Abstract
BackgroundAutonomic dysfunction, characterized by sympathetic activation and vagal withdrawal, contributes to the progression of heart failure (HF). We hypothesized that chronic vagus nerve stimulation (VNS) could prevent left ventricular (LV) remodeling and dysfunction in a canine HF model induced by chronic mitral regurgitation (MR).Methods and resultsAfter the MR inducing procedure, 12 survived canines were randomly divided into the control (n = 6) and the VNS (n = 6) groups. At month 2, a VNS stimulator system was implanted in all canines. From month 3 to month 6, VNS therapy was applied in the VNS group but not in the control group. At month 6, compared with the control group, the canines in VNS group had significantly higher cardiac output (2.3 ± 0.3 versus 2.9 ± 0.4 L/min, P < 0.05, LV forward stroke volume (20.1 ± 3.7 versus 24.8 ± 3.9 ml, P < 0.05), and end-systolic stiffness constant (2.2 ± 0.3 versus 2.7 ± 0.3, P < 0.05). NT-proBNP and C-reactive protein were decreased significantly in the VNS group. However, no statistical difference was found in LV ejection fraction, LV end-diastolic dimension, LV end-diastolic volume, myocyte cross-sectional area, or collagen volume fraction between two groups.ConclusionsChronic VNS therapy may ameliorate MR-induced LV contractile dysfunction and improve the expression of biomarkers, but has less effect in improving LV chamber remodeling.
Highlights
Autonomic dysfunction, characterized by sympathetic activation and vagal withdrawal, contributes to the progression of heart failure (HF)
One of the key features of chronic heart failure (CHF) is the autonomic sympathetic/parasympathetic imbalance, which is usually characterized by excessive sympathetic drive accompanied by parasympathetic withdrawal [1,2]
This study was designed to test the hypothesis that chronic vagus nerve stimulation (VNS) can attenuate left ventricular (LV) remodeling and improve LV function for CHF caused by chronic mitral regurgitation (MR)
Summary
Autonomic dysfunction, characterized by sympathetic activation and vagal withdrawal, contributes to the progression of heart failure (HF). One of the key features of chronic heart failure (CHF) is the autonomic sympathetic/parasympathetic imbalance, which is usually characterized by excessive sympathetic drive accompanied by parasympathetic withdrawal [1,2]. It directly affects the heart and blood vessels, and indirectly modulates the blood volume through the reninangiotensin-aldosterone (RAA) system and vasopressin signaling. By suppressing cardiac sympathetic activities, β-blockade had been demonstrated to be an effective treatment for contractile dysfunction caused by valvular heart disease [8]. Whether enhancing cardiac parasympathetic activities by VNS can be an alternative effective treatment for such contractile dysfunction is unknown. This study was designed to test the hypothesis that chronic VNS can attenuate LV remodeling and improve LV function for CHF caused by chronic mitral regurgitation (MR)
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