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Published on: January 28, 2020
Association between inflammation, lipid and hemostatic factors in patients with stable angina
José D Sagastagoitia1, Yolanda Sáez, Marta Vacas
1Servicio de Cardiología, Hospital de Basurto, Departamento Medicina, Universidad del País Vasco UPV/EHU, Bilbao, Spain.
Insights
Inflammation, indicated by C-reactive protein, correlates with prothrombotic factors like fibrinogen and D-dimer in stable angina patients. Apolipoprotein A1 shows an inverse association, suggesting anti-inflammatory properties.
Area of Science:
- Cardiovascular Medicine
- Clinical Chemistry
- Atherosclerosis Research
Background:
- Atherosclerosis involves dyslipidemia, thrombosis, and inflammation.
- Understanding the interplay between these factors is crucial for managing stable angina.
Purpose of the Study:
- To investigate the association between inflammation, lipid profiles, and thrombotic markers in patients with stable angina.
- To explore the relationship between C-reactive protein, lipid parameters, and coagulation factors.
Main Methods:
- Study included 295 patients (mean age 65.69 years) with stable angina.
- Measured levels of C-reactive protein, total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, lipoprotein(a), apolipoproteins A1 and B100, fibrinogen, and D-dimer.
- Utilized correlation and multivariate analyses to assess associations.
Main Results:
- Elevated C-reactive protein correlated positively with fibrinogen and D-dimer.
- High C-reactive protein showed an inverse correlation with HDL cholesterol and apolipoprotein A1.
- Fibrinogen and D-dimer were independently associated with high C-reactive protein; apolipoprotein A1 was inversely associated.
Conclusions:
- Confirms a link between prothrombotic states and inflammation in stable angina.
- Suggests apolipoprotein A1 may possess anti-inflammatory effects.
- Highlights the complex relationship between lipids, thrombosis, and inflammation in cardiovascular disease.
Introduction:
Dyslipidemia and thrombotic processes are both clearly involved in atherogenesis and its secondary complications. Moreover, inflammation has also been shown to play an important role in the pathophysiology of atherosclerosis. Our objective was to determine the association between inflammation, lipids and thrombosis in a group of patients with stable angina.
Patients And Methods:
295 patients (217 males and 78 females) with a mean age of 65.69+/-11.24 years. Levels of C-reactive protein, total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, lipoprotein(a), apolipoproteins A1 and B100, fibrinogen and D-dimer were determined for each.
Results:
Arithmetic and geometric means of C-reactive protein in the sample were 10.7 and 1.4 mg/l, respectively. Distributing the sample by quartiles of C-reactive protein, we found a positive correlation between C-reactive protein, fibrinogen and D-dimer levels (p<0.000), and an inverse correlation for HDL cholesterol and apolipoprotein A1 (p<0.000). In multivariate analysis, fibrinogen (p<0.000) and D-dimer (p<0.01) levels were independently associated with high levels of C-reactive protein. Of the lipid factors, only apolipoprotein A1 (p<0.000) was independently and inversely associated with high levels of C-reactive protein.
Conclusions:
These data confirm the association between prothrombotic and inflammatory states and suggest the anti-inflammatory effect of apolipoprotein A1.
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