TY - JOUR
T1 - Assessment of Cardiac, Vascular, and Pulmonary Pathobiology In Vivo During Acute COVID-19
AU - Alam, Shirjel R.
AU - Vinayak, Sudhir
AU - Shah, Adeel
AU - Doolub, Gemina
AU - Kimeu, Redemptar
AU - Horn, Kevin P.
AU - Bowen, Stephen R.
AU - Jeilan, Mohamed
AU - Lee, Kuan Ken
AU - Gachoka, Sylvia
AU - Riunga, Felix
AU - Adam, Rodney D.
AU - Vesselle, Hubert
AU - Joshi, Nikhil
AU - Obino, Mariah
AU - Makhdomi, Khalid
AU - Ombati, Kevin
AU - Nganga, Edward
AU - Gitau, Samuel
AU - Chung, Michael H.
AU - Shah, Anoop S.V.
N1 - Publisher Copyright:
© The Authors.
PY - 2022/9/20
Y1 - 2022/9/20
N2 - BACKGROUND: Acute COVID-19– related myocardial, pulmonary, and vascular pathology and how these relate to each other remain unclear. To our knowledge, no studies have used complementary imaging techniques, including molecular imag-ing, to elucidate this. We used multimodality imaging and biochemical sampling in vivo to identify the pathobiology of acute COVID-19. Specifically, we investigated the presence of myocardial inflammation and its association with coronary artery disease, systemic vasculitis, and pneumonitis. METHODS AND RESULTS: Consecutive patients presenting with acute COVID-19 were prospectively recruited during hospital admission in this cross-sectional study. Imaging involved computed tomography coronary angiography (identified coronary disease), cardiac 2-deoxy-2-[fluorine-18]fluoro-D-glucose positron emission tomography/computed tomography (identified vascular, cardiac, and pulmonary inflammatory cell infiltration), and cardiac magnetic resonance (identified myocardial dis-ease) alongside biomarker sampling. Of 33 patients (median age 51 years, 94% men), 24 (73%) had respiratory symptoms, with the remainder having nonspecific viral symptoms. A total of 9 patients (35%, n=9/25) had cardiac magnetic resonance– defined myocarditis. Of these patients, 53% (n=5/8) had myocardial inflammatory cell infiltration. A total of 2 patients (5%) had elevated troponin levels. Cardiac troponin concentrations were not significantly higher in patients with and without myocarditis (8.4 ng/L [interquartile range, IQR: 4.0– 55.3] versus 3.5 ng/L [IQR: 2.5– 5.5]; P=0.07) or myocardial cell infiltration (4.4 ng/L [IQR: 3.4– 8.3] versus 3.5 ng/L [IQR: 2.8–7.2]; P=0.89). No patients had obstructive coronary artery disease or vasculitis. Pulmonary inflammation and consolidation (percentage of total lung volume) was 17% (IQR: 5%– 31%) and 11% (IQR: 7%–18%), respec-tively. Neither were associated with the presence of myocarditis. CONCLUSIONS: Myocarditis was present in a third patients with acute COVID-19, and the majority had inflammatory cell infil-tration. Pneumonitis was ubiquitous, but this inflammation was not associated with myocarditis. The mechanism of cardiac pathology is nonischemic and not attributable to a vasculitic process. REGISTRATION: URL: https://www.isrctn.com; Unique identifier: ISRCTN12154994.
AB - BACKGROUND: Acute COVID-19– related myocardial, pulmonary, and vascular pathology and how these relate to each other remain unclear. To our knowledge, no studies have used complementary imaging techniques, including molecular imag-ing, to elucidate this. We used multimodality imaging and biochemical sampling in vivo to identify the pathobiology of acute COVID-19. Specifically, we investigated the presence of myocardial inflammation and its association with coronary artery disease, systemic vasculitis, and pneumonitis. METHODS AND RESULTS: Consecutive patients presenting with acute COVID-19 were prospectively recruited during hospital admission in this cross-sectional study. Imaging involved computed tomography coronary angiography (identified coronary disease), cardiac 2-deoxy-2-[fluorine-18]fluoro-D-glucose positron emission tomography/computed tomography (identified vascular, cardiac, and pulmonary inflammatory cell infiltration), and cardiac magnetic resonance (identified myocardial dis-ease) alongside biomarker sampling. Of 33 patients (median age 51 years, 94% men), 24 (73%) had respiratory symptoms, with the remainder having nonspecific viral symptoms. A total of 9 patients (35%, n=9/25) had cardiac magnetic resonance– defined myocarditis. Of these patients, 53% (n=5/8) had myocardial inflammatory cell infiltration. A total of 2 patients (5%) had elevated troponin levels. Cardiac troponin concentrations were not significantly higher in patients with and without myocarditis (8.4 ng/L [interquartile range, IQR: 4.0– 55.3] versus 3.5 ng/L [IQR: 2.5– 5.5]; P=0.07) or myocardial cell infiltration (4.4 ng/L [IQR: 3.4– 8.3] versus 3.5 ng/L [IQR: 2.8–7.2]; P=0.89). No patients had obstructive coronary artery disease or vasculitis. Pulmonary inflammation and consolidation (percentage of total lung volume) was 17% (IQR: 5%– 31%) and 11% (IQR: 7%–18%), respec-tively. Neither were associated with the presence of myocarditis. CONCLUSIONS: Myocarditis was present in a third patients with acute COVID-19, and the majority had inflammatory cell infil-tration. Pneumonitis was ubiquitous, but this inflammation was not associated with myocarditis. The mechanism of cardiac pathology is nonischemic and not attributable to a vasculitic process. REGISTRATION: URL: https://www.isrctn.com; Unique identifier: ISRCTN12154994.
KW - CMR
KW - COVID-19
KW - FDG-PET
KW - myocarditis
KW - pneumonitis
UR - http://www.scopus.com/inward/record.url?scp=85138460337&partnerID=8YFLogxK
U2 - 10.1161/JAHA.122.026399
DO - 10.1161/JAHA.122.026399
M3 - Article
C2 - 36102258
AN - SCOPUS:85138460337
SN - 2047-9980
VL - 11
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
IS - 18
M1 - e026399
ER -