Adrenergic dependent torsades despointes ventricular tachycardia (ADTdpVT) is a genetic defect caused by multiple ion channel abnormalities due to multiple genetic mutations, resulting in prolonged Q-T interval, recurrent TDP, recurrent syncope and sudden death. The causes of adrenergic dependence: ADTdp has been previously classified into the following three types: 1. Jervell-Lange-Nielson syndrome (JLNS): characterized by congenital deafness, prolonged Q-T interval, T-wave abnormalities, tip-twisting ventricular tachycardia (TDP) or ventricular fibrillation under stress and stress, and even syncope and sudden death, which is an autosomal It is an autosomal recessive disorder. Ganstorp syndrome is a subtype of RWS, showing no congenital deafness and reduced serum potassium. The rest is the same as JLNS. In recent years, it has been recognized that genetic mutations are the basic motive of its genetic basis. ADTdp is genetically heterogeneous and at least six LQTS (LQT1 to LQT6) variant loci are known to be autosomal dominant, five of which have been localized on chromosomes and four of which have established associated mutant genes. jLNS belongs to When both parents of JLNS patients contain KVLQT1 and the abnormal gene is inherited from both parents as a pure heterozygote, KVLQT1 causes abnormal ion channel function in the heart, i.e., abnormal potassium channel regulation. It makes myocardial repolarization significantly delayed as Q-T interval significantly prolonged, and is autosomal dominant. KVLQT1 also causes congenital hearing abnormalities and deafness by encoding the hearing component, which is autosomal recessive. Because the conditions that form JLNS are so specific, JLNS is rare. The other types of LQT, which constitute RWS, so RWS is caused by multiple genetic defects and is autosomal dominant. Its known related genes are LQT2, LQT3 (HERG), LQT4 (SCN5A), LQT5, and LQT6 (KCNE4). Defective genes mediate abnormalities in the regulation of cell membrane ion channels: SCN5A encodes a sodium channel that increases Na inward current, and its ion mediation is likely to be associated with Cl- abnormalities. kVLQT1, KCNE1 and HERG encode potassium channels that decrease K outward current. Thus, either one or more of these genetic mutations can lead to a decrease in K outflow and/or an increase in Na inward current. This results in prolonged action potential phase 2 and phase 3 timing and increased membrane potential. Delayed and incomplete repolarization occurs. The ECG shows a prolonged Q-T interval and abnormal TU waves. The formation and maintenance of EAD and TDP are also related to the midmyocardial M-cells, and the maintenance of arrhythmia is related to the folding mechanism. JLNS mostly presents with TDP when the heart rate increases due to emotional excitement, mental stress, exercise and exertion, which manifests as episodic syncope or even sudden death. This is associated with increased sympathetic tone, increased catecholamines that lead to the opening of calcium channels, and increased Ca2 inward flow, which increases the inward current and aggravates the imbalance of ion flow inside and outside the cell membrane, making it easier to produce post-depolarization, especially EAD and triggered arrhythmias. Some ADTdp do not normally show prolonged Q-T interval, but only when sympathetic tone is increased and inward current is more pronounced. Therefore, JLNS and RWS and their concurrent TDP are referred to as adrenergic-dependent TDP, but there are a few ADTdp patients with sleep or quiet onset (HERG and SCN5A gene-deficient types), which are intermittent-dependent, and adrenergic neuroexcitation can also contribute to the onset of TDP in patients with drug-induced secondary LQTS, suggesting that the mechanisms of onset Both types have a little crossover.