Lung Injury (Pulmonary Edema) in COVID-19: Treatment With Furosemide and Negative Fluid Balance (NEGBAL)
NCT ID: NCT05304702
Last Updated: 2022-04-22
Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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Recruitment Status
COMPLETED
Total Enrollment
120 participants
Study Classification
OBSERVATIONAL
Study Start Date
2021-11-28
Study Completion Date
2022-03-31
Brief Summary
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In COVID-19, pulmonary edema has been attributed to "cytokine storm". However, it is known that SARS-CoV-2 promotes angiotensin-converting enzyme 2 deficiency, it increases angiotensin II and this triggers volume overload. The current study is based on patients with COVID-19, tomographic evidence of pulmonary edema and volume overload. These patients received a standard goal-guided diuretic (furosemide) treatment: Negative Fluid Balance (NEGBAL) approach. This retrospective observational study consists of comparing two groups. The cases show patients with COVID-19 and lung injury treated with NEGBAL approach comparing it to the control group consisting of patients with COVID-19 and lung injury receiving standard treatment. Medical records of 120 critically ill patients (60 in NEGBAL group and 60 in control group) were reviewed: demographic, clinical, laboratory, blood gas and chest tomography (CT) before and during NEGBAL.
Once NEGBAL strategy started, different aspects were evaluated: clinical, gasometric and biochemical evolution until the 8th day, tomography until the 12th day, ICU stay, hospital stay and morbidity and mortality until the 30th day.
Once NEGBAL strategy started, different aspects were evaluated: clinical, gasometric and biochemical evolution until the 8th day, tomography until the 12th day, ICU stay, hospital stay and morbidity and mortality until the 30th day.
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Detailed Description
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In December 2019, a new coronavirus, known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in Wuhan, China and spread throughout the world.
In COVID-19, pulmonary edema has been described; however, the dominant paradigm is focused on cytokine storm as responsible for lung injury and subsequent acute respiratory distress syndrome (ARDS). Not everyone agreed with this paradigm. Sinha et al. challenged the role of this cytokine storm given that median interleukin-6 (IL-6) levels in non-COVID patients ARDS were up to 200 times higher than in patients with severe COVID-19. Gattinoni et al. maintained that COVID-19 presented as an "atypical form" of ARDS. On the other hand, Kuba et al. and Imai et al. reported that angiotensin-converting enzyme 2 (ACE2) levels during a SARS-CoV infection are decreased. Furthermore, in patients with COVID-19, plasma levels of Angiotensin II are higher than in healthy population and stimulate an upregulation of aldosterone level, triggering sodium and water retention. SARS-CoV-2 enters through ACE2 and downregulates ACE2 expression so that this enzyme is unable to exert its protective effects. The dysregulated activity of the renin angiotensin aldosterone system (RAAS) is partly responsible for pulmonary edema in COVID-19. ACE2 is known for its effect as the main counter-regulatory mechanism for the renin-angiotensin aldosterone system (RAAS), which is an essential player in blood pressure control by retaining sodium and water and increasing the intravascular fluid volume. SARS-CoV-2 binds ACE2 and accelerates the degradation of ACE2, and thus decreases the counteraction of ACE2 on RAAS. The final effect is increasing reabsorption of sodium and water and subsequent volume overload. The RAAS can be envisioned as a dual function system in which the vasoconstrictor/proliferative or vasodilator/antiproliferative actions are primarily driven by the ACE-ACE2 balance. According to that, an increased ACE/ACE2 activity ratio generated by the downregulation action of SARS-CoV-2 on ACE2 will lead to increased Angiotensin II and increased catabolism of Angiotensin 1-7, towards vasoconstriction, endothelial dysfunction, prothrombosis, proinflammatory, and antinatriuretic effect.
Acute pulmonary edema is caused mostly by one of the following mechanisms: pulmonary venous pressure elevation-volume overload-or augmentation of the alveolar capillary membrane permeability-inflammation. In fact, both mechanisms sometimes coexist and the distinction is irrelevant. There are bibliographic references of pulmonary edema in COVID-19, as well as evidence of volume overload in COVID-19: Lang et al. describes frequent and pronounced vasculature in affected lung areas that may be suggestive of disordered vasoregulation. Eslami et al. observed increased cardiothoracic ratio and it is also described as right ventricular dilatation. In this setting, a different approach emerged: moderate or severe COVID-19 could experience a severe acute pulmonary edema with a "dual hit". A "first hit" of pneumonitis-augmentation of the alveolar capillary membrane permeability-can lead to low hydrostatic pressure pulmonary edema. The "second hit" is high pressure pulmonary edema, caused by increase of hydrostatic pressure secondary to volume overload, a result of dysregulation of the RAAS. This results in a "dual hit" that triggers severe acute pulmonary edema. If this edema is not solved, then a "third hit" appears with secondary inflammation, superinfection, fibrosis and finally the typical ARDS. Consequently, the study group looked for patients with pulmonary edema before ARDS was triggered. Cases of moderate and severe COVID-19 were searched, with tomographic evidence of pulmonary edema: dilated superior vena cava, large pulmonary arteries, diffuse interstitial infiltrates and dilated right ventricle. At the detection of pulmonary edema in patients with COVID-19, a standard treatment consisting of oral hydric restriction and diuretics (NEGBAL approach) was initiated. The effects of furosemide on pulmonary edema were well established decades ago. To date there is no evidence that had suggested the model of pulmonary edema and volume overload secondary to the dysregulation of the renin angiotensin aldosterone system in COVID-19. The objective of this study is to compare patients with COVID-19 undergoing NEGBAL approach with a control group of patients with COVID-19 of similar demographic, clinical, gasometric and tomographic characteristics. Medical records of 120 adult patients were reviewed: demographic; clinical, laboratory; Pro b-type natriuretic peptide (pro-BNP): (negative: below 125 pg/mL); high-sensitivity cardiac troponin (hs-cTnT): (negative: \<14 ng/L); blood gas; chest tomography (CT); oxygen therapy support and mechanical ventilation (MV) requirements, all of which were reviewed and recorded by investigators. With the purpose of knowing the patient's basal hematocrit before COVID-19, prior hematocrit, if any, defined as hematocrit previous to COVID-19 infection (hematocrit prior to admission to NEGBAL) was also reviewed.
Once the NEGBAL strategy began, the clinical, tomographic, gasometric, biochemical evolution was evaluated until the 8th day (until the 12th day for tomography), ICU stay, hospital stay and morbidity and mortality until the 30th day.
In COVID-19, pulmonary edema has been described; however, the dominant paradigm is focused on cytokine storm as responsible for lung injury and subsequent acute respiratory distress syndrome (ARDS). Not everyone agreed with this paradigm. Sinha et al. challenged the role of this cytokine storm given that median interleukin-6 (IL-6) levels in non-COVID patients ARDS were up to 200 times higher than in patients with severe COVID-19. Gattinoni et al. maintained that COVID-19 presented as an "atypical form" of ARDS. On the other hand, Kuba et al. and Imai et al. reported that angiotensin-converting enzyme 2 (ACE2) levels during a SARS-CoV infection are decreased. Furthermore, in patients with COVID-19, plasma levels of Angiotensin II are higher than in healthy population and stimulate an upregulation of aldosterone level, triggering sodium and water retention. SARS-CoV-2 enters through ACE2 and downregulates ACE2 expression so that this enzyme is unable to exert its protective effects. The dysregulated activity of the renin angiotensin aldosterone system (RAAS) is partly responsible for pulmonary edema in COVID-19. ACE2 is known for its effect as the main counter-regulatory mechanism for the renin-angiotensin aldosterone system (RAAS), which is an essential player in blood pressure control by retaining sodium and water and increasing the intravascular fluid volume. SARS-CoV-2 binds ACE2 and accelerates the degradation of ACE2, and thus decreases the counteraction of ACE2 on RAAS. The final effect is increasing reabsorption of sodium and water and subsequent volume overload. The RAAS can be envisioned as a dual function system in which the vasoconstrictor/proliferative or vasodilator/antiproliferative actions are primarily driven by the ACE-ACE2 balance. According to that, an increased ACE/ACE2 activity ratio generated by the downregulation action of SARS-CoV-2 on ACE2 will lead to increased Angiotensin II and increased catabolism of Angiotensin 1-7, towards vasoconstriction, endothelial dysfunction, prothrombosis, proinflammatory, and antinatriuretic effect.
Acute pulmonary edema is caused mostly by one of the following mechanisms: pulmonary venous pressure elevation-volume overload-or augmentation of the alveolar capillary membrane permeability-inflammation. In fact, both mechanisms sometimes coexist and the distinction is irrelevant. There are bibliographic references of pulmonary edema in COVID-19, as well as evidence of volume overload in COVID-19: Lang et al. describes frequent and pronounced vasculature in affected lung areas that may be suggestive of disordered vasoregulation. Eslami et al. observed increased cardiothoracic ratio and it is also described as right ventricular dilatation. In this setting, a different approach emerged: moderate or severe COVID-19 could experience a severe acute pulmonary edema with a "dual hit". A "first hit" of pneumonitis-augmentation of the alveolar capillary membrane permeability-can lead to low hydrostatic pressure pulmonary edema. The "second hit" is high pressure pulmonary edema, caused by increase of hydrostatic pressure secondary to volume overload, a result of dysregulation of the RAAS. This results in a "dual hit" that triggers severe acute pulmonary edema. If this edema is not solved, then a "third hit" appears with secondary inflammation, superinfection, fibrosis and finally the typical ARDS. Consequently, the study group looked for patients with pulmonary edema before ARDS was triggered. Cases of moderate and severe COVID-19 were searched, with tomographic evidence of pulmonary edema: dilated superior vena cava, large pulmonary arteries, diffuse interstitial infiltrates and dilated right ventricle. At the detection of pulmonary edema in patients with COVID-19, a standard treatment consisting of oral hydric restriction and diuretics (NEGBAL approach) was initiated. The effects of furosemide on pulmonary edema were well established decades ago. To date there is no evidence that had suggested the model of pulmonary edema and volume overload secondary to the dysregulation of the renin angiotensin aldosterone system in COVID-19. The objective of this study is to compare patients with COVID-19 undergoing NEGBAL approach with a control group of patients with COVID-19 of similar demographic, clinical, gasometric and tomographic characteristics. Medical records of 120 adult patients were reviewed: demographic; clinical, laboratory; Pro b-type natriuretic peptide (pro-BNP): (negative: below 125 pg/mL); high-sensitivity cardiac troponin (hs-cTnT): (negative: \<14 ng/L); blood gas; chest tomography (CT); oxygen therapy support and mechanical ventilation (MV) requirements, all of which were reviewed and recorded by investigators. With the purpose of knowing the patient's basal hematocrit before COVID-19, prior hematocrit, if any, defined as hematocrit previous to COVID-19 infection (hematocrit prior to admission to NEGBAL) was also reviewed.
Once the NEGBAL strategy began, the clinical, tomographic, gasometric, biochemical evolution was evaluated until the 8th day (until the 12th day for tomography), ICU stay, hospital stay and morbidity and mortality until the 30th day.
Conditions
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COVID-19
Study Design
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Observational Model Type
CASE_CONTROL
Study Time Perspective
RETROSPECTIVE
Study Groups
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NEGBAL
Negative Fluid Balance (NEGBAL) Approach:
COVID-19 patients with tomographic detection of pulmonary edema (dilated superior vena cava, large pulmonary arteries, diffuse interstitial infiltrates with Kerley lines, and dilated right ventricle or dilated cardiac axis) treated with NEGBAL approach. This consisted of oral hydric restriction and use of diuretics (20 mg of furosemide, intravenous bolus, followed by furosemide in endovenous continuous infusion, starting at 60 mg/day).
The objective of this approach was to achieve negative fluid balance, between 600 to 1400 mL/day adjusted to body surface area, with a final target of 8-10% of body weight in up to 8 days. The furosemide dose was titrated considering heart rate and blood pressure, target fluid balance, hematocrit, and serum creatinine.
No interventions assigned to this group
NO-NEGBAL
Treatment for COVID-19 pneumonia in this series were based on standard recommendations.
All patients in this group received dexamethasone 6 mg/day and thromboembolic prevention with enoxaparin 40 mg/day.
Participants in the NO-NEGBAL group, did not received a NEGBAL approach as treatment.
No interventions assigned to this group
Eligibility Criteria
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Inclusion Criteria
* confirmed diagnosis of COVID-19
* PaO2/FiO2 (ratio of arterial oxygen partial pressure to fractional inspired oxygen) \<300;
* Patients over 18 years of age and
* tomographic evidence of acute pulmonary edema, defined as dilated superior vena cava, large pulmonary arteries, diffuse interstitial infiltrates with Kerley lines, and dilated right ventricle or dilated cardiac axis.
Patients subjected to NEGBAL underwent a treatment with furosemide in continuous intravenous infusion, guided by objectives: Negative Fluid Balance approach (NEGBAL).
* confirmed diagnosis of COVID-19 through real-time reverse transcriptase polymerase chain reaction (RT-PCR) assay with samples obtained from nasopharyngeal swab or positive antinucleocapsid immunoglobulin M (IgM) antibodies;
* ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2) \<300;
* age older than 18 years, and
* tomographic evidence of acute pulmonary edema, defined as dilated superior vena cava, large pulmonary arteries, diffuse interstitial infiltrates with Kerley lines, and dilated right ventricle or dilated cardiac axis.
Patients subjected to NO-NEGBAL group, did not receive NEGBAL approach as treatment.
* PaO2/FiO2 (ratio of arterial oxygen partial pressure to fractional inspired oxygen) \<300;
* Patients over 18 years of age and
* tomographic evidence of acute pulmonary edema, defined as dilated superior vena cava, large pulmonary arteries, diffuse interstitial infiltrates with Kerley lines, and dilated right ventricle or dilated cardiac axis.
Patients subjected to NEGBAL underwent a treatment with furosemide in continuous intravenous infusion, guided by objectives: Negative Fluid Balance approach (NEGBAL).
* confirmed diagnosis of COVID-19 through real-time reverse transcriptase polymerase chain reaction (RT-PCR) assay with samples obtained from nasopharyngeal swab or positive antinucleocapsid immunoglobulin M (IgM) antibodies;
* ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2) \<300;
* age older than 18 years, and
* tomographic evidence of acute pulmonary edema, defined as dilated superior vena cava, large pulmonary arteries, diffuse interstitial infiltrates with Kerley lines, and dilated right ventricle or dilated cardiac axis.
Patients subjected to NO-NEGBAL group, did not receive NEGBAL approach as treatment.
Exclusion Criteria
* patients with prior indication of diuretics for another reason,
* renal failure,
* cardiac failure (diagnosis by echocardiography),
* hepatic failure,
* hypernatremia or hyponatremia,
* hypotension or shock.
* renal failure,
* cardiac failure (diagnosis by echocardiography),
* hepatic failure,
* hypernatremia or hyponatremia,
* hypotension or shock.
Minimum Eligible Age
18 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
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Clinica Colon
OTHER
Sponsor Role
lead
Responsible Party
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José Luis Francisco Santos
Chief of Intensive Care Unit
Responsibility Role
PRINCIPAL_INVESTIGATOR
Principal Investigators
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José LF Santos, MD
Role: PRINCIPAL_INVESTIGATOR
Clínica Colón - Mar del Plata - Argentina
Locations
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Clínica Colón
Mar del Plata, Buenos Aires, Argentina
Site Status
Countries
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Argentina
References
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Cui X, Chen W, Zhou H, Gong Y, Zhu B, Lv X, Guo H, Duan J, Zhou J, Marcon E, Ma H. Pulmonary Edema in COVID-19 Patients: Mechanisms and Treatment Potential. Front Pharmacol. 2021 Jun 7;12:664349. doi: 10.3389/fphar.2021.664349. eCollection 2021.
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Mangalmurti N, Hunter CA. Cytokine Storms: Understanding COVID-19. Immunity. 2020 Jul 14;53(1):19-25. doi: 10.1016/j.immuni.2020.06.017. Epub 2020 Jun 28.
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Langer-Gould A, Smith JB, Gonzales EG, Castillo RD, Figueroa JG, Ramanathan A, Li BH, Gould MK. Early identification of COVID-19 cytokine storm and treatment with anakinra or tocilizumab. Int J Infect Dis. 2020 Oct;99:291-297. doi: 10.1016/j.ijid.2020.07.081. Epub 2020 Aug 6.
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Hu B, Huang S, Yin L. The cytokine storm and COVID-19. J Med Virol. 2021 Jan;93(1):250-256. doi: 10.1002/jmv.26232. Epub 2020 Sep 30.
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Fara A, Mitrev Z, Rosalia RA, Assas BM. Cytokine storm and COVID-19: a chronicle of pro-inflammatory cytokines. Open Biol. 2020 Sep;10(9):200160. doi: 10.1098/rsob.200160. Epub 2020 Sep 23.
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BACKGROUND
Marini JJ, Gattinoni L. Management of COVID-19 Respiratory Distress. JAMA. 2020 Jun 9;323(22):2329-2330. doi: 10.1001/jama.2020.6825. No abstract available.
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BACKGROUND
Sinha P, Matthay MA, Calfee CS. Is a "Cytokine Storm" Relevant to COVID-19? JAMA Intern Med. 2020 Sep 1;180(9):1152-1154. doi: 10.1001/jamainternmed.2020.3313. No abstract available.
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Gattinoni L, Coppola S, Cressoni M, Busana M, Rossi S, Chiumello D. COVID-19 Does Not Lead to a "Typical" Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med. 2020 May 15;201(10):1299-1300. doi: 10.1164/rccm.202003-0817LE. No abstract available.
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BACKGROUND
Kuba K, Imai Y, Rao S, Gao H, Guo F, Guan B, Huan Y, Yang P, Zhang Y, Deng W, Bao L, Zhang B, Liu G, Wang Z, Chappell M, Liu Y, Zheng D, Leibbrandt A, Wada T, Slutsky AS, Liu D, Qin C, Jiang C, Penninger JM. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. Nat Med. 2005 Aug;11(8):875-9. doi: 10.1038/nm1267. Epub 2005 Jul 10.
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BACKGROUND
Imai Y, Kuba K, Rao S, Huan Y, Guo F, Guan B, Yang P, Sarao R, Wada T, Leong-Poi H, Crackower MA, Fukamizu A, Hui CC, Hein L, Uhlig S, Slutsky AS, Jiang C, Penninger JM. Angiotensin-converting enzyme 2 protects from severe acute lung failure. Nature. 2005 Jul 7;436(7047):112-6. doi: 10.1038/nature03712.
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Liu Y, Yang Y, Zhang C, Huang F, Wang F, Yuan J, Wang Z, Li J, Li J, Feng C, Zhang Z, Wang L, Peng L, Chen L, Qin Y, Zhao D, Tan S, Yin L, Xu J, Zhou C, Jiang C, Liu L. Clinical and biochemical indexes from 2019-nCoV infected patients linked to viral loads and lung injury. Sci China Life Sci. 2020 Mar;63(3):364-374. doi: 10.1007/s11427-020-1643-8. Epub 2020 Feb 9.
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Santos RA, Ferreira AJ, Simoes E Silva AC. Recent advances in the angiotensin-converting enzyme 2-angiotensin(1-7)-Mas axis. Exp Physiol. 2008 May;93(5):519-27. doi: 10.1113/expphysiol.2008.042002. Epub 2008 Feb 29.
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Chen D, Li X, Song Q, Hu C, Su F, Dai J, Ye Y, Huang J, Zhang X. Assessment of Hypokalemia and Clinical Characteristics in Patients With Coronavirus Disease 2019 in Wenzhou, China. JAMA Netw Open. 2020 Jun 1;3(6):e2011122. doi: 10.1001/jamanetworkopen.2020.11122.
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Connell JM, Davies E. The new biology of aldosterone. J Endocrinol. 2005 Jul;186(1):1-20. doi: 10.1677/joe.1.06017.
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Vaduganathan M, Vardeny O, Michel T, McMurray JJV, Pfeffer MA, Solomon SD. Renin-Angiotensin-Aldosterone System Inhibitors in Patients with Covid-19. N Engl J Med. 2020 Apr 23;382(17):1653-1659. doi: 10.1056/NEJMsr2005760. Epub 2020 Mar 30. No abstract available.
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Gurwitz D. Angiotensin receptor blockers as tentative SARS-CoV-2 therapeutics. Drug Dev Res. 2020 Aug;81(5):537-540. doi: 10.1002/ddr.21656. Epub 2020 Mar 4.
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Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med. 2005 Dec 29;353(26):2788-96. doi: 10.1056/NEJMcp052699. No abstract available.
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Lang M, Som A, Carey D, Reid N, Mendoza DP, Flores EJ, Li MD, Shepard JO, Little BP. Pulmonary Vascular Manifestations of COVID-19 Pneumonia. Radiol Cardiothorac Imaging. 2020 Jun 18;2(3):e200277. doi: 10.1148/ryct.2020200277. eCollection 2020 Jun.
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Eslami V, Abrishami A, Zarei E, Khalili N, Baharvand Z, Sanei-Taheri M. The Association of CT-measured Cardiac Indices with Lung Involvement and Clinical Outcome in Patients with COVID-19. Acad Radiol. 2021 Jan;28(1):8-17. doi: 10.1016/j.acra.2020.09.012. Epub 2020 Oct 1.
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Argulian E, Sud K, Vogel B, Bohra C, Garg VP, Talebi S, Lerakis S, Narula J. Right Ventricular Dilation in Hospitalized Patients With COVID-19 Infection. JACC Cardiovasc Imaging. 2020 Nov;13(11):2459-2461. doi: 10.1016/j.jcmg.2020.05.010. Epub 2020 May 15. No abstract available.
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BACKGROUND
Li YL, Zheng JB, Jin Y, Tang R, Li M, Xiu CH, Dai QQ, Zuo S, Wang HQ, Wang HL, Zhao MY, Ye M, Yu KJ. Acute right ventricular dysfunction in severe COVID-19 pneumonia. Rev Cardiovasc Med. 2020 Dec 30;21(4):635-641. doi: 10.31083/j.rcm.2020.04.159.
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Patil VP, Salunke BG. Fluid Overload and Acute Kidney Injury. Indian J Crit Care Med. 2020 Apr;24(Suppl 3):S94-S97. doi: 10.5005/jp-journals-10071-23401.
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BACKGROUND
Gluecker T, Capasso P, Schnyder P, Gudinchet F, Schaller MD, Revelly JP, Chiolero R, Vock P, Wicky S. Clinical and radiologic features of pulmonary edema. Radiographics. 1999 Nov-Dec;19(6):1507-31; discussion 1532-3. doi: 10.1148/radiographics.19.6.g99no211507.
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Gandhi SK, Powers JC, Nomeir AM, Fowle K, Kitzman DW, Rankin KM, Little WC. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med. 2001 Jan 4;344(1):17-22. doi: 10.1056/NEJM200101043440103.
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BACKGROUND
Pan F, Ye T, Sun P, Gui S, Liang B, Li L, Zheng D, Wang J, Hesketh RL, Yang L, Zheng C. Time Course of Lung Changes at Chest CT during Recovery from Coronavirus Disease 2019 (COVID-19). Radiology. 2020 Jun;295(3):715-721. doi: 10.1148/radiol.2020200370. Epub 2020 Feb 13.
Reference Type
BACKGROUND
Santos JLF, Zanardi P, Alo V, Rodriguez M, Magdaleno F, De Langhe V, Dos Santos V, Murialdo G, Villoldo A, Coria M, Quiros D, Milicchio C, Garcia Saiz E. Pulmonary Edema in COVID-19 Treated with Furosemide and Negative Fluid Balance (NEGBAL): A Different and Promising Approach. J Clin Med. 2021 Nov 28;10(23):5599. doi: 10.3390/jcm10235599.
Reference Type
BACKGROUND
Other Identifiers
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UTI-ESI-002
Identifier Type: -
Identifier Source: org_study_id
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UNKNOWN
Ultrasound in Acute Dyspnea in the Field
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COMPLETED
Exhaled Breath Particles as a Clinical Indicator for Lung Injury and Acute Respiratory Distress Syndrome (ARDS)
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UNKNOWN
RALE Versus CORADS/CT-Severity Score in COVID-19
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COMPLETED
Portable Ultrasound to Predict Heart Failure Readmission Risk
NCT05980533
WITHDRAWN
NA