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Heart failure and plasminogen activator inhibitor 1 in acute ST elevation myocardial infarction treated with primary percutaneous coronary intervention

Session Poster Session 1

Speaker Doctor Marin Pavlov

Event : Acute Cardiovascular Care 2019

  • Topic : heart failure
  • Sub-topic : Biomarkers
  • Session type : Poster Session

Authors : M Pavlov (Zagreb,HR), Z Babic (Zagreb,HR), V Nikolic Heitzler (Zagreb,HR), A Djuzel (Zagreb,HR), K Kordic (Zagreb,HR), I Celap (Zagreb,HR), V Degoricija (Zagreb,HR)

M Pavlov1 , Z Babic1 , V Nikolic Heitzler1 , A Djuzel1 , K Kordic1 , I Celap2 , V Degoricija3 , 1University Hospital Sestre Milosrdnice, Cardiac intensive care unit - Zagreb - Croatia , 2University Hospital Sestre Milosrdnice, Department of Clinical Chemistry - Zagreb - Croatia , 3University Hospital Sestre Milosrdnice, Department of Medicine - Zagreb - Croatia ,

Acute Heart Failure: Biomarkers

To investigate whether plasminogen activator inhibitor 1 (PAI-1) activity detected during first 24 hours of treatment of ST elevation myocardial infarction (STEMI) differs in patients with and without acute onset heart failure (HF).
A total of 87 STEMI patients treated with primary percutaneous coronary intervention (PCI) were enrolled in the prospective observational single center cohort study. PAI-1 activity was determined on admission (prior to PCI) and after exactly 24 hours by using commercially available test Berichrom PAI (Siemens, Marburg, Germany). PAI-1 activity rise was defined as activity in second sample subtracted by activity at admission. Primary end-point was defined as an episode of HF requiring intravenous therapy within index hospital treatment, regardless of ejection fraction. Secondary end-point was defined as death at 5-year follow-up.
Primary end-point occured in 9 patients (10.3%). In this group of patients, cardiogenic shock was more common (22.2% vs. 1.3%, chi square, test P=0.001), and ejection fraction was lower (median 45% vs. 55%, Mann-Whitney U test, P=0.001), while differences in other variables did not reach statistical significance level. Median PAI-1 activity rise in patients with HF was 4.10 U/mL (interquartile range (IQR) 1.75-7.65 U/mL), and in patients without HF 1.18 U/mL (IQR -0.04-2.22 U/mL). In linear regression model, PAI-1 rise was independently related to HF (odds ratio (OR) 4.4), use of thrombus aspiration (OR 3.8) and body weight (OR -2.2). Secondary endpoint occured in 2 patients during hospital treatment, and in 11 during follow up. Higher mortality was found in patients older than 65 (chi square test, P=0.034), females (chi square test, P=0.030), patients with occurrence of HF (Fisher exact test, P=0.026), worse final Thrombolysis in myocardial infarction (TIMI) flow (Fisher-Halton-Freeman test, P=0.001), higher PAI-1 activity rise (Mann-Whitney U test, P=0.004), lower left ventricular ejection fraction (Mann-Whitney U test, P=0.014) and lower body mass index (Mann-Whitney U test, P=0.024). In multivariate Cox regression analysis, with dichotomised PAI-1 activity rise (expressed as >3.7 U/mL; cut-off point found by receiver operating characteristic curve analysis), independent predictors of death were final TIMI flow and PAI-1 activity rise >3.7 U/mL, but not HF.
Higher PAI-1 activity rise was observed in STEMI patients treated with primary PCI in whom acute HF occured during index hospitalisation. Whether the detected association is clinically significant, and contributes to long term outcome of the patients with HF in coronary artery disease, is to be determined in further studies.

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