Evidence mapPaperPMID 42393752Full record

Observational studyCritical care (London, England)2026

Coronary microvascular function in patients with sepsis and myocardial injury: an invasive coronary physiology study.

Samantha Lörstad, Per Åstrand, Patrik Gille-Johnson, Yunzhang Wang, Christina Ekenbäck, Fadi Jokhaji, Felix Böhm, Patrik Hjalmarsson, Shajan Shekarestan, Tomas Jernberg and 3 more

Registry-linked trialAbstract readObservational Study
In one paragraph

Observational study in Critical care (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06294730 (Coronary Microcirculation and Troponin Elevation in Septic Shock), which is not on this map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06294730 completednot on this map

Coronary Microcirculation and Troponin Elevation in Septic Shock

TypeobservationalSponsorKarolinska InstitutetRan2019 to 2025Enrolled62ConditionsSepsis, Myocardial Injury, Coronary Microvascular Dysfunction, Endothelial Dysfunction
3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Samantha LörstadDepartment of Clinical Sciences, Division of Internal Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden. samantha.rutherford.lorstad@ki.se.ORCID http://orcid.org/0000-0003-3422-7943
Per ÅstrandInternal Medicine Clinic, Danderyd University Hospital, Stockholm, Sweden.
Patrik Gille-JohnsonInfectious Diseases Clinic, Danderyd University Hospital, Stockholm, Sweden.
Yunzhang WangDepartment of Clinical Sciences, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Christina EkenbäckDepartment of Clinical Sciences, Division of Cardiovascular Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Fadi JokhajiDepartment of Clinical Sciences, Division of Cardiovascular Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Felix BöhmDepartment of Clinical Sciences, Division of Cardiovascular Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Patrik HjalmarssonDepartment of Clinical Sciences, Division of Cardiovascular Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Shajan ShekarestanDepartment of Clinical Sciences, Division of Cardiovascular Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Tomas JernbergDepartment of Clinical Sciences, Division of Cardiovascular Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Sara TehraniDepartment of Clinical Sciences, Division of Internal Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Kambiz ShahgaldiDepartment of Clinical Sciences, Division of Cardiovascular Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Jonas PerssonDepartment of Clinical Sciences, Division of Cardiovascular Medicine, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial injury is common in sepsis and associated with increased mortality, but its underlying mechanisms remain incompletely understood. Coronary microvascular dysfunction (CMD) has been proposed as a contributor, although in vivo evidence is limited. We characterised coronary microvascular function in patients with sepsis and myocardial injury and its relationship with cardiac troponin release.

methodsConsecutive adults with sepsis (Sepsis-3 criteria) and myocardial injury (hs-cTnT ≥ 15 ng/L) were prospectively enrolled between June 2019 and December 2024. Patients underwent coronary angiography, invasive thermodilution-based assessment of coronary microvascular function, and transthoracic echocardiography after clinical stabilisation. CMD was defined as an index of microcirculatory resistance (IMR) > 25 and/or microvascular resistance reserve (MRR) ≤ 3. Associations between hs-cTnT concentrations and coronary microvascular indices, obstructive coronary artery disease (CAD), and echocardiographic variables were assessed using regression analyses. Coronary microvascular indices were compared with those of age-, sex-, and CAD-matched patients with chronic coronary syndrome (CCS) using mixed-effects models.

resultsFifty-five patients underwent coronary angiography and 49 completed invasive coronary microvascular assessment. Obstructive CAD was identified in 12/55 (22%). CMD was present in 30/49 (61%). Among these, 8/49 (16%) had elevated IMR only, 9/49 (18%) had functional CMD (MRR ≤ 3 and IMR ≤ 25), and 13/49 (27%) had structural CMD (MRR ≤ 3 and IMR > 25). Restricted cubic spline analyses demonstrated no evidence of associations between hs-cTnT and IMR (overall P = 0.899; non-linearity P = 0.687) or MRR (overall P = 0.987; non-linearity P = 0.954). CMD was associated with a higher prevalence of ventriculo-arterial uncoupling, right ventricular systolic dysfunction, and impaired right ventricular-pulmonary arterial coupling. Patients with sepsis demonstrated reduced coronary microvascular vasodilatory capacity compared with matched CCS controls (MRR 3.2 [IQR 2.4-4.5] vs. 4.0 [2.7-6.2]). IMR was similar between groups.

conclusionsCMD was common and heterogeneous and exhibited distinct phenotypes in patients with sepsis and myocardial injury. Measures of coronary microvascular function were not associated with troponin release. Previously unrecognised obstructive CAD was identified in 22% of patients, supporting consideration of underlying CAD in patients with sepsis and myocardial injury.

trial registrationClinicalTrials.gov identifier NCT06294730.

Indexed as

Coronary CirculationMicrocirculationSepsisAgedCoronary AngiographyEchocardiographyFemaleHumansMaleMiddle AgedProspective StudiesCoronary microcirculationCoronary microvascular dysfunction.EchocardiographyMyocardial injurySepsisTroponin

Identifiers

PMID42393752
PMCPMC13330245

What Socratic holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.