myocardial¹²³I-MIBG uptake might progress independently of SMD.     

Myocardial clearance of I-123 metaiodobenzylguanidine in dilated cardiomyopathy

We present the results of sequential imaging studies conducted in two patients with dilated cardiomyopathy whose responses to long-term beta-blocker therapy differed. We evaluated the time course of the myocardial clearance and the heart to upper mediastinal ratios of I-123 metaiodobenzylguanidine (MIBG) scintigraphy. In the first patient, the left ventricular ejection fraction as well as the clinical symptoms were improved by long-term beta-blocker therapy with a concurrent normalization of the myocardial clearance and the heart to upper mediastinal ratio of I-123 MIBG scintigraphy. The myocardial clearance and the upper mediastinal ratio of I-123 MIBG indicated no improvement in the second patient, and the left ventricular function did not change. The myocardial clearance and the heart to upper mediastinal ratio of I-123 MIBG scintigraphy were useful in evaluating the efficacy of long-term beta-blocker therapy in patients with dilated cardiomyopathy.     

The reversibility of cardiac neuronal function after removal of a pheochromocytoma: an I-123 MIBG Scintigraphic Study.

PURPOSE: Twelve patients with proved pheochromocytoma evaluated in our institution between 1991 and 1997 are described. METHODS: The patients' urinary excretion rates and their metabolites (vanylmandelic acid and metanephrines) were significantly greater than normal before surgery. Echocardiography showed normal left ventricular ejection fractions (72% +/- 8%). All of the patients underwent planar I-123 metaiodobenzylguanidine (MIBG) scintigraphy to assess cardiac neuronal uptake 4 hours after and locate a pheochromocytoma 24 hours after intravenous injection of 185 MBq (3 mCi) I-231 MIBG. Ten patients with pheochromocytoma had positive tumoral findings with I-123 MIBG scintigraphy. Twelve patients had significant impairment of cardiac neuronal uptake of MIBG, with a heart:mediastinum ratio averaging 142% +/- 18% (normal value, 230% +/- 30%, P < 0.05). Postoperative cardiac MIBG imaging was performed in all patients (at 6 +/- 3 months). RESULTS: After surgical removal of the pheochromocytoma, cardiac MIBG uptake and the heart:mediastinum uptake ratios improved significantly (197% +/- 20%, P < 0.05) in all the patients. Urinary excretion rates and metabolites returned to the normal range. However, no significant correlation was found between cardiac MIBG uptake and urinary excretion rates and metabolites after the tumors were removed. CONCLUSION: Removing a pheochromocytoma reversed cardiac neuronal function as assessed by MIBG scintigraphy.     

Cardiac 123I-MIBG reflects left ventricular functional reserve in patients with nonobstructive hypertrophic cardiomyopathy.

Little is known about the relation between left ventricular (LV) functional reserve in response to exercise and cardiac sympathetic nervous function in patients with nonobstructive hypertrophic cardiomyopathy (HCM). We investigated whether an assessment of cardiac sympathetic nervous function by myocardial (123)I-metaiodobenzylguanidine ((123)I-MIBG) scintigraphy might provide a sign of an abnormal LV functional reserve in response to exercise-induced beta-adrenergic stimulation in patients with HCM. METHODS: Thirty HCM patients underwent (123)I-MIBG scintigraphy and echocardiography at rest and subsequent biventricular cardiac catheterization at rest and during dynamic exercise. LV pressures were measured using a micromanometer-tipped catheter system. The early and delayed (123)I-MIBG images were quantified as a heart-to-mediastinum ratio (H/M). The plasma levels of brain natriuretic peptide (BNP) and norepinephrine (NE) were also measured. RESULTS: Patients were divided into 2 groups according to the delayed (123)I-MIBG H/M: group I consisted of 12 patients with a delayed H/M of < or =1.8 and group II had 18 patients with a delayed H/M of >1.8. Both the percentage increase from rest to exercise in LV isovolumic contraction (LV dP/dt(max)) and the percentage shortening of LV pressure half-time (T(1/2)) as an index of isovolumic relaxation were significantly less in group I than in group II (P < 0.05, respectively). A significant linear correlation was observed between the percentage increase in LV dP/dt(max) and (123)I-MIBG H/Ms (early H/M: r = 0.49, P < 0.01; delayed H/M: r = 0.54, P < 0.005, respectively). A significant linear correlation was also observed between the percentage shortening in T(1/2) and (123)I-MIBG H/Ms (early H/M: r = 0.58, P < 0.001; delayed H/M: r = 0.64, P < 0.0005, respectively). The plasma NE levels were significantly higher in group I than in group II (P < 0.01), whereas the plasma BNP levels were comparable in the 2 HCM groups. CONCLUSION: beta-Adrenergic enhancement of LV function during exercise may depend on the extent of cardiac sympathetic nervous innervation in HCM patients. Resting myocardial (123)I-MIBG scintigraphy can noninvasively evaluate LV functional reserve in response to exercise in patients with nonobstructive HCM.