Introduction
In recent years, COVID-19 has posed substantial challenges for health care systems in managing a growing number of patients in the acute phase of the disease and pneumonia. An equally significant challenge has been the long phase of the disease, the so-called long COVID. The occurrence of this long phase is independent of the severity of the acute phase.1 It affects more than 80% of COVID-19 survivors and can manifest in several ways, including cardiovascular diseases.2,3 Its most common symptoms include fatigue, headache, attention disorders, hair loss, and dyspnea.2
D-dimer, a fibrin degradation product,4 is a parameter whose elevated levels are the most frequent laboratory finding.2 Its elevated value is associated with previous severe infections requiring hospitalization,5 but is also frequently observed in patients after mild infections. In a study by Townsend et al,6 25.3% of the patients at least 6 weeks post–COVID-19 had elevated D-dimer levels. The scale of this problem highlights its relevance. Elevated postinfection D-dimer concentration may result from an imbalance in coagulation and fibrinolysis in the lungs during the acute phase.6 However, studies conflict on whether elevated D-dimer levels are more common in COVID-19 survivors with persistent symptoms or asymptomatic individuals.3 D-dimer has proven useful in the acute phase of COVID-19, as it can help predict pulmonary embolism (PE),7 severe disease course, and death.8 Its levels shortly after hospitalization for COVID-19 are independent of the degree of respiratory support.9 In the long phase, D-dimer may be associated with patients’ clinical parameters.5 Some studies have demonstrated its role in predicting clinical outcomes after COVID-19—Zhao et al10 showed its value in predicting pulmonary dysfunction 3 months after hospitalization, while Son et al11 found that D-dimer predicted fatigue and dyspnea 3 months after the acute phase.
Aim
This study aimed to assess long-term D-dimer levels and their associations with other clinical and laboratory parameters in patients with elevated post–COVID-19 D-dimer concentrations.
Methods
Study design and patients
This was an observational, prospective study conducted at the St. John Paul II Hospital in Kraków, Poland. We included patients with a history of COVID-19 confirmed by a diagnostic test, who attended a control visit after infection at our center between December 23, 2020 and April 26, 2021 (data extracted from the hospital database), and had elevated D-dimer levels in a peripheral blood sample obtained during that visit (cutoff value ≥500 μg/l). The D-dimer level was measured routinely in all post–COVID-19 patients. They were invited to attend a second control visit after a follow-up period. The patients who did not attend the second visit were excluded. The first postinfection consultation was considered the baseline (short term), while the second was regarded as follow-up (long term). The short- and long-term periods reflected the time elapsed since COVID-19.
The patients were divided into 2 groups based on D-dimer levels at follow-up: the elevated D-dimer group (EDG) and the normalized D-dimer group (NDG). D-dimer levels were considered normalized at follow-up when the value was below 500 μg/l during the second postinfection visit.
The study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of the Regional Medical Chamber in Kraków (OIL/KBL/48/2021). Verbal informed consent was obtained from all participants before the start of the study. Consent was verbal because the study was observational and consisted of standard medical diagnostics and treatment based on clinical indications.
Investigation and clinical evaluation
The data collected at the first postinfection visit included a medical interview, physical examination, transthoracic echocardiogram, 24-hour Holter monitoring, serum D-dimer levels, complete blood count with differential, as well as creatinine, alanine aminotransferase, aspartate aminotransferase, cardiac troponin T (cTnT), C-reactive protein (CRP), fibrinogen, and N-terminal pro–B-type natriuretic peptide (NT-proBNP) serum concentrations. At the second postinfection visit, the same data were collected, except for transthoracic echocardiogram, 24-hour Holter monitoring, and serum cTnT levels. During this visit, the medical interview was conducted using a standardized questionnaire. It included questions about the presence of: reduced exercise tolerance, angina pectoris, heart palpitations, stabbing chest pain, cough, nasal discharge, sore throat or swallowing difficulties, smell or taste disturbances, headache, dizziness, sleep disturbances, memory dysfunction, anxiety, depression or low mood, musculoskeletal pain, hair loss, and fatigue. Based on clinical indications, some patients underwent additional imaging, including chest computed tomography (CT; high-resolution CT when required), and / or pulmonary CT angiography for PE, and / or lung scintigraphy. During both post–COVID-19 visits, the patients were examined by cardiologists. All laboratory tests were performed using routine laboratory techniques.
Statistical analysis
Statistical analysis was performed using Statistica software, versions a13.3 and 14.1 (TIBCO Software Inc., Palo Alto, California, United States). Categorical variables were presented as numbers and percentages, while numerical variables were reported as mean (SD) or median with interquartile range (IQR), depending on normality. Normality was assessed using the Shapiro–Wilk test. Homogeneity of variances was assessed with the Levene test. The study groups were compared at baseline and at follow-up in terms of clinical and laboratory parameters and changes in the parameters between baseline and follow-up, also in the form of percentage of baseline values. Numerical variables were compared using the t test for normally distributed variables. The Mann–Whitney test was applied for non-normally distributed numerical variables. Categorical variables were compared using the Pearson χ2 test or the 1-tailed Fisher exact test. We investigated the correlations between baseline D-dimer, follow-up D-dimer, and changes in D-dimer levels and the following parameters: baseline age, cTnT, and ejection fraction, as well as baseline, follow-up, and change in complete blood count parameters, creatinine, estimated glomerular filtration rate (eGFR), alanine aminotransferase, aspartate aminotransferase, cTnT, CRP, fibrinogen, and NT-proBNP. Correlations between 2 numerical variables were determined using the Pearson linear correlation coefficient (r) for normally distributed variables, and the Spearman rank correlation coefficient (R) for non-normally distributed variables.
Significance was set at a P value below 0.05. The box plots were created using Statistica software, version 13.3 (TIBCO Software Inc.) and transformed into line art using Adobe Illustrator 2024 (Adobe Inc., San Jose, California, United States). Theflow chart was created using Adobe Illustrator 2026 (Adobe Inc.).
Results
Baseline characteristics
A total of 152 post–COVID-19 patients had elevated D-dimer levels at the time of the control postinfection visit, and were originally included in the study (Figure 1). This represented 60.8% of the 250 post–COVID-19 individuals who attended the control postinfection visit at our center during the previously mentioned period. A total of 96 patients did not attend the second postinfection visit and were excluded, whereas 56 did so between July 15 and August 11, 2022, and were considered for the final study group. The participants did not differ in age (P = 0.65), or sex (P = 0.94) from the patients lost to follow-up. Median (IQR) time from COVID-19 to the first postinfection visit was 85 (31–124) days. All patients had elevated D-dimer levels at baseline, with median (IQR) value of 716.5 (570–885.5) μg/l. The patients in the EDG were older, had lower eGFR, and had higher cTnT levels at baseline, as compared with those in the NDG (Figure 2; Table 1). Baseline laboratory parameters with nonsignificant differences between the EDG and NDG are not reported.
Figure 1. Flowchart of the study recruitment process
Figure 2. Box plots of baseline age (A), cTnT (B), and eGFR (C), grouped by normalization of D-dimer level at follow-up
Abbreviations: see Table 1
Characteristic | All patients (n = 56) | NDG (n = 25) | EDG (n = 31) | P value (NDG vs EDG) | |
|---|---|---|---|---|---|
Men | 19 (33.93) | 11 (44) | 8 (25.81) | 0.15 | |
Age, y | 65 (50.5–72.5) | 59 (48–67) | 70 (59–74) | 0.003 | |
Medical history and clinical presentation | Hospitalization during COVID-19 | 15 (26.79) | 6 (24) | 9 (29.03) | 0.67 |
EF on TTE | 62 (60–65) | 62 (60–66) | 62 (60–65) | 0.44 | |
Diastolic dysfunction on TTE | 16 (34.78) | 4 (20) | 12 (46.15) | 0.07 | |
Cardiac hypertrophy on TTE | 21 (47.73) | 7 (41.18) | 14 (51.85) | 0.49 | |
Reduced exercise tolerance | 42 (75) | 18 (72) | 24 (77.42) | 0.64 | |
NYHA class III–IV | 7 (12.5) | 2 (8) | 5 (16.13) | 0.27 | |
Angina pectoris | 21 (37.5) | 8 (32) | 13 (41.94) | 0.44 | |
Heart palpitations | 29 (51.79) | 12 (48) | 17 (54.84) | 0.61 | |
Stabbing chest pain | 8 (14.29) | 1 (4) | 7 (22.58) | 0.052 | |
Medications | ACEIs | 20 (35.71) | 7 (28) | 13 (41.94) | 0.28 |
ARBs | 4 (7.14) | 1 (4) | 3 (9.68) | 0.39 | |
β-Blockers | 31 (55.36) | 15 (60) | 16 (51.61) | 0.53 | |
Statins | 26 (46.43) | 11 (44) | 15 (48.39) | 0.74 | |
Diuretics | 18 (32.14) | 7 (28) | 11 (35.48) | 0.55 | |
Platelet antagonists | 15 (26.79) | 6 (24) | 9 (29.03) | 0.67 | |
VKAs or DOACs | 2 (3.57) | 1 (4) | 1 (3.23) | 0.7 | |
Heparins | 2 (3.57) | 0 | 2 (6.45) | 0.3 | |
DTIs | 1 (1.79) | 1 (4) | 0 | 0.45 | |
OCs or HRT | 1 (1.79) | 0 | 1 (3.23) | 0.55 | |
eGFR, ml/min/1.73 m2, mean (SD) | 82.04 (17.25) | 88.57 (13.34) | 76.86 (18.42) | 0.01 | |
cTnT, ng/ml | 0.007 (0.005–0.011) | 0.006 (0.003–0.009) | 0.009 (0.006–0.012) | 0.04 | |
Data are presented as number (percentage) or median (interquartile range) unless indicated otherwise. Abbreviations: ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; cTnT, cardiac troponin T; DOAC, direct oral anticoagulant; DTI, direct thrombin inhibitor; EDG, elevated D-dimer group; EF, ejection fraction; eGFR, estimated glomerular filtration rate; HRT, hormone replacement therapy; NDG, normalized D-dimer group; NYHA, New York Heat Association; OC, oral contraceptive; TTE, transthoracic echocardiography; VKA, vitamin K antagonist | |||||
Median (IQR) age of the participants was higher in the EDG than NDG (70 [59–74] vs 59 [48–67] y; P = 0.003). Nineteen patients (33.93%) were men, with 8 (25.81%) in the EDG and 11 (44%) in the NDG (P = 0.15).
No significant differences were found at baseline between the study groups with respect to heparin or glucocorticoid use during COVID-19, medical history of myocardial infarction, venous thromboembolism, stroke, syncope, or pneumonia, Holter monitoring results (number of supraventricular extrasystoles, number of ventricular extrasystoles, or presence of ventricular tachycardia), or baseline comorbidities, including arterial hypertension, diabetes mellitus, coronary artery disease, atrial fibrillation, or congenital heart disease. None of the patients had a history of PE.
Follow-up
Median (IQR) follow-up time was 16.73 (15.83–18.02) months: 16.83 (15.83–17.27) months in the EDG and 16.6 (15.9–18.37) months in the NDG (P = 0.37). A total of 31 patients (55.36%) still had elevated D-dimer levels and constituted the EDG, while D-dimer levels normalized in 25 patients (44.64%) at the second postinfection visit, forming the NDG. Median (IQR) D-dimer level was 510 (338.5–662.5) μg/l for all patients: 648 (539–789) μg/l in the EDG and 322 (206–410) μg/l in the NDG. Median (IQR) decrease in D-dimer levels during follow-up was greater in the NDG than EDG (–349 [–513 to –176] vs –126 [–281 to 42] μg/l; P <0.001; Figure 3). The patients in the EDG had a higher prevalence of fatigue, higher neutrophil count, monocyte count, neutrophil percentage, fibrinogen, and NT-proBNP levels, as well as lower eGFR and lymphocyte percentage, as compared with the NDG (Figure 4; Table 2). Follow-up clinical and laboratory parameters with nonsignificant differences between the EDG and NDG are not reported.
Figure 3. Box plots of baseline (A) and follow-up (B) D-dimer levels grouped by normalization of D-dimer level at follow-up
Figure 4. Box plots of follow-up laboratory parameters grouped by normalization of D-dimer level at follow-up: NT-proBNP (A), fibrinogen (B), neutrophil count (C), monocyte count (D), neutrophil percentage (E), lymphocyte percentage (F), and eGFR (G)
Abbreviations: see Tables 1 and 2
Characteristic | All patients (n = 56) | NDG (n = 25) | EDG (n = 31) | P value (NDG vs EDG) | |
|---|---|---|---|---|---|
Fatigue, n (%) | 37 (66.07) | 13 (52) | 24 (77.42) | 0.046 | |
Laboratory workup | NT-proBNP, pg/ml | 95.5 (48–228) | 54 (27–117) | 160 (84–248) | <0.001 |
eGFR, ml/min/1.73 m2 | 80.2 (18.53) | 87.96 (14.66) | 73.94 (19.16) | 0.004 | |
Fibrinogen, g/l | 3.15 (0.5) | 2.89 (0.41) | 3.35 (0.48) | <0.001 | |
Neutrophils, × 103/μl | 3.16 (2.63–4.05) | 2.83 (2.51–3.45) | 3.52 (2.93–4.99) | 0.01 | |
Monocytes, × 103/μl | 0.525 (0.45–0.605) | 0.52 (0.38–0.58) | 0.53 (0.49–0.71) | 0.046 | |
Neutrophils, % | 54.16 (8.29) | 51.62 (7.39) | 56.2 (8.52) | 0.04 | |
Lymphocytes, % | 33.13 (7.61) | 35.66 (6.97) | 31.09 (7.59) | 0.02 | |
Data are presented as mean (SD) or median (interquartile range) unless indicated otherwise. SI conversion factors: to convert NT-proBNP to pmol/l, multiply by 0.1182. Abbreviations: NT-proBNP, N-terminal pro–B-type natriuretic peptide; others, see Table 1 | |||||
The most frequent long-term clinical symptoms at follow-up were musculoskeletal pain (76.79%), reduced exercise tolerance (75%), fatigue (66.07%), sleep disturbances (66.07%), and memory dysfunction (58.92%).
Eight patients (14.26%) had pneumonia: 7 (22.58%) in the EDG and 1 (4%) in the NDG, which showed a tendency toward significance (P = 0.052).
Chest CT (including high-resolution CT) was performed in 30 participants (53.57%), including 21 (67.74%) in the EDG and 9 (36%) in the NDG (P = 0.02). Pulmonary CT angiography for PE was performed in 5 patients (8.93%) and lung scintigraphy in 2 individuals (3.57%), with no significant differences between the study groups in performing those procedures. Changes in the levels of D-dimer, NT-proBNP, and CRP and lymphocyte percentage between baseline and follow-up (also as percentages of baseline values) differed between the groups (Table 3). Median (IQR) decreases in NT-proBNP (10 [–20 to 44] vs –20 [–68 to –3] pg/ml; P = 0.003) and CRP (0.4 [–0.9 to 1.8] vs –0.4 [–2.2 to 0.2] mg/l; P = 0.03) were smaller in the EDG than the NDG. Median (IQR) decrease in lymphocyte percentage was greater in the EDG, as compared with the NDG (1.4% [–1.1% to 5.4%] vs 6.6% [2.3%–9.5%]; P = 0.01). Median (IQR) decrease in white blood cell count was 0.46 (–0.45 to 1.14) × 103/μl in the EDG and –0.15 (–0.65 to 0.16) × 103/μl in the NDG, which showed a tendency toward significance (P = 0.06).
Laboratory parameter | All patients (n = 56) | NDG (n = 25) | EDG (n = 31) | P value (NDG vs EDG) | |
|---|---|---|---|---|---|
D-dimer | Change in D-dimer, μg/l | –222.5 (–395 to –75) | –349 (–513 to –176) | –126 (–281 to 42) | <0.001 |
Change in D-dimer as percentage of baseline value, % | –31.81 (–59.56 to –13.51) | –55.97 (–65.23 to –32.35) | –16.28 (–31.76 to 5.1) | <0.001 | |
NT-proBNP | Change in NT-proBNP, pg/ml | –8.5 (–31.5 to 31.5) | –20 (–68 to –3) | 10 (–20 to 44) | 0.003 |
Change in NT-proBNP as percentage of baseline value, % | –10.66 (–29.52 to 21.73) | –28.866 (–47.84 to –16.67) | 9.78 (–20.41 to 31.74) | <0.001 | |
CRP | Change in CRP, mg/l | 0 (–1.5 to 0.75) | –0.4 (–2.2 to 0.2) | 0.4 (–0.9 to 1.8) | 0.3 |
Change in CRP as percentage of baseline value, % | 0 (–47.05 to 42.26) | –40 (–63.77 to 16.25) | 18.18 (–40 to 81.81) | 0.03 | |
Lymphocytes | Change in lymphocytes, % | 4 (–0.2 to 8.05) | 6.6 (2.3–9.5) | 1.4 (–1.1 to 5.4) | 0.01 |
Change in lymphocytes as percentage of baseline value, % | 12.98 (–0.64 to 26.3) | 23.31 (9.39–34.32) | 5.07 (–3.69 to 22.28) | 0.02 | |
Data are presented as median (interquartile range). SI conversion factors: to convert NT-proBNP to pmol/l, multiply by 0.1182; CRP to nmol/l, by 9.5238. Abbreviations: CRP, C-reactive protein; others, see Tables 1 and 2 | |||||
Various correlations with D-dimer levels at baseline and at follow-up were found. Only significant and at least moderate correlations are reported (Table 4).
Variable 1 | Variable 2 | Correlation factor | P value |
|---|---|---|---|
Follow-up D-dimer | Baseline age | R = 0.44 | <0.001 |
Baseline D-dimer | Change in D-dimer | R = 0.552l | <0.001 |
Follow-up D-dimer | Change in D-dimer | R = –0.535 | <0.001 |
Follow-up D-dimer | Fibrinogen | r = 0.591 | <0.001 |
Follow-up D-dimer | NT-proBNP | R = 0.435 | <0.001 |
Follow-up D-dimer | Change in NT-proBNP | R = –0.436 | <0.001 |
Follow-up D-dimer | eGFR | r = –0.401 | 0.002 |
Abbreviations: see Tables 1 and 2 | |||
There were no significant differences between the study groups at follow-up regarding the presence of pulmonary fibrosis, ground glass opacity, COVID-19 reinfection, hospitalization due to COVID-19 reinfection, or newly diagnosed arterial hypertension, diabetes mellitus, or atrial fibrillation. Likewise, no differences were observed in the follow-up numbers of myocardial infarction events, syncope, venous thromboembolism, or PE. No patients experienced a stroke during follow-up.
Discussion
In their meta-analysis, Lopez-Leon et al2 reported that in a population analyzed 2–12 weeks post–COVID-19, the most frequent symptoms were: fatigue (58%), headache (44%), attention disorder (27%), hair loss (25%), and dyspnea (24%), which is, in majority, different from our observations. In a work by Meisinger et al,12 38.69% of the patients shortly after COVID-19 experienced fatigue, but D-dimer levels were not associated with it, unlike in our study. Other studies have shown fatigue in 69%13 and 53.1%14 of the patients shortly after COVID-19. At 12 or more weeks after infection, this percentage has been reported at 32%.15
Our study showed that the patients whose D-dimer levels did not normalize in the long term were older. This finding is consistent with other data on the characteristics of D-dimer testing16 as well as previous COVID-19 studies.6
Shortly after COVID-19, 60.8% of all post–COVID-19 patients in our study had elevated D-dimer levels. Existing data indicate that 46.4% of the individuals in the acute phase of COVID-19 have elevated D-dimer levels,17 and 30.1% of the patients with abnormal D-dimer values at discharge showed their persistent elevation in short-term follow-up.13 Lehmann et al5 reported that 14.7% of all COVID-19 survivors had elevated D-dimer levels at a median of 94 days after infection. Interestingly, these percentages are lower than those observed in our study. The strong positive correlation between the decrease in D-dimer levels during follow-up and baseline D-dimer concentrations in our study suggests that patients with the highest short-term postinfection D-dimer levels do not necessarily have the highest D-dimer concentrations or worse outcomes in the long term. Multiple associations of D-dimer with various variables highlight the complexity of interactions among numerous factors in long COVID.
We observed several associations between fibrinogen and D-dimer. It has also been investigated by other authors in relation to long COVID. Proteomic analyses demonstrated that fibrinogen chains are more prevalent in the plasma of long COVID patients than that of controls or acute COVID-19 patients. Furthermore, fibrinolysis-resistant microclots have been detected in the plasma of long COVID patients.18 Similar microclots have been confirmed in the plasma of those with acute PE.19 High fibrinogen levels in long COVID have also been associated with myalgia.20
The study groups differed in parameters directly related to inflammation. D-dimer itself is considered an inflammatory marker, which may suggest that chronic inflammation with concomitant coagulation exists in some long COVID patients. The findings of Maamar et al20 were consistent with ours: long COVID was associated with higher neutrophil counts, CRP, and fibrinogen levels; neutrophil counts in men with long COVID were significantly higher in those with fatigue. High levels of inflammatory markers may reflect underlying processes, responsible for fatigue and other long COVID symptoms. Other studies have indicated that neutrophilia and lymphopenia,21 as well as the monocyte-to-lymphocyte ratio,22 can be associated with the severity of the acute phase of COVID-19. Persistent lymphopenia has been observed in the short term in 7.3% of the patients with abnormal discharge lymphocyte counts.13 Moreover, in women, a neutrophil-to-lymphocyte ratio in the highest tertile is associated with a higher risk of long COVID.20 In our work, changes in CRP, also when reported as percentage of baseline values, differed significantly between the study groups. Other authors have reported significantly higher CRP levels in patients with elevated D-dimer levels 94 days after infection.5
Our study results, particularly baseline and follow-up NT-proBNP levels and normal ejection fraction at baseline in both groups, suggest that the observed higher NT-proBNP levels may be caused by diastolic dysfunction, and tend to decrease along with D-dimer normalization. In the long term, cTnT levels, similarly to NT-proBNP concentrations, are higher in long COVID patients than in asymptomatic individuals.23 Myocardial injury with elevated troponin levels is present in 7%–17% of hospitalized COVID-19 patients,24 and approximately one-third of the individuals with myocarditis develop persistent cardiac impairment.25 The higher baseline cTnT values observed in the EDG in our study may reflect more frequent acute-phase myocardial injury, which later manifested as higher follow-up NT-proBNP levels in this group. It is possible that augmented autoimmunization is responsible for heart damage in long COVID rather than chronic inflammation itself, as has been suggested in systemic lupus erythematosus.26 Acanfora et al23 reported that long COVID patients had significantly higher D-dimer and NT-proBNP levels than those not having undergone this form of the disease. In long COVID, higher NT-proBNP concentrations have been associated with new-onset heart palpitations and / or reduced exercise tolerance,27 as well as 1-year mortality.28
The study groups also differed in terms of kidney function. It is worth noting that chronic kidney disease is itself a hypercoagulable state. Patients with chronic kidney disease have higher D-dimer levels than those without it,29 and they are largely independent of GFR.30 This likely explains our observation that elevated long-term D-dimer levels were associated with worse renal function, although the correlation between the D-dimer concertation and eGFR was not always present.
Limitations
Our study has several limitations. The population (n = 56) was limited to the participants who attended the second postinfection visit at our center. With a larger sample size, the results that had a tendency toward significance may have reached it. Also, large number of patients lost to follow-up means that our findings apply to a selected subgroup and may not reflect all patients with elevated post–COVID-19 D-dimer levels. We performed several univariate tests across many variables, so findings should be considered hypothesis-generating, and some associations may reflect multiple-testing effects. The study groups differed significantly at baseline in terms of age and eGFR, which likely confounded many associations. In addition, the patient interview during the first postinfection visit was not standardized with a questionnaire. Finally, we were unable to repeat all laboratory tests and diagnostic procedures performed at the first visit during the second postinfection visit, which limited our ability to identify certain associations.
Conclusions
In patients with elevated postinfection D-dimer levels, long-term values remain elevated in the majority. In long COVID, D-dimer levels show several associations with other clinical and laboratory parameters. Further studies with larger cohorts are needed to better determine the long-term role of D-dimer after COVID-19.
Tomasz Sternalski, MD, Jagiellonian University Medical College, ul. św. Anny 12, 31-008 Kraków, Poland, phone: +48 12 422 54 44, email: tomasz.sternalski.1@gmail.com
August 25, 2025.
February 23, 2026.
February 24, 2026.
None.
None.
Conceptualization: TS and LT-P; methodology: LT-P; validation: TS and LT-P; formal analysis: TS; investigation: TS, MS-Ś, ND, PS, DS, and LT-P; resources: LT-P; data curation: TS; writing (original draft preparation): TS; writing (review and editing): TS, MS-Ś, ND, PS, DS, and LT-P; visualization: TS; supervision: LT-P; project administration: LT-P. All authors edited and approved the final version of the manuscript.
None declared.
Artificial intelligence was not used in the preparation of this manuscript.
Sternalski T, Smaś-Suska M, Dłużniewska N, et al. D-dimer changes and associations in long COVID: a prospective observational study. Prz Lek Jagiellonian Med Rev. 2026; 78: 20033. doi:10.20452/jmr.2026.20033
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