Angiotensin-converting enzyme inhibition is associated with reduced troponin release in non-ST-elevation acute
S Kennon1, K Barakat, G A Hitman
1Department 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
Insights
Angiotensin-converting enzyme (ACE) inhibition significantly reduces troponin release in patients with non-ST-elevation acute coronary syndrome (ACS). This finding suggests ACE inhibitors may mitigate myocardial damage in ACS.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Troponin is a critical risk marker in acute coronary syndrome (ACS).
- Determinants of troponin release in ACS remain incompletely defined.
- Understanding these determinants is crucial for risk stratification and treatment optimization.
Purpose of the Study:
- To investigate the impact of angiotensin-converting enzyme (ACE) inhibition on troponin release in non-ST-elevation ACS.
- To identify other clinical factors influencing troponin release.
- To explore the role of ACE gene polymorphism in troponin release.
Main Methods:
- Prospective cohort study of 301 patients with non-ST-elevation ACS.
- Collection of baseline clinical data and ACE gene polymorphism.
- Serial troponin-I assays to quantify release levels.
Main Results:
- ACE inhibitor pretreatment was independently associated with a significant reduction in troponin-I release (OR 0.25).
- Patients pretreated with ACE inhibitors had substantially lower maximum troponin-I concentrations.
- Aspirin pretreatment showed a trend towards lower troponin levels but did not significantly reduce troponin release odds.
- No association was found between ACE genotype and troponin release.
Conclusions:
- ACE inhibition effectively reduces troponin release in non-ST-elevation ACS.
- This effect is likely mediated by improved vascular reactivity and coagulation modulation.
- ACE inhibitors represent a valuable therapeutic strategy in managing ACS to limit myocardial injury.
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 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.
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