scholarly journals Imaging cardiac sympathetic innervation with MIBG: linear conversion of the heart-to-mediastinum ratio between different collimators

2019 ◽  
Vol 6 (1) ◽  
Author(s):  
Joachim Brumberg ◽  
Ganna Blazhenets ◽  
Nils Schröter ◽  
Lars Frings ◽  
Wolfgang H. Jost ◽  
...  
EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
HS Chen ◽  
C Jungen ◽  
Y Kimura ◽  
P Dibbets-Schneider ◽  
SRD Piers ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Background   Occurrence of ventricular tachycardias (VT) has been related to changes in sympathetic innervation and myocardial tissue in ischemic cardiomyopathy. In non-ischemic cardiomyopathy (NICM) patients with VT, the relation between global cardiac sympathetic innervation and non-ischemic fibrosis is less clear. The current gold standard in electrophysiology to identify non-ischemic fibrosis relies on unipolar endocardial voltage mapping. Objective To establish the relationship between global cardiac sympathetic innervation and global fibrosis. Methods 29 patients (93% male, 58 ± 14 years, mean LVEF 38%±13) from the ‘Leiden Nonischemic Cardiomyopathy Study’ undergoing VT ablation between 2011-2018 were included. Endocardial voltage mapping was performed and the mean endocardial unipolar voltage (UV) was taken as a surrogate for global fibrosis. Global cardiac sympathetic innervation was analyzed by 123-I-MIBG imaging using heart-to-mediastinum ratio (HMR). A cut-off of 1.8 was used to delineate between normal (>1.8) and denervated (<1.8). HMR was correlated with mean UV. Results For patients with global cardiac sympathetic denervation a linear relationship was present between HMR and mean UV (R = 0.5278, P = 0.0431. There was no significant linear relationship for patients with normal cardiac sympathetic innervation between HMR and mean UV (R=-0.1696, P = 0.5795). Conclusion Global cardiac sympathetic denervation is related to myocardial fibrosis in patients with NICM and VT. The data support an interplay between denervation and fibrosis which may contribute to arrhythmogeneity, as observed in ICM. Abstract Figure.


2008 ◽  
Vol 14 (4) ◽  
pp. 347-355
Author(s):  
D. Ryzhkova ◽  
E. M. Zykov ◽  
E. V. Shlyakhto

This article summarizes data of the studies with the use of positron emission tomography (PET) and devotes technical aspects and clinical application of PET for assessment of the autonomic nervous system of the heart in patients with cardiac diseases. According to the results of experimental and clinical studies PET with radiolabeled сatecholamines and adrenoreceptor ligands provides us with information about alteration of cardiac sympathetic innervation at different steps of neurotransmission. It plays a key role in the progression of various heart diseases such as ischemia, diabetes mellitus, heart failure and noncoronary arrhythmia. Cardiac sympathetic neuronal PET imaging seems to be a good tool for the stratification of the risk of the severe cardiovascular complications.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
F Marsico ◽  
S Paolillo ◽  
P Gargiulo ◽  
I Esposito ◽  
S Dell'aversana ◽  
...  

Abstract Introduction In heart failure (HF) a strict interaction exists between heart and kidney. Previous studies reported a significant impact of sympathetic overdrive, that causes beta-adrenoceptor desensitization, in both renal and heart failure progression. It can be hypothesized that renal failure might be associated with impaired sympathetic activity assessed directly at the myocardial level in patients affected by HF. Purpose Aim of the present observational study was to assess the relationship between renal dysfunction and cardiac sympathetic innervation in HF patients with mildly and severely reduced ejection fraction (HFrEF and HFmEF). Methods Two-hundred and sixty-three patients (84% males; 66±10.8 years) with mild-to-severe HF (EF 31±6.8%) underwent iodine-123 meta-iodobenzylguanidine (123I-MIBG) myocardial scintigraphy to assess sympathetic innervation, evaluating early and late heart to mediastinum (H/M) ratios and washout rate. All patients also underwent clinical evaluation and venous blood sample collection for the assessment of serum creatinine and consequently the estimation of glomerular filtration rate (eGFR) by EPI formula. Results A direct correlation was found between EPI-eGFR and late H/M (r=0,215; p<0.001) (figure 1), with an inverse correlation between NYHA class and late H/M (r=0,152; p=0.013), and a direct correlation between left ventricular EF and late H/M (r=0,348; p<0.001). These results were not confirmed for early H/M, nor washout rate. Dividing the population in reduced eGFR and normal eGFR (cut-off ≤60 ml/min/1,73m2), a statistical significant reduction of late H/M value was found in patients with reduced eGFR (late H/M = 1,49±0,21) compared with patients with preserved eGFR (late H/M = 1,56±0,26) (p=0.020). In a multivariate model, adjusting eGFR for NYHA class and left ventricular EF, reduced eGFR and left ventricular EF remained significant predictors of reduced late H/M (p=0.006 and p<0.001, respectively). Figure 1. linear regression curve Conclusions Patients with impaired renal function and HF show impaired cardiac sympathetic activity compared to HF patients with preserved renal function, and reduced eGFR estimated by EPI formula is a significant predictor of reduced late H/M evaluated by 123I-MIBG. Thus, in future studies, the combination of these two parameters might provide addictive prognostic information in HF patients.


1991 ◽  
Vol 261 (3) ◽  
pp. H969-H973 ◽  
Author(s):  
L. S. Sun ◽  
P. C. Ursell ◽  
R. B. Robinson

The onset of sympathetic innervation induces a developmental change in the cardiac alpha 1-adrenergic chronotropic response from an increase to a decrease in rate. The mechanism by which innervation induces this alteration is unknown. Neuropeptide Y (NPY), which is found abundantly in cardiac sympathetic nerve terminals, was considered as a possible mediator for this effect. Chronic conditioning by NPY in noninnervated myocyte cultures stimulated the effect of sympathetic innervation in inducing the alpha 1-inhibitory chronotropic response. Chronic conditioning by the NPY antagonist PYX-2 blocked the effect of innervation. Thus endogenous NPY may modulate alpha 1-adrenergic responsiveness during the ontogeny of cardiac sympathetic innervation.


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