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Sympathetic activation has been long appreciated exclusively as a fundamental compensatory mechanism of the failing heart and, thus, welcome and to be supported. In the initial clinical phases of heart failure (HF), the sympathetic nervous system overdrive plays a compensatory function aimed at maintaining an adequate cardiac output despite the inotropic dysfunction affecting the myocardium. However, when the sympathetic reflex response is exaggerated it triggers a sequence of unfavourable remodelling processes causing a further contractile deterioration that unleashes major adverse cardiovascular consequences, favouring the HF progression and the occurrence of fatal events. Eventually, the sympathetic nervous system in HF was demonstrated to be a ‘lethality factor’ and thus became a prominent therapeutic target. The existence of an effective highly specialized intracardiac neuronal network immediately rules out the old concept that sympathetic activation in HF is merely the consequence of a drop in cardiac output. When a cardiac damage occurs, such as myocardial ischaemia or a primary myocardial disorder, the adaptive capability of the system may be overcame, leading to excessive sympatho-excitation coupled with attenuation till to abolishment of central parasympathetic drive. Myocardial infarction causes, within a very short time, both a functional and anatomical remodelling with a diffuse up-regulation of nerve growth factor (NGF). The subsequent nerve sprouting signal, facilitated by a rise in the levels of NGF in the left stellate ganglion and in the serum, triggers an increase in cardiac nerve density in both peri-infarct and non-infarcted areas. Finally, NFG production decreases over time, supposedly as an adaptative response to the prolonged exposure to sympathetic overactivity, leading in the end to a reduction in sympathetic nerve density. Accordingly, NGF levels were markedly reduced in patients with severe congestive heart failure. The kidney is the other key player of the sympathetic response to HF as it indeed reacts to under-perfusion and to loop diuretics to preserve filtration at the cost of many pathological consequences on its physiology. This vicious loop ultimately participates to the chronic and disruptive sympathetic overdrive.In conclusion, sympathetic activation is the natural physiological consequence to life stressors but also to any condition that may harm our body. It is the first system of reaction to any potential life-threatening event. However, in any aspect of life over reaction is never effective but, in many instances, is, actually, life threatening. One for all is the case of ischaemia-related ventricular fibrillation which is, strongly facilitated by sympathetic hyperactivity. The take home message? When, in a condition of harm, everybody is yelling failure is just around the corner.

Percutaneous left stellate ganglion block (PLSGB) has been recently implemented for the acute treatment of refractory ventricular arrhythmias (VAs). The beneficial effect on supraventricular arrhythmias susceptibility and their ventricular response is well characterized in animal models, less so in humans. Available data suggest a significant prolongation of atrial refractory period, a reduction in inducibility and duration of atrial fibrillation and of all spontaneous intra– and postoperative atrial arrhythmias after thoracic and cardiac surgery. Here we describe a case of PLSGB for focal atrial tachycardia (AT). Case: we present a 68–year–old men with hypertension, obesity, OSAS and previous anterior myocardial infarction in the setting of a trivessel coronary disease, treated with PCI and complicated by apical aneurysm, with a LVEF of 38% and a moderate mitral and aortic regurgitation. He was on chronic antiarrhythmic therapy with bisoprolol 1.25 mg and ranolazine. He presented in the ED due to palpitations, pre–syncopal episodes, and worsening dyspnea. The ECG showed very frequent, self–limiting episodes of AT with a 1:1 atrioventricular (AV) conduction and a variable heart rate (HR) between 100 and 160 bpm, alternating with sinus rhythm at 45–50 bpm, sometimes conducted with aberrancy. Isolated and repetitive premature ventricular beats (PVB, maximum 8 beats) were also documented. Amiodarone, lidocaine, and intravenous unloading therapy were tried, without benefit. Coronary angiography was negative. PLSGB with an ultrasound–guided lateral approach (local bolus of lidocaine 100 mg+ropivacaine 20 mg) was performed, without complications, inducing palpebral ptosis. Over the next 15 hours we observed the disappearance of non–sustained VAs, the reduction of PVBs, and a progressive reduction of AT burden, of mean hourly HR (from 84 to 50 bpm, –40%) and of mean HR during AT (from 158 to 84 bpm, –47%, with AV 1:1 conduction). The patient subsequently underwent ablation of an extra systolic focus found near the ostium of the right inferior pulmonary vein, with no recurrences after 18 months.