尖端扭转型室性心动过速（torsades de points,TdP）于1966年由法国学者Dessertenne首先描述.其心电图特点包括：基础心律QT间期延长,U波明显,室性心动过速（室速）常由长间歇后舒张早期室早诱发,心率多在160～280次/min,QRS波宽大畸形...尖端扭转型室性心动过速（torsades de points,TdP）于1966年由法国学者Dessertenne首先描述.其心电图特点包括：基础心律QT间期延长,U波明显,室性心动过速（室速）常由长间歇后舒张早期室早诱发,心率多在160～280次/min,QRS波宽大畸形,振幅不一,围绕基线不断扭转其主波方向,每5 ～ 20个心动周期转向反向.目前认为,其发生机理与折返有关,在心肌跨壁复极离散度（TDR）增大的基础上因早后除极（EAD）而诱发.常见病因为长QT间期综合征、严重心肌缺血或心肌病变、使用延长心肌复极药物及电解质紊乱等,为自身及临床因素共同决定.但对其扭转机制,目前尚未见相关报道.本文结合心肌电生理及心电图形成原理,探讨其发生扭转的可能机制,加深对该心电现象的理解和认识,为临床预防和治疗提供依据.展开更多
Electrical remodeling in atrial fibrillation(AF)is considered to beget AF.However,in AF,decreased expressions of introverted ion currents INa and ICa channel proteins are corresponding to the induced increase of ion c...Electrical remodeling in atrial fibrillation(AF)is considered to beget AF.However,in AF,decreased expressions of introverted ion currents INa and ICa channel proteins are corresponding to the induced increase of ion concentration in cells to maintain the membranes’polarity;ITo is phase 1 instantaneous extraverted K+current,IKur is the important extraverted K+current in phases 1 and 2,IKr,IKs are the main extraverted current in phase 2,and the ion channel proteins of them are down-regulated in AF to prolong atrial effective refractory period(AERP),which is disadvantageous to reentry;IK1,IKAch,IKATP work in phase 3,and their up-regulated channel proteins amplify myocardium diastolic potential,lower the myocardium excitability and reduce the ectopic excitement.Therefore,in AF,atrial electrical remodeling is not to beget AF,but to restore its physiological function.AF begets AF in that it can cause atrial structural remodeling,and the structural remodeling facilitates AF initiation and perpetuation.The interaction eventually aggravates atrial muscle injury and induces myocardial electrical disorder.展开更多
文摘尖端扭转型室性心动过速（torsades de points,TdP）于1966年由法国学者Dessertenne首先描述.其心电图特点包括：基础心律QT间期延长,U波明显,室性心动过速（室速）常由长间歇后舒张早期室早诱发,心率多在160～280次/min,QRS波宽大畸形,振幅不一,围绕基线不断扭转其主波方向,每5 ～ 20个心动周期转向反向.目前认为,其发生机理与折返有关,在心肌跨壁复极离散度（TDR）增大的基础上因早后除极（EAD）而诱发.常见病因为长QT间期综合征、严重心肌缺血或心肌病变、使用延长心肌复极药物及电解质紊乱等,为自身及临床因素共同决定.但对其扭转机制,目前尚未见相关报道.本文结合心肌电生理及心电图形成原理,探讨其发生扭转的可能机制,加深对该心电现象的理解和认识,为临床预防和治疗提供依据.
文摘Electrical remodeling in atrial fibrillation(AF)is considered to beget AF.However,in AF,decreased expressions of introverted ion currents INa and ICa channel proteins are corresponding to the induced increase of ion concentration in cells to maintain the membranes’polarity;ITo is phase 1 instantaneous extraverted K+current,IKur is the important extraverted K+current in phases 1 and 2,IKr,IKs are the main extraverted current in phase 2,and the ion channel proteins of them are down-regulated in AF to prolong atrial effective refractory period(AERP),which is disadvantageous to reentry;IK1,IKAch,IKATP work in phase 3,and their up-regulated channel proteins amplify myocardium diastolic potential,lower the myocardium excitability and reduce the ectopic excitement.Therefore,in AF,atrial electrical remodeling is not to beget AF,but to restore its physiological function.AF begets AF in that it can cause atrial structural remodeling,and the structural remodeling facilitates AF initiation and perpetuation.The interaction eventually aggravates atrial muscle injury and induces myocardial electrical disorder.
