背景:心脏骤停是由心电不稳定引起的,慢性癫痫患者的发生频率是普通人群的3倍。我们假设,双侧强直阵挛性癫痫发作(FTBTCS)会严重影响T波交替(TWA),心脏电不稳定的标志与心脏猝死的风险升高有关,超过局灶性癫痫发作(FS)[局灶性意识癫痫发作(FAS)和局灶性意识受损癫痫发作(FIAS)],由于他们对心脏的交感神经刺激更大。由于压力已被证明会导致心脏病患者的TWA显着升高,我们还假设,与慢性癫痫患者住院天数相比,癫痫监测单位(EMU)住院的早期TWA水平较高,大概是由于压力。
方法:我们分析了癫痫发作的急性影响[FAS,FIAS,FTBTCS,使用高分辨率无线心电图(ECG)贴片监测仪入院的18例患者的TWA和非癫痫发作(NES)]和住院天数。
结果:共有5例患者出现FTBTCS,7例患者有FS(2例FAS,5FIAS),3例患者仅在住院期间有NES。四名患者没有任何临床电癫痫发作或NES。FTBTCS导致发作TWA从基线(2±0.3µV)到发作最大值(70±6.1µV,p<0.0001),超过60µV切割点的后者被定义为严重异常。相比之下,而FAS和FIAS也引起了TWA的显着增加(从2±0.5µV到30±3.3µV,p<0.0001),最大发作TWA水平未达到定义为异常的47µV切点.在FTBTCS期间,心率从基线(62±5.8次/分钟)增加到发作最大值(134±8.6次/分钟,增加72±7.2次/分钟,p<0.02)也大于(p=0.014)FS期间的心率增加(从70±5.2次/分钟到118±6.2次/分钟,增加48±2.6次/分钟,p<0.03)。在3例NES患者中,TWA在患者典型发作期间温和上升(从2±0.6µV上升至14±2.6µV,p<0.0004),远低于异常的临界点,同时观察到心率增加(从75±1.3到112±8.7次/分钟,增加37±8.9次/分钟,p=0.03)。在EMU中记录的EEG确认的临床电癫痫发作的患者在EMU入院当天表现出发作间TWA最大值(61±3.4µV)显着升高,其幅度与FTBTCS期间所见的发作最大值(70±6.1µV,p=0.21)。在随后的住院期间,在FS和FTBTCS患者中,每天的发作间TWA最大值显示出逐渐习惯,但仅在NES患者中没有.
结论:这是我们了解到的第一项研究,表明FTBTCS急性引起TWA高度显著增加,达到与其他患者人群心脏猝死风险增加相关的水平。我们推测与FTBTCS暂时相关的死亡率可能,在某些情况下,是由于心脏猝死而不是呼吸衰竭。在EEG证实的癫痫患者中,入院与发作间TWA最大值相关,接近FTBTCS期间看到的最大值,与住院早期相比,与住院后期的压力有关,表明心脏电不稳定和潜在的心源性猝死的脆弱性与压力相关,而与癫痫发作的时间关系无关。在癫痫发作和医院第1天时观察到的心率升高与高肾上腺素能状态以及交感神经输出量升高对易损心脏基质的影响一致。一种被称为“癫痫心”的现象。
BACKGROUND: Sudden cardiac arrest results from cardiac electrical instability and is 3-fold more frequent in patients with chronic epilepsy than in the general population. We hypothesized that focal to bilateral tonic-clonic seizures (FTBTCS) would acutely impact T-wave alternans (TWA), a marker of cardiac electrical instability linked to an elevated risk for sudden cardiac death, more than focal seizures (FS) [focal aware seizures (FAS) and focal with impaired awareness seizures (FIAS)], due to their greater sympathetic stimulation of the heart. Since stress has been shown to cause significant TWA elevations in patients with heart disease, we also hypothesized that the early days of an inpatient admission to an epilepsy monitoring unit (EMU) would be associated with higher TWA levels compared to later hospital days in patients with chronic epilepsy, presumably due to stress.
METHODS: We analyzed the acute effects of seizures [FAS, FIAS, FTBTCS, and nonepileptic seizures (NES)] and day of hospital stay on TWA in 18 patients admitted to the EMU using high-resolution wireless electrocardiographic (ECG) patch monitors.
RESULTS: A total of 5 patients had FTBTCS, 7 patients had FS (2 FAS, 5 FIAS), and 3 patients had NES only during the index hospital stay. Four patients did not have any electroclinical seizures or NES. FTBTCS resulted in marked acute increases in ictal TWA from baseline (2 ± 0.3 µV) to ictal maximum (70 ± 6.1 µV, p < 0.0001), the latter exceeding the 60 µV cut point defined as severely abnormal. By comparison, while FAS and FIAS also provoked significant increases in TWA (from 2 ± 0.5 µV to 30 ± 3.3 µV, p < 0.0001), maximum ictal TWA levels did not reach the 47 µV cut point defined as abnormal. Heart rate increases during FTBTCS from baseline (62 ± 5.8 beats/min) to ictal maximum (134 ± 8.6 beats/min, an increase of 72 ± 7.2 beats/min, p < 0.02) were also greater (p = 0.014) than heart rate increases during FS (from 70 ± 5.2 beats/min to 118 ± 6.2 beats/min, an increase of 48 ± 2.6 beats/min, p < 0.03). In 3 patients with NES, TWA rose mildly during the patients\' typical episodes (from 2 ± 0.6 µV to 14 ± 2.6 µV, p < 0.0004), well below the cut point of abnormality, while heart rate increases were observed (from 75 ± 1.3 to 112 ± 8.7 beats/min, an increase of 37 ± 8.9 beats/min, p = 0.03). Patients with EEG-confirmed electroclinical seizures recorded while in the EMU exhibited significantly elevated interictal TWA maxima (61 ± 3.4 µV) on EMU admission day which were similar in magnitude to ictal maxima seen during FTBTCS (70 ± 6.1 µV, p = 0.21). During subsequent days of hospitalization, daily interictal TWA maxima showed gradual habituation in patients with both FS and FTBTCS but not in patients with NES only.
CONCLUSIONS: This is the first study to our knowledge demonstrating that FTBTCS acutely provoke highly significant increases in TWA to levels that have been associated with heightened risk for sudden cardiac death in other patient populations. We speculate that mortality temporally associated with FTBTCS may, in some cases, be due to sudden cardiac death rather than respiratory failure. In patients with EEG-confirmed epilepsy, hospital admission is associated with interictal TWA maxima that approach those seen during FTBTCS, presumably related to stress during the early phase of hospitalization compared to later in the hospitalization, indicating cardiac electrical instability and potential vulnerability to sudden cardiac death related to stress independent of temporal relationships to seizures. The elevated heart rates observed acutely with seizures and on hospital Day 1 are consistent with a hyperadrenergic state and the effect of elevated sympathetic output on a vulnerable cardiac substrate, a phenomenon termed \"the Epileptic Heart.\"