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

Recruiting
Conditions
I21
Acute myocardial infarction
Registration Number
DRKS00033039
Lead Sponsor
niversitätsklinikum Freiburg Abteilung Kardiologie und Angiologie
Brief Summary

Not available

Detailed Description

Not available

Recruitment & Eligibility

Status
Recruiting
Sex
All
Target Recruitment
100
Inclusion Criteria

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

Exclusion Criteria

None.

Study & Design

Study Type
observational
Study Design
Not specified
Primary Outcome Measures
NameTimeMethod
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.<br><br>
Secondary Outcome Measures
NameTimeMethod
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).<br>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.
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