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Clinical Characteristics and Comparative Proteomics Analysis of COVID-19-Related Atrioventricular Block
Yuan Gao1, Zhongli Chen1, Sijin Wu1
1State Key Laboratory of Cardiovascular Disease, Arrhythmia Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 100037 Beijing, China.
Insights
Coronavirus disease 2019 (COVID-19) can cause atrioventricular block (AVB), leading to myocardial damage and pneumonia. Proteomics analysis identified key proteins involved in inflammation and immune response, offering insights into COVID-19-related AVB pathogenesis.
Area of Science:
- Cardiology
- Infectious Diseases
- Proteomics
Background:
- Atrioventricular block (AVB) is a potential cardiovascular complication of COVID-19, but data beyond case reports are limited.
- This study aimed to characterize patients with COVID-19-related AVB, including their proteomics profile and outcomes.
Purpose of the Study:
- To describe the baseline characteristics, proteomics profile, and outcomes of patients experiencing AVB due to COVID-19.
- To identify potential biomarkers and understand the pathogenesis of COVID-19-related AVB.
Main Methods:
- Prospective recruitment of 17 patients with COVID-19-related AVB and 24 controls with COVID-19 but without AVB.
- Analysis of patient characteristics, outcomes, and comparative plasma proteomics.
- Laboratory tests for myocardial damage, inflammation, and coagulation markers.
Main Results:
- COVID-19 patients with AVB had higher rates of pneumonia and elevated biomarkers of myocardial damage, inflammation (CRP, D-dimer), and cardiac strain (NT-proBNP).
- Proteomics identified 397 proteins, with significant alterations in those related to inflammatory response (e.g., Serum amyloid A protein), complement/coagulation cascades (e.g., Tetranectin), and immune response (e.g., Neutrophil defensin 3).
- All AVB patients required permanent pacemaker implantation.
Conclusions:
- COVID-19-related AVB is associated with increased myocardial damage and pneumonia.
- Differential expression of specific proteins involved in inflammation, coagulation, and immune response provides insights into the pathogenesis of COVID-19-related AVB and suggests potential biomarkers.
Background:
Atrioventricular block (AVB) is thought to be a rare cardiovascular complication of the coronavirus disease 2019 (COVID-19), though limited data are available beyond case reports. We aim to describe the baseline characteristics, proteomics profile, and outcomes for patients with COVID-19-related AVB.
Methods:
We prospectively recruited patients diagnosed with COVID-19-related AVB between November 2022 and March, 2023. Inclusion criteria were hospitalization for COVID-19 with the diagnosis of AVB. A total of 24 patients diagnosed with COVID-19 without AVB were recruited for control. We analyzed patient characteristics and outcomes and performed a comparative proteomics analysis on plasma samples of those patients and controls.
Results:
A total of 17 patients diagnosed with COVID-19-related AVB and 24 individuals diagnosed with COVID-19 infection without AVB were included. Among patients with COVID-19-related AVB, the proportion of concurrent pneumonia was significantly higher than controls (7/17 versus 2/24, p 0.05). All 17 AVB patients (9 of permanent AVB, 8 of paroxysmal AVB) received permanent pacemaker implantation. No procedural-related complication occurred. In laboratory tests, the level of biomarkers indicating myocardial damage were substantially higher than controls, including high-sensitivity cardiac troponin-I (median 0.005 versus 0.002 ng/mL, p 0.05), myoglobulin (median 39.0 versus 27.6 ng/mL, p 0.05), and MB isoenzyme of creatine kinase (median 1.2 versus 0.8 U/L, p 0.05). The level of N-terminal pro-b-type natriuretic peptide (median 241.0 versus 33.5 pg/mL, p 0.05), C-reactive protein (median 4.8 versus 2.0 mg/L, p 0.05), D-dimer (median 1.2 versus 0.2 µg/mL, p 0.05), left ventricular end-diastolic diameter (median 49.3 versus 45.7 mm, p 0.05) in patients with COVID-19-related AVB were significantly higher than controls. The level of albumin (median 41.9 versus 44.5 g/L, p 0.05) was significantly lower than controls. In comparative proteomics analysis, we identified 397 human proteins. Several significantly altered plasma proteins related to inflammatory response (Serum amyloid A protein, C-reactive protein, Protein Adenosine 5'-monophosphate-activated protein kinase (AMPK), Alpha-2-macroglobulin), complement and coagulation cascades (Tetranectin, haptoglobin), and immune response (Neutrophil defensin 3, Fibrinogen beta chain) may contribute to the pathogenesis of COVID-19-related AVB.
Conclusions:
Patients with COVID-19-related AVB are more prone to have myocardial damage and concurrent pneumonia. Through laboratory tests and comparative proteomics analysis, we identified several differential expressed proteins (Serum amyloid A protein, Tetranectin, Neutrophil defensin 3) releated to the inflammatory response, complement and coagulation cascades, and immune response, which provides evidence of potential biomarkers and sheds light on the pathogenesis of COVID-19-related AVB.
