title: [Is the reduction of the plasma levels of endothelin in the acute and sub-acute stage of myocardial infarct one of the beneficial effects of early treatment with ace inhibitors?].
abstract: BACKGROUND
  Studies showed that endothelin-1 (ET-1) was increased in the acute myocardial infarction (AMI). Experimental studies reported that captopril was able to reduce ET-1 secretion. In addition increased levels of ET-1 were reported as a negative prognostic index. The study was aimed to verify whether captopril was able to reduce plasma ET-1 levels in the acute and subacute phases of AMI.
  
  
  METHODS
  Forty five patients, hospitalized for suspected anterior AMI within 4 h since the onset of symptoms, suitable for thrombolysis (first episode), in Killip class 1-2, were randomized (double blind) into two groups: Group A (23 patients, pts), 7 females and 16 males, received captopril 6.25 mg orally (as first dose) 2-4 h after starting thrombolysis, and the doses of captopril were successively increased up to 25 mg every 8 h. Group B: (22 pts), 5 females and 17 males, received placebo after thrombolysis. All the patients met the reperfusion criteria.
  
  
  RESULTS
  The two groups were similar for age, sex, CK peak, ejection fraction, end systolic volume and risk factors. Plasma ET levels were checked on admission, and 2, 12, 24, 48, 72 hours, after starting thrombolysis. Mean concentrations of ET +/- SD: Group A: basal 1.50 +/- 0.67, at 2 h 2.31 +/- 1.24, 12 h 1.84 +/- 1.45, 24 h 1.30 +/- 0.72, 48 h 0.95 +/- 0.50, 72 h 0.60 +/- 0.15 fmol/ml (p < 0.001). Group B: basal 1.58 +/- 0.83, at 2 h 2.38 +/- 1.35, 12 h 2.33 +/- 1.71, 24 h 1.80 +/- 1.41, 48 h 1.46 +/- 0.88, 72 h 0.93 +/- 0.44 fmol/ml (p < 0.001). Difference between the two groups was significant at 48 h (p < 0.05), and 72 h (p < 0.001).
  
  
  CONCLUSIONS
  Our data suggest that captopril affects plasma endothelin levels in the acute and subacute phases of AMI. In addition, our results seem to be an additional support to the beneficial effects of early captopril treatment in patients with AMI.
authors.affiliation: Divisione di Cardiologia, Ospedale G.F. Ingrassia, Palermo.
authors.forename: P
authors.initials: P
authors.lastname: Di Pasquale
authors.forename: V
authors.initials: V
authors.lastname: Bucca
authors.forename: S
authors.initials: S
authors.lastname: Scalzo
authors.forename: S
authors.initials: S
authors.lastname: Cannizzaro
authors.forename: A M
authors.initials: AM
authors.lastname: Longo
authors.forename: V
authors.initials: V
authors.lastname: Alessi
authors.forename: M
authors.initials: M
authors.lastname: D'Amato
authors.forename: F
authors.initials: F
authors.lastname: Manusia
authors.forename: M F
authors.initials: MF
authors.lastname: Magatti
mesh_terms: D000284:Administration, Oral; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002216:Captopril / Q000627:therapeutic use*; D003402:Creatine Kinase / Q000097:blood; D004311:Double-Blind Method; D019332:Endothelin-1 / Q000097:blood*; D005260:Female; D006801:Humans; D007527:Isoenzymes; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000201:enzymology; D015912:Thrombolytic Therapy; D013997:Time Factors
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D019332:Endothelin-1; D007527:Isoenzymes; D002216:Captopril; D003402:Creatine Kinase