Moak Jeffrey P, Goldstein David S, Eldadah Basil A, Saleem Ahmed, Holmes Courtney, Pechnik Sandra, Sharabi Yehonatan
Children's National Medical Center, Washington, DC, USA.
Heart Rhythm. 2007 Dec;4(12):1523-9. doi: 10.1016/j.hrthm.2007.07.019. Epub 2007 Jul 18.
Power spectral analysis of heart rate variability (HRV) has been used to indicate cardiac autonomic function. High-frequency power relates to respiratory sinus arrhythmia and therefore to parasympathetic cardiovagal tone; however, the relationship of low-frequency (LF) power to cardiac sympathetic innervation and function has been controversial. Alternatively, LF power might reflect baroreflexive modulation of autonomic outflows.
We studied normal volunteers and chronic autonomic failure syndrome patients with and without loss of cardiac noradrenergic nerves to examine the relationships of LF power with cardiac sympathetic innervation and baroreflex function.
We compared LF power of HRV in patients with cardiac sympathetic denervation, as indicated by low myocardial concentrations of 6-[(18)F] fluorodopamine-derived radioactivity or low rates of norepinephrine entry into coronary sinus plasma (cardiac norepinephrine spillover) to values in patients with intact innervation, at baseline, during infusion of yohimbine, which increases exocytotic norepinephrine release from sympathetic nerves, or during infusion of tyramine, which increases non-exocytotic release. Baroreflex-cardiovagal slope (BRS) was calculated from the cardiac interbeat interval and systolic pressure during the Valsalva maneuver.
LF power was unrelated to myocardial 6-[(18)F] fluorodopamine-derived radioactivity or cardiac norepinephrine spillover. In contrast, the log of LF power correlated positively with the log of BRS (r=0.72, P <0.0001). Patients with a low BRS (<or=3 msec/mm Hg) had low LF power, regardless of cardiac innervation. Tyramine and yohimbine increased LF power in subjects with normal BRS but not in those with low BRS. BRS at baseline predicted LF responses to tyramine and yohimbine.
LF power reflects baroreflex function, not cardiac sympathetic innervation.
心率变异性（HRV）的功率谱分析已被用于指示心脏自主神经功能。高频功率与呼吸性窦性心律不齐相关，因此与副交感神经的心迷走神经张力有关；然而，低频（LF）功率与心脏交感神经支配和功能的关系一直存在争议。另外，LF功率可能反映了自主神经输出的压力反射调节。
我们研究了正常志愿者以及患有和未患有心脏去甲肾上腺素能神经丧失的慢性自主神经功能衰竭综合征患者，以检查LF功率与心脏交感神经支配和压力反射功能之间的关系。
我们比较了心脏交感神经去神经支配患者（以心肌中6-[(18)F]氟多巴胺衍生的放射性低或去甲肾上腺素进入冠状窦血浆的速率低（心脏去甲肾上腺素溢出）为指标）与神经支配完整患者在基线时、输注育亨宾（可增加交感神经胞吐性去甲肾上腺素释放）期间或输注酪胺（可增加非胞吐性释放）期间的HRV的LF功率。通过瓦尔萨尔瓦动作期间的心搏间期和收缩压计算压力反射 - 心迷走斜率（BRS）。
LF功率与心肌6-[(18)F]氟多巴胺衍生放射性或心脏去甲肾上腺素溢出无关。相比之下，LF功率的对数与BRS 的对数呈正相关（r = 0.72，P <0.0001）。无论心脏神经支配情况如何，BRS低（≤3毫秒/毫米汞柱） 的患者LF功率都低。酪胺和育亨宾使BRS正常的受试者的LF功率增加，但对BRS低的受试者无效。基线时的BRS可预测LF对酪胺和育亨宾的反应。
LF功率反映压力反射功能，而非心脏交感神经支配。
