房室传导间期(A-V)的自动测量及频谱特征

目的 探讨房室传导间期(A-V)的自动测量,频谱特点及心率对其影响。方法 实验是在去神经的猫上进行,由右颈总动脉插入主动脉根部,测出希氏束(His)电图,通过模板匹配的方法自动检测His电图中心房(A)、希氏(H)波及心室(V)波,并将AA、AV间期数据通过快速傅立叶(FFT)转换,获得其频谱特征。再通过程序控制心房起搏观察了AA间期变化对AV频谱的影响。结果His束中A、H、V波可以自动重复检测,AV频谱与AA频谱均相似,但密度(PSD)较AA小,经标准化后,两者的高频(HF),低频(LF)及高频/低频(HF/LF)相同(P>0.05),通过心房起搏表明AA间期与AV间期呈非线形关系,AV频谱中HF与AA间期的变化率呈负相关(R=-0.97,P<0.01),LF与AA间期的变化率呈正相关关系(R=0.96,P<0.01)。结论心脏His束自动测量揭示了房室传导的频域特征以及心率对AV频谱各成份的相关关系,为研究心脏房室传导障碍性疾病以及心率对心电频谱的影响提供了一个新的方法。     

病变心肌组织多普勒频谱分析

目的探讨病变心肌组织多普勒(DTI)频谱各速度波及其变化.方法开胸犬13只,于冠状动脉左旋支的分支结扎前、后分别记录乳头肌水平左心室后壁短轴方向的DTI运动频谱,结合同步记录的心电图、左心室压力(P)曲线及其一阶导数(dP/dt)曲线、心音图辨认DTI频谱各速度波,并对照比较冠状动脉结扎前、后DTI频谱的变化.临床连续观察19例心肌梗死患者,6例接受原位心脏移植患者,记录左心室壁及二尖瓣环DTI频谱和组织速度图(TVI),结合心电图辨认各速度波.结果正常开胸犬左心室后壁短轴方向运动等容收缩期以正向为主(IVC1),急性缺血时出现明显的反向运动波(IVC2)并可延至射血期,冠状动脉结扎前、后IVC1和IVC2峰值均发生显著变化[(16.60±4.11)cm/s对(4.60±5.38)cm/s 和(5.97±6.25)cm/s对(19.57±3.58)cm/s,P<0.01];冠脉结扎后射血期S波峰值显著降低[(11.30±1.58)cm/s对(7.16±1.80)cm/s,P<0.01],舒张早期E波反向或双向变化[(10.86±3.32)cm/s对-(10.72±6.36)cm/s,P<0.01],左心房收缩期A波峰值速度降低[(11.08±3.35)cm/s对(6.71±4.81)cm/s,P<0.05].临床定性观察心肌梗死和接受心脏移植的患者亦发现类似犬急性缺血心肌DTI频谱的变化.结论在心肌病变较严重的情况下,等容收缩期出现反向DTI频谱,S波峰值降低,E波反向或双向,如不结合心电图等确定心动时相,频谱分析结果可能会出现分歧或误差.     

应用组织多普勒观察缺血心肌等容收缩波的变化

目的:研究缺血心肌等容收缩波(isovolumetriccontraction,IVC)幅度和时相的变化。方法:7只开胸犬,冠状动脉左旋支后壁分支结扎前、后分别录得左室后壁短轴方向等容收缩期组织多普勒(dopplertissueimaging,DTI)运动频谱,并进行结扎前后对照分析。结果:冠状动脉结扎前后比较,等容收缩波IVC1显著降低犤(17.31±2.88),(6.01±3.25)cm/s,t>5×106,P<0.05犦,持续时间显著缩短犤(31.77±14.69),(13.77±9.94)ms,t=3.01,P<0.05犦,IVC2波显著增高犤(-0.53±11.37),(-17.44±4.92)cm/s,t=3.36,P<0.05犦,持续时间显著延长犤(19.00±9.01),(59.09±11.99)ms,t=6.20,P<0.05犦。结论:心肌供血状态的改变可以引起等容收缩波显著变化。     

牛磺酸对大鼠缺血心肌缺血再损伤的保护作用

目的探讨大鼠心肌缺血损伤与凋亡蛋白 Bcl-2和 Bax的关系及牛磺酸的影响. 方法选择健康 SD大鼠 30只,随机分为假结扎组、结扎组和牛磺酸保护组,每组 10只.结扎大鼠冠状动脉左前降支建立心肌缺血模型.检测 3组心肌线粒体中超氧化物歧化酶( superoxide dismutase,SOD)、 Ca2+-ATP酶活性和丙二醛含量,用免疫组化法检测心肌中的 Bcl-2和 Bax蛋白. 结果结扎冠状动脉左前降支可致心肌线粒体丙二醛含量升高 [假结扎组 (4.89± 0.54) μ mol/g;结扎组( 9.85± 0.68) μ mol/g], SOD和 Ca2+-ATP酶活性下降 [假结扎组( 8.63± 0.35) μ mol/( g· s) ,(13.97± 1.97) mmol/( g· s) ;结扎组( 6.73± 0.39) μ mol/( g· s), (8.54± 2.28) mmol/( g· s) ].缺血心肌 Bax蛋白表达呈显著升高 (t=3.931, P< 0.01),牛磺酸能明显减少缺血心肌线粒体丙二醛的生成 [牛磺酸保护组 (5.46± 0.72) μ mol/g],降低心肌 Bax蛋白的表达,增加 Bcl-2蛋白的表达 ( t=3.716, P< 0.01). 结论结扎大鼠冠状动脉左前降支所致心肌缺血损伤与 Bcl-2和 Bax蛋白的表达有关 ,牛磺酸对缺血心肌 Bcl-2和 Bax蛋白的表达有较好的调控作用.     

运动疗法对轻度原发性高血压的疗效及心率变异性的影响

目的:观察运动对轻度原发性高血压患者的疗效和心率变异性的影响。方法:40例轻度高血压患者进行3个月的中低强度运动疗法,记录并比较运动疗法前后的血压、心率及心率变异时域、频域指标,并与36例健康对照组比较。结果:与对照组相比,高血压患者相邻正常R-R间期标准差,正常相邻R-R间期差值的方差,高频功率明显下降,低频功率/高频功率比值增加(P<0.05)。运动疗法后血压从(150.2±8.5)(/85.3±7.3)mmHg下降至(137.2±7.6)/(77.3±7.0)mmHg,同时和运动疗法前相比R-R间期标准差、正常相邻R-R间期差值的方差、高频功率增加,低频功率/高频功率比值降低(P<0.05),且和对照组相比差异有显著性意义(P<0.05)。结论:轻度高血压采用中低强度运动疗法可降低血压,同时提高心率变异指标,改善自主神经功能。     

超声指导下优化心脏再同步化治疗扩张型心肌病心衰患者临床研究

目的超声评价扩张型心肌病心衰患者再同步化治疗(CRT)的术后参数优化。方法12例扩张型心肌病心衰患者(心功能分别为Ⅲ级或Ⅳ级),其中8例伴完全性左束支传导阻滞患者,在充分抗心衰药物治疗基础上植入人工心脏三腔起搏器(InsyncⅢ),行CRT,术后继续接受抗心衰药物治疗。术后1周在超声指导下对起搏器进行优化,设置合理的AV间期和VV间期。评价优化前、后LVEDD、LVEF、主动脉瓣VTI、二尖瓣VTI、Ts-SD、6MHW、QRS间期。结果12例患者CRT治疗1周后,LVEDD由优化前的66.12±5.32mm减少到64.79±5.31mm(P>0.05);LVEF由优化前的(30.91±6.22)%增加到(32.25±5.96)%(P<0.01);主动脉瓣VTI由优化前的14.47±2.42 cm增加到16.35±2.31 cm(P<0.01);二尖瓣VTI由优化前的16.23±3.33 cm增加到21.78±4.40 cm(P<0.01);Ts-SD由优化前的42.17±23.88m s减少到37.74±22.38m s(P>0.05);6MHW由优化前的324.62±25.49m增加到367.31±22.01m(P>0.01);QRS间期由优化前的129.00±6.65m s减少到128.65±6.31m s(P>0.05)。结论本研究显示超声在优化扩张型心肌病心衰患者同步化治疗中发挥作用。     

关于缺血心肌组织多普勒频谱识别的探讨

【目的】确认缺血心肌组织多普勒 (DTI)频谱各速度波及缺血前后的变化。【方法】开胸犬 13条 ,于冠脉左旋支的分支结扎前、后记录乳头肌水平左室后壁短轴方向的DTI运动频谱 ,结合同步记录的心电图、心内压力曲线 (P ,dP/dt)及心音图辨认DTI频谱的各速度波 ,比较冠脉结扎前、后DTI频谱的变化 ;观察19例心肌梗死患者 ,记录左室壁及二尖瓣环DTI频谱和组织速度图 (TVI) ,结合心电图辨认各速度波。【结果】正常开胸犬左室后壁短轴方向运动速度波 ,等容收缩期以正向为主 (IVC1) ,急性缺血时出现明显的反向运动波 (IVC2 )并可延至射血期 ,冠脉结扎前、后IVC1和IVC2 峰值均发生显著变化 [(16 .6 0± 4 .11)cm/s对(4 .6 0± 5 .38)cm/s和 (5 .97± 6 .2 5 )cm/s对 (19.5 7± 3.5 8)cm/s,P <0 .0 1];冠脉结扎后射血期S波峰值显著降低 [(11.30± 1.5 8)cm/s对 (7.16± 1.80 )cm/s ,P <0 .0 1],舒张早期E波反向或双向变化 [(10 .86±3.32 )cm/s对 (- 10 .72± 6 .36 )cm/s,P <0 .0 1],左房收缩期A波峰值速度降低 [(11.0 8± 3.35 )cm/s对 (6 .71± 4 .81)cm/s ,P <0 .0 5 ]。临床观察心肌梗死患者亦发现类似犬急性缺血心肌DTI频谱的变化。【结论】在心肌严重缺血或梗死的情况下 ,DTI频谱等容收缩期出现反向 ,S波峰值     

运动疗法对经皮冠状动脉介入治疗后患者心肌缺血和自主神经功能的影响

目的:探讨康复运动疗法对冠心病经皮冠状动脉介入治疗(percutaneouscoronaryintervention,PCI)后患者心肌缺血的改善和自主神经功能的影响,以评价康复运动疗法对改善PCI患者心功能的价值。方法:2001-07/2003-10在中国汕头大学医学院第一附属医院心内科住院的PCI后患者186例。符合标准的患者32例,对32例PCI后患者进行运动前评定,制定康复运动方案,行8周运动疗法,应用运动心电图和心率变异对运动前后进行评价。结果:PCI后患者康复运动后心电图最大心率,最大收缩压,最大舒张压、最大ST段压低犤(131.8±6.5)次/min,(154.0±7.1),(86.2±7.9)mmHg,(0.58±0.35)mV犦明显低(或少)于运动前犤(136.4±8.3)次/min,(172.6±6.2),(97.6±9.2)mmHg,(0.96±0.34)mV犦(P<0.05～0.01;PCI后患者运动后心率增值、运动时间、最大运动负荷明显高(或长)于治疗前(P<0.05～0.01);康复运动前24h内全部正常心动周期的标准、24h内5min节段平均心动周期的标准差、24h内5min节段正常心动周期的标准差的均方根、相邻正常心动周期差值的均方根及频域指标的总频谱、低频和高频明显低于对照组(P<0.01);运动后全部正常心动周期的标准、相邻正常心动周期差值的均方根、频域指标的总频谱、低频和高频较运动前均明显升高,(P<0.01);5min节段平     

高氧液对家兔心肌缺血/再灌注细胞凋亡的影响

目的观察高氧液对心肌缺血/再灌注心肌梗死面积、心肌结构和细胞凋亡参数的影响,探讨高氧液抗心肌缺血/再灌注损伤的保护作用机制。方法家兔心脏左冠状动脉前降支缺血/再灌注动物模型,缺血30min,再灌注2h。60只家兔随机数字表法分成3组:对照组(I组,n=20)只暴露左冠状动脉前降支,不结扎;缺血/再灌注组(Ⅱ组,I/R组,n=20),在缺血再灌注前10min静脉注射生理盐水(20ml/kg);高氧液治疗组(Ⅲ组,n=20),在缺血前10min静脉注射高氧液(20ml/kg)。分别按TCC法染色,用图像分析系统计算梗死面积;原位末端TUNEL法检测细胞凋亡指数;免疫组化ABC法检测Fas、Bcl-2的含量,同时电镜观察心肌细胞的超微结构。结果III组心肌梗死细胞面积为(2.29±0.02)cm,与II组的(3.38±0.07)cm比较,梗死面积明显缩小。II组的AI(20.8±0.36),明显高于I组(4.1±0.25),P<0.01,t=170.4,III组的AI(13.3±0.35)显著低于II组,P<0.01,t=66.8,但仍高于I组,P<0.01,t=92.8。I组Fas的OD值为2.80±0.07,II组3.70±0.05,III组3.10±0.04。I组Bcl-2的OD值为2.7±0.02,II组0.60±0.03,III组2.90±0.02。结论高氧液具有抗心肌缺血/再灌注损伤的作用,其作用机制可能是通过调节Fas和Bcl-2介导的心肌缺血/再灌注细胞凋亡而实现。     

太极拳运动中心率变异性指标的检测及意义

目的:检测太极拳爱好者在安静状态下的心率变异性(heartratevariabil-ity,HRV)范围,为进一步探索HRV与健身运动的关系打下工作基础。方法:测定49名太极拳拳龄5～15年,年龄45～70岁的中老年太极拳运动爱好者在安静状态下的心电图,由计算机获取RR间期变化,并做功率频谱密度(powerspectrumdensity,PSD)分析。得出正常人在安静状态下的总变异性、低频成分、高频成分以及低频成分/高频成分比值。结果:安静状态下男性心率总变异性为2973.07±2309.23,低频成分/高频成分为1.09±1.32;女性的上述两项指标分别为3495.95±2819.32及1.02±1.21;男女之间各组数据差异均无显著性意义(P>0.05)。结论:HRV分析方法具有无创伤、准确定量等其他方法无可替代的优点;本研究检测结果为将HRV作为检测自主神经系统功能的指标应用于运动生理领域打下了工作基础。     

Autonomic Effects of Dipyridamole Stress Testing on Frequency Distribution of RR and QT Interval Variability

Transient myocardial ischemia and associated changes in the autonomic nervous system may influence heart rate and ventricular repolarization to variable degrees. This study evaluated the effect of dipyridamole (DIP) induced ischemia on the autonomic balance by spectral analysis of RR and QT intervals variability. Patients with coronary artery disease undergoing DIP stress echocardiography were studied. From high resolution ECG recordings, RR and QT interval measurements were performed by a dynamic template-matching algorithm. A time-variant analysis was used to estimate power in the LF (0.05–0,15 Hz) and in the HF (0.15–0.4 Hz) band of RR and QT interval spectra. Patients were grouped in ischemic and nonischemic subgroups based on the echocardiographic detection of wall-motion abnormalities. In patients without ischemia (n = 28), DIP caused a decrease in LF power and an increase in HF power of the RR and QT interval variability, indicating concordant changes of both intervals. In contrast, patients with inducible ischemia (n = 11) showed a decrease in HF power of the RR interval spectra and an increase of HF power of QT interval spectra. Furthermore, LF power was increased for RR but decreased for QT interval spectra. Our study suggests that DIP induced ischemia causes a loss of autonomic coupling between heart rate and ventricular repolarization for sympathetic and parasympathetic activities. This lability in ventricular repolarization may constitute an arrhythmogenic substrate during acute ischemia in patients with coronary artery disease.     

右冠状动脉阻塞时交感神经对房室传导调节功能的实验研究

目的 研究右冠状动脉阻塞时交感神经对房室传导调节功能的影响. 方法 在去自主传出神经的动物上,结扎右冠状动脉造成急性下壁心肌梗死(AIMI)的动物模型,通过模板匹配的方法检测His束的A、H、V波,自动检测两心房波(AA)间期,心房波与His渡(AH)间期,并刺激双侧交感神经. 结果 正常动物刺激交感神经使得AH问期在未起搏与起搏时减少(14±5)%和(23±7)%;而心肌梗死时,刺激交感神经使AH间期在未起搏与起搏时减少(7±5)%和(12±2)%.后者只有前者减少幅度的50%和48%(P<0.05). 结论 在AIMI时,交感神经对心脏传导调节功能减弱,这种减弱可能参与AIMI伴房室传导阻滞发生的机制.     

Lorenz散点图在慢性心力衰竭患者心率变异性分析中的应用研究

目的探讨洛伦兹(Lorenz)散点图在慢性心力衰竭患者图心率变异性(HRV)分析中的应用。方法回顾性分析2017年9月至2020年9月安庆市立医院收治的34例心力衰竭患者的动态心电图检查资料,作为心衰组;选取同期行动态心电图检查的30例非心力衰竭患者作为对照组。比较2组HRV指标,包括时域频域指标:24 h内相邻窦性R-R间期标准差(SDNN)、相邻5 min R-R均值标准差(SDANN)、相邻R-R间期差值均方根(RMSSD)、相邻R-R间期>50 ms占正常心动周期比例(PNN50)、HRV三角指数;频域指标:高频(HF)、低频(LF)、LF/HF;观察2组Lorenz散点图形态、散点图长度(L)及离散度(D);分析Lorenz散点图测量值与HRV指标的相关性。结果心衰组HRV频域指标SDANN[(73.56±34.309)ms]、HRV三角指数(24.99±10.91)和时域指标LF/HF(1.0)均显著低于对照组[(103.13±23.41)ms、33.26±9.71、1.9],频域指标RMSSD(56 ms)、PNN50(21%)显著高于对照组(30 ms、5%),差异均有统计学意义(P<0.05)。2组Lorenz散点图形态分布比较差异有统计学意义(P<0.05);心衰组Lorenz散点图测量值D(174.71±74.15)显著低于对照组(222.76±92.69),差异有统计学意义(P<0.05)。Pearson相关性分析显示,心衰组Lorenz散点图测量值L与D均与HRV频域指标SDNN、PNN50、HRV三角指数呈显著正相关(P<0.05);与HRV时域指标HF、LF呈显著负相关(P<0.05)。结论慢性心力衰竭患者HRV指标、Lorenz散点图形态与离散度均与非心力衰竭患者有显著差异;Lorenz散点图测量值与HRV指标具有一定相关性。     

Evaluation of Autonomic Influences on QT Dispersion Using the Head-Up Tilt Test in Healthy Subjects

Our objective was to examine the autonomic influence on QT interval dispersion using the head-up tilt test in healthy subjects. RR and QT intervals, heart rate variability, and plasma norepinephrine concentration were measured in the supine position and tilting to 70 degrees for 20 minutes using a footboard support in 15 healthy male volunteers (mean age +/- SD: 28.0 +/- 4.5 years). The rate-corrected QT interval (QTc) was calculated using Bazett's formula, and QT and QTc dispersions were defined as the maximum minus minimum values for the QT and QTc, respectively, from the 12-lead ECG. Spectral analysis of the heart rate variability generated values for the low- and high-frequency powers (LF and HF) and their ratio (LF/HF). Compared with values obtained in the supine position, tilting significantly increased QT (P < 0.05) and QTc dispersion (P < 0.01), the LF/HF ratio (P < 0.0001), and plasma norepinephrine concentration (P < 0.0001), and significantly decreased HF (P < 0.0001). QTc dispersion was positively correlated with the LF/HF ratio and plasma norepinephrine concentration, and negatively correlated with HF. These results suggest that head-up tilt testing increases QT dispersion by increasing sympathetic tone and/or decreasing vagal tone in healthy subjects.     

慢性肺心病患者的心率变异性

目的：观察慢性肺心病患者心率变异性，了解其自主神经功能的变化。方法：对25例慢性肺心病，25例健康对照者（对照组）作前瞻性对照研究，记录24h动态心电图，作时域和频域分析，结果：与对照组比较，肺心病组相邻心搏的R－R间期之差＞50ms的心搏数占R－R间期数的百分(pNN50)，每5min正常R－R间期标准差的平均值（SDANN），频域指标的高频（HF）明显降低，低频与高频的比值（LF／HF），明显升高，差异均有非常显著意义（P均＜0．01），而频域指标的低频（LF）无明显变化（P＞0．05），经过治疗后，肺心病组处于缓解期，与治疗前比较，HF，PNN50，SDANN等指标明显增加，而LF／HF明显降低，差异均有非常显著意义（P均＜0．01），肺心病组病人治疗后HF，pNN50,SDANN等指标均低于对照组，而LF／HF明显高于对照组，差异均有非常显著意义（P均＜0．01），肺心病组治疗后LF与治疗前及对照组比较，差异不具显著意义（P＞0．05）。结论：肺心中层得不仅交感神经活动占优势，同时并存迷走神经功能受损，自主神经功能可能存在连续性障碍。     

急性下壁心肌梗死患者的临床特点分析

目的 分析研究急性下壁心肌梗死患者的临床特点. 方法 将急性下壁心肌梗死患者100例根据冠状动脉造影结果分为两组:76例为右冠状动脉(RCA)闭塞(A组),24例为左回旋支冠状动脉(LCX)闭塞(B组). 结果 心电图ST段抬高STⅢ>STⅡ及ST段压低STAVL>ST I A组显著高于B组(均P<0.05);ST段抬高STⅢ0.1 mV A组显著高于B组(P<0.05);胸前导联V1～6ST段压低患者中,合并左前降支冠状动脉(LAD)病变的患者显著高于胸前导联V1～6ST段无压低者(P<0.05);左心室射血分数(LVEF)A组[(51±14)%]显著低于B组[(57±10)%](P<0.05);合并右心室心肌梗死A组显著高于B组(P<0.05);急性下壁心肌梗死患者总的住院病死率6%,均为A组,但心源性休克、心力衰竭、Ⅱ、Ⅲ度房室传导阻滞,室性心动过速/心室颤动及住院病死率,两组差异均无统计学意义(均P>0.05);死亡者中心源性休克占83.3%. 结论 心电图Ⅲ、Ⅱ、I、AVL、及V4R导联ST段变化能预测急性下壁心肌梗死相关血管,急性下壁心肌梗死患者伴胸前导联ST段压低提示LAD病变,RCA闭塞所致下壁心肌梗死LVEF低于LCX闭塞者,心源性休克为死亡主要原因.     

Effect of antiarrhythmic agents on heart rate variability indices after myocardial infarction: comparative experimental study of aprindine and procainamide

The cardiac arrhythmic suppression trial (CAST) reported that antiarrhythmic treatments in post-myocardial infarction (MI) patients resulted in poor outcome and decreased in heart rate variability indices (HRV). The goal of the present study was to determine whether aprindine and procainamide, antiarrhythmic agents that increase HRV, result in beneficial effects in post-MI rabbits. Four weeks before experiment, MI was induced in four rabbits by ligating the major branch of left coronary artery. A total of eight rabbits (four post-MI and four normal rabbits) were randomly assigned to treatment with either intravenous aprindine (1 mg/kg) or intravenous procainamide (15 mg/kg). Frequency domain HRV (low frequency spectra, LF, 0.04–0.15 Hz; high frequency spectra, HF, 0.15–0.40 Hz) were assessed by MemCalc software. Aprindine significantly increased HF and LF in both MI and normal rabbits, whereas procainamide tended to decrease HF and LF in MI and normal rabbits (in total rabbits; aprindine, LF, from 6.3 ± 7.9 to 16.5 ± 15.0 ms²/Hz, P < 0.05; HF, from 8.0 ± 11.7 to 17.5 ± 15.0 ms²/Hz, P < 0.05; procainamide, LF, from 4.9 ± 7.4 to 4.8 ± 8.5 ms²/Hz, NS; HF, from 11.1 ± 23.0 to 5.1 ± 10.6 ms²/Hz, NS). Under pharmacological denervation with propranolol (0.1 mg/kg) and atropine (0.04 mg/kg), aprindine increased LF and HF (LF, from 0.2 ± 0.2 to 0.8 ± 0.7 ms²/Hz, P < 0.05; HF, from 0.1 ± 0.0 to 0.2 ± 0.0 ms²/Hz, P < 0.05). These data suggest that aprindine can increase HRV in post-MI rabbits. Further experiments in human subjects would be of benefit.     

Effect of Radiofrequency Catheter Ablation on Parasympathetic Denervation: A Comparison of Three Different Ablation Sites

Radiofrequency (RF) catheter ablation of supraventricular tachycardias (SVT) has been shown to result in local parasympathetic denervation. The purpose of this study was to estimate the correlation between RF cumulative energy and parasympathetic denervation at three different ablation sites. Methods: 45 patients who underwent RF ablation of 36 AV reentrant tachycardias and 9 AV nodal reentrant tachycardias were studied. Twenty patients had left free-wall accessory pathways (group L), 8 patients right free-wall accessory pathways (group R), and 17 patients septal accessory path ways (n = 8) or slow pathways (n -9)(groupS). Time and frequency domain analysis of heart rate variability on 24-hour ambulatory ECG recordings was performed before and after RF ablation, pNN50 and the high frequency (0.15 to 0.40 Hz, HF) component were measured to examine the effects on parasympathetic nerve activity. The values of Δ pNN50 and Δ HF were expressed as the percent change of pNN50 and HF that occurred after versus before RF ablation. Results: Both pNN50 and HF significantly decreased after RF ablation in all three groups. In group S, there was a significant correlation between RF cumulative energy and Δ pNN50r = 0.66, P < 0.01) or Δ HF (r = 0.58, P < 0,05). In contrast, there was no correlation between RF cumulative energy and Δ pNNSO or Δ HF in either group L or group R. Conclusion: These data suggest that RF ablation produces parasympathetic denervation at all three sites along the mitral or tricuspid annulus and that parasympathetic fibers may be located predominantly in the septal area.     

The effects of metronome breathing on the variability of autonomic activity measurements

BACKGROUND: Many chiropractors hypothesize that spinal manipulation affects the autonomic nervous system (ANS). However, the ANS responses to chiropractic manipulative therapy are not well documented, and more research is needed to support this hypothesis. This study represents a step toward the development of a reliable method by which to document that chiropractic manipulative therapy does affect the ANS by exploring the use of paced breathing as a way to reduce the inherent variability in ANS measurements. OBJECTIVE: To examine the hypothesis that the variability of ANS measurements would be reduced if breathing were paced to a metronome at 12 breaths/min. SETTING: The study was performed at Parker College Research Institute. Eight normotensive subjects were recruited from the student body and staff. METHODS: Respiration frequency was measured through a strain gauge. A 3-lead electrocardiogram (ECG) was used to register the electric activity of the heart, and arterial tonometry monitors were used to record the left and right radial artery blood pressures. Signals were recorded on an IBM-compatible computer with a sampling frequency of 100 Hz. Normal breathing was used for the first 3 recordings, and breathing was paced to a metronome for the final 3 recordings at 12 breaths/min. Fourier analysis was performed on the beat-by-beat fluctuations of the ECG-determined R-R interval and systolic arterial pressure (SBP). Low-frequency fluctuations (LF; 0.04-0.15 Hz) reflected sympathetic activity, whereas high-frequency fluctuations (HF; 0.15-0.4 Hz) represented parasympathetic activity. Sympathovagal indices were determined from the ratio of the two bandwidths (LF/HF). The coefficient of variation (CV%) for autonomic parameters was calculated ([average/SD] x 100%) to compare breathing normally and breathing to a metronome with respect to variability. One-way analysis of variance was used to detect differences. A value of P < 0.05 was considered statistically significant; all results are presented as average +/- SD. RESULTS: Three male and 5 female normotensive subjects were studied. Metronome breathing did not produce any significant changes in blood pressure for the left and right radial arteries, heart rate, or pressure pulse transmission time. Breathing to a metronome increased ECG-HF power (0.25 +/- 0.07 vs 0.35 +/- 0.09, P < 0.04), decreased ECG-LF/HF (1.08 +/- 0.55 vs 0.57 +/- 0.35, P < 0.05), and reduced the CV% for ECG-LF (47.6% +/- 23.4% vs 23.8% +/- 14.6%, P < 0.03), ECG-HF (46.2% +/- 14.2% vs 25.8% +/- 17.0%, P < 0.03) and ECG-LF/HF (50.1% +/- 27.6% vs 23.4% +/- 12.3%, P < 0.03) in comparison with normal breathing. Metronome breathing increased the left and right radial artery SBP-HF fluctuations (left, 0.11 +/- 0.05 vs 0.30 +/- 0.16, P < 0.007; right, 0.09 +/- 0.05 vs 0.27 +/- 0.15, P < 0.008) and decreased the SBP-LF/HF components (left, 3.42 +/- 2.36 vs 1.14 +/- 0.88, P > 0.03; right, 3.08 +/- 1.77 vs 1.20 +/- 0.93, P < 0.02). Metronome breathing did not significantly alter the CV% for SBP-HF, SBP-LF, and SBP-LF/HF. CONCLUSIONS: Metronome breathing increased parasympathetic activity, as evidenced by augmented HF power in the ECG and SBP data. The variability (CV%) of ECG-determined ANS measurements was significantly reduced with paced breathing at 12 breaths/min, but no significant reductions were observed for the SBP-determined ANS measurements. These findings indicate that ECG data are more sensitive than SBP data for future clinical trials.