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Acute release of plasminogen activator inhibitor-1 in ST-segment elevation myocardial infarction predicts mortality
J P Collet1, G Montalescot, E Vicaut
1Institut de Cardiologie, Pitié-Salpêtrière Hospital, Paris, France.
Insights
The acute release of von Willebrand factor (vWF) and plasminogen activator inhibitor-1 (PAI-1) in ST-segment elevation myocardial infarction (STEMI) is linked to patient death and heart failure. Elevated PAI-1 levels are a significant independent predictor of mortality within 30 days.
Area of Science:
- Cardiology
- Biomarkers
- Acute Coronary Syndromes
Background:
- Previous studies suggest a link between von Willebrand factor (vWF) and plasminogen activator inhibitor-1 (PAI-1) and outcomes in acute coronary syndromes.
- The role of acute marker release in ST-segment elevation myocardial infarction (STEMI) requires further investigation.
Purpose of the Study:
- To evaluate the acute release of vWF and PAI-1 in STEMI patients.
- To determine the association of these markers with mortality and heart failure development.
Main Methods:
- 153 consecutive STEMI patients had vWF and PAI-1 antigen levels measured at admission (H0) and 24 hours later (H24).
- Outcomes including 30-day mortality and heart failure (Killip stage ≥3) were assessed.
- Statistical analysis identified predictors of death.
Main Results:
- The 30-day death rate was 7.2%, with 13.7% experiencing heart failure on admission.
- Acute release of PAI-1 and vWF was significantly higher in patients who died versus survivors.
- Increased PAI-1 and vWF release was also observed in patients who developed heart failure.
- Postangioplasty TIMI-3 flow and acute PAI-1 release were independent predictors of 30-day death.
Conclusions:
- Acute release of vWF and PAI-1 within 24 hours of STEMI correlates with increased risk of death and heart failure.
- The acute rise in PAI-1 is a potent independent predictor of 30-day mortality in STEMI patients.
Background:
A few studies have suggested that von Willebrand factor (vWF) or plasminogen activator inhibitor-1 (PAI-1) can be associated with outcomes of acute coronary syndromes. The present study was designed to assess the acute release of these markers in ST-segment elevation myocardial infarction (STEMI) and their relations to death.
Methods And Results:
In 153 consecutive patients with STEMI, vWF and PAI-1 antigens were measured on admission (H0) and 24 hours later (H24). At 30 days, the death rate was 7.2%. Heart failure (Killip stage > or =3) on admission was present in 13.7% of patients. The acute release of PAI-1 (H24-H0, in ng/mL) and of vWF (H24-H0, in %) was dramatically higher in patients who died than in those who survived (46.9+/-26.3 versus -0.6+/-2.8 ng/mL, P=0.0001 and 65.8+/-20.0% versus 10.0+/-5.1%, P=0.004 for PAI-1 and vWF, respectively) and in patients developing heart failure compared with those without (24.8+/-10.1 versus -1.1+/-3.3 ng/mL, P=0.004 and 47.3+/-11.0% versus 8.1+/-5.6%, P=0.005 for PAI-1 and vWF, respectively). The release of PAI-1 correlated weakly with the left ventricular ejection fraction (R=-0.195, P=0.01) and the peak of troponin (R=0.149, P=0.045). Postangioplasty TIMI-3 flow and the acute release of PAI-1 were the only 2 independent predictors of death at 30 days.
Conclusions:
The acute release of vWF and PAI-1 over the first 24 hours of STEMI is associated with death and heart failure. The acute rise of PAI-1 is also a strong independent predictor of death at 30 days.
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