Clinical Outcomes and Prognosis
Lorenzo R. Sewanan, MD, PhD
Physician
Columbia University, United States
Lorenzo R. Sewanan, MD, PhD
Physician
Columbia University, United States
J. Thomas Vaughan
Professor of Biomedical Engineering and Radiology
Columbia University, United States
Marco R. Di Tullio, MD
Professor
Columbia University, United States
Andrew Laine
Professor
Columbia University, United States
Belinda D’Souza
Professor
Columbia University, United States
Jay Leb
Professor
Columbia University, United States
Alexander Mironov
Cardiologist
New York University, United States
Ahsan Khan
Cardiologist
Columbia University, United States
Elisa Konofagou
Professor
Columbia University, United States
Rochelle Goldsmith
Professor
Columbia University, United States
Sachin Jambawalikar
Professor
Columbia University, United States
Cole Hirschfeld
Fellow
Weill Cornell Medical College, United States
Michelle Castillo, BSc
Clinical Research Coordinator
Columbia University
New York, New York, United States
Kathleen Durkin
Professor
Columbia University, United States
Stephen Dashnaw
Director, Imaging Services
Columbia University
NYC, New York, United States
Andrew J. Einstein, MD, PhD, FSCMR
Professor
Columbia University
New York, New York, United States
COVID-19, particularly from the pandemic’s early phase, has been reported to have diverse manifestations of cardiac injury including symptoms, troponinemia, imaging, and ECG abnormalities, and hypercoagulability. CMR can be particularly revealing of COVID’s myocardial effects since it can capture structure, function, and tissue properties that might be altered by this inflammatory and prothrombotic state. CMR findings in COVID-19 patients have been varied, and few studies have assessed long-term changes to the myocardium of early COVID cases.
Methods:
We performed CMR using a 3T GE SIGNA™ Premier scanner with gadoterate meglumine (Clariscan, GE Healthcare) in cases of the initial pandemic (2020) without pre-existing cardiac disease and matched controls at long-term follow up >6 months after infection. Comprehensive myocardial characterization was performed using T2-weighted imaging with short tau inversion recovery, native T1 mapping using a modified Look Locker inversion recovery sequence, gadolinium enhanced T1 mapping and ECV fraction assessment, T2 mapping using a T2-prepared single-shot bSSFP sequence, and late gadolinium enhancement (LGE) with phase-sensitive inversion recovery. CMR analysis was performed using cvi v5.11 (Circle Cardiovascular Imaging, Calgary). T tests for continuous and c2 tests for categorical variables were used. P< 0.05 was considered significant.
Results:
We performed CMR in 40 COVID-19 cases and 12 healthy controls with 35% of patients hospitalized and 28% intubated during acute COVID presentation. Cases and controls were closely matched by age, sex, and race-ethnic distribution with median age 46, 50% female, 48% Hispanic, 28% Black, and mean BMI 27 (Table 1). Most had presented with initial symptoms of fever, dyspnea, and chest pain, though none had acute coronary syndrome or thromboembolism. Imaging was performed median 308 days after initial infection. At that time, there was no difference in median d-dimer or high sensitivity troponin T, and few cases had symptoms of ongoing chest pain, dyspnea, or palpitations. Using CMR, we found no difference in median LV or RV EF or EDVi, or LV mass index for controls vs. cases; no cases had wall motion abnormalities, and only one had a pericardial effusion (Table 2). We found no difference in median T1 (1278 v 1306), T2 (47 v 46), and ECV (29 v 30). Only one case had LGE, which involved only 1 of 17 segments. We similarly found no difference in these parameters between hospitalized and non-hospitalized cases (Table 3).
Conclusion:
Using CMR, we did not detect meaningful differences in heart structure and function in COVID cases vs. controls irrespective of COVID severity almost 10 months post-COVID. While additional work should be done to investigate long-term outcomes in COVID-19 patients presenting with myocarditis, acute coronary syndromes and thromboembolism, it is reassuring that in this cohort of patients there is limited lasting damage to the heart from COVID-19.