Chlamydia pneumoniae serology is associated with thrombosis-related but not with plaque-related microembolization during carotid endarterectomy.

نویسندگان

  • Tryfon Vainas
  • Harrie A J M Kurvers
  • Werner H Mess
  • Rick de Graaf
  • Rajaa Ezzahiri
  • Jan H M Tordoir
  • Geert-Willem H Schurink
  • Cathrien A Bruggeman
  • Peter J E H M Kitslaar
چکیده

BACKGROUND AND PURPOSE Chlamydia pneumoniae has repeatedly been associated with atherosclerotic disease. Our study was designed to clarify whether this association is based on C pneumoniae-induced transformation of a stable into an unstable atherosclerotic plaque or on stimulation of hypercoagulability leading to increased thrombotic arterial occlusions by C pneumoniae infection. Transcranial Doppler ultrasonographic monitoring of the middle cerebral artery during carotid endarterectomy offers the opportunity to study, before removal of the plaque, atherothrombotic emboli dislodging from an unstable carotid plaque (plaque-related emboli) and emboli related to (excessive) thrombus formation at the endarterectomy site after removal of the plaque and restoration of flow (thrombosis-related emboli). METHODS C pneumoniae IgA (> or =1/16) and IgG (> or =1/64) seropositivity was assessed in 53 patients with symptomatic carotid artery disease undergoing carotid endarterectomy. The removed carotid plaques were studied histologically to assess plaque instability. RESULTS Plaque- and thrombosis-related emboli were registered in 43 patients with an adequate transtemporal window. IgA seropositivity (58%) was associated significantly with thrombosis-related embolization (P=0.030) but not with plaque-related embolization or with histological plaque instability. CONCLUSIONS C pneumoniae serology is associated with microembolization after endarterectomy and restoration of flow. Since these microemboli represent platelet aggregations and are related to cerebrovascular complications, our data suggest that C pneumoniae infection contributes to cerebrovascular events in patients with carotid artery disease through stimulation of thrombosis.

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عنوان ژورنال:
  • Stroke

دوره 33 5  شماره 

صفحات  -

تاریخ انتشار 2002