[Thrombophilic state inpatients suffering from myocardial infarction with or without carotid atherosclerotic lesions]

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G Avellone1, V Di Garbo, R Cordova

  • 1Istituto di Clinica Medica, Università degli Studi, Palermo.

Cardiologia (Rome, Italy)
|November 1, 1995
PubMed

Insights

Myocardial infarction survivors show heightened blood clot formation and impaired clot breakdown, especially those with carotid artery disease. This suggests a pro-thrombotic state contributes to atherosclerosis and related complications.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Vascular Biology

Background:

  • Myocardial infarction (MI) survivors often face risks of recurrent events and thromboembolic complications.
  • Carotid atherosclerotic lesions are common comorbidities in cardiovascular disease patients.
  • Understanding the hemostatic balance in these patients is crucial for risk stratification.

Purpose of the Study:

  • To investigate metabolic, coagulation, and fibrinolytic profiles in MI survivors.
  • To compare these parameters between patients with and without carotid atherosclerotic lesions.
  • To identify potential thrombophilic markers associated with vascular disease progression.

Main Methods:

  • 35 MI survivors were categorized into groups with (n=16) or without (n=19) carotid plaques.
  • Extracranial carotid arteries were assessed using B-mode duplex scanning.
  • Metabolic markers (lipids, apolipoproteins), coagulation factors (Factor VII, fibrinogen), and fibrinolytic markers (PAI, t-PA) were measured.

Main Results:

  • MI patients exhibited dyslipidemia and altered apolipoprotein profiles compared to controls.
  • Patients with carotid lesions showed higher triglycerides and Lipoprotein(a) [Lp(a)].
  • Both MI groups displayed enhanced coagulation (Factor VII, Fibrinogen, F1+2, Thrombin-Antithrombin) and impaired fibrinolysis (lower t-PA, higher PAI) post-venous occlusion.

Conclusions:

  • MI survivors exhibit a pro-thrombotic state characterized by activated coagulation and deficient fibrinolysis.
  • The presence of carotid atherosclerotic lesions exacerbates this thrombophilic tendency.
  • These hemostatic abnormalities may contribute to the pathogenesis of atherosclerotic vascular disease and thromboembolic events.

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