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Updated: Aug 30, 2026

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
The pre-existence of an acute coronary event predicts differences in biological parameters and clinical evolution
Andrei C Sposito1, Pedro A Lemos, Raul C Maranhão
1Heart Institute (InCor), University of São Paulo Medicine School, São Paulo, Brazil. sposito@zerbini.org.br
Insights
Patients with stable coronary artery disease (CAD) and a prior myocardial infarction (MI) have distinct biological markers and a higher risk of developing refractory angina compared to those with uneventful angina.
Area of Science:
- Cardiology
- Biochemistry
Background:
- Stable angina patients are often treated similarly, regardless of prior acute coronary events.
- Clinical experience suggests potential differences in disease behavior between these patient groups.
Purpose of the Study:
- To investigate differences in clinical, angiographic, and biological parameters between stable angina patients with and without a prior myocardial infarction (MI).
Main Methods:
- Compared cardiovascular risk factors, clinical evolution, angiographic data, white blood cell (WBC) count, lipids, and fibrinogen between 160 MI patients and 226 patients with uneventful angina.
- Utilized multivariate logistic regression to identify independent predictors.
Main Results:
- Myocardial infarction (MI) patients showed higher WBC count, fibrinogen, and lipoprotein(a), with lower HDL cholesterol and apoA1.
- Fibrinogen, lipoprotein(a), and HDL cholesterol were independently associated with prior MI.
- Prior MI patients were more likely to develop refractory angina, with fibrinogen levels independently predicting this outcome.
Conclusions:
- Stable coronary artery disease (CAD) patients with prior myocardial infarction (MI) possess a distinct biological profile.
- These patients exhibit a different clinical evolution, with a higher propensity towards refractory angina.
- Biological markers like fibrinogen are linked to disease progression in this cohort.
Background:
To date, patients displaying stable angina with or without a previous acute coronary event have been grouped together and are offered nowadays, similar clinical approach. However, from clinical experience, increasing doubt exists whether they behave clinically in the same way. In the current study, we investigated whether differences might exist in the clinical, angiographic and biological parameters between these two distinct clinical presentations.
Methods:
The cardiovascular risk factor profile, clinical evolution, angiographic data, white blood cell (WBC) count and plasma concentrations of lipids and fibrinogen were compared between two groups of patients with longstanding stable angina. The first group consisted of 160 subjects who had undergone myocardial infarction (MI) as the first manifestation of coronary artery disease (CAD) and had no further coronary event. The second group was composed of 226 subjects who had effort-induced angina but never experienced an acute coronary event. The mean period between the first CAD manifestation and entry into the study was 7+/-6 years for MI group and 7+/-4 years for patients with uneventful angina.
Results:
MI patients displayed 8% higher WBC count (P=0.038), 20% higher fibrinogen (P=0.001), 12% lower HDL cholesterol (P=0.02), 8% lower apoA1 (P=0.005) and 46% higher lipoprotein (a) (P=0.005) than patients who presented an uneventful clinical course. Upon multivariate logistic regression analysis, fibrinogen (OR=1.14; 95% CI=1.08-1.28; P=0.033), lipoprotein (a) (OR=1.19; 95% CI=1.05-1.34; P=0.0036) and HDL cholesterol levels (OR=0.97; 95% CI=0.94-0.99; P=0.0095) remained independently associated with the pre-existence of MI. Patients with prior MI evolved more frequently towards clinically refractory angina (P=0.04). In addition, fibrinogen levels were independently associated with evolution to clinically refractory angina (OR=1.03; 95% CI=1.005-1.550; P=0.0448).
Conclusions:
Stable CAD patients with a prior MI differ from those who display an uneventful effort-induced angina in their biological profile and their evolution towards clinically refractory angina.
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