Duma Andreas, Pal Swatilika, Johnston Joshua, Helwani Mohammad A, Bhat Adithya, Gill Bali, Rosenkvist Jessica, Cartmill Christopher, Brown Frank, Miller J Philip, Scott Mitchell G, Sanchez-Conde Francisco, Jarvis Michael, Farber Nuri B, Zorumski Charles F, Conway Charles, Nagele Peter
From the Division of Clinical and Translational Research, Department of Anesthesiology (A.D., S.P., J.J., M.A.H., A.B., B.G., C.Cartmill, F.B., F.S.-C., P.N.), Department of Psychiatry (J.R., M.J., N.B.F., C.F.Z., C.Conway), Division of Biostatistics (J.P.M.), Department of Pathology and Immunology (M.G.S.), and Taylor Family Institute for Innovative Psychiatric Research (N.B.F., C.F.Z., C.Conway, P.N.), Washington University School of Medicine in St. Louis, Missouri. Current position: Department of Anesthesiology and Critical Care, Medical University of Vienna, Vienna, Austria (A.D.).
Anesthesiology. 2017 Apr;126(4):643-652. doi: 10.1097/ALN.0000000000001531.
While electroconvulsive therapy is widely regarded as a lifesaving and safe procedure, evidence regarding its effects on myocardial cell injury is sparse. The objective of this investigation was to determine the incidence and magnitude of new cardiac troponin elevation after electroconvulsive therapy using a novel high-sensitivity cardiac troponin I assay.
This was a prospective cohort study in adult patients undergoing electroconvulsive therapy in a single academic center (up to three electroconvulsive therapy treatments per patient). The primary outcome was new high-sensitivity cardiac troponin I elevation after electroconvulsive therapy, defined as an increase of high-sensitivity cardiac troponin I greater than 100% after electroconvulsive therapy compared to baseline with at least one value above the limit of quantification (10 ng/l). Twelve-lead electrocardiogram and high-sensitivity cardiac troponin I values were obtained before and 15 to 30 min after electroconvulsive therapy; in a subset of patients, an additional 2-h high-sensitivity cardiac troponin I value was obtained.
The final study population was 100 patients and a total of 245 electroconvulsive therapy treatment sessions. Eight patients (8 of 100; 8%) experienced new high-sensitivity cardiac troponin I elevation after electroconvulsive therapy with a cumulative incidence of 3.7% (9 of 245 treatments; one patient had two high-sensitivity cardiac troponin I elevations), two of whom had a non-ST-elevation myocardial infarction (incidence 2 of 245; 0.8%). Median high-sensitivity cardiac troponin I concentrations did not increase significantly after electroconvulsive therapy. Tachycardia and/or elevated systolic blood pressure developed after approximately two thirds of electroconvulsive therapy treatments.
Electroconvulsive therapy appears safe from a cardiac standpoint in a large majority of patients. A small subset of patients with preexisting cardiovascular risk factors, however, may develop new cardiac troponin elevation after electroconvulsive therapy, the clinical relevance of which is unclear in the absence of signs of myocardial ischemia.
虽然电休克疗法被广泛认为是一种挽救生命且安全的治疗方法,但关于其对心肌细胞损伤影响的证据却很稀少。本研究的目的是使用一种新型的高敏心肌肌钙蛋白I检测方法,确定电休克治疗后新出现的心肌肌钙蛋白升高的发生率和幅度。
这是一项针对在单一学术中心接受电休克治疗的成年患者的前瞻性队列研究(每位患者最多接受三次电休克治疗)。主要结局是电休克治疗后新出现的高敏心肌肌钙蛋白I升高,定义为电休克治疗后高敏心肌肌钙蛋白I较基线升高超过100%,且至少有一个值高于定量限(10 ng/l)。在电休克治疗前和治疗后15至30分钟获取12导联心电图和高敏心肌肌钙蛋白I值;在部分患者中,还获取了治疗后2小时的高敏心肌肌钙蛋白I值。
最终研究人群为100例患者,共进行了245次电休克治疗。8例患者(100例中的8例;8%)在电休克治疗后出现新的高敏心肌肌钙蛋白I升高,累积发生率为3.7%(245次治疗中的9例;1例患者出现两次高敏心肌肌钙蛋白I升高),其中2例发生非ST段抬高型心肌梗死(发生率为245次治疗中的2例;0.8%)。电休克治疗后高敏心肌肌钙蛋白I的中位数浓度没有显著增加。约三分之二的电休克治疗后出现心动过速和/或收缩压升高。
从心脏角度来看,电休克疗法在大多数患者中似乎是安全的。然而,一小部分有心血管危险因素的患者在电休克治疗后可能会出现新的心肌肌钙蛋白升高,在没有心肌缺血迹象的情况下,其临床意义尚不清楚。