High baseline fibrinogen concentration as a risk factor of no tissue reperfusion in ST-segment elevation acute myocardial infarction treated with successful primary percutaneous coronary intervention
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Published on: May 28, 2019
Jarosław Wasilewski1, Tadeusz Osadnik, Lech Poloński
1III Katedra i Oddział Kliniczny Kardiologii SlAM, ul. Szpitalna 2, 41-800 Zabrze, Poland. jaroslaw-wasilewski@wp.pl
Insights
High baseline fibrinogen concentration is linked to poor myocardial reperfusion after angioplasty. This finding suggests fibrinogen impacts blood flow and heart tissue recovery following artery recanalization.
Area of Science:
- Cardiology
- Hematology
- Vascular Biology
Background:
- Myocardial infarction (MI) patients often experience impaired tissue reperfusion post-successful epicardial artery recanalization.
- Microcirculation blood flow is influenced by vascular structure and blood rheology.
Purpose of the Study:
- To determine the relationship between initial fibrinogen levels and myocardial reperfusion success after coronary angioplasty.
- Investigate fibrinogen as a predictor for myocardial reperfusion in acute MI.
Main Methods:
- Compared baseline fibrinogen in 105 acute ST-segment elevation MI patients.
- Grouped patients based on successful tissue reperfusion (n=79) versus no reperfusion (n=26) via ST-segment normalization.
- Analyzed correlation with cardiac biomarkers and chest pain duration.
Main Results:
- No-reperfusion group had significantly higher baseline fibrinogen (523 mg/dl) vs. reperfusion group (395 mg/dl).
- Fibrinogen correlated positively with peak creatine kinase-MB and chest pain duration.
- Higher fibrinogen and longer chest pain duration independently increased no-reflow risk.
Conclusions:
- Baseline fibrinogen is an independent risk factor for failed myocardial reperfusion post-angioplasty.
- Elevated fibrinogen may impair blood rheology, contributing to the no-reflow phenomenon.
- Fibrinogen concentration correlates with infarct size and symptom duration.
Background:
In a large group of patients with myocardial infarction, lack of tissue reperfusion following successful recanalisation of the infarct-related epicardial artery is seen. Blood flow in the microcirculation depends not only on structural changes in the microvasculature but also on rheological features of the blood itself.
Aim:
To investigate the association between baseline fibrinogen concentration and myocardial reperfusion following successful coronary angioplasty.
Methodology:
In 105 patients with acute ST-segment elevation myocardial infarction, baseline fibrinogen concentration was compared between patients with successful tissue reperfusion (n=79) and with no myocardial reperfusion (n=26) measured as the degree of ST-segment normalisation after successful recanalisation of the infarct-related artery.
Results:
Baseline fibrinogen concentration was significantly higher in the no-reperfusion group than in the reperfusion group (523+/-198.02 mg/dl vs 395.56+/-144.98 mg/dl, p=0.0004). In the overall study population, fibrinogen level correlated positively with maximum creatine kinase MB fraction concentration (r=0.25, p=0.012) and duration of chest pain (r=0.31, p=0.002). Mean fibrinogen concentration was higher in patients with anterior myocardial infarction than in patients with the infarct-related artery other than the left anterior descending artery. The risk of no-reflow phenomenon assessed in multivariate analysis was higher if duration of chest pain was longer (OR=1.46, CI 95% 1.06-2.16, p=0.001) and baseline fibrinogen concentration higher (OR=1.51, CI 95% 1.011-4.58, p=0.021).
Conclusions:
Baseline fibrinogen concentration following successful mechanical recanalisation of the infarct-related coronary artery is an independent risk factor of a lack of myocardial reperfusion and it positively correlates with maximum creatine kinase MB fraction concentration and duration of chest pain. High fibrinogen concentration may affect rheological parameters of the blood and play an important role in the pathomechanism of myocardial no-reperfusion phenomenon following successful mechanical recanalisation of the infarct-related coronary artery.
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