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[Evaluation of resistance to activated protein C in myocardial infarction patients]
G Avellone1, V Di Garbo, D Di Raimondo
1Istituto di Clinica Medica, Centro per Diagnosi delle Dislipidemie e del Rischio Trombotico, Università degli Studi, Palermo, Italy.
Insights
Resistance to activated protein C (APCR) was found in 30% of men who had myocardial infarction. This finding suggests APCR may play a role in arterial thrombosis and warrants further investigation for prevention strategies.
Area of Science:
- Hematology
- Cardiovascular Medicine
- Genetics
Context:
- Activated protein C resistance (APCR) is a common inherited coagulation disorder, primarily linked to venous thromboembolism.
- The association between APCR and arterial thrombosis, particularly myocardial infarction, remains less understood.
- This study investigates APCR prevalence in male myocardial infarction survivors without traditional cardiovascular risk factors.
Purpose:
- To determine the prevalence of APCR in men who have experienced myocardial infarction.
- To assess potential links between APCR and specific coagulation and lipid parameters in these patients.
Summary:
- Thirty percent of male myocardial infarction patients (n=20) exhibited APCR, compared to none in the control group (n=20).
- APCR patients showed elevated fibrinogen, LDL-C, APO B100, oxidized LDL antibodies, and C4 levels.
- Positive correlations were found between the APCR ratio and fibrinogen/oxidized LDL antibodies.
Impact:
- The high prevalence of APCR in this cohort suggests its potential significance in arterial thrombosis.
- Findings support considering APCR screening for primary prevention of arterial thrombosis.
- This research may inform secondary prevention strategies for thromboembolic complications.
Background:
It is known that resistance to activated protein C (APCR), often associated with a single point mutation (Arg506-->Gln) in the coagulation factor V gene (factor V Leiden), is the most frequent inherited abnormality of blood coagulation. It plays a key role as pathogenetic factor of venous thromboembolism, but its association with an increased risk of arterial thrombosis is uncertain. Aim of the present study was to evaluate the prevalence of APCR in men, who suffered myocardial infarction more than 6 months earlier and without cardiovascular risk factors (hypercholesterolemia, smoking, diabetes, obesity and hypertension).
Methods:
The study was carried on 20 men aged <65 years who have suffered myocardial infarction. Twenty healthy subjetcs matched for sex and age were recruited as controls. We determined: PTT, PTT-PCA (Activated Protein C), PTT-PCA/PTT, AntiThrombin III, Protein C, Protein S, Fibrinogen, Glucose, Triglycerides, Cholesterol, HDL-C, LDL-C, APO A1, APO B100, Lp(a), oxizided LDL antibody and some components of the complement system (C3c, C4).
Results:
In the group of patients there were six subjects (30%) with APCR, while there were no subjects in the control group (0%) with APCR. Patients were subdivided into two groups: with and without APCR. Patients with APCR displayed significantly higher levels of fibrinogen (367.5+/-48.4 vs 268.3+/-37.7), LDL-C (147.0 +/-20.7 vs 125.8+/-25,6), APO B100 (133.8+/-29.8 vs 121.8+/-31.5), oxizide LDL antibody (596.8+/-357 vs 315.3+/-179.6) and C4 (45.6+/-10 vs 37.85+/-11,3). Significant positive correlations (p<0.05) were observed between PTT-PCA/PTT ratio and fibrinogen (r=0.68) and between PTT-PCA/PTT ratio and oxidized LDL antibody (r=0.61).
Conclusions:
In conclusion, the high prevalence of APCR (30%) in our patients seems to be important in order to carry out a primary prevention of arterial thrombosis and a secondary prevention of new thromboembolic complications.