Hydroxyl radical generation, levels of tumor necrosis factor-alpha, and progression to heart failure after acute myocardial infarction

Valgimigli, Marco; Merli, E; Malagutti, Patrizia; Soukhomovskaia, Olga; Cicchitelli, Giordano; Antelli, Alessandra; Canistro, Donatella; Francolini, Gloria; Macrì, Gaetano; Mastrorilli, Francesca; Paolini, Moreno; Ferrari, Roberto

doi:10.1016/j.jacc.2004.01.036

Cited by 46 publications

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“…Accordingly, results of an unadjusted analysis in this setting should be considered with caution. 16 Our multivariate analysis suggests that only levels of sTNFR-1 during acute MI predict the occurrence of death and new-onset HF independently from LV systolic function, Killip class, and peak CK-MB.…”

Section: Discussionmentioning

confidence: 69%

Tumor Necrosis Factor-α Receptor 1 Is a Major Predictor of Mortality and New-Onset Heart Failure in Patients With Acute Myocardial Infarction

et al. 2005

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Background-Tumor necrosis factor alpha-␣ (TNF-␣) activation is an independent prognostic indicator of mortality in patients with heart failure (HF). Despite the recognition that several TNF family cytokines are elevated during myocardial infarction, their role in predicting subsequent prognosis in these setting remains poorly understood. Methods and Results-We performed a systematic evaluation of TNF-␣ and its type 1 and 2 soluble receptors, together with interleukin (IL)-6, IL-1 receptor antagonist, and IL-10, in 184 patients (132 men; mean age, 64Ϯ12) consecutively admitted for myocardial infarction. We correlated their values to short-and long-term incidence of death and HF (primary outcome). In 10 patients, we also studied the presence of transcardiac gradients for TNF-␣ and its soluble receptors. The control group comprised 45 healthy subjects who were sex and age matched (33 men; mean age, 65Ϯ6 years) to the patients. All tested cytokines were increased in patients, and no transcardiac or systemic AV difference was found. After a median follow-up of 406 days (range, 346 to 696 days), 24 patients died and 32 developed HF. Univariate analysis showed that all cytokines were related to outcome, whereas after adjustment for baseline and clinical characteristics, sTNFR-1 remained the only independent predictor of death and HF (hazard ratio, 2.9; 95% CI, 1.9 to 3.8, tertile 1 versus 3), together with left ventricular ejection fraction, Killip class, and creatine kinase-MB at peak. Conclusions-sTNFR-1 is a major short-and long-term predictor of mortality and HF in patients with acute myocardial infarction. (Circulation. 2005;111:863-870.)

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Section: Discussionmentioning

confidence: 69%

Tumor Necrosis Factor-α Receptor 1 Is a Major Predictor of Mortality and New-Onset Heart Failure in Patients With Acute Myocardial Infarction

et al. 2005

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“…Serum oxidative stress (OS) level is a crucial element of the inflammatory process, owing to the accumulation of reactive oxygen/nitrogen species that might provoke and exacerbate the myocardial damage of the already failing heart. 1 Several medications claim to have at least some beneficial effects through the antioxidant potential. 2 -6 The thermochemiluminescence (TCL) oxidiziability assay (Lumitest Ltd., Haifa, Israel), measures the OS level via photon emission counting from excited carbonyls in biological macromolecules.…”

Section: Introductionmentioning

confidence: 99%

Serum Oxidative Stress Level Correlates with Clinical Parameters in Chronic Systolic Heart Failure Patients

Amir

Rogowski

Bar-Shai³

et al. 2009

Clinical Cardiology

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Background: Serum oxidative stress (OS) level has an important role in the inflammatory process of heart failure. Hypothesis:The study was designed to analyze serum OS levels in chronic heart failure (HF) patients and to examine the relation between OS levels and other clinical and prognostic parameters of HF. Methods: We studied 82 consecutive chronic symptomatic HF patients with systolic LV dysfunction (ejection fraction < 45%). The serum OS level was determined using thermochemiluminescence assay. We compared the serum OS levels with patients' clinical and prognostic parameters. Results: Higher serum OS levels were associated with higher New York Heart Association class (P = .01), worse renal function (serum urea, creatinine, and creatinine clearance) (P<.001) and higher serum levels of hs-C-reactive protein and N-terminal pro brain natriuretic peptide (P = .001, P<.001, respectively). Conclusions: In chronic systolic HF patients, high serum OS levels correlate with advanced disease and known markers of poor prognosis. IntroductionHeart failure (HF) is a major cardiovascular health problem, associated with high mortality and morbidity. Several studies suggested that inflammation has an important role in HF progression. Serum oxidative stress (OS) level is a crucial element of the inflammatory process, owing to the accumulation of reactive oxygen/nitrogen species that might provoke and exacerbate the myocardial damage of the already failing heart. 1 Several medications claim to have at least some beneficial effects through the antioxidant potential. 2 -6 The thermochemiluminescence (TCL) oxidiziability assay (Lumitest Ltd., Haifa, Israel), measures the OS level via photon emission counting from excited carbonyls in biological macromolecules. 7 TCL measurements were previously compared to other well accepted methods, which measure serum oxidative stress level via oxidation of lipids or proteins. 8 As we demonstrated before, TCL measurements were highly correlated with thiobarbituric acid reactive substances-(TBA assay), as well as with protein carbonyl formation (r = 0.99, r = 0.98, P<.01, respectively). 7 In this study, we investigated serum OS levels in chronic HF patients and examined the relation between OS levels and other clinical and laboratory prognostic parameters.

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“…Importantly, evidence indicates that inactivity alone cannot fully account for congestive heart failure-induced reductions in muscle function (25). Recent work indicates, however, that congestive heart failure is associated with an increase in generation of free radicals (i.e., molecules derived from superoxide anions) and other reactive oxygen species in some tissues (2,32). Moreover, in several conditions (e.g., sepsis, wasting syndromes), heightened free radical formation in skeletal muscle has been recently linked to the development of muscle weakness and protein loss (4,24).…”

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Diaphragmatic free radical generation increases in an animal model of heart failure

Supinski

Callahan²

2005

Journal of Applied Physiology

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Supinski, Gerald S., and Leigh A. Callahan. Diaphragmatic free radical generation increases in an animal model of heart failure. J Appl Physiol 99: 1078 -1084, 2005; doi:10.1152/japplphysiol.01145.2004.-Heart failure evokes diaphragm weakness, but the mechanism(s) by which this occurs are not known. We postulated that heart failure increases diaphragm free radical generation and that free radicals trigger diaphragm dysfunction in this condition. The purpose of the present study was to test this hypothesis. Experiments were performed using halothaneanesthetized sham-operated control rats and rats in which myocardial infarction was induced by ligation of the left anterior descending coronary artery. Animals were killed 6 wk after surgery, the diaphragms were removed, and the following were assessed: 1) mitochondrial hydrogen peroxide (H2O2) generation, 2) free radical generation in resting and contracting intact diaphragm using a fluorescent-indicator technique, 3) 8-isoprostane and protein carbonyls (indexes of free radical-induced lipid and protein oxidation), and 4) the diaphragm force-frequency relationship. In additional experiments, a group of coronary ligation animals were treated with polyethylene glycol-superoxide dismutase (PEG-SOD, 2,000 units⅐kg Ϫ1 ⅐day Ϫ1) for 4 wk. We found that coronary ligation evoked an increase in free radical formation by the intact diaphragm, increased diaphragm mitochondrial H2O2 generation, increased diaphragm protein carbonyl levels, and increased diaphragm 8-isoprostane levels compared with controls (P Ͻ 0.001 for the first 3 comparisons, P Ͻ 0.05 for 8-isoprostane levels). Force generated in response to 20-Hz stimulation was reduced by coronary ligation (P Ͻ 0.05); PEG-SOD administration restored force to control levels (P Ͻ 0.03). These findings indicate that cardiac dysfunction due to coronary ligation increases diaphragm free radical generation and that free radicals evoke reductions in diaphragm force generation. oxidative stress CONGESTIVE HEART FAILURE IS known to evoke significant changes in skeletal muscle function, inducing muscle wasting, reductions in muscle force-generating capacity, and alterations in muscle energy metabolism (9,16,20). Both limb and respiratory skeletal muscle are thought to be affected in this condition (28). Some work indicates that limb skeletal muscle dysfunction plays an important role in determining exercise capacity in patients with congestive heart failure (22). In addition, respiratory muscle dysfunction may predispose these patients to respiratory failure under conditions in which the respiratory workload increases (28).The mechanism by which congestive heart failure alters skeletal muscle function remains unclear. Importantly, evidence indicates that inactivity alone cannot fully account for congestive heart failure-induced reductions in muscle function (25). Recent work indicates, however, that congestive heart failure is associated with an increase in generation of free radicals (i.e., molecules derived from superoxide anions) an...

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Hydroxyl radical generation, levels of tumor necrosis factor-alpha, and progression to heart failure after acute myocardial infarction

Abstract: 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.

Cited by 46 publications

References 45 publications

Tumor Necrosis Factor-α Receptor 1 Is a Major Predictor of Mortality and New-Onset Heart Failure in Patients With Acute Myocardial Infarction

Tumor Necrosis Factor-α Receptor 1 Is a Major Predictor of Mortality and New-Onset Heart Failure in Patients With Acute Myocardial Infarction

Serum Oxidative Stress Level Correlates with Clinical Parameters in Chronic Systolic Heart Failure Patients

Diaphragmatic free radical generation increases in an animal model of heart failure

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