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Published on: June 14, 2016
Cardiac sympathetic dysfunction in left ventricular hypertrophy caused by arterial hypertension and degenerative
Riccardo Liga1, Alessia Gimelli2, Marco De Carlo3
1Cardiac, Thoracic and Vascular Department, University Hospital of Pisa, Via Paradisa 2, 56124, Pisa, Italy. riccardo.liga@gmail.com.
Insights
Cardiac sympathetic innervation is impaired in patients with left ventricular hypertrophy (LVH), with or without aortic stenosis (AS). The transcatheter aortic valve implantation (TAVI) procedure did not significantly impact cardiac sympathetic function.
Area of Science:
- Cardiology
- Nuclear Medicine
- Cardiovascular Imaging
Background:
- Hypertension and aortic stenosis (AS) can lead to left ventricular hypertrophy (LVH).
- Cardiac sympathetic dysfunction is implicated in cardiovascular disease progression.
- Assessing cardiac sympathetic innervation is crucial in patients with LVH and AS.
Purpose of the Study:
- To evaluate cardiac sympathetic innervation in patients with LVH and AS undergoing transcatheter aortic valve implantation (TAVI).
- To compare sympathetic innervation in patients with LVH and AS, essential hypertension (HT), and controls.
- To assess the impact of TAVI on cardiac sympathetic innervation.
Main Methods:
- Utilized 123I-metaiodobenzylguanidine (MIBG) and 99mTc-tetrofosmin SPECT imaging.
- Assessed sympathetic innervation and left ventricular (LV) perfusion.
- Calculated innervation/perfusion mismatch score as an indicator of cardiac sympathetic dysfunction.
Main Results:
- Patients with AS and LVH, and those with essential HT and LVH, showed higher innervation/perfusion mismatch scores than controls.
- Significant LVH was identified as the primary predictor of impaired LV sympathetic innervation.
- No significant changes in LV sympathetic innervation were observed 6 months post-TAVI, despite a marginal reduction in LV mass.
Conclusions:
- Cardiac sympathetic innervation is demonstrably impaired in patients with LVH, irrespective of AS.
- The TAVI procedure does not significantly alter cardiac sympathetic innervation in this patient cohort.
- LVH is a key factor influencing cardiac sympathetic dysfunction.
Background:
To evaluate cardiac sympathetic innervation in hypertensive patients with left ventricular (LV) hypertrophy (H) and aortic stenosis (AS) submitted to transcatheter aortic valve implantation (TAVI).
Methods And Results:
Twenty-two hypertensive elders (82 ± 5 years) with severe AS and significant LVH (> 122 g·m-2 in women and > 149 g·m-2 in men) were compared with 14 patients with uncomplicated essential hypertension (HT) with similar degree of LVH and 10 controls. 123I-metaiodobenzylguanidine (MIBG) and 99mTc-tetrofosmin SPECT acquisitions were obtained to assess sympathetic innervation and LV perfusion. The innervation/perfusion mismatch score was taken as an indicator of cardiac sympathetic dysfunction. The imaging protocol was repeated 6 months after TAVI. Regional MIBG uptake was more heterogeneous in HT and AS patients than controls, and therefore, innervation/perfusion mismatch score was higher in both AS (9 ± 8) and HT (5 ± 2) than controls (1 ± 1, P < .001). On multivariate analysis, significant LVH was the major predictor of impaired LV sympathetic innervation (OR 19.45, 95% CI 1.87-201.92; P = .013). After TAVI, no differences in measures of LV sympathetic innervation were evident, although only a marginal LV mass reduction was observed (- 5.4 ± 2.4 g).
Conclusions:
Cardiac sympathetic innervation is impaired in patients with LVH, either with AS or not, and is not impacted significantly by TAVI procedure.
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