Marwick Thomas H, Wexler Noah, Smith Joel, Wright Leah, Ho Felicia, Oreto Marc, Sherriff Ashleigh-Georgia, Allwood Richard, Sata Yusuke, Manca Stefano, Howden Erin, Huynh Quan
Imaging Research Lab, Baker Heart and Diabetes Institute, Hobart, Tasmania, Australia; Baker Department of Cardiometabolic Health, University of Melbourne, Melbourne, Victoria, Australia; Department of Cardiology, Western Health, Melbourne, Victoria, Australia; Department of Cardiology, Royal Hobart Hospital, Hobart, Tasmania, Australia; Cardiovascular Health Flagship, Menzies Institute for Medical Research, Hobart, Tasmania, Australia.
Imaging Research Lab, Baker Heart and Diabetes Institute, Hobart, Tasmania, Australia; Department of Cardiology, Western Health, Melbourne, Victoria, Australia.
J Am Soc Echocardiogr. 2025 Jan;38(1):16-23.e1. doi: 10.1016/j.echo.2024.09.006. Epub 2024 Sep 17.
Cardiac impairment has been associated with acute COVID-19 since the earliest reports of the pandemic. However, its role in postacute sequelae of COVID-19 ("long COVID") is undefined, and many existing observations about cardiovascular involvement in postacute sequelae of COVID-19 are uncontrolled.
To compare the prevalence of cardiac dysfunction in patients with long COVID and noninfected controls from the same community and explore their association with functional capacity.
Echocardiography was used to assess cardiac structure and function, including the measurement of global longitudinal strain (GLS), in 190 participants with long COVID. All underwent assessment of functional impairment by subjective (Duke Activity Status Index) and objective tests (6-minute walk test). The 190 participants from the long COVID group were matched with those from 979 patients who underwent the same tests in the pre-COVID-19 era, using a propensity score.
The 190 patients with long COVID had similar age and risk factor profiles to those of their matched controls. Left ventricular dimensions and geometry, but not diastolic parameters, were significantly altered in the long COVID group. The long COVID group had subclinical systolic dysfunction (GLS 18.5% ± 2.6% vs 19.3% ± 2.7%, P = .005), and more long COVID patients had abnormal (<16%) GLS (13% vs 8%, P = .035). The association of long COVID with abnormal GLS (odds ratio, 1.49 [1.04, 2.45]) was independent of-and had a similar or greater effect size than-age and risk factors. There was no interaction of long COVID with the association of risk factors with GLS. As expected, the long COVID group had significant subjective (<85% predicted METS; 72% vs 5%, P < .001) and objective functional impairment (29% vs 24%, P = .026), but GLS was only weakly associated with both subjective (r = 0.30, P = .005) and objective (r = 0.21, P = .05) functional impairment. The presence of long COVID was independently associated with subjective (odds ratio = 159.7 [95% CI, 61.6-414.2]) and objective functional impairment (odds ratio = 2.8 [95% CI, 1.5-5.2]).
Impaired GLS and left ventricular dimensions are the echocardiographic features that are overrepresented in long COVID, and this association is similar to and independent of other risk factors. Impaired GLS is weakly associated with functional impairment.
自新冠疫情最早报告以来,心脏损害就与急性新冠病毒病(COVID-19)相关。然而,其在新冠病毒病急性后遗症(“长新冠”)中的作用尚不清楚,而且许多关于心血管系统参与新冠病毒病急性后遗症的现有观察结果未得到对照验证。
比较长新冠患者与来自同一社区的未感染对照者中心脏功能障碍的患病率,并探讨其与功能能力的关联。
对190例长新冠患者使用超声心动图评估心脏结构和功能,包括测量整体纵向应变(GLS)。所有患者均通过主观(杜克活动状态指数)和客观测试(6分钟步行试验)进行功能损害评估。使用倾向评分法,将190例长新冠组患者与979例在新冠疫情前时代接受相同测试的患者进行匹配。
190例长新冠患者的年龄和危险因素分布与其匹配的对照组相似。长新冠组患者的左心室大小和形态发生了显著改变,但舒张参数未改变。长新冠组存在亚临床收缩功能障碍(GLS为18.5%±2.6%,对照组为19.3%±2.7%,P = 0.005),更多长新冠患者的GLS异常(<16%)(13% vs 8%,P = 0.035)。长新冠与GLS异常的关联(优势比为1.49[1.04, 2.45])独立于年龄和危险因素,且效应大小相似或更大。长新冠与危险因素和GLS的关联之间没有相互作用。正如预期的那样,长新冠组存在显著的主观(<预测代谢当量的85%;72% vs 5%,P < 0.001)和客观功能损害(29% vs 24%,P = 0.026),但GLS仅与主观(r = 0.30,P = 0.005)和客观(r = 0.21,P = 0.05)功能损害存在弱关联。长新冠的存在与主观(优势比 = 159.7[95%CI,61.6 - 414.2])和客观功能损害(优势比 = 2.8[95%CI,1.5 - 5.2])独立相关。
GLS受损和左心室大小是长新冠患者超声心动图中表现突出的特征,这种关联与其他危险因素相似且独立。GLS受损与功能损害存在弱关联。