https://scholars.lib.ntu.edu.tw/handle/123456789/187946
標題: | 慢性心房顫動病人的竇房結功能及心房電生理:心房加速驅動與抗心律不整藥物的角色 | 其他標題: | Sinus Node Function and Atrial Electrophysiologic Property in Patients with Chronic Atrial Fibrillation: The Role of Atrial Overdrive Pacing and Antiarrhythmic Drugs | 作者: | 林俊立 | 關鍵字: | 心房顫動;竇房結功能;直流電電擊;心房電生理;Atrial fibrillation;sinus node function;electrical cardioversion | 公開日期: | 1999 | 出版社: | 臺北市:國立臺灣大學醫學院內科 | 摘要: | 慢性心房顫動的病患往往併發不可預期之血栓栓塞,造成個人及社會之損 失。本研究針對此類長時間之心房顫動病患,分析其臨床、心臟結構、心房電生 理藥理,以及竇房結功能,以瞭解回復正常心律及心房功能的病生理。 三十六位慢性心房顫動病患之全心房電生理分析,顯示左心房之局部訊號間 距明確小於右心房(160±14 msec vs 170±15 msec, P<0.01)。平均而言,直流電電 擊須247±98 焦耳之能量方能中止心房顫動。使用Sotalol 之下,能量可降為206±85 焦耳(P<0.05),但Propafenone 則不變(244±89 焦耳,P>0.05)。Sotalol 與Propafenone 均明顯增加左、右心房內之局部訊號間距,亦即迴旋波波長增加,但電擊能量則 有不同。慢性心房顫動終止之後,正常竇房結心律之穩定性常受到不安定的心房 早期收縮病灶干擾,而再發心房快速不整脈。這些不安定之病灶雖然多見於肺靜 脈入口處、左心耳及右心房之竇房結附近,但分佈上相當濔漫;此種情形雖以 Sotalol 與Propafenone 控制,亦無法全面改善,此顯示慢性心房顫動之病患常有 心房本身的多部位病變,而非只是竇房結功能異常。且即使後者輕微變化,所有 回復正常心律者均無心跳過慢的症狀。綜合各項因素分析,可惜卻只有體表心電 圖之P 波長度可以預測慢性心房顫動終止之後是否復發;若P 波大於125 msec ,其預測復發正確度為70%。慢性心房顫動(>6 個月)確對病患之心房電生理、病理及藥理產生長時間的變 化,且有相當程度的不可逆性,欲求長期穩定回復正常心律仍須進一步研究。 Chronic persistent atrial fibrillation is at risk of multiple cerebral and peripheral embolization and causes great socio-economic burden. For the purpose of investigation of the atrial electro-pathophysiology and relevant sinus node functional reserve, we studied 36 consecutive patients of chronic persistent atrial fibrillation by sequential clinical assessment, cardiac echocardiography and invasive cardiac electrophysiology study with bi-atrial basket electrodes. The underlying clinical-pathophysiological property of chronic persistent atrial fibrillation is correlated with the efficacy of electrical cardioversion and the subsequent maintenance of stable sinus rhythm and adequate sinus node function. Global atrial mapping of the chronic atrial fibrillation revealed a significantly shorter local A-A intervals in the left atrium than that in the right atrium (160±14 ms vs 170±15 ms, P<0.01). The electrophysiological gradient of reentrant wavelets was not changed under the use of sotalol and propafenone. However, the energy requirement for electrical cardioversion could be lessened by sotalol, but not propafenone, although both drugs help facilitate the success rate of direct current shocks. Meanwhile, the vulnerable atrial ectopies appearing after successful electrical cardioversion were located mostly at the pulmonary vein convergence area of the left atrium, the left atrial appendage and the sinus node and crista terminalis area of the right atrium. Nevertheless, the ectopies from the remaining areas of the atria were not uncommon. Sotalol and propafenone could decrease the number, but not the distribution of the vulnerable atrial foci. Apparently, in patients with chronic atrial fibrillation, the abnormalities in atrial pathology and electrophysiology are wide-spread and inter-relevant, which may disturb the restoration of stable sinus node activity after successful conversion. Despite of the deepened atrial pathophysiology, the sinus node function was generally acceptable, with only mild prolongation of post-suppression sinus node recovery time or intrinsic heart rate in half of the patients evaluated 3 months after conversion of chronic atrial fibrillation. None of these patients has had bradyarrhythmia-relevant symptoms, nor needing the implantation of a permanent pacemaker. Chronic persistent atrial fibrillation in humans deteriorated the structrual, functional and electrophysiological properties of the atria, which may not always be reversible. Fortunately, the underlying sinus node function remained competent after the conversion of long-term atrial fibrillation. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/23426 | 其他識別: | 882314B002286 | Rights: | 國立臺灣大學醫學院內科 |
顯示於: | 醫學系 |
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