TY - JOUR
T1 - Hydroxyl radical generation, levels of tumor necrosis factor-alpha, and progression to heart failure after acute myocardial infarction
AU - Valgimigli, Marco
AU - Merli, Elisa
AU - Malagutti, Patrizia
AU - Soukhomovskaia, Olga
AU - Cicchitelli, Giordano
AU - Antelli, Alessandra
AU - Canistro, Donatella
AU - Francolini, Gloria
AU - Macrì, Gaetano
AU - Mastrorilli, Francesca
AU - Paolini, Moreno
AU - Ferrari, Roberto
PY - 2004/6/2
Y1 - 2004/6/2
N2 - 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.
AB - 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.
KW - OH
KW - acetylsalicylic acid
KW - ASA
KW - DHBA
KW - dihydroxybenzoic acid
KW - heart failure
KW - HF
KW - hydroxyl radical
KW - IL
KW - interleukin
KW - left ventricular
KW - LV
KW - MI
KW - myocardial infarction
KW - OSS
KW - oxidative stress status
KW - reactive oxygen species
KW - ROS
KW - SA
KW - salicylic acid
KW - sTNFR
UR - http://www.scopus.com/inward/record.url?scp=2542461010&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=2542461010&partnerID=8YFLogxK
U2 - 10.1016/j.jacc.2004.01.036
DO - 10.1016/j.jacc.2004.01.036
M3 - Article
C2 - 15172404
AN - SCOPUS:2542461010
VL - 43
SP - 2000
EP - 2008
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 11
ER -