Dynamics of serum-induced endothelial cell apoptosis in patients with myocardial infarction
Maria J Forteza1, Susana Novella, Isabel Trapero
1Cardiology Department, Hospital Clínico Universitario, Valencia, Spain; Universidad de Valencia, Valencia, Spain; INCLIVA, Fundación Hospital Clínico Universitario de Valencia, Valencia, Spain.
Insights
Endothelial cell viability decreases after ST-segment elevation myocardial infarction (STEMI) treated with primary coronary intervention, primarily due to increased apoptosis, and is linked to myocardial edema.
Area of Science:
- Cardiology
- Cell Biology
- Biomedical Science
Background:
- ST-segment elevation myocardial infarction (STEMI) patients treated with primary percutaneous coronary intervention (PCI) experience dynamic changes in endothelial cell (EC) health.
- The relationship between EC viability, apoptosis, necrosis, and left ventricular structural changes post-STEMI has not been previously investigated.
Purpose of the Study:
- To investigate the dynamics of endothelial cell (EC) viability, apoptosis, and necrosis in STEMI patients after primary PCI.
- To explore the association between these EC changes and left ventricular structural consequences, specifically myocardial edema.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) were incubated with serum from 20 STEMI patients before and after reperfusion (24h, 96h, 30 days).
- EC viability, apoptosis, and necrosis were quantified using flow cytometry.
- Cardiac magnetic resonance (CMR) imaging was performed to assess left ventricular structure, including myocardial edema.
Main Results:
- Serum from STEMI patients significantly reduced EC viability, with a nadir at 96 hours post-reperfusion (67.7%).
- This reduction in viability was primarily driven by increased EC apoptosis, peaking at 96 hours (15.2%).
- Extensive myocardial edema (>30% of left ventricular mass) on CMR was significantly associated with higher EC apoptosis at 96 hours.
Conclusions:
- Endothelial cell viability undergoes dynamic changes following STEMI treated with primary PCI, with a late peak in apoptosis.
- These EC alterations are significantly associated with the extent of myocardial edema detected by CMR.
- The findings highlight the impact of reperfusion injury on endothelial cells and their link to cardiac remodeling in STEMI.
Background:
In patients with ST-segment elevation myocardial infarction (STEMI) reperfused with primary coronary intervention (PCI), the dynamics of endothelial cell (EC) viability, apoptosis and necrosis and its relationship with the structural consequences on the left ventricle have not been addressed so far.
Design:
In 20 STEMI patients, we incubated human umbilical vein endothelial cells (HUVECs) with serum drawn before reperfusion and subsequently afterwards (24, 96 h, 30 days). Viability, apoptosis and necrosis percentages were evaluated by flow cytometry. Values were compared with 12 age- and sex-matched control subjects with normal coronary arteries. Cardiac magnetic resonance (CMR) was performed during the first week after infarction.
Results:
Serum from STEMI patients induced a progressive loss of EC viability, with a nadir of 67.7 ± 10.2% at 96 h (baseline: 75 ± 6% and controls: 80.2 ± 3.9%, P < 0.001 in both cases). This is due to an increase in apoptosis that peaked at 96 h after reperfusion (15.2 ± 7.1% vs. 11 ± 6 at baseline and 5.8 ± 1.6% in controls, P < 0.001 in both cases). However, no significant dynamic changes in EC necrosis were detected. Extensive myocardial oedema (> 30%, median of left ventricular mass) was the only CMR variable significantly associated with a higher percentage of EC apoptosis at 96 h (extensive vs. nonextensive oedema: 18.3 ± 6.8% vs. 12.1 ± 6.3%, P < 0.05).
Conclusions:
Dynamic changes in EC viability occur in the setting of STEMI patients reperfused with PCI, these changes peak late after reperfusion, they are mainly the result of an increase of apoptosis and are associated with the presence of extensive myocardial oedema.
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