Interaction between Endothelin-1 and Left Stellate Ganglion Activation: A Potential Mechanism of Malignant Ventricular Arrhythmia during Myocardial Ischemia

Figure 8

Schematic diagram depicting the potential role of ET-1 in the LSG and the aggravation of VA. ET-1 is mainly synthesized by vascular endothelial cells and contributes to cardiac sympathetic hyperactivity, aggravating LADO-induced VA. The underlying mechanisms may be correlated directly with activated ETA-R signaling in the LSG or correlated indirectly with an increased inflammatory response.