[AF-FORUM] 104E 副交感神经相关房颤. Dr. Perez Riera

星期二四月 24 14:04:16 ART 2007

亲爱的Vazquez-Tanus医生：变化的心律动态性，比如通 
过复杂性以及不规则性的分析，会在自发性房颤发作 
前出现。减少的估计熵和样本熵（可以反映心率变异 
的非线性复杂性）是房颤发作前心率动态变化的标志 
（1）。

窦律时的心率是通过自主神经系统调节的，有时会发 
生短时的振动。而这些振动的高频成分与呼吸相关， 
并通过副交感神经介导产生窦性心律不齐。控制呼吸 
在长期房颤患者中可以导致周期性的房颤频率波动。 
这些现象可能与副交感神经对房颤不应期的调节相 
关 （2）。

增强的迷走神经张力在试验室房颤的发生和维持上起 
重要作用。变化的心率动态特点，提示迷走输出的一 
过性增高与临床上房颤的自发发作相关（3）。

在Brugada综合症患者，大多数房颤和多形性室速夜间 
发生（85%）提示自主神经的影响。 夜间的心动过 
缓，恶心呕吐，体位性心动过速综合症可以恶化 
Brugada综合症的心电图表现。与年龄性别匹配的对照 
组相比，Brugada综合症24小时心率变异性降低，日间QT/ 
RR 曲线降低。Brugada综合症患者窦律常见；然而Brugada 
综合症患者房性心律失常发病率也较高（10-25%），显 
然其病变不仅局限于心室。在最初Brugada兄弟报道的 
病人中曾提到过阵发性房颤的病史（4）。

阵发性迷走神经介导性的房颤可见于30%的Brugada综合 
症患者。

Eckardt等（5）2001年 报道室上性心律失常发生率29%。 
他们当时描述这些为房室折返性的室上性心动过速。

狗试验显示，心儿在胆碱能房颤的发生中起重要作 
用。然而，肺静脉和上腔静脉在迷走性阵发性房颤中 
作用相对减少（6）。

倾斜试验中显示的房颤发作前张力反射敏感度增加提 
示迷走介导机制的参与（7）。

RG2(一种新的III类抗心律失常药)可以在试验中终止和 
预防房颤再发，似乎也与显著增加的心房有效不应期 
相关（8）。

在迷走神经介导的房颤终止后出现的钙超载可以形成 
早期后除极诱发触发电活动，这一机制可能与早搏形 
成进而再发房颤相关（9）。

参考文献
1)        Shin DG, YooCS, Yu SH, et al.  Prediction of paroxysmal
atrial fibrillation using nonlinear analysis of the R-R interval
dynamics before the spontaneous onset of atrial fibrillation. Circ J.
2006;70:94-99.
2)        Holmqvist F, Stridh M, Waktare JE,  et al. Rapid
fluctuations in atrial fibrillatory electrophysiology detected during
controlled respiration. Am J Physiol Heart Circ Physiol. 2005;
289:H754-760.
3)        Vikman S, Lindgren K, Makikallio TH, et al.Heart rate
turbulence after atrial premature beats before spontaneous onset of
atrial fibrillation. J Am Coll Cardiol. 2005; 45:278-284.
4)        Pierre B, Babuty D, Poret P. et al. Abnormal Nocturnal
Heart Rate Variability and QT Dynamics in Patients with Brugada
Syndrome. Pacing Clin Electrophysiol. 2007;30: S188-191.
5)        Eckardt L, Kirchhof P, Johna R, et al. Wolff-Parkinson-
White syndrome associated with Brugada syndrome. Pacing Clin
Electrophysiol 2001;24:1423-1424.
6)        Zhao QY, Huang CX, Jiang H, et al. The research of
molecular and ionic mechanisms in vagally mediated atrial
fibrillation in canine. Int J Cardiol. 2007; 117: 425-426.
7)        De Casto RR, Mesquita ET, da Nobrega AC. Parasympathetic-
mediated atrial fibrillation during tilt test associated with
increased baroreflex sensitivity. Europace. 2006;8:349-351.
8)        Fedorov VV, Rozenshtraukh LV,  Reznik AV, et al.
Antiarrhythmic Efficacy of a New Class III Antiarrhythmic Drug RG-2
Kardiologiia. 2004; 44:66-73.
9)        Burashnikov A, Antzelevitch C. Reinduction of atrial
fibrillation immediately after termination of the arrhythmia is
mediated by late phase 3 early afterdepolarization-induced triggered
activity. Circulation. 2003;107:2355-2360.

All the best for all
Andrés Ricardo Pérez Riera MD
Chief of Electro-Vectocardiology Sector of the Discipline of
Cardiology,
ABC Faculty of Medicine (FMABC), Foundation of ABC (FUABC) - Santo
André 圣保罗– 巴西.
riera在uol.com.br

-----------------------------
Dear Dr Vazquez-Tanus: Altered HR dynamics, as analyzed with
complexity and fractal measures, may precede the spontaneous onset of
paroxysmal AF. A reduction in the approximate entropy  and sample
entropy, which reflects the nonlinear complexity of HR variability,
is a hallmark of altered HR dynamics preceding the spontaneous onset
of AF(1).

HR during SR is modulated through the autonomic nervous system, which
generates short-term oscillations. The high-frequency components in
these oscillations are associated with respiration, causing sinus
arrhythmia, mediated by the parasympathetic nervous system.
Controlled respiration causes cyclic fluctuations in the AF frequency
in patients with long-duration AF. This phenomenon seems to be
related to parasympathetic modulations of the AF refractory period (2).

Enhanced vagal activity plays a major role in the onset and
perpetuation of experimental AF. Altered HR dynamics, suggesting
transient enhancement of vagal outflow after premature atrial
excitation, are temporally related to spontaneous onset of clinical
AF (3).

In Brugada Syndrome(BrS) most of the AF and PVT events are nocturnal
( 85% of cases), suggesting an influence of the autonomic nervous
system by selective stimulation of muscarinic receptors. Nocturnal
bradycardia by vagal predominance; nausea, vomiting,  postural
Orthostatic Tachycardia Syndrome worst BrS ECG pattern. Compared to a
control group matched for age and sex, Heart Rate Variability (HRV)
was decreased over 24 hours and QT/RR slopes and during nighttime in
patients with BrS4. Sinus rhythm is the usual inBrS; however, BrS
patients exhibit an abnormally high proportion of atrial arrhythmias
that are found in 10 to 25% of cases since the arrhythmogenic
substrate is not limited to the ventricles. In the original discovery
by the Brugada brothers (1992) temporary AF was mentioned.

Paroxysmal vagal mediate form of AF is observed in a 30% of cases in
BrS.

A publication by Eckardt L et al (2001)5, indicates a frequency for
supraventricular arrhythmias of 29%. These authors described episodes
of AV supraventricular tachycardia with reentry.

Experimentally in dogs atrial appendage play an important role in
initiation of cholinergic AF. However, pulmonary veins and and
superior vena cava less often play an important role in vagotonic
paroxysmal AF(6).

Increased barorereflex sensitivity preceding the onset of AF during
the tilt test may indicate the involvement of a vagally mediated
mechanism(7).

The ability of RG-2(a new class III antiarrhythmic drug) to terminate
and prevent reinduction of experimental AF appears to be associated
with a significant increased atrial effective refractory period(8).

Calcium overload conditions present after termination of vagally
mediated AF contribute to the development of late phase 3 early
afterdepolarizations-induced triggered activity and that this
mechanism may be responsible for the extrasystolic activity that
reinitiates AF(9).

References
1)        Shin DG, YooCS, Yu SH, et al.  Prediction of paroxysmal
atrial fibrillation using nonlinear analysis of the R-R interval
dynamics before the spontaneous onset of atrial fibrillation. Circ J.
2006;70:94-99.
2)        Holmqvist F, Stridh M, Waktare JE,  et al. Rapid
fluctuations in atrial fibrillatory electrophysiology detected during
controlled respiration. Am J Physiol Heart Circ Physiol. 2005;
289:H754-760.
3)        Vikman S, Lindgren K, Makikallio TH, et al.Heart rate
turbulence after atrial premature beats before spontaneous onset of
atrial fibrillation. J Am Coll Cardiol. 2005; 45:278-284.
4)        Pierre B, Babuty D, Poret P. et al. Abnormal Nocturnal
Heart Rate Variability and QT Dynamics in Patients with Brugada
Syndrome. Pacing Clin Electrophysiol. 2007;30: S188-191.
5)        Eckardt L, Kirchhof P, Johna R, et al. Wolff-Parkinson-
White syndrome associated with Brugada syndrome. Pacing Clin
Electrophysiol 2001;24:1423-1424.
6)        Zhao QY, Huang CX, Jiang H, et al. The research of
molecular and ionic mechanisms in vagally mediated atrial
fibrillation in canine. Int J Cardiol. 2007; 117: 425-426.
7)        De Casto RR, Mesquita ET, da Nobrega AC. Parasympathetic-
mediated atrial fibrillation during tilt test associated with
increased baroreflex sensitivity. Europace. 2006;8:349-351.
8)        Fedorov VV, Rozenshtraukh LV,  Reznik AV, et al.
Antiarrhythmic Efficacy of a New Class III Antiarrhythmic Drug RG-2
Kardiologiia. 2004; 44:66-73.
9)        Burashnikov A, Antzelevitch C. Reinduction of atrial
fibrillation immediately after termination of the arrhythmia is
mediated by late phase 3 early afterdepolarization-induced triggered
activity. Circulation. 2003;107:2355-2360.

All the best for all
Andrés Ricardo Pérez Riera MD
Chief of Electro-Vectocardiology Sector of the Discipline of
Cardiology,
ABC Faculty of Medicine (FMABC), Foundation of ABC (FUABC) - Santo
André São
Paulo - Brazil.
riera在uol.com.br

--
Dr. Sergio Dubner
President of Scientific Committee

Dr. Edgardo Schapachnik
President of Steering Committee