Transition from pro-inflammatory to reparative phase following acute myocardial infarction: Role of the innate immune system.

Transition from pro-inflammatory to reparative phase following acute myocardial infarction: Role of the innate immune system. - IRIS

Status

Recruiting

Phases

Unknown

Study type

Observational

Source

DRKS

Registry ID

DRKS00033039

Enrollment

100

Registered

2023-11-29

Start date

2023-10-16

Completion date

Unknown

Last updated

2025-04-07

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

I21

Interventions

Group 1: Patients with ST-segment elevation myocardial infarction After inclusion, a blood sample (approx. 14mL) is taken at 0,4,12,24 hours after PCI. After about 3 months, an echocardiography and/o

Eligibility

Sex/Gender

All

Age

18 Years to 99 Years

Inclusion criteria

Inclusion criteria: ST-Segment elevation in ECG and interventional recanalisation with stenting.

Exclusion criteria

Exclusion criteria: None.

Design outcomes

Primary

Measure	Time frame
At indicated timepoints NLRP3 expression in neutrophils is absolutely quantified using digital droplet PCR as well as the intercellular levels of the NLRP3 protein determined using ELISA. The hypothesis being that 1) Elevated NLRP3 expression and transcription in neutrophils is characteristic of ischemia-reperfusion injury following acute myocardial infarction and 2) the timeline of alteration in neutrophil NLRP3 expression and transcription is indicative of the switch from the inflammatory phase to the reparative phase following myocardial infarction indicated by corresponding changes in plasma inflammatory markers measured using ELISA.	—

Measure

Time frame

At indicated timepoints NLRP3 expression in neutrophils is absolutely quantified using digital droplet PCR as well as the intercellular levels of the NLRP3 protein determined using ELISA. The hypothesis being that 1) Elevated NLRP3 expression and transcription in neutrophils is characteristic of ischemia-reperfusion injury following acute myocardial infarction and 2) the timeline of alteration in neutrophil NLRP3 expression and transcription is indicative of the switch from the inflammatory phase to the reparative phase following myocardial infarction indicated by corresponding changes in plasma inflammatory markers measured using ELISA.

—

Secondary

Measure	Time frame
Within 24 hours of inclusion and after 30 days, the resulting myocardial damage is quantified using 3D speckle tracking echocardiography (STE) and the ejection fraction is determined. In addition, after 30 days, the size of the resulting infarction is precisely quantified using contrast-enhanced magnetic resonance imaging (CE-MRI). The hypothesis is that the extent and temporal dynamics of neutrophil NLRP3 activation correlates with the extent of the inflammatory immune response after myocardial infarction and thereby significantly affects the extent of myocardial damage.	—

Measure

Time frame

Within 24 hours of inclusion and after 30 days, the resulting myocardial damage is quantified using 3D speckle tracking echocardiography (STE) and the ejection fraction is determined. In addition, after 30 days, the size of the resulting infarction is precisely quantified using contrast-enhanced magnetic resonance imaging (CE-MRI). The hypothesis is that the extent and temporal dynamics of neutrophil NLRP3 activation correlates with the extent of the inflammatory immune response after myocardial infarction and thereby significantly affects the extent of myocardial damage.

—

Countries

Germany

Contacts

Public ContactLukas Heger

Universitätsklinikum Freiburg

lukas.heger@uniklinik-freiburg.de004976127034010

Outcome results

None listed

Source: DRKS (via WHO ICTRP) · Data processed: Feb 4, 2026