心房的自主神经节丛及其临床意义_中国医学科学院阜外心血管病医院_姚焰_心血管网（Atrial autonomic ganglia plexus and its clinical significance _ China Academy of Medical Sciences Fuwai Hospital of C..

心房的自主神经节丛及其临床意义_中国医学科学院阜外心血管病医院_姚焰_心血管网（Atrial autonomic ganglia plexus and its clinical significance _ China Academy of Medical Sciences Fuwai Hospital of C.. 心房的自主神经节丛及其临床意义_中国医学科学院阜外心血管病医 院_姚焰_心血管网(Atrial autonomic ganglia plexus and its clinical significance _ China Academy of Medical Sciences Fuwai Hospital of Cardiovascular Disease _ Yao Yan _ cardiovascular network I. distribution and physiological function of cardiac autonomic nerve The heart is inherent and from central autonomic common control, which is the intrinsic ganglia autonomic nerve plexus (Ganglion Plexi, GP), mainly in the left atrial surface fat pad and Marshall ligament, right atrial surface near the left atrium have also been distributed [1]. The atrium's own autonomic nervous system receives signals from the autonomic nervous system of the central nervous system, but independently regulates the functioning of the heart, including autonomic, contractile, and conduction functions, [2,3]. Self contained within the atrium from ganglionic plexus and afferent neurons from central nervous system efferent cholinergic and adrenergic neurons (around GP in the pulmonary vein ostium muscle and atrial muscle in a large distribution) and a large number of connections between neurons. The latter constructs a network of connections between different GP and GP and atrial and pulmonary venous myocardium. The surface of the left atrial autonomic ganglia plexus (GP) mainly distributed in the top of the left superior pulmonary vein (LSGP), the top right pulmonary vein before (RSGP), along the ligament of Marshall (LLGP), posterior wall of left inferior pulmonary vein extraoral LIGP and right pulmonary veins outside the RIGP. In addition, the GP between the superior vena cava, the aorta, and the right pulmonary vein is thought to be the "head station" between the autonomic nerve fibers originating from the center and the autonomic nerve fibers which are the autonomic structures of the left atrium (Head Station). The specific site of the left atrium GP can be determined by high frequency stimulation (High-frequency, Stimulation, HFS). Can use 20~50 Hz frequency, front degree 10~15 V, pulse width up to 10 MS, at least 5 seconds at a time. If high frequency stimulation leads to sinus arrest, sinus bradycardia, atrioventricular node block, or even hypotension, vagal reflexes suggest that there is GP present. An in vivo study revealed that 4 GP (2~6) were recorded on the left atrium by high frequency stimulation of the intima. An increase in sympathetic tension in the cardiovascular system can lead to increased heart rate, visceral vasoconstriction, coronary artery dilatation, and increased blood pressure. An increase in vagal tension leads to heart rate slowing and vasodilation and blood pressure decline. Two 、 left atrium vagus nerve and atrial fibrillation Atrial GP is associated with atrial fibrillation, which is first isolated from the pulmonary veins around the endocardium, and in the treatment of atrial fibrillation, some patients experience severe vagal reflexes. In the study of the relationship between vagus nerve and the occurrence and maintenance of atrial fibrillation, it was found that acetylcholine can trigger atrial fibrillation by local injection of the neurotransmitter acetylcholine in the vagus nerve. Scherlag found that the GP release of acetylcholine can cause atrial and pulmonary vein muscle sleeves should not be shortened, the same period of adrenergic neurotransmitter release increased intracellular calcium, calcium concentration increased early repolarization and prolonged release of intracellular calcium, sodium ion influx and calcium ion flow is 3: 1. Result in a net flow, thus forming early repolarization and trigger excited trigger atrial fibrillation. They believe that ablation for GP may increase the ablation success rate of paroxysmal atrial fibrillation, [4, 5]. In fact, Pokushalov et al claimed that for atrial fibrillation only ablation of the left atrium GP without isolation of the pulmonary vein could achieve good results. But its subsequent trial with Greek scholars was depressing. Compared with the success rate of 77.5% for pulmonary vein isolation, the success rate of single left atrial GP ablation for paroxysmal atrial fibrillation was only 42.5%[6]. However, its rigorous, realistic, self denial of academic spirit worthy of recognition. To be sure, GP can be accurately calibrated by endometrial stimulation or by destruction by ablation, which was subsequently confirmed by a series of clinical studies. Of course, the outer membrane stimulation is more accurate for the calibration of GP. Because the left atrium GP is located in the fat pad of the outer membrane, clinical studies have confirmed that the ablation of left atrium GP by thoracoscopic external membrane ablation is more accurate, and, It can improve postoperative life therapy, relieve symptoms and increase exercise tolerance. It is worth pointing out that after GP ablation, it is possible that the sympathetic tone is relatively dominant, leading to a marked improvement in sinus rhythm. This effect is beneficial to patients with dysfunction and paroxysmal sinus, but quite a few scholars have observed that this effect usually lasts less than 2 years, and that the recovery caused by atrial autonomic innervation. Such inferences may be flawed because sinus node dysfunction and atrial fibrillation are all manifestations of atrial fibrosis. Ablation destroys the sinus rhythm caused by increased sympathetic tension in the vagus component of GP, and may be counteracted by the increase in atrial fibrosis, so we cannot simply assume that GP is restored to dominance. In addition, it may also be related to the ablation intensity. Pokushalov increased the RR interval by 50% during stimulation of GP, and decreased by more than 20% in blood pressure, as the criterion of vagal reflex, and repeated high frequency stimulation after ablation could not induce vagal reflex as the end point. From our experience, the end point may not be reliable. Because the endometrial ablation may be due to local myocardial dehydration, necrosis, resulting in high frequency stimulation effectiveness discounts, affecting the efficacy of judgment. However, the reconstruction of autonomic innervation does have animal epicardial ablation after evidence, but confusingly, necrosis of neuron and nerve fiber regeneration should not be possible, if the existence of the restored phenomenon of left atrial autonomic nerve innervation, what is the regeneration of the nervous system and autonomic nervous system function compensation. It is worth to study the exact mechanism. A recent study presented an unexpected phenomenon. Previous clinical and experimental studies confirmed that all the ablation of left atrial GP can reduce atrial fibrillation episodes of atrial fibrillation, improve the cure rate, but for the superior vena cava and right pulmonary vein between the aorta as the central autonomic nerve and intrinsic heart autonomic nervous system between the "head" of the SVC-AoGP in the acute period while the ablation of atrial effective should not be prolonged, but in the long term, the local effective should not be more episodes of atrial fibrillation and the shortening of atrial tachycardia, suggesting that central nervous system inhibited the activity of [7] intrinsic heart autonomic nervous system. The mechanism is also worthy of study in the future. Three, left atrial vagal treatment for vasovagal syncope Vasovagal syncope (Vaso, vagal Syncope (VVS) is the most common cause of syncope in the clinic, accounting for about 2/3 of all syncope patients. Although it is not fatal, a clinical study from Spain suggests that its impact on the quality of life is comparable to that of heart failure. It is not uncommon for a patient to have a fall due to frequent attacks in the clinic. Many factors contribute to VVS, including long standing, postural changes, drugs, temperature, alcohol consumption, and mood changes. Interestingly, VVS is the most common cause of nocturnal urination in Chinese men. The resulting VVS mechanism is not entirely clear, from the tilt test, because of lower extremity blood stasis, blood volume decreased, increased sympathetic tone and ventricular contractility, excessive stimulation of left ventricular baroreceptor, leads to increased activity of the vagus nerve, feedback inhibition of the sympathetic nerve, resulting in peripheral vasodilatation, decreased blood pressure and / or heart rate, cardiac output decreased, brain ischemia and sudden, syncope, this is the classic Bezold-Jarisch reflection. The diagnosis of VVS mainly depends on tilt test, and can be divided into vascular type, heart type and mixed type according to the tilt test results. The current treatment methods, physical exercise and drug therapy are major drawbacks or side effects of poor compliance, only with pacemakers pacemaker with closed loop sympathetic tone perception prevent syncope effect, but the economic burden and psychological pressure has greatly restricted its use. In view of the above left atrial GP distribution and its physiological significance, we have since 2005 attempted a VVS ablation of the left atrium GP catheter for frequent episodes of syncope. The first two cases were paroxysmal atrial fibrillation with frequent VVS, we measured the left atrial linear ablation under the guidance of the most common LSGP, just covering RSGP, RIGP and LLGP in non contact location. In order to improve the curative effect and prevent the atrial reinnervation, we used a relatively large power (8 mm, 60 W power head cap and 60 DEG C temperature limit), and to each of the GP ablation until vagal reflex disappeared as the ablation end point. This means that certain sites of GP may need to be ablated for 1~2 minutes or longer, significantly higher than the GP ablation time and intensity reported by other investigators. A typical left atrial GP position and ablation of VVS in a patient with LSGP lead to a typical vagal reflex of sinus arrest (Fig. 1). The current follow-up was satisfactory, [8]. In the extended series, more than 85% of the patients were not fainting during the follow-up period. The longest one has not occurred again for 8 years, and the patient may swoon before bending or lowering his head.