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Sympathetic nervous system hyperactivity has a well-recognized role in the pathophysiology of heart failure with reduced left ventricular ejection fraction. Alterations in sympathetic nervous system have been related to the pathophysiology of pulmonary arterial hypertension, but it is unclear whether cardiac sympathetic nervous system is impaired and how sympathetic dysfunction correlates with hemodynamics and clinical status in pulmonary arterial hypertension patients. The aim of this study was to evaluate the cardiac sympathetic nervous system activity by means of 123 Iodine-metaiodobenzylguanidine nuclear imaging in pulmonary arterial hypertension patients and to explore its possible correlation with markers of disease severity. Twelve consecutive pulmonary arterial hypertension patients (nine women, median age 56.5 (17.8), eight idiopathic and four connective tissue-associated pulmonary arterial hypertension) underwent cardiac 123 Iodine-metaiodobenzylguanidine scintigraphy. The results were compared with those of 12 subjects with a negative history of cardiovascular or pulmonary disease who underwent the same nuclear imaging test because of a suspected paraganglioma or pheochromocytoma, with a negative result (controls), and 12 patients with heart failure with reduced left ventricular ejection fraction. Hemodynamics, echocardiography, six-minute walking distance, cardiopulmonary exercise testing, and N-terminal pro brain natriuretic peptide were collected in pulmonary arterial hypertension patients within one week from 123 Iodine-metaiodobenzylguanidine scintigraphy. Cardiac 123 Iodine-metaiodobenzylguanidine uptake, assessed as early and late heart-to-mediastinum ratio, was significantly lower in pulmonary arterial hypertension compared to controls (p = 0.001), but similar to heart failure with reduced left ventricular ejection fraction. Myocardial 123 Iodine-metaiodobenzylguanidine turnover, expressed as washout rate, was similar in pulmonary arterial hypertension and heart failure with reduced left ventricular ejection fraction and significantly higher compared to controls (p = 0.016). In the pulmonary arterial hypertension group, both early and late heart-to-mediastinum ratios and washout rate correlated with parameters of pulmonary arterial hypertension severity including pulmonary vascular resistance, right atrial pressure, tricuspid annular plane systolic excursion, N-terminal pro brain natriuretic peptide, and peak VO 2 . Although we evaluated a small number of subjects, our study showed a significant impairment in cardiac sympathetic nervous system in pulmonary arterial hypertension, similarly to that observed in heart failure with reduced left ventricular ejection fraction. This impairment correlated with indices of pulmonary arterial hypertension severity. Cardiac sympathetic dysfunction may be a contributing factor to the development of right-sided heart failure in pulmonary arterial hypertension.

PURPOSE: Cardiac sympathetic denervation may be detectable in patients with Anderson-Fabry disease (AFD), suggesting its usefulness for early detection of the disease. However, the relationship between sympathetic neuronal damage measured by 123I-metaiodobenzylguanidine (MIBG) imaging with myocardial fibrosis on cardiac magnetic resonance (CMR) is still unclear. METHODS: Cardiac sympathetic innervation was assessed by 123I-MIBG single-photon emission computed tomography (SPECT) in 25 patients with genetically proved AFD. Within one month from MIBG imaging, all patients underwent contrast-enhanced CMR. MIBG defect size and fibrosis size on CMR were measured for the left ventricle (LV) and expressed as %LV. RESULTS: Patients were divided into three groups according to MIBG and CMR findings: (1) matched normal, without MIBG defects and without fibrosis on CMR (n = 10); (2) unmatched, with MIBG defect but without fibrosis (n = 5); and (3) matched abnormal, with MIBG defect and fibrosis (n = 10). The three groups did not differ with respect to age, gender, α-galactosidase, proteinuria, glomerular filtration rate, and troponin I, while New York Heart Association class (p = 0.008), LV hypertrophy (p = 0.05), and enzyme replacement therapy (p = 0.02) were different among groups. Although in patients with matched abnormal findings, there was a significant correlation between MIBG defect size and area of fibrosis at CMR (r2 = 0.98, p < 0.001), MIBG defect size was larger than fibrosis size (26 ± 23 vs. 18 ± 13%LV, p = 0.02). CONCLUSION: Sympathetic neuronal damage is frequent in AFD patients, and it may precede myocardial damage, such as fibrosis. Thus, 123I-MIBG imaging can be considered a challenging technique for early detection of cardiac involvement in AFD.

This study was designed to assess the impact of obesity and acquisition protocol on (123)I-metaiodobenzylguanidine (MIBG) indexes of cardiac sympathetic innervation.Forty-five patients with heart failure (HF) (38 men, age 58±15 years) underwent (123)I-MIBG cardiac imaging. Of these patients, 10 were obese [body mass index (BMI) ≥30 kg/m(2)]. Ten-minute planar images of the thorax in anterior view were performed 15 minutes ("early" image) and 3 hours and 50 minutes ("late" image) after tracer administration in both supine- and prone-position. Early and late (123)I-MIBG heart-to-mediastinum (H/M) ratios and washout rate were computed.In overall study population, early and late (123)I-MIBG H/M ratios and washout rate were comparable between supine- and prone-position acquisitions. Obese patients had a lower early and late (123)I-MIBG H/M ratios both in supine (P0.01) and prone (P0.05) positions compared to non-obese subjects.Our results indicate that in HF patients, obesity has a significant impact on (123)I-MIBG indexes of cardiac sympathetic innervation. Prone-position did not change early and late (123)I-MIBG H/M ratios and washout rate compared to supine position both in obese and non-obese HF patients.

Objective Unfavourable effects of sleep-disordered breathing (SDB) in heart failure (HF) are mainly mediated by impaired sympathetic activity. Few data are available on SDB and cardiac adrenergic impairment evaluated at myocardial level. The aim of the study was to assess the relationship between SDB, cardiac sympathetic innervation assessed by 123 I-metaiodobenzylguanidine ( 123 I-MIBG) imaging and prognosis in HF. Methods Observational, prospective study enrolling patients with HF and reduced systolic function. Patients underwent nocturnal cardiorespiratory monitoring to assess SDB presence by apnoea/hypopnoea index (AHI), and 123 I-MIBG imaging to calculate heart-to-mediastinum (H/M) ratios and washout rate. Patients were prospectively followed for 29±18 months for the combined endpoint of cardiovascular death and HF hospitalisation. Results Ninety-four patients (66.1±9.8 years; left ventricular ejection fraction 32±7%) were enrolled; 72 (77%) showed SDB and, compared with non-SDB, significantly reduced early (1.67±0.22 vs 1.77±0.13; p=0.019) and late H/M ratios (1.50±0.22 vs 1.61±0.23; p=0.038). Dividing patients into two groups according to SDB severity, patients with a moderate–severe disturbance (AHI >15; n=43) showed significantly worse survival for the composite study outcome (log-rank test, p=0.001) with respect to patients with mild or no disorder (AHI ≤15; n=51). Adding SDB variables to the already known prognostic role of 123 I-MIBG imaging, we observed a worse survival in patients with both SDB and H/M impairment. Conclusions Patients with systolic HF and SDB show more impaired cardiac adrenergic innervation assessed by 123 I-MIBG imaging, and more adverse prognosis compared with HF patients without SDB.

The heart is richly innervated with sympathetic and parasympathetic fibers that work in conjunction with norepinephrine to accurately preserve hemodynamic and electrophysiological stability at rest and during periods of increased cardiovascular demand. Imaging of the cardiac sympathetic system is an area of active investigation in a wide variety of conditions, such as heart failure, arrhythmias, and ischemic heart diseases, providing an independent ability to risk stratify and a potential guide for improving patient management. 123I-metaiodobenzylguanidine (MIBG), an analog of the false neurotransmitter guanethidine, represents the most widely studied tracer for imaging of the cardiac autonomic system. Myocardial scintigraphy with 123I-MIBG is widely used in Europe and Japan but to date there is no established standard for tracer administration, imaging acquisition, and interpretation. We discuss the current literature regarding methods and interpretation of 123I-MIBG cardiac innervation imaging.