title: Significant prostacyclin/thromboxane level imbalance after lower limb arterial angioplasty: a possible platelet function alteration.
abstract: OBJECTIVE
  The authors investigated prostacyclin (PGI2) and thromboxane (TX) productions in peripheral venous blood after lower limb revascularization by percutaneous transluminal angioplasty (PTA) versus diagnostic angiography. The purpose of this study was to investigate PGI2/TX imbalance after PTA. This imbalance is of pathophysiologic importance and it is a potential sign of platelet function alteration.
  
  
  METHODS
  Twenty-five patients requiring PTA were compared with 20 patients undergoing angiography alone from April 2004-December 2005 from a single vascular unit. Patient age range was 42-90 years, and the majority of patients were men. Prostaglandin F2-alpha (PGF2-alpha) and thromboxane B2 (TXB2) were measured sequentially (preprocedure, at 1 hour, and 24 hours after procedure). Differences between postprocedure and preprocedure level were compared statistically between angiography and PTA.
  
  
  RESULTS
  Baseline demographics were distributed equally between the two groups except presence of critical ischemia and ankle brachial pressure index, which were two significant confounders. TXB2 was significantly higher after PTA at 1 hour and 24 hours after PTA (P = .005 and P = .014 respectively), PGF2-alpha was significantly higher 24 hours after PTA only (P = .018) (Mann-Whitney U test).
  
  
  CONCLUSIONS
  PGI2/TX balance homeostasis is of significant pathophysiologic importance. The authors found that PTA results in significant PGI2/TX imbalance and shifts more toward increased TX production. This finding is partly suggestive of significant platelet activation. This imbalance in PGI2/TX level may have implications for future failure of PTA. Future research in reducing this platelet activation is recommended.
authors.affiliation: Vascular Surgery Department, Hammersmith Hospital, London, England. jitsparmar@yahoo.co.uk
authors.forename: Jitesh H
authors.initials: JH
authors.lastname: Parmar
authors.forename: Mo
authors.initials: M
authors.lastname: Aslam
authors.forename: Nigel J
authors.initials: NJ
authors.lastname: Standfield
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017130:Angioplasty / Q000009:adverse effects; D055109:Ankle Brachial Index; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000378:metabolism*; D003251:Constriction, Pathologic; D015237:Dinoprost / Q000097:blood; D004739:England; D011464:Epoprostenol / Q000097:blood; D005260:Female; D005263:Femoral Artery / Q000000981:diagnostic imaging; D006801:Humans; D007083:Iliac Artery / Q000000981:diagnostic imaging; D035002:Lower Extremity / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D058729:Peripheral Arterial Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000628:therapy*; D015539:Platelet Activation; D044062:Prostaglandins I / Q000097:blood*; D015641:Radiography, Interventional / Q000009:adverse effects; D013928:Thromboxane A2 / Q000097:blood; D013929:Thromboxane B2 / Q000097:blood; D013931:Thromboxanes / Q000097:blood*; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D044062:Prostaglandins I; D013931:Thromboxanes; D013929:Thromboxane B2; D013928:Thromboxane A2; D015237:Dinoprost; D011464:Epoprostenol