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Alterations in endothelial activation biomarkers ICAM-1 and VCAM-1 following mitral regurgitation surgery
Saša Kostovski1, Jelena Milenkovic2, Boris Djindjic2
1Clinic for Cardiosurgery, The Military Medical Academy, Belgrade, Serbia.
Insights
Surgical correction of mitral regurgitation (MR) significantly reduces ICAM-1 levels, an inflammatory marker. This decline is linked to left ventricular (LV) size changes after surgery, indicating improved endothelial function.
Area of Science:
- Cardiology
- Vascular Biology
- Surgical Research
Background:
- Degenerative mitral regurgitation (MR) causes hemodynamic changes and left ventricular (LV) remodeling.
- Endothelial activation, marked by adhesion molecules like ICAM-1 and VCAM-1, plays a role in inflammation and LV dysfunction.
Purpose of the Study:
- To evaluate endothelial activation during surgical correction of chronic MR.
- To assess the association between adhesion molecules (ICAM-1, VCAM-1) and postsurgical LV dysfunction (LVD).
Main Methods:
- Asymptomatic patients with severe degenerative MR (grade 3-4) were studied.
- Transthoracic echocardiography and blood samples were collected pre- and post-surgery.
- Circulating ICAM-1 and VCAM-1 levels were measured using ELISA.
Main Results:
- Post-surgery, ejection fraction and LV dimensions decreased significantly.
- ICAM-1 levels significantly declined (p=0.031), while VCAM-1 levels did not change.
- Postoperative LVD occurred in 35.7% but wasn't correlated with adhesion molecules; however, ICAM-1 levels were associated with LV dilatation (EDD >5.6 cm).
Conclusions:
- Serum ICAM-1 levels decrease after MR surgical correction, correlating with LV enlargement.
- Endothelial activity dynamically changes post-surgery in MR patients.
- Further research is needed to fully understand endothelial processes in MR.
Objective:
Severe chronic degenerative mitral regurgitation (MR) is characterised by altered hemodynamics and high-shear stress, which initiate left ventricular (LV) remodelling, including upregulation of various cytokines. We evaluated endothelial activation during surgical correction of chronic MR by assessing adhesion molecules ICAM-1 and VCAM-1, classic markers of inflammation, and their association with postsurgical LV dysfunction (LVD).
Material And Methods:
The study included asymptomatic patients with grade 3-4 degenerative MR. Transthoracic echocardiography data and blood samples were collected before and five days after surgical correction of MR. Circulating levels of adhesion molecules were measured by ELISA.
Results:
Ejection fraction, end-diastolic diameter (EDD), and volume all decreased significantly after surgery. A significant decline in ICAM-1 concentration was observed between the two periods (457.11±256.12 vs. 240.29±157.14 ng/mL; p=0.031), whereas VCAM-1 levels did not change significantly. Leukocyte count and C-reactive protein were significantly higher in the postoperative period. Early postoperative LVD (in 35.7% of patients) was not correlated with adhesion molecule levels. However, we observed significant changes in ICAM-1 levels associated with postoperative EDD >5.6 cm, which indicates LV dilatation. These patients had markedly lower preoperative and postoperative ICAM-1 values than others.
Conclusion:
Serum ICAM-1 levels significantly decline following surgical correction of MR and are associated with postoperative enlargement of the LV. Our study highlights dynamic changes in endothelial activity and underscores the need for a better understanding of this process in MR.
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