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Angiotensin-converting enzyme inhibition is associated with reduced troponin release in non–ST-elevation acute coronary syndromes

2001; Elsevier BV; Volume: 38; Issue: 3 Linguagem: Inglês

10.1016/s0735-1097(01)01426-7

1558-3597

Simon Kennon, Khalid Barakat, G. A. Hitman, Christopher P. Price, Peter Mills, Kulasegaram Ranjadayalan, Jackie Cooper, Heather D. Clark, Adam Timmis,

Heart Failure Treatment and Management

OBJECTIVES 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 μg/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 μg/l [0.19 to 2.65 μg/l] vs. 4.18 μg/l [0.91 to 12.41 μg/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 μg/l [0.72 to 8.02 μg/l] vs. 5.85 μg/l [1.19 to 12.79 μg/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.