Cardiac ArrestNCT02785224
Arterial Pressure and Stress-Dose Steroids in Cardiac Arrest.
An observational study of Cardiac Arrest, run by University of Athens at 3 sites in Greece.
Trial summary
Early stress-dose steroids are of uncertain efficacy in cardiac arrest. The current authors plan to conduct a pertinent mediation analysis using prospectively collected data from 2 prior randomized clinical trials of in-hospital cardiac arrest. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Cardiac Arrest
- What is being tested?
- Vasopressin Steroids Epinephrine
- How many people
- 0 participants
- Where
- 3 sitesGreece
- Study dates
- Dec 2025to Dec 2026
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Adult patients with vasopressor-requiring, inhospital cardiac arrest, i.e., with asystole, pulseless electrical activity, or ventricular fibrillation/pulseless ventricular tachycardia not responsive to two attempts at defibrillation. Patients have already participated in 2 prior RCTs (references 3 and 4). Thus, the below-provided Eligibility Criteria are the Criteria already employed by the prior RCTs.
Who may be able to join
- Adult patients with vasopressor-requiring inhospital cardiac arrest according to guidelines for resuscitation 2005, defined as:
- epinephrine requirement for ventricular fibrillation/tachycardia
- or asystole, or
- pulseless electrical activity
Who cannot join
- Age < 18 years;
- Terminal illness or do-not resuscitate status;
- Cardiac arrest due to exsanguination;
- Cardiac arrest before hospital admission;
- Pre-arrest treatment with intravenous corticosteroids;
- Previous enrollment in or exclusion from the 2 studies included in the analysis.
Trial locations and contacts
3 sites in 1 country.
Greece3 sites
Evaggelismos General Hospital
Athens, Attica, 10676
401 General Military Hospital of Athens
Athens, Attica, GR-11526
Larisa University General Hospital
Larissa, Thessaly, GR-41110
About this study
Official title: Arterial Pressure and Stress-Dose Steroids in In-hospital Cardiac Arrest: a Mediation Analysis of Prior Randomized Clinical Trial Data.
Early stress-dose steroids are of uncertain efficacy in cardiac arrest. The current authors plan to conduct a pertinent mediation analysis using prospectively collected data from 2 prior randomized clinical trials of in-hospital cardiac arrest. These trials reported positive results on the vasopressin-steroids-epinephrine (VSE) combination. The current analysis is aimed at identifying mediators of the benefit associated with VSE, potentially attributable to its stress-dose steroid subcomponent. Tested mediators will include arterial pressure in the early postresuscitation period (primary), and arterial blood lactate in the early postresuscitation period and renal failure free days (secondary).
Read the detailed description
BACKGROUND AND RATIONALE The usefulness of stress-dose hydrocortisone in cardiac arrest is uncertain, especially when its administration starts at 10 hours after the return of spontaneous circulation (ROSC) (1). Such delay, probably exceeds the therapeutic window for the prevention of detrimental episodes of postresuscitation hypotension (2) through a steroid-induced hemodynamic stabilization (3,4).
In the context of NCT02408939, recent post hoc exploratory analyses in postresuscitation shock (n=191) showed an improved early post-ROSC hemodynamic profile in patients treated with the vasopressin-steroids-epinephrine (VSE) combination. Pooled data originated from our prior VSE 1 and VSE 2 randomized clinical trials (RCTs) (3,4) Recordings of "early post-ROSC systolic arterial pressure (SAP) >90" mmHg [i.e. "absence of early postresuscitation hypotension" (2)], and "≥1 recorded/analyzed, day-1 mean arterial pressure (MAP) value of >80mmHg (2)," were significantly more frequent in VSE patients vs. controls. After considering the short vasopressin half-life of 24 min and that the VSE protocol mandates vasopressin use solely during cardiopulmonary resuscitation (CPR) (3,4), we postulate that the more frequent "day-1 MAP>80 mmHg" can be attributed to the MAP-stabilizing effects of early stress-dose steroids (3,4). Under this assumption, a mediation analysis of VSE outcome benefits through day-1 MAP might further address the knowledge gap of steroids' usefulness in cardiac arrest (5).
METHODS Study Design. Intention-to-treat, retrospective analysis of prospectively collected data from two RCTs (3,4). Study participants were hospitalized in intensive or coronary care units (ICUs or CCUs) of three tertiary care centers: Evaggelismos General Hospital and 401 Greek Army Hospital (both in Athens, Greece), and University Hospital of Larissa, Larissa, Greece.
Ethics and Approval. The present analysis of de-identified, previously collected and electronically stored patient data (see also Detailed Descriptions of NCT00729794 and NCT02408939) is not associated with any clinical intervention, and therefore, the investigators have applied for a waiver of informed consent from either the patient or his/her next of kin.
Analysis Endpoints are presented in the dedicated subsection. Patients. The reference study population consists of 368 patients (Evaggelismos Hospital, n=288/368=78.2%) with in-hospital cardiac arrest, who required epinephrine during CPR according to the 2005 Guidelines for Resuscitation (6). During CPR, VSE group patients (n=178) also received vasopressin and methylprednisolone and controls (n=190) the respective saline placebos. At 4 hours after CPR, there were 211 surviving patients (VSE group, n=115), who were evaluated for postresuscitation shock (3,4). One hundred three VSE group patients were then assigned to stress-dose hydrocortisone and 88 controls to saline placebo. Of the 103 VSE group patients, 102 received stress-dose hydrocortisone, whereas 1 did not because of study pharmacist error; of the 88 control group patients, 73 actually received saline placebo, whereas 15 received open-label stress-dose hydrocortisone by protocol violation and according to the orders of their attending physicians (4).
Multivariable Analysis - Effect Modifiers In addition to variables described in the Outcomes subsection, the multivariable analysis will include the following potential effect modifiers: Data Source (VSE2 vs. VSE1 study), Study Center (4), group (VSE vs, control), cardiac arrest cause (cardiac vs. non-cardiac), area of cardiac arrest occurrence (monitored vs. non-monitored), initial cardiac arrest rhythm (shockable vs. non-shockable) atropine use (yes vs. no), prescribed total dose of sodium bicarbonate, cardiac arrest occurrence on holiday vs. working day; Cardiac arrest occurrence at night (23:00-07:00) vs. morning-to-late evening (07:00-23:00), total dose of epinephrine during CPR, and therapeutic hypothermia (use vs. no use).
All analyses will be conducted with SPSS version 22.0 (IBM, Armonk, NY) and the Process Procedure for SPSS, release 2.15. Statistical methodology reference: Hayes AF. Part II, Mediation Analysis. In: Hayes AF, ed. Introduction to Mediation, Moderation, and Conditional Process Analysis. A Regression-based Approach. The Guilford Press, New York. 2013, 3-419. 85-207.
- Conditions
- Cardiac Arrest
- Being tested
- Vasopressin Steroids Epinephrine
- Medical subject headings
- Heart Arrest
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Vasopressin Steroids EpinephrineDrug
Also called VSE
Vasopressin Steroids Epinephrine: Vasopressin (up to 5 doses of 20 IU) and methylprednisolone (single dose - 40 mg) in addition to epinephrine during cardiopulmonary resuscitation, and stress dose hydrocortisone (300 mg/day for 7 days maximum followed by gradual taper) for postresuscitation shock.
| Study group | Role | What they receive |
|---|---|---|
| Vasopressin Steroids Epinephrine (VSE) | Patients with in-hospital cardiac arrest treated with vasopressin, methylprednisolone, and epinephrine during cardiopulmonary resuscitation, and also with stress-dose hydrocortisone for postresuscitation shock. Receives: Drug: Vasopressin Steroids Epinephrine | |
| Control | Patients with in-hospital cardiac arrest treated with normal saline placebo, normal saline placebo, and epinephrine during cardiopulmonary resuscitation, and also with normal saline placebo for postresuscitation shock. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Early postresuscitation systolic arterial pressure (SAP) as mediator of observed intervention benefit.
Determination of the possible mediating role of SAP with respect to the observed vasopressin-steroids-epinephrine (VSE) outcome benefit. Multivariable mediation analysis of the following possible relationship: VSE intervention - postresuscitation SAP>90 mmHg at 20 min post-ROSC - Survival with good neurological recovery i.e. Cerebral Performance Category (CPC) score of 1 or 2.This will result in the primary mediation analysis "SAP" model.
Measured: 20 min after return of spontaneous circulation (ROSC)
Early postresuscitation mean arterial pressure (MAP) as mediator of observed intervention benefit
Determination of the possible mediating role of MAP with respect to the observed VSE outcome benefit. Multivariable mediation analysis of the following possible relationship: VSE intervention - at least 1 day-1 postrandomization MAP value>80 mmHg - Survival with good neurological recovery i.e. CPC score of 1 or 2. This will result in the primary mediation analysis "MAP" model.
Measured: 24 hours after ROSC
Secondary outcomes (6)
Renal failure free days and SAP
Addition of renal failure free days to the primary mediation analysis "SAP" model - this will result in a first "multiple mediator" SAP model.
Measured: Days 1-60 after ROSC
Renal failure free days and MAP
Addition of renal failure free days to the primary mediation analysis "MAP" model - this will result in a first "multiple mediator" MAP model.
Measured: Days 1-60 after ROSC
Arterial blood lactate level > 4.65 mmol/L at 4 hours post-ROSC and SAP
Addition of arterial blood lactate at 4 hours post-ROSC > 4.65 mmol/L (median value in 191 patients) to the first "multiple mediator" SAP model - this will result in the second "multiple mediator" SAP model.
Measured: 4 hours post-ROSC
Arterial blood lactate level > 4.65 mmol/L at 4 hours post-ROSC and MAP
Addition of arterial blood lactate at 4 hours post-ROSC > 4.65 mmol/L (median value in 191 patients) to the first "multiple mediator" MAP model - this will result in the second "multiple mediator" MAP model.
Measured: 4 hours post-ROSC
Arterial blood lactate level > 2.80 mmol/L at 4 hours post-ROSC and SAP
Addition of arterial blood lactate at 4 hours post-ROSC > 2.80 mmol/L (lower bound of interquartile range in 191 patients) to the first "multiple mediator" SAP model - this will result in the third "multiple mediator" SAP model.
Measured: 4 hours post-ROSC
Arterial blood lactate level > 2.80 mmol/L at 4 hours post-ROSC and MAP
Addition of arterial blood lactate at 4 hours post-ROSC > 2.80 mmol/L (lower bound of interquartile range in 191 patients) to the first "multiple mediator" MAP model - this will result in the third "multiple mediator" MAP model.
Measured: 4 hours post-ROSC
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted27 May 2016 (estimated)
- Study startDec 2025 (estimated)
- Primary completionDec 2026 (estimated)
- Study completionDec 2026 (estimated)
Why it stopped: No funding could be obtained for this study
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (6)Papers the sponsor has linked to this study.
- Other trials for Cardiac ArrestStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Other
- Time perspective
- Retrospective
- Enrolment
- 0 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Athens
- Sponsor type
- University, hospital or other
- Collaborators
- University of Thessaly
- Responsible party
- Principal investigator, Spyros D. Mentzelopoulos, University of Athens
- Investigators
- Spyros D. Mentzelopoulos, MD, PhD, Principal investigator, University of AthensSpyros G. Zakynthinos, MD, PhD, Study chair, University of Athens
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02785224
- Sponsor's protocol ID
- AP-MEDIATION-15516/23/5/16
- Status last verified
- Mar 2025
- First submitted
- 22 May 2016
- Last updated
- 30 Mar 2025
- Results posted
- No
- Data monitoring committee
- No
- Individual data sharing
- No
Publications
Donnino MW, Andersen LW, Berg KM, Chase M, Sherwin R, Smithline H, Carney E, Ngo L, Patel PV, Liu X, Cutlip D, Zimetbaum P, Cocchi MN; Collaborating Authors from the Beth Israel Deaconess Medical Center's Center for Resuscitation Science Research Group. Corticosteroid therapy in refractory shock following cardiac arrest: a randomized, double-blind, placebo-controlled, trial. Crit Care. 2016 Apr 3;20:82. doi: 10.1186/s13054-016-1257-x.
PubMed 27038920Trzeciak S, Jones AE, Kilgannon JH, Milcarek B, Hunter K, Shapiro NI, Hollenberg SM, Dellinger P, Parrillo JE. Significance of arterial hypotension after resuscitation from cardiac arrest. Crit Care Med. 2009 Nov;37(11):2895-903; quiz 2904. doi: 10.1097/ccm.0b013e3181b01d8c.
PubMed 19866506Link MS, Berkow LC, Kudenchuk PJ, Halperin HR, Hess EP, Moitra VK, Neumar RW, O'Neil BJ, Paxton JH, Silvers SM, White RD, Yannopoulos D, Donnino MW. Part 7: Adult Advanced Cardiovascular Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015 Nov 3;132(18 Suppl 2):S444-64. doi: 10.1161/CIR.0000000000000261. No abstract available.
PubMed 26472995Nolan JP, Deakin CD, Soar J, Bottiger BW, Smith G; European Resuscitation Council. European Resuscitation Council guidelines for resuscitation 2005. Section 4. Adult advanced life support. Resuscitation. 2005 Dec;67 Suppl 1:S39-86. doi: 10.1016/j.resuscitation.2005.10.009. No abstract available.
PubMed 16321716Mentzelopoulos SD, Zakynthinos SG, Tzoufi M, Katsios N, Papastylianou A, Gkisioti S, Stathopoulos A, Kollintza A, Stamataki E, Roussos C. Vasopressin, epinephrine, and corticosteroids for in-hospital cardiac arrest. Arch Intern Med. 2009 Jan 12;169(1):15-24. doi: 10.1001/archinternmed.2008.509.
PubMed 19139319Mentzelopoulos SD, Malachias S, Chamos C, Konstantopoulos D, Ntaidou T, Papastylianou A, Kolliantzaki I, Theodoridi M, Ischaki H, Makris D, Zakynthinos E, Zintzaras E, Sourlas S, Aloizos S, Zakynthinos SG. Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial. JAMA. 2013 Jul 17;310(3):270-9. doi: 10.1001/jama.2013.7832.
PubMed 23860985
Study at a glance
From the registry record, last updated by the sponsor on 30 Mar 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Arterial Pressure and Stress-Dose Steroids in In-hospital Cardiac Arrest: a Mediation Analysis of Prior Randomized Clinical Trial Data.
- ClinicalTrials.gov ID
- NCT02785224
- Acronym / sponsor ID
- AP-MEDIATION-15516/23/5/16
- Conditions
- Cardiac Arrest
- Study type
- Observational
- Recruitment status
- WithdrawnReason stopped: No funding could be obtained for this study
- Enrolment
- 0 participants (actual)
- Lead sponsor
- University of AthensUniversity, hospital or other
- Collaborators
- University of Thessaly
- Study start
- Dec 2025 (estimated)
- Primary completion
- Dec 2026 (estimated)
- Study completion
- Dec 2026 (estimated)
- First posted
- 27 May 2016 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Early stress-dose steroids are of uncertain efficacy in cardiac arrest. The current authors plan to conduct a pertinent mediation analysis using prospectively collected data from 2 prior randomized clinical trials of in-hospital cardiac arrest. These trials reported positive results on the vasopressin-steroids-epinephrine (VSE) combination. The current analysis is aimed at identifying mediators of the benefit associated with VSE, potentially attributable to its stress-dose steroid subcomponent. Tested mediators will include arterial pressure in the early postresuscitation period (primary), and arterial blood lactate in the early postresuscitation period and renal failure free days (secondary).
Detailed description
BACKGROUND AND RATIONALE The usefulness of stress-dose hydrocortisone in cardiac arrest is uncertain, especially when its administration starts at 10 hours after the return of spontaneous circulation (ROSC) (1). Such delay, probably exceeds the therapeutic window for the prevention of detrimental episodes of postresuscitation hypotension (2) through a steroid-induced hemodynamic stabilization (3,4).
In the context of NCT02408939, recent post hoc exploratory analyses in postresuscitation shock (n=191) showed an improved early post-ROSC hemodynamic profile in patients treated with the vasopressin-steroids-epinephrine (VSE) combination. Pooled data originated from our prior VSE 1 and VSE 2 randomized clinical trials (RCTs) (3,4) Recordings of "early post-ROSC systolic arterial pressure (SAP) >90" mmHg [i.e. "absence of early postresuscitation hypotension" (2)], and "≥1 recorded/analyzed, day-1 mean arterial pressure (MAP) value of >80mmHg (2)," were significantly more frequent in VSE patients vs. controls. After considering the short vasopressin half-life of 24 min and that the VSE protocol mandates vasopressin use solely during cardiopulmonary resuscitation (CPR) (3,4), we postulate that the more frequent "day-1 MAP>80 mmHg" can be attributed to the MAP-stabilizing effects of early stress-dose steroids (3,4). Under this assumption, a mediation analysis of VSE outcome benefits through day-1 MAP might further address the knowledge gap of steroids' usefulness in cardiac arrest (5).
METHODS Study Design. Intention-to-treat, retrospective analysis of prospectively collected data from two RCTs (3,4). Study participants were hospitalized in intensive or coronary care units (ICUs or CCUs) of three tertiary care centers: Evaggelismos General Hospital and 401 Greek Army Hospital (both in Athens, Greece), and University Hospital of Larissa, Larissa, Greece.
Ethics and Approval. The present analysis of de-identified, previously collected and electronically stored patient data (see also Detailed Descriptions of NCT00729794 and NCT02408939) is not associated with any clinical intervention, and therefore, the investigators have applied for a waiver of informed consent from either the patient or his/her next of kin.
Analysis Endpoints are presented in the dedicated subsection. Patients. The reference study population consists of 368 patients (Evaggelismos Hospital, n=288/368=78.2%) with in-hospital cardiac arrest, who required epinephrine during CPR according to the 2005 Guidelines for Resuscitation (6). During CPR, VSE group patients (n=178) also received vasopressin and methylprednisolone and controls (n=190) the respective saline placebos. At 4 hours after CPR, there were 211 surviving patients (VSE group, n=115), who were evaluated for postresuscitation shock (3,4). One hundred three VSE group patients were then assigned to stress-dose hydrocortisone and 88 controls to saline placebo. Of the 103 VSE group patients, 102 received stress-dose hydrocortisone, whereas 1 did not because of study pharmacist error; of the 88 control group patients, 73 actually received saline placebo, whereas 15 received open-label stress-dose hydrocortisone by protocol violation and according to the orders of their attending physicians (4).
Multivariable Analysis - Effect Modifiers In addition to variables described in the Outcomes subsection, the multivariable analysis will include the following potential effect modifiers: Data Source (VSE2 vs. VSE1 study), Study Center (4), group (VSE vs, control), cardiac arrest cause (cardiac vs. non-cardiac), area of cardiac arrest occurrence (monitored vs. non-monitored), initial cardiac arrest rhythm (shockable vs. non-shockable) atropine use (yes vs. no), prescribed total dose of sodium bicarbonate, cardiac arrest occurrence on holiday vs. working day; Cardiac arrest occurrence at night (23:00-07:00) vs. morning-to-late evening (07:00-23:00), total dose of epinephrine during CPR, and therapeutic hypothermia (use vs. no use).
All analyses will be conducted with SPSS version 22.0 (IBM, Armonk, NY) and the Process Procedure for SPSS, release 2.15. Statistical methodology reference: Hayes AF. Part II, Mediation Analysis. In: Hayes AF, ed. Introduction to Mediation, Moderation, and Conditional Process Analysis. A Regression-based Approach. The Guilford Press, New York. 2013, 3-419. 85-207.
Study design
- Observational model
- Other
- Time perspective
- Retrospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Vasopressin Steroids Epinephrine (VSE) | – | Drug: Vasopressin Steroids EpinephrinePatients with in-hospital cardiac arrest treated with vasopressin, methylprednisolone, and epinephrine during cardiopulmonary resuscitation, and also with stress-dose hydrocortisone for postresuscitation shock. |
| Control | – | –Patients with in-hospital cardiac arrest treated with normal saline placebo, normal saline placebo, and epinephrine during cardiopulmonary resuscitation, and also with normal saline placebo for postresuscitation shock. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Adult patients with vasopressor-requiring, inhospital cardiac arrest, i.e., with asystole, pulseless electrical activity, or ventricular fibrillation/pulseless ventricular tachycardia not responsive to two attempts at defibrillation. Patients have already participated in 2 prior RCTs (references 3 and 4). Thus, the below-provided Eligibility Criteria are the Criteria already employed by the prior RCTs.
Key inclusion criteria (4 listed)
- Adult patients with vasopressor-requiring inhospital cardiac arrest according to guidelines for resuscitation 2005, defined as:
- epinephrine requirement for ventricular fibrillation/tachycardia
- or asystole, or
- pulseless electrical activity
Key exclusion criteria (6 listed)
- Age < 18 years;
- Terminal illness or do-not resuscitate status;
- Cardiac arrest due to exsanguination;
- Cardiac arrest before hospital admission;
- Pre-arrest treatment with intravenous corticosteroids;
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Vasopressin Steroids EpinephrineAlso: VSEVasopressin Steroids Epinephrine: Vasopressin (up to 5 doses of 20 IU) and methylprednisolone (single dose - 40 mg) in addition to epinephrine during cardiopulmonary resuscitation, and stress dose hydrocortisone (300 mg/day for 7 days maximum followed by gradual taper) for postresuscitation shock. | Drug | Vasopressin Steroids Epinephrine (VSE) |
Primary outcome
Early postresuscitation systolic arterial pressure (SAP) as mediator of observed intervention benefit.
Time frame: 20 min after return of spontaneous circulation (ROSC)
Determination of the possible mediating role of SAP with respect to the observed vasopressin-steroids-epinephrine (VSE) outcome benefit. Multivariable mediation analysis of the following possible relationship: VSE intervention - postresuscitation SAP>90 mmHg at 20 min post-ROSC - Survival with good neurological recovery i.e. Cerebral Performance Category (CPC) score of 1 or 2.This will result in the primary mediation analysis "SAP" model.
Early postresuscitation mean arterial pressure (MAP) as mediator of observed intervention benefit
Time frame: 24 hours after ROSC
Determination of the possible mediating role of MAP with respect to the observed VSE outcome benefit. Multivariable mediation analysis of the following possible relationship: VSE intervention - at least 1 day-1 postrandomization MAP value>80 mmHg - Survival with good neurological recovery i.e. CPC score of 1 or 2. This will result in the primary mediation analysis "MAP" model.
6 secondary outcomes
Renal failure free days and SAP
Time frame: Days 1-60 after ROSC
Renal failure free days and MAP
Time frame: Days 1-60 after ROSC
Arterial blood lactate level > 4.65 mmol/L at 4 hours post-ROSC and SAP
Time frame: 4 hours post-ROSC
Arterial blood lactate level > 4.65 mmol/L at 4 hours post-ROSC and MAP
Time frame: 4 hours post-ROSC
Arterial blood lactate level > 2.80 mmol/L at 4 hours post-ROSC and SAP
Time frame: 4 hours post-ROSC
Arterial blood lactate level > 2.80 mmol/L at 4 hours post-ROSC and MAP
Time frame: 4 hours post-ROSC
Results and safety
The study was withdrawn before enrolling participants, so there are no results.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 30 Mar 2025.
- Background: PubMed 27038920Donnino MW, Andersen LW, Berg KM, Chase M, Sherwin R, Smithline H, Carney E, Ngo L, Patel PV, Liu X, Cutlip D, Zimetbaum P, Cocchi MN; Collaborating Authors from the Beth Israel Deaconess Medical Center's Center for Resuscitation Science Research Group. Corticosteroid therapy in refractory shock following cardiac arrest: a randomized, double-blind, placebo-controlled, trial. Crit Care. 2016 Apr 3;20:82. doi: 10.1186/s13054-016-1257-x.
- Background: PubMed 19866506Trzeciak S, Jones AE, Kilgannon JH, Milcarek B, Hunter K, Shapiro NI, Hollenberg SM, Dellinger P, Parrillo JE. Significance of arterial hypotension after resuscitation from cardiac arrest. Crit Care Med. 2009 Nov;37(11):2895-903; quiz 2904. doi: 10.1097/ccm.0b013e3181b01d8c.
- Background: PubMed 26472995Link MS, Berkow LC, Kudenchuk PJ, Halperin HR, Hess EP, Moitra VK, Neumar RW, O'Neil BJ, Paxton JH, Silvers SM, White RD, Yannopoulos D, Donnino MW. Part 7: Adult Advanced Cardiovascular Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015 Nov 3;132(18 Suppl 2):S444-64. doi: 10.1161/CIR.0000000000000261. No abstract available.
- Background: PubMed 16321716Nolan JP, Deakin CD, Soar J, Bottiger BW, Smith G; European Resuscitation Council. European Resuscitation Council guidelines for resuscitation 2005. Section 4. Adult advanced life support. Resuscitation. 2005 Dec;67 Suppl 1:S39-86. doi: 10.1016/j.resuscitation.2005.10.009. No abstract available.
- Results publication: PubMed 19139319Mentzelopoulos SD, Zakynthinos SG, Tzoufi M, Katsios N, Papastylianou A, Gkisioti S, Stathopoulos A, Kollintza A, Stamataki E, Roussos C. Vasopressin, epinephrine, and corticosteroids for in-hospital cardiac arrest. Arch Intern Med. 2009 Jan 12;169(1):15-24. doi: 10.1001/archinternmed.2008.509.
- Results publication: PubMed 23860985Mentzelopoulos SD, Malachias S, Chamos C, Konstantopoulos D, Ntaidou T, Papastylianou A, Kolliantzaki I, Theodoridi M, Ischaki H, Makris D, Zakynthinos E, Zintzaras E, Sourlas S, Aloizos S, Zakynthinos SG. Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial. JAMA. 2013 Jul 17;310(3):270-9. doi: 10.1001/jama.2013.7832.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Spyros D. Mentzelopoulos, MD, PhD principal investigator
University of Athens
Spyros G. Zakynthinos, MD, PhD study chair
University of Athens
3 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Cardiac Arrest, run by University of Athens at 3 sites in Greece.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 6 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: withdrawn, as of the sponsor's last update on 30 Mar 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 3 sites in Greece. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study was withdrawn before enrolling participants, so there are no results.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Early postresuscitation systolic arterial pressure (SAP) as mediator of observed intervention benefit. (time frame: 20 min after return of spontaneous circulation (ROSC)). The study lists 2 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02785224, which also lists 6 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 30 Mar 2025.