4 research outputs found
Hydroxyl radical generation, levels of tumor necrosis factor-alpha, and progression to heart failure after acute myocardial infarction
OBJECTIVES We used acetylsalicylic acid (ASA) as a probing agent to quantify hydroxyl radical (˙OH) in
Controls and patients with coronary artery disease and to prospectively investigate ˙OH
production in patients with myocardial infarction (MI) complicated by heart failure (HF).
BACKGROUND Oxidative stress status (OSS) is a mechanism for transition to HF in experimental heart injury
models, but evidence for its causal role in humans is still limited.
METHODS Thirty healthy subjects (Controls), 12 patients with stable angina (Group 1), and 74 patients
with ST-segment elevation MI (Group 2) were enrolled. A dose of 250 mg Flectadol was
given intravenously before each blood collection to determine the 2,3-dihydroxybenzoic
acid/salicylic acid (DHBA/SA) ratio. We also quantified vitamin E and coenzyme Q10 to
monitor antioxidant reserve, as well as tumor necrosis factor (TNF)-alpha, TNF-soluble
receptors, interleukin (IL)-6, and IL-1ra to assess inflammatory status. All measurements
were repeated at month 6 in Group 2.
RESULTS There were no differences between Controls and Group 1. Group 2 showed increased ˙OH
production, peaking at 24 h, whereas vitamin E and coenzyme Q10 progressively declined.
Group 2 patients developing HF during hospitalization (Group 2Bi) presented with an
increase of both ˙OH production at discharge and inflammatory status, as compared with
patients without HF (Group 2Ai), persisting at month 6 in post-MI patients with HF
(Group 2Bii).
CONCLUSIONS We found a distinct pattern of ˙OH generation in post-MI patients who show progression to
HF. The interplay between OSS and inflammatory status should be targeted as a possible
mechanism of progression to post-MI left ventricular dysfunction. (J Am Coll Cardiol
2004;43:2000–8) © 2004 by the American College of Cardiology Foundatio