Steffen Johansson Rebecka, Loewenstein Daniel, Lodin Klara, Bruchfeld Judith, Runold Michael, Ståhlberg Marcus, Xue Hui, Kellman Peter, Caidahl Kenneth, Engblom Henrik, Nickander Jannike
Department of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
JAMA Netw Open. 2025 Jun 2;8(6):e2514411. doi: 10.1001/jamanetworkopen.2025.14411.
COVID-19 can lead to long-term cardiopulmonary symptoms and is associated with coronary microvascular dysfunction (CMD). However, long-term data on CMD after severe COVID-19 are lacking.
To investigate long-term left ventricular function and the presence of CMD after severe COVID-19.
DESIGN, SETTING, AND PARTICIPANTS: This case-control study was conducted among patients at a single center from the prospective Follow-Up of Patients With Severe COVID-19 (UppCov) study, with follow-up multiparametric perfusion cardiovascular magnetic resonance (CMR) at 10 months after discharge from November 2020 to February 2021. Patients previously hospitalized due to severe COVID-19 (ventilatory support, oxygen flow ≥5 L/min, or both) with or without cardiac involvement (troponin t > 14 ng/L, pulmonary artery pressure >34 mm Hg, or both) were compared with historical sex- and age-matched volunteers without symptomatic ischemic heart disease. Standard contraindications to adenosine CMR were applied. Data were analyzed between March 2023 and March 2025.
Hospitalization due to severe COVID-19.
Comprehensive CMR included native T1, native T2, extracellular volume, adenosine stress and rest perfusion mapping, gadolinium enhancement, and cine imaging. Comorbidities, medications, symptoms at follow-up, and details regarding hospitalization were obtained from patient records.
The study included 37 patients with COVID-19 (mean age, 56 years [95% CI, 53 to 61 years]; 28 male [75.7%]) and 22 healthy volunteers (mean age, 51 years [95% CI, 45 to 57 years]; 12 male [54.4%]). Patients with COVID-19 compared with healthy patients demonstrated reduced mean stress perfusion (2.80 mL/min/g [95% CI, 2.53 to 3.07 mL/min/g] vs 3.43 mL/min/g [95% CI, 3.13 to 3.74 mL/min/g]; P = .003), impaired mean global longitudinal strain (-17% [95% CI, -18% to -16%] vs -19% [-20% to -18%]; P = .003), and impaired mean global circumferential strain (-16% [95% CI, -17% to -15%] vs -19% [-20% to -18%]; P = .001). There were no differences in stress perfusion or myocardial perfusion reserve in the COVID-19 group between patients with vs without cardiovascular risk factors or cardiac symptoms.
In this study, patients with COVID-19 exhibited long-term reduced stress perfusion indicating CMD, along with declined left ventricular function by global longitudinal strain and global circumferential strain. Lack of variation in stress perfusion between patients with and without cardiovascular risk factors may suggest CMD due to severe COVID-19, warranting further investigation to elucidate mechanisms and guide potential therapies.
新冠病毒感染（COVID-19）可导致长期心肺症状，并与冠状动脉微血管功能障碍（CMD）相关。然而，关于重症COVID-19后CMD的长期数据尚缺。
研究重症COVID-19后的长期左心室功能及CMD的存在情况。
设计、背景和参与者：本病例对照研究在一个中心的患者中进行，这些患者来自重症COVID-19患者前瞻性随访（UppCov）研究，于2020年11月至2021年2月出院后10个月进行多参数灌注心血管磁共振成像（CMR）随访。将既往因重症COVID-19住院（接受通气支持、氧流量≥5L/分钟或两者皆有）且有或无心脏受累（肌钙蛋白t＞14ng/L、肺动脉压＞34mmHg或两者皆有）的患者与无症状性缺血性心脏病的年龄和性别匹配的历史对照志愿者进行比较。采用腺苷CMR的标准禁忌证。于2023年3月至2025年3月期间分析数据。
因重症COVID-19住院。
全面的CMR包括原生T1、原生T2、细胞外容积、腺苷负荷及静息灌注成像、钆增强成像和电影成像。从患者记录中获取合并症、用药情况、随访时的症状以及住院详情。
该研究纳入了37例COVID-19患者（平均年龄56岁[95%CI，53至61岁]；28例男性[75.7%]）和22名健康志愿者（平均年龄51岁[95%CI，45至57岁]；12例男性[54.4%]）。与健康患者相比，COVID-19患者的平均负荷灌注降低（2.80mL/分钟/g[95%CI，2.53至3.07mL/分钟/g]对3.43mL/分钟/g[95%CI，3.13至3.74mL/分钟/g]；P = 0.003），平均整体纵向应变受损（-17%[95%CI，-18%至-1/%]对-19%[-20%至-18%]；P = 0.003），平均整体圆周应变受损（-16%[95%CI，-17%至-15%]对-19%[-20%至-18%]；P = 0.001）。在COVID-19组中，有心血管危险因素或心脏症状的患者与无这些情况的患者在负荷灌注或心肌灌注储备方面无差异。
在本研究中，COVID-1患者表现出长期负荷灌注降低，提示存在CMD，同时左心室功能通过整体纵向应变和整体圆周应变下降。有和无心血管危险因素的患者在负荷灌注方面缺乏差异，这可能提示重症COVID-19导致了CMD，需要进一步研究以阐明机制并指导潜在治疗。
