Effect of High Thoracic Sympathetic Nerve Block on Serum Collagen Biomarkers in Patients with Chronic Heart Failure

Abstract

Objectives: The impact of high thoracic sympathetic block (HTSB) on myocardial fibrosis in chronic heart failure (HF) is unclear. Myocardial collagen synthesis can be assessed by measuring circulating biomarkers. Weobserved the effect of HTSB on serum collagen biomarkers in HF. Methods: Forty-four patients were randomized to a control and a HTSB group. They received routine medications. Repeated epidural injections were given to the HTSB group for 4 weeks. Echocardiography and measurements of serum carboxy-terminal propeptide of procollagen type I (PICP) and amino-terminal propeptide of procollagen type III (PIIINP) were performed at baseline and 4 weeks later. Results: There were significant reductions in left atrial diameter, left ventricular (LV) diameter and volume, LV weight index (LVWI) and serum PICP and PIIINP levels in the HTSB group (p < 0.05). The changes in LV end-systolic volume and ejection fraction (LVEF) were greater in the HTSB group than in the control group (p < 0.05). In the HTSB group, the decreases in PICP and PIIINP were correlated with the decrease in LVWI (PICP: r = 0.695, p = 0.000; PIIINP: r = 0.642, p = 0.001), and the decrease in PICP was negatively associated with the rise in LVEF (r = -0.813, p = 0.000). Conclusion: HTSB reduces myocardial fibrosis in HF, which may accompany the improvement of LV hypertrophy anddysfunction.

Targeted ablation of cardiac sympathetic neurons attenuates adverse postinfarction remodelling and left ventricular dysfunction

“…Previous studies have shown that HF increases SG nerve activity and induces remodelling of cardiac ganglia (Ogawa et al., ; Singh et al., ). Sympathectomy and SG block have been demonstrated to be effective therapeutic options in the treatment of ventricular arrhythmias and cardiac dysfunction in HF patients (Pêgo‐Fernandes et al., ; Sun, Liu, & Qu, ; Vaseghi et al., ). Targeted ablation of cardiac sympathetic neurons (TACSN) is an effective approach to decrease cardiac noradrenergic drive by injection of the retrogradely transported cholera toxin B subunit–saporin (CTB‐SAP) compound into the SG (Llewellyn‐Smith, Martin, Arnolda, & Minson, ).…”