Transient intermittent lymphocyte activation is responsible for the instability of angina

Gian Gastone Neri Serneri, Rosanna Abbate, Anna Maria Gori, Monica Attanasio, Francesca Martini, Betti Giusti, Piero Dabizzi, Loredana Poggesi, Pietro Amedeo Modesti, Francesco Trotta, Carlo Rostagno, Maria Boddi, Gian Franco Gensini

Research output: Contribution to journalArticlepeer-review


Background. Blood clotting activation is an important component of the inflammatory response; the outbursts of unstable angina are usually associated with increased thrombin formation and coronary mural thrombosis. Methods and Results. To investigate 1) whether monocyte activation is responsible for the enhanced thrombin formation during bursts of unstable angina and 2) what mechanism(s) might be responsible for monocyte activation, we studied patients with unstable angina (n=31), stable effort angina (n=23), left endoventricular thrombosis (n=8), and control subjects (n=44), measuring plasma fibrinopeptide A (FPA) levels and the capacity of monocytes to express procoagulant activity (PCA) and of lymphocytes to modulate this expression. Patients with unstable angina and patients with endoventricular thrombosis had significantly (p5 monocytes, median and range; 120, 1.1-463.2 versus 10.8, 0.8-39.1 in control subjects; p

Original languageEnglish
Pages (from-to)790-797
Number of pages8
Issue number3
Publication statusPublished - Sep 1992


  • Angina, effort
  • Angina, unstable
  • Monocytes
  • Tissue factor

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine


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