CLINICAL STUDY: ACUTE CORONARY SYNDROME
Angiotensin-converting enzyme inhibition is associated with reduced troponin release in non–ST-elevation acute coronary syndromes
Simon Kennon, MB, MRCP*,
Khalid Barakat, MA, MRCP*,
Graham A. Hitman, MD, FRCP ,
Christopher P. Price, PhD, FRCPath ,
Peter G. Mills, MA, FRCP*,
Kulasegaram Ranjadayalan, MPhil, MRCP ,
Jackie Cooper, MSc||,
Heather Clark, PhD, MRCPath and
Adam D. Timmis, MD, FRCP*
* Department of Cardiology, St. Bartholomew’s and the Royal London School of Medicine and Dentistry, Queen Mary, University of London, London, United Kingdom
Department of Clinical Biochemistry, St. Bartholomew’s and the Royal London School of Medicine and Dentistry, Queen Mary, University of London, London, United Kingdom
Department of Diabetes and Metabolic Medicine, St. Bartholomew’s and the Royal London School of Medicine and Dentistry, Queen Mary, University of London, London, United Kingdom
Department of Cardiology, Newham Healthcare Trust, London, United Kingdom
|| MRC Epidemiology and Medical Care Unit, Charterhouse Square, London, United Kingdom
Manuscript received January 10, 2001;
revised manuscript received May 8, 2001,
accepted May 22, 2001.
Reprint requests and correspondence: Dr. Simon Kennon, The London Chest Hospital, Bonner Road, London E2 9JX, UK
srok{at}dircon.co.uk
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.
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Abbreviations and Acronyms
| | ACE | = angiotensin-converting enzyme | | ACS | = acute coronary syndromes | | CAD | = coronary artery disease | | ECG | = electrocardiogram, electrocardiographic | | MI | = myocardial infarction |
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