SepsisCOMTESSNCT06294730
COronary Microcirculation and Troponin Elevation in Septic Shock
An observational study of Sepsis and Myocardial Injury, run by Karolinska Institutet at 1 site in Sweden.
Trial summary
Plasma cardiac troponin (cTn) elevation is an indicator of increased mortality in patients with sepsis yet the underlying cause of troponin elevation in sepsis is not known. The COMTESS study investigates whether elevated high-sensitive cardiac Troponin T (hs-cTnT) levels in hemodynamically unstable patients with… Read more about this study
- Who is it for?
- Ages 40 to 85 years
- Conditions the study is for
- Sepsis, Myocardial Injury, Coronary Microvascular Dysfunction
- How many people
- 62 participants
- Where
- 1 siteSweden
- Study dates
- 13 Jun 2019to 28 Feb 2025
- 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 40 to 85 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Sepsis- or septic shock-patients with a life expectancy of >1year and non-normal high-sensitive cardiac troponin T values (>15 ng/L)
Who may be able to join
- Patients fulfilling the Sepsis-3 definition of and diagnostic criteria for sepsis or septic shock
- Age 40 - 85 years
- Life expectancy > 1 year
- hs-cTnT values >15 ng/L
Who cannot join
- pregnancy
- previous medical history of coronary artery by-pass grafting
- heart transplant
- previously verified ejection fraction (EF) ≤39% prior to hospital admission
- Hypertrophic cardiomyopathy (Septum > 15 mm)
- severe aortic stenosis
Show all 11Show fewer
- amyloidosis or sarcoidosis with myocardial engagement
- estimated glomerular filtration rate (eGFR) <30 mL/min/1.73m2 prior to hospital admission
- asthma
- infectious endocarditis
- a medical history of abdominal, thoracic, or orthopaedic surgery within the last three months prior to hospital admission.
Trial locations and contacts
1 site in 1 country.
Sweden1 site
Karolinska Institutet, Danderyd University Hospital
Stockholm, 182 88
About this study
Official title: Coronary Microcirculation and Troponin Elevation in Septic Shock
Plasma cardiac troponin (cTn) elevation is an indicator of increased mortality in patients with sepsis yet the underlying cause of troponin elevation in sepsis is not known. The COMTESS study investigates whether elevated high-sensitive cardiac Troponin T (hs-cTnT) levels in hemodynamically unstable patients with sepsis can be explained by an underlying coronary artery disease or a process within the coronary microcirculation. Fifty patients with sepsis and with hs-cTnT elevation (>15 ng/L) will undergo coronary angiography, including an assessment of coronary flow using a method called thermo-dilution to record the index of microcirculatory resistance (IMR) in the left anterior descending artery (LAD). The relationship between IMR and hs-cTnT will subsequently be analysed. It is important to identify the underlying causes of elevated cTn during sepsis to target further research with an aim to improve the survival in patients suffering from this condition.
Read the detailed description
Severe sepsis and septic shock are frequent primary causes of morbidity and mortality in intensive care units worldwide with a mortality rate of 28.3 - 41.1%. Our research group has previously shown that increasing level of high-sensitive cardiac troponin T (hs-cTnT) taken in sepsis patients is associated with 30-day and one-year mortality. Importantly, our group showed that hs-cTnT is also associated with mortality during the convalescence phase (30-365-day) in sepsis survivors.
Serum cardiac troponin (cTn) measurement is used to detect myocardial injury in patients with acute ischemic heart disease. Cardiac-specific troponins (troponin I and T) are, under normal physiological conditions, only detectable in the blood in small concentrations. In the event of myocyte damage, cardiac-specific troponins I and T enter the systemic circulation and can be detected and measured using modern immunoassay methods. This has led to the use of these biomarkers to identify both the presence and even estimated extent of myocardial injury which can then in turn facilitate an early risk stratification and identification of patients suitable for coronary intervention. Since 2018, the high-sensitive cardiac troponin assays have become the recommended assays for use within the clinical setting. In stark contrast to the treatment of patients with acute myocardial infarction and elevated cTn levels, there are currently no clinical guidelines to help physicians treat, investigate or follow-up sepsis patients with sepsis-related myocardial injury.
The COMTESS study is a pioneering observational prospective clinical study of 50 critically ill sepsis patients with a sampled hs-cTnT >15 ng/L investigating the relationship between hs-cTnT level and concurrent microvascular dysfunction. Following informed consent, coronary angiography with measurements of coronary flow reserve (CFR), basal resistance index (BRI) and index of microcirculatory resistance (IMR) using thermo-dilution in the left anterior descending artery (LAD) is performed in each patient to ascertain underlying coronary microvascular dysfunction (CMVD). Fractional flow reserve (FFR) will be measured in cases where there is a coronary stenosis in the LAD. A research echocardiography is also performed on day 2-10 to examine right and left ventricular function.
Our primary hypothesis is that increasing level of hs-cTnT is associated with increasing level of CMVD in patients with sepsis and that myocardial injury thus contributes to excess death in sepsis and sepsis-survivors. The mechanisms behind myocardial injury in sepsis are not known. Disturbed sublingual microcirculatory alterations are associated with mortality in septic shock, but whether these alterations in proxy vessels translates to clinically relevant CMVD and myocardial injury in patients with sepsis is not known.
The physiological properties of endothelial cells (ECs) in the microcirculation are dependent on a complex carbohydrate-rich layer covering the EC luminal surface called the glycocalyx. Studies have shown that the disseminated dysfunctional immune response which is the hallmark of sepsis causes glycocalyx and EC injury and widespread coagulopathy leading to microvascular thrombosis. Pro-thrombotic components (e.g., neutrophile extracellular traps [NETs], and prothrombin) and components from EC and glycocalyx damage (e.g., Syndecan-1, thrombomodulin) can subsequently be analysed in plasma. Elevated level of Syndecan-1 in sepsis is associated with greater risk of death. Blood samples will be drawn during the coronary angiography for each patient and will be stored in a biobank. Our aim is to investigate if there is an association between plasma level of different microvascular components in relation to IMR level.
- Keywords
- sepsis, cardiac troponin, myocardial injury, coronary microvascular dysfunction, Index of microcirculatory resistance, survival
- Medical subject headings
- Sepsis
What is being measured
The primary outcome is the main question the study is designed to answer.
Relationship between hs-cTnT and IMR
Spline regression between the highest hs-cTnT at 0-72 hrs from vasopressor initiation and IMR at day 2-10 from sepsis onset
Measured: Day 2-10 from the onset of sepsis symptoms.
Secondary outcomes (10)
Relationship between hs-cTnT and CFR
Spline regression between the highest log hs-cTnT at 0-72 hrs from vasopressor initiation and CFR at day 2-10 from sepsis onset
Measured: Day 2-10 from the onset of sepsis symptoms.
Relationship between hs-cTnT and BRI
Spline regression between the highest hs-cTnT at 0-72 hrs from vasopressor initiation and and BRI at day 2-10 from sepsis onset
Measured: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and number of diseased epicardial coronary vessels
ANOVA for the relationship between the highest hs-cTnT at 0-72 hrs from vasopressor initiation and number of diseased epicardial coronary vessels
Measured: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and Synergy Between PCI With Taxus and Cardiac Surgery (SYNTAX)-score
Spline regression between the highest hs-cTnT at 0-72 hrs from vasopressor initiation and SYNTAX-score
Measured: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and left ventricular end diastolic pressure (LVEDP)
Spline regression between the highest hs-cTnT at 0-72 hrs from vasopressor initiation and LVEDP (mmHg)
Measured: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and Tricuspid annular plane systolic excursion (TAPSE)
Spline regression between the highest hs-cTnT at 0-72 hrs and Tricuspid annular plane systolic excursion TAPSE (mm)
Measured: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and echocardiographic measurements of left ventricular global strain
Spline regression between the highest hs-cTnT at 0-72 hrs from vasopressor initiation and left ventricular global strain from speckle tracking (units)
Measured: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and echocardiographic measurements of left diastolic dysfunction
ANOVA between the highest hs-cTnT at 0-72 hrs from vasopressor initiation and left ventricular diastolic function grouping (none; grade I, impaired relaxation; grade II, pseudonormalization; grade III, restrictive filling)
Measured: Day 2-10 from the onset of sepsis symptoms
Relationship between measures of endothelial dysfunction and IMR
Spline regression between plasma levels of syndecan-1 and IMR (units)
Measured: Day 2-10 from the onset of sepsis symptoms
Relationship between measures NETs and IMR
Spline regression between NETs in plasma and IMR
Measured: Day 2-10 from the onset of sepsis symptoms
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted5 Mar 2024
- Study start13 Jun 2019
- Primary completion20 Dec 2024
- Study completion28 Feb 2025
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (17)Papers the sponsor has linked to this study.
- Other trials for SepsisStudies of the same condition, open and under way.
- More trials run by Karolinska InstitutetThe sponsor's other registered studies.
- 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
- Cohort
- Time perspective
- Prospective
- Enrolment
- 62 participants (actual)
Sponsor and investigators
- Lead sponsor
- Karolinska Institutet
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Jonas Persson, Karolinska Institutet
- Investigators
- Jonas Persson, MD, PhD, Principal investigator, Karolinska Institutet Danderyd University Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06294730
- Sponsor's protocol ID
- 2018/1891-31
- Acronym
- COMTESS
- Status last verified
- Jun 2025
- First submitted
- 16 Feb 2024
- Last updated
- 29 Jun 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Yes: Will be provided upon reasonable request.
Publications
Lorstad S, Shekarestan S, Jernberg T, Tehrani S, Astrand P, Gille-Johnson P, Persson J. First Sampled High-Sensitive Cardiac Troponin T is Associated With One-Year Mortality in Sepsis Patients and 30- to 365-Day Mortality in Sepsis Survivors. Am J Med. 2023 Aug;136(8):814-823.e8. doi: 10.1016/j.amjmed.2023.04.029. Epub 2023 May 6.
PubMed 37156347Levy MM, Artigas A, Phillips GS, Rhodes A, Beale R, Osborn T, Vincent JL, Townsend S, Lemeshow S, Dellinger RP. Outcomes of the Surviving Sepsis Campaign in intensive care units in the USA and Europe: a prospective cohort study. Lancet Infect Dis. 2012 Dec;12(12):919-24. doi: 10.1016/S1473-3099(12)70239-6. Epub 2012 Oct 26.
PubMed 23103175Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, White HD; Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018 Oct 30;72(18):2231-2264. doi: 10.1016/j.jacc.2018.08.1038. Epub 2018 Aug 25. No abstract available.
PubMed 30153967Neumann FJ, Sousa-Uva M, Ahlsson A, Alfonso F, Banning AP, Benedetto U, Byrne RA, Collet JP, Falk V, Head SJ, Juni P, Kastrati A, Koller A, Kristensen SD, Niebauer J, Richter DJ, Seferovic PM, Sibbing D, Stefanini GG, Windecker S, Yadav R, Zembala MO; ESC Scientific Document Group. 2018 ESC/EACTS Guidelines on myocardial revascularization. Eur Heart J. 2019 Jan 7;40(2):87-165. doi: 10.1093/eurheartj/ehy394. No abstract available.
PubMed 30165437Fearon WF, Nakamura M, Lee DP, Rezaee M, Vagelos RH, Hunt SA, Fitzgerald PJ, Yock PG, Yeung AC. Simultaneous assessment of fractional and coronary flow reserves in cardiac transplant recipients: Physiologic Investigation for Transplant Arteriopathy (PITA Study). Circulation. 2003 Sep 30;108(13):1605-10. doi: 10.1161/01.CIR.0000091116.84926.6F. Epub 2003 Sep 8.
PubMed 12963639De Bruyne B, Pijls NH, Smith L, Wievegg M, Heyndrickx GR. Coronary thermodilution to assess flow reserve: experimental validation. Circulation. 2001 Oct 23;104(17):2003-6. doi: 10.1161/hc4201.099223.
PubMed 11673336Fearon WF, Balsam LB, Farouque HM, Caffarelli AD, Robbins RC, Fitzgerald PJ, Yock PG, Yeung AC. Novel index for invasively assessing the coronary microcirculation. Circulation. 2003 Jul 1;107(25):3129-32. doi: 10.1161/01.CIR.0000080700.98607.D1. Epub 2003 Jun 23.
PubMed 12821539Aarnoudse W, Fearon WF, Manoharan G, Geven M, van de Vosse F, Rutten M, De Bruyne B, Pijls NH. Epicardial stenosis severity does not affect minimal microcirculatory resistance. Circulation. 2004 Oct 12;110(15):2137-42. doi: 10.1161/01.CIR.0000143893.18451.0E. Epub 2004 Oct 4.
PubMed 15466646Fearon WF, Aarnoudse W, Pijls NH, De Bruyne B, Balsam LB, Cooke DT, Robbins RC, Fitzgerald PJ, Yeung AC, Yock PG. Microvascular resistance is not influenced by epicardial coronary artery stenosis severity: experimental validation. Circulation. 2004 May 18;109(19):2269-72. doi: 10.1161/01.CIR.0000128669.99355.CB. Epub 2004 May 10.
PubMed 15136503Ong P, Camici PG, Beltrame JF, Crea F, Shimokawa H, Sechtem U, Kaski JC, Bairey Merz CN; Coronary Vasomotion Disorders International Study Group (COVADIS). International standardization of diagnostic criteria for microvascular angina. Int J Cardiol. 2018 Jan 1;250:16-20. doi: 10.1016/j.ijcard.2017.08.068. Epub 2017 Sep 8.
PubMed 29031990De Backer D, Donadello K, Sakr Y, Ospina-Tascon G, Salgado D, Scolletta S, Vincent JL. Microcirculatory alterations in patients with severe sepsis: impact of time of assessment and relationship with outcome. Crit Care Med. 2013 Mar;41(3):791-9. doi: 10.1097/CCM.0b013e3182742e8b.
PubMed 23318492Fernandez-Sarmiento J, Molina CF, Salazar-Pelaez LM, Florez S, Alarcon-Forero LC, Sarta M, Hernandez-Sarmiento R, Villar JC. Biomarkers of Glycocalyx Injury and Endothelial Activation are Associated with Clinical Outcomes in Patients with Sepsis: A Systematic Review and Meta-Analysis. J Intensive Care Med. 2023 Jan;38(1):95-105. doi: 10.1177/08850666221109186. Epub 2022 Jun 19.
PubMed 35722738Piotti A, Novelli D, Meessen JMTA, Ferlicca D, Coppolecchia S, Marino A, Salati G, Savioli M, Grasselli G, Bellani G, Pesenti A, Masson S, Caironi P, Gattinoni L, Gobbi M, Fracasso C, Latini R; ALBIOS Investigators. Endothelial damage in septic shock patients as evidenced by circulating syndecan-1, sphingosine-1-phosphate and soluble VE-cadherin: a substudy of ALBIOS. Crit Care. 2021 Mar 19;25(1):113. doi: 10.1186/s13054-021-03545-1.
PubMed 33741039Sun T, Wang Y, Wu X, Cai Y, Zhai T, Zhan Q. Prognostic Value of Syndecan-1 in the Prediction of Sepsis-Related Complications and Mortality: A Meta-Analysis. Front Public Health. 2022 Apr 11;10:870065. doi: 10.3389/fpubh.2022.870065. eCollection 2022.
PubMed 35480580Colicchia M, Perrella G, Gant P, Rayes J. Novel mechanisms of thrombo-inflammation during infection: spotlight on neutrophil extracellular trap-mediated platelet activation. Res Pract Thromb Haemost. 2023 Mar 11;7(2):100116. doi: 10.1016/j.rpth.2023.100116. eCollection 2023 Feb.
PubMed 37063765
Study at a glance
From the registry record, last updated by the sponsor on 29 Jun 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Coronary Microcirculation and Troponin Elevation in Septic Shock
- ClinicalTrials.gov ID
- NCT06294730
- Acronym / sponsor ID
- COMTESS / 2018/1891-31
- Keywords
- sepsis, cardiac troponin, myocardial injury, coronary microvascular dysfunction, Index of microcirculatory resistance, survival
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 62 participants (actual)
- Lead sponsor
- Karolinska InstitutetUniversity, hospital or other
- Study start
- 13 Jun 2019 (actual)
- Primary completion
- 20 Dec 2024 (actual)
- Study completion
- 28 Feb 2025 (actual)
- First posted
- 5 Mar 2024 (actual)
- 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.
Plasma cardiac troponin (cTn) elevation is an indicator of increased mortality in patients with sepsis yet the underlying cause of troponin elevation in sepsis is not known. The COMTESS study investigates whether elevated high-sensitive cardiac Troponin T (hs-cTnT) levels in hemodynamically unstable patients with sepsis can be explained by an underlying coronary artery disease or a process within the coronary microcirculation. Fifty patients with sepsis and with hs-cTnT elevation (>15 ng/L) will undergo coronary angiography, including an assessment of coronary flow using a method called thermo-dilution to record the index of microcirculatory resistance (IMR) in the left anterior descending artery (LAD). The relationship between IMR and hs-cTnT will subsequently be analysed. It is important to identify the underlying causes of elevated cTn during sepsis to target further research with an aim to improve the survival in patients suffering from this condition.
Detailed description
Severe sepsis and septic shock are frequent primary causes of morbidity and mortality in intensive care units worldwide with a mortality rate of 28.3 - 41.1%. Our research group has previously shown that increasing level of high-sensitive cardiac troponin T (hs-cTnT) taken in sepsis patients is associated with 30-day and one-year mortality. Importantly, our group showed that hs-cTnT is also associated with mortality during the convalescence phase (30-365-day) in sepsis survivors.
Serum cardiac troponin (cTn) measurement is used to detect myocardial injury in patients with acute ischemic heart disease. Cardiac-specific troponins (troponin I and T) are, under normal physiological conditions, only detectable in the blood in small concentrations. In the event of myocyte damage, cardiac-specific troponins I and T enter the systemic circulation and can be detected and measured using modern immunoassay methods. This has led to the use of these biomarkers to identify both the presence and even estimated extent of myocardial injury which can then in turn facilitate an early risk stratification and identification of patients suitable for coronary intervention. Since 2018, the high-sensitive cardiac troponin assays have become the recommended assays for use within the clinical setting. In stark contrast to the treatment of patients with acute myocardial infarction and elevated cTn levels, there are currently no clinical guidelines to help physicians treat, investigate or follow-up sepsis patients with sepsis-related myocardial injury.
The COMTESS study is a pioneering observational prospective clinical study of 50 critically ill sepsis patients with a sampled hs-cTnT >15 ng/L investigating the relationship between hs-cTnT level and concurrent microvascular dysfunction. Following informed consent, coronary angiography with measurements of coronary flow reserve (CFR), basal resistance index (BRI) and index of microcirculatory resistance (IMR) using thermo-dilution in the left anterior descending artery (LAD) is performed in each patient to ascertain underlying coronary microvascular dysfunction (CMVD). Fractional flow reserve (FFR) will be measured in cases where there is a coronary stenosis in the LAD. A research echocardiography is also performed on day 2-10 to examine right and left ventricular function.
Our primary hypothesis is that increasing level of hs-cTnT is associated with increasing level of CMVD in patients with sepsis and that myocardial injury thus contributes to excess death in sepsis and sepsis-survivors. The mechanisms behind myocardial injury in sepsis are not known. Disturbed sublingual microcirculatory alterations are associated with mortality in septic shock, but whether these alterations in proxy vessels translates to clinically relevant CMVD and myocardial injury in patients with sepsis is not known.
The physiological properties of endothelial cells (ECs) in the microcirculation are dependent on a complex carbohydrate-rich layer covering the EC luminal surface called the glycocalyx. Studies have shown that the disseminated dysfunctional immune response which is the hallmark of sepsis causes glycocalyx and EC injury and widespread coagulopathy leading to microvascular thrombosis. Pro-thrombotic components (e.g., neutrophile extracellular traps [NETs], and prothrombin) and components from EC and glycocalyx damage (e.g., Syndecan-1, thrombomodulin) can subsequently be analysed in plasma. Elevated level of Syndecan-1 in sepsis is associated with greater risk of death. Blood samples will be drawn during the coronary angiography for each patient and will be stored in a biobank. Our aim is to investigate if there is an association between plasma level of different microvascular components in relation to IMR level.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
Who may qualify
- Ages
- 40 to 85 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Sepsis- or septic shock-patients with a life expectancy of >1year and non-normal high-sensitive cardiac troponin T values (>15 ng/L)
Key inclusion criteria (4 listed)
- Patients fulfilling the Sepsis-3 definition of and diagnostic criteria for sepsis or septic shock
- Age 40 - 85 years
- Life expectancy > 1 year
- hs-cTnT values >15 ng/L
Key exclusion criteria (11 listed)
- pregnancy
- previous medical history of coronary artery by-pass grafting
- heart transplant
- previously verified ejection fraction (EF) ≤39% prior to hospital admission
- Hypertrophic cardiomyopathy (Septum > 15 mm)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Relationship between hs-cTnT and IMR
Time frame: Day 2-10 from the onset of sepsis symptoms.
Spline regression between the highest hs-cTnT at 0-72 hrs from vasopressor initiation and IMR at day 2-10 from sepsis onset
10 secondary outcomes
Relationship between hs-cTnT and CFR
Time frame: Day 2-10 from the onset of sepsis symptoms.
Relationship between hs-cTnT and BRI
Time frame: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and number of diseased epicardial coronary vessels
Time frame: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and Synergy Between PCI With Taxus and Cardiac Surgery (SYNTAX)-score
Time frame: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and left ventricular end diastolic pressure (LVEDP)
Time frame: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and Tricuspid annular plane systolic excursion (TAPSE)
Time frame: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and echocardiographic measurements of left ventricular global strain
Time frame: Day 2-10 from the onset of sepsis symptoms
Relationship between hs-cTnT and echocardiographic measurements of left diastolic dysfunction
Time frame: Day 2-10 from the onset of sepsis symptoms
Relationship between measures of endothelial dysfunction and IMR
Time frame: Day 2-10 from the onset of sepsis symptoms
Relationship between measures NETs and IMR
Time frame: Day 2-10 from the onset of sepsis symptoms
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 29 Jun 2025.
- Background: PubMed 37156347Lorstad S, Shekarestan S, Jernberg T, Tehrani S, Astrand P, Gille-Johnson P, Persson J. First Sampled High-Sensitive Cardiac Troponin T is Associated With One-Year Mortality in Sepsis Patients and 30- to 365-Day Mortality in Sepsis Survivors. Am J Med. 2023 Aug;136(8):814-823.e8. doi: 10.1016/j.amjmed.2023.04.029. Epub 2023 May 6.
- Background: PubMed 23103175Levy MM, Artigas A, Phillips GS, Rhodes A, Beale R, Osborn T, Vincent JL, Townsend S, Lemeshow S, Dellinger RP. Outcomes of the Surviving Sepsis Campaign in intensive care units in the USA and Europe: a prospective cohort study. Lancet Infect Dis. 2012 Dec;12(12):919-24. doi: 10.1016/S1473-3099(12)70239-6. Epub 2012 Oct 26.
- Background: PubMed 30153967Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, White HD; Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018 Oct 30;72(18):2231-2264. doi: 10.1016/j.jacc.2018.08.1038. Epub 2018 Aug 25. No abstract available.
- Background: PubMed 30165437Neumann FJ, Sousa-Uva M, Ahlsson A, Alfonso F, Banning AP, Benedetto U, Byrne RA, Collet JP, Falk V, Head SJ, Juni P, Kastrati A, Koller A, Kristensen SD, Niebauer J, Richter DJ, Seferovic PM, Sibbing D, Stefanini GG, Windecker S, Yadav R, Zembala MO; ESC Scientific Document Group. 2018 ESC/EACTS Guidelines on myocardial revascularization. Eur Heart J. 2019 Jan 7;40(2):87-165. doi: 10.1093/eurheartj/ehy394. No abstract available.
- Background: PubMed 12963639Fearon WF, Nakamura M, Lee DP, Rezaee M, Vagelos RH, Hunt SA, Fitzgerald PJ, Yock PG, Yeung AC. Simultaneous assessment of fractional and coronary flow reserves in cardiac transplant recipients: Physiologic Investigation for Transplant Arteriopathy (PITA Study). Circulation. 2003 Sep 30;108(13):1605-10. doi: 10.1161/01.CIR.0000091116.84926.6F. Epub 2003 Sep 8.
- Background: PubMed 11673336De Bruyne B, Pijls NH, Smith L, Wievegg M, Heyndrickx GR. Coronary thermodilution to assess flow reserve: experimental validation. Circulation. 2001 Oct 23;104(17):2003-6. doi: 10.1161/hc4201.099223.
- Background: PubMed 12821539Fearon WF, Balsam LB, Farouque HM, Caffarelli AD, Robbins RC, Fitzgerald PJ, Yock PG, Yeung AC. Novel index for invasively assessing the coronary microcirculation. Circulation. 2003 Jul 1;107(25):3129-32. doi: 10.1161/01.CIR.0000080700.98607.D1. Epub 2003 Jun 23.
- Background: PubMed 15466646Aarnoudse W, Fearon WF, Manoharan G, Geven M, van de Vosse F, Rutten M, De Bruyne B, Pijls NH. Epicardial stenosis severity does not affect minimal microcirculatory resistance. Circulation. 2004 Oct 12;110(15):2137-42. doi: 10.1161/01.CIR.0000143893.18451.0E. Epub 2004 Oct 4.
- Background: PubMed 15136503Fearon WF, Aarnoudse W, Pijls NH, De Bruyne B, Balsam LB, Cooke DT, Robbins RC, Fitzgerald PJ, Yeung AC, Yock PG. Microvascular resistance is not influenced by epicardial coronary artery stenosis severity: experimental validation. Circulation. 2004 May 18;109(19):2269-72. doi: 10.1161/01.CIR.0000128669.99355.CB. Epub 2004 May 10.
- Background: PubMed 29031990Ong P, Camici PG, Beltrame JF, Crea F, Shimokawa H, Sechtem U, Kaski JC, Bairey Merz CN; Coronary Vasomotion Disorders International Study Group (COVADIS). International standardization of diagnostic criteria for microvascular angina. Int J Cardiol. 2018 Jan 1;250:16-20. doi: 10.1016/j.ijcard.2017.08.068. Epub 2017 Sep 8.
- Background: PubMed 23318492De Backer D, Donadello K, Sakr Y, Ospina-Tascon G, Salgado D, Scolletta S, Vincent JL. Microcirculatory alterations in patients with severe sepsis: impact of time of assessment and relationship with outcome. Crit Care Med. 2013 Mar;41(3):791-9. doi: 10.1097/CCM.0b013e3182742e8b.
- Background: PubMed 35722738Fernandez-Sarmiento J, Molina CF, Salazar-Pelaez LM, Florez S, Alarcon-Forero LC, Sarta M, Hernandez-Sarmiento R, Villar JC. Biomarkers of Glycocalyx Injury and Endothelial Activation are Associated with Clinical Outcomes in Patients with Sepsis: A Systematic Review and Meta-Analysis. J Intensive Care Med. 2023 Jan;38(1):95-105. doi: 10.1177/08850666221109186. Epub 2022 Jun 19.
- Individual participant dataSharing planned: Yes. Will be provided upon reasonable request.
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A Study to Evaluate AZD7760 Safety and Pharmacokinetics in Healthy Adults (Phase I) and Adults With End-stage Kidney Disease on Hemodialysis With a Central Venous Catheter (Phase IIa)
Staphylococcus Aureus
Recruiting
Veno-arterial Carbon Dioxide Partial Pressure Difference (CO2gap) for Early Resuscitation of Septic Shock
Sepsis - to Reduce Mortality in the Intensive Care Unit, Septic Shock
Not yet recruiting
Hemodynamic Resuscitation Guided by Non-Invasive Mean Systemic Filling Pressure to Prevent Acute Kidney Injury in Septic Shock
Acute Kidney Injury Due to Sepsis
RecruitingPhase 3
CLARITHROMYCIN TO PREVENT SECONDARY INFECTIONS IN PATIENTS WITH SEPSIS FOLLOWING LOWER RESPIRATORY TRACT INFECTIONS: THE CLASSIFY TRIAL
Sepsis
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.
Jonas Persson, MD, PhD principal investigator
Karolinska Institutet Danderyd University Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Sepsis and Myocardial Injury, run by Karolinska Institutet at 1 site in Sweden.
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 11 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: finished, as of the sponsor's last update on 29 Jun 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Sweden. 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 is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
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?
Relationship between hs-cTnT and IMR (time frame: Day 2-10 from the onset of sepsis symptoms.). 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 NCT06294730, which also lists 17 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 29 Jun 2025; AzTrials last refreshed its copy on 30 Oct 2026.