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Published on: January 28, 2020
Relationship between PCSK9 and endothelial function in patients with acute myocardial infarction
Paolo Cimaglia1, Francesca Fortini1, Francesco Vieceli Dalla Sega1
1Maria Cecilia Hospital, GVM Care and Research, via Corriera 1, 48033, Cotignola RA, Italy.
Insights
Proprotein convertase subtilisin/kexin type 9 (PCSK9) levels and endothelial dysfunction, measured by apoptosis rate, are linked in patients with ST-elevation myocardial infarction. Changes in PCSK9 correlate with endothelial function variations post-myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Endothelial Function
- Lipid Metabolism
Background:
- The role of PCSK9 in lipid metabolism is established, but its association with endothelial function requires further investigation.
- Endothelial dysfunction is a critical factor in acute myocardial infarction (AMI).
Purpose of the Study:
- To evaluate the relationship between PCSK9 and endothelial dysfunction in patients experiencing acute myocardial infarction (specifically STEMI).
Main Methods:
- Serum samples from 74 STEMI patients were analyzed at admission and 5 days post-admission.
- Endothelial dysfunction was assessed by measuring the apoptosis rate (AR) of endothelial cells incubated with patient serum.
- Correlations between PCSK9 levels and AR were examined.
Main Results:
- A significant positive correlation was observed between PCSK9 levels and AR at baseline (r=0.649) and 5-day (r=0.648).
- PCSK9 levels significantly increased post-STEMI (p<0.001), while AR did not (p=0.491).
- Patients with reduced PCSK9 showed a greater decrease in AR (p=0.002), and PCSK9 change was the sole predictor of AR change (p=0.001).
Conclusions:
- Variations in endothelial function and PCSK9 are related in the initial days following acute myocardial infarction.
- Further research is needed to validate these findings and explore their clinical implications.
Background And Aims:
While the role of PCSK9 in lipid metabolism is well established, its link with endothelial function is less clear. The aim of the present study is to evaluate the relationship between PCSK9 and endothelial dysfunction in the setting of acute myocardial infarction.
Methods And Results:
To this purpose, we analyzed the serum of 74 patients with ST-elevation myocardial infarction (STEMI) at the time of admission and after 5 days. Endothelial dysfunction was evaluated as rate of apoptosis (AR) of human umbilical vein endothelial cells incubated with patients' serum. There was a good correlation between PCSK9 and the apoptosis rate values, both at baseline (r = 0.649) and 5-day (r = 0.648). In the 5 days after STEMI, PCSK9 increased significantly (242-327 ng/ml, p < 0.001), while AR did not (p = 0.491). Overall, 21 (28%) patients showed a reduction of PCSK9, and they had a significantly higher decrease of AR as compared to others (-13.87 vs 5.8%, p = 0.002). At the univariable analysis, the 5-day change of PCSK9 resulted to be the only variable associated with the 5-day change of the apoptosis rate (beta 0.217, 95%CI 0.091-0.344, p = 0.001).
Conclusion:
The variation of endothelial function and PCKS9 in the first days after an acute myocardial infarction are related. Further validation and research are necessary to confirm our findings.
Clinical Trial:
NCT02438085.
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