Angiotensin-converting enzyme inhibition is associated with reduced troponin release in non-ST-elevation acute coronary syndromes.
OBJECTIVE
This study was done to determine the effects of angiotensin-converting enzyme (ACE) inhibition and other clinical factors on troponin release in non-ST-elevation acute coronary syndrome (ACS).


BACKGROUND
Troponin is now widely used as a marker of risk in ACS, but determinants of its release have not been defined.


METHODS
This was a prospective cohort study of 301 consecutive patients admitted with non-ST-elevation ACS. Baseline clinical data were recorded, ACE gene polymorphism was determined and serial blood samples were obtained for troponin-I assay.


RESULTS
Significant troponin-I release (>0.1 microg/l) was detected in 93 (31%) patients. Pretreatment with ACE inhibitors, recorded in 53 patients (17.6%), independently reduced the odds of troponin-I release (odds ratio 0.25; 95% confidence intervals 0.10 to 0.64) and was associated with lower maximum troponin-I concentrations (median [interquartile range]) compared with patients not pretreated with ACE inhibitors (0.44 microg/l [0.19 to 2.65 microg/l] vs. 4.18 microg/l [0.91 to 12.41 microg/l], p = 0.01). Pretreatment with aspirin, recorded in 173 patients (57.5%), did not significantly reduce the odds of troponin-I release after adjustment but was associated with lower maximum troponin-I concentrations compared with patients not pretreated with aspirin (2.31 microg/l [0.72 to 8.02 microg/l] vs. 5.85 microg/l [1.19 to 12.79 microg/l], p = 0.05). The ACE genotyping (n = 268) showed 81 patients (30%) DD homozygous and 77 (29%) II homozygous. There was no association between ACE genotype and troponin release.


CONCLUSIONS
We conclude that ACE inhibition reduces troponin release in non-ST-elevation ACS. This is likely to be mediated by the beneficial effects of treatment on vascular reactivity and the coagulation system.
Kennon
S
S
Department of Cardiology, St. Bartholomew's and the Royal London School of Medicine and Dentistry, Queen Mary, University of London, London, United Kingdom. srok@dircon.co.uk
Barakat
K
K
Hitman
G A
GA
Price
C P
CP
Mills
P G
PG
Ranjadayalan
K
K
Cooper
J
J
Clark
H
H
Timmis
A D
AD
D000368:Aged; D000789:Angina, Unstable / Q000097:blood* / Q000503:physiopathology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D005838:Genotype; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood* / Q000503:physiopathology; D011446:Prospective Studies; D012084:Renin-Angiotensin System / Q000187:drug effects*; D013577:Syndrome; D014336:Troponin / Q000097:blood*; D014664:Vasodilation / Q000187:drug effects
D000806:Angiotensin-Converting Enzyme Inhibitors; D014336:Troponin