背景:COVID-19感染的一个相对常见的并发症是心律失常。关于出现室性心律失常的有症状的COVID后患者的心肌变形和心率变异性(HRV)的信息有限。
目的:我们的目的是评估COVID-19后室性心律失常患者的2D心室应变和心率变异性指数(通过动态心电图监测评估)。
方法:目前的观察性病例对照研究是在60例患者从COVID-19感染中康复1个月后进行的。30名健康志愿者作为对照组。每个参与者都有完整的病史回顾,验血,12导联体表心电图(ECG),24小时动态心电图监测,和回声多普勒检查以评估左心室(LV)尺寸,组织多普勒速度,和左心室和右心室(RV)应变的2D斑点追踪超声心动图(2D-STE)。
结果:患有单形性室性早搏(PVC)的COVID后症状性患者显示LV/RV收缩和舒张功能严重受损,LV/RV心肌表现(MPI),HRV指数降低。心室负荷较高和较低的患者功能状态较差,较高水平的炎症生物标志物和降低的HRV参数(纽约心脏协会(NYHA)等级:2.1±0.9vs.1.5±0.6,p<0.001,C反应蛋白(CRP):13.3±4.1vs.8.3±5.9mg/L,p<0.0001,低频/高频(LF/HF):3.6±2.4vs.2.2±1.2,p<0.002,连续正常间隔之间差异的均方根(rMSSD):21.8±4.7vs.29.3±14.9ms,p<0.039,RR间隔的标准偏差(SDNN):69.8±19.1vs.108.8±37.4ms,p<0.0001)。心室负荷与中性粒细胞/淋巴细胞比值(NLR)呈正相关(r=0.33,p<0.001),CRP(r=0.60,p<0.0001),而与左心室整体纵向应变(GLS)呈负相关(r=-0.38,p<0.0001),和RV-GLS(r=-0.37,p<0.0001)。
结论:出现室性心律失常的COVID后症状患者的功能状态较差。有COVID后症状和室性心律失常的患者有亚临床心肌损害,斑点追踪超声心动图证明,同时明显保留了LV收缩功能。COVID后患者室性心律失常的负担与炎症生物标志物增加和双心室应变减少显著相关。
BACKGROUND: A relatively common complication of COVID -19 infection is arrhythmia. There is limited information about myocardial deformation and heart rate variability (HRV) in symptomatic post COVID patients presented by ventricular arrhythmia.
OBJECTIVE: Our goal was to assess 2D-ventricular strain and heart rate variability indices (evaluated by ambulatory ECG monitoring) in post-COVID-19 patients suffering from ventricular arrhythmia.
METHODS: The current observational case-control study performed on 60 patients one month after they had recovered from the COVID-19 infection. Thirty healthy volunteers served as the control group. Each participant had a full medical history review, blood tests, a 12-lead surface electrocardiogram (ECG), 24-h ambulatory ECG monitoring, and an echo-Doppler examination to evaluate the left ventricular (LV) dimensions, tissue Doppler velocities, and 2D-speckle tracking echocardiography (2D-STE) for both the LV and right ventricular (RV) strain.
RESULTS: Symptomatic post-COVID patients with monomorphic premature ventricular contractions (PVCs) showed a substantial impairment of LV/RV systolic and diastolic functions, LV/RV myocardial performance (MPI) with reduced indices of HRV. Patients with higher versus lower ventricular burden had poorer functional status, higher levels of inflammatory biomarkers and reduced parameters of HRV (New York Heart Association (NYHA) class: 2.1 ± 0.9 vs. 1.5 ± 0.6, p < 0.001, C-reactive protein (CRP): 13.3 ± 4.1 vs. 8.3 ± 5.9 mg/L, p < 0.0001, low frequency/high frequency (LF/HF): 3.6 ± 2.4 vs. 2.2 ± 1.2, p < 0.002, the root mean square of the difference between successive normal intervals (rMSSD): 21.8 ± 4.7 vs. 29.3 ± 14.9 ms, p < 0.039 and the standard deviation of the RR interval (SDNN): 69.8 ± 19.1 vs.108.8 ± 37.4 ms, p < 0.0001). The ventricular burden positively correlated with neutrophil/lymphocyte ratio (NLR) (r = 0.33, p < 0.001), CRP (r = 0.60, p < 0.0001), while it negatively correlated with LV-global longitudinal strain (GLS) (r = -0.38, p < 0.0001), and RV-GLS (r = -0.37, p < 0.0001).
CONCLUSIONS: Patients with post-COVID symptoms presented by ventricular arrhythmia had poor functional status. Patients with post-COVID symptoms and ventricular arrhythmia had subclinical myocardial damage, evidenced by speckle tracking echocardiography while having apparently preserved LV systolic function. The burden of ventricular arrhythmia in post-COVID patients significantly correlated with increased inflammatory biomarkers and reduced biventricular strain.