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Elevated CETP activity during acute phase of myocardial infarction is independently associated with endothelial
Luiz Sergio F Carvalho1, Vitor W M Virginio2, Natalia B Panzoldo2
1Cardiology Division, State University of Campinas School of Medicine (Unicamp), Campinas, SP, Brazil.
Insights
Elevated cholesteryl ester transfer protein (CETP) activity in ST-elevation myocardial infarction (STEMI) patients is linked to endothelial dysfunction and worse clinical outcomes, including sudden death and recurrent heart attacks.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Clinical Research
Background:
- Cholesteryl ester transfer protein (CETP) activity may be influenced by acute stress, inflammation, oxidative stress, and thrombosis.
- Previous research suggests a potential link between CETP activity and adverse cardiovascular events.
Purpose of the Study:
- To investigate the association between CETP activity and inflammatory-oxidative response, thrombogenesis, and clinical outcomes in patients with ST-elevation myocardial infarction (STEMI).
Main Methods:
- 116 STEMI patients were enrolled within 24 hours of symptom onset and followed for 180 days.
- Plasma levels of inflammatory markers (CRP, IL-2, TNFα), oxidative stress markers (8-isoprostane, NOx), and CETP activity were measured.
- Flow-mediated dilation (FMD) and coronary thrombus burden (CTB) were assessed.
Main Results:
- Higher baseline CETP activity was associated with reduced nitric oxide (NOx) levels and lower FMD.
- Increased thiobarbituric acid reactive substances (TBARS) in HDL particles correlated with CETP activity and impaired FMD.
- High CETP activity at admission predicted sudden death and recurrent myocardial infarction (MI) within 30 and 180 days.
Conclusions:
- Enhanced CETP activity during the acute phase of STEMI is an independent predictor of endothelial dysfunction.
- Elevated CETP activity is associated with adverse clinical outcomes in STEMI patients.
Objective:
Recent data suggests that cholesteryl ester transfer protein (CETP) activity may interact with acute stress conditions via inflammatory-oxidative response and thrombogenesis. We investigated this assumption in patients with ST-elevation myocardial infarction (STEMI).
Methods:
Consecutive patients with STEMI (n = 116) were enrolled <24-h of symptoms onset and were followed for 180 days. Plasma levels of C-reactive protein (CRP), interleukin-2 (IL-2), tumor necrosis factor (TNFα), 8-isoprostane, nitric oxide (NOx) and CETP activity were measured at enrollment (D1) and at fifth day (D5). Flow-mediated dilation (FMD) was assessed by ultrasound and coronary thrombus burden (CTB) was evaluated by angiography.
Results:
Neither baseline nor the change of CETP activity from D1 to D5 was associated with CRP, IL-2, TNFα, 8-isoprostane levels or CTB. The rise in NOx from D1 to D5 was inferior [3.5(-1; 10) vs. 5.5(-1; 12); p < 0.001] and FMD was lower [5.9(5.5) vs. 9.6(6.6); p = 0.047] in patients with baseline CETP activity above the median value than in their counterparts. Oxidized HDL was measured by thiobarbituric acid reactive substances (TBARS) in isolated HDL particles and increased from D1 to D5, and remaining elevated at D30. The change in TBARS content in HDL was associated with CETP activity (r = 0.72; p = 0.014) and FMD (r = -0.61; p = 0.046). High CETP activity at admission was associated with the incidence of sudden death and recurrent MI at 30 days (OR 12.8; 95% CI 1.25-132; p = 0.032) and 180 days (OR 3.3; 95% CI 1.03-10.7; p = 0.044).
Conclusions:
An enhanced CETP activity during acute phase of STEMI is independently associated with endothelial dysfunction and adverse clinical outcome.
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