ArticleJAMA network open2025
Long-Term Coronary Microvascular and Cardiac Dysfunction After Severe COVID-19 Hospitalization.
Article in JAMA network open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Microvascular Dysfunction and Redox Imbalance in Long COVID.Microcirculation (New York, N.Y. : 1994) · 2026Article
- eNOS Uncoupling, Shear-Stress Tolerance, and the Two-Threshold Model of Post-Exertional Malaise in Long COVID: A Mechanistic Hypothesis With Implications for Physiotherapy and Recovery Protocols.Microcirculation (New York, N.Y. : 1994) · 2026Review
- Community-acquired pneumonia withJournal of thoracic disease · 2026Article
- Errors in Results.JAMA network open · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Importance: 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. Objective: 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. Exposure: Hospitalization due to severe COVID-19. Main Measures and Outcomes: 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. Results: 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. Conclusions and Relevance: 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.
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