Evidence for enhanced free radical activity in chronic congestive heart failure secondary to coronary artery disease

McMurray, John J.V.; McLay, JS; Chopra, Mridula; Bridges, A. B.; Belch, J. J. F.

doi:10.1016/0002-9149(90)90985-a

Cited by 128 publications

(66 citation statements)

References 15 publications

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“…In heart failure, circulating free radicals may contribute to disease progression and possibly mediate the process of apoptosis. By measuring byproducts of lipid peroxidation, several studies [17][18][19] have shown that patients with heart failure have increased oxygen-derived free radical production and/or decreased reducing ability compared with age-matched controls. Despite the laboratory evidence of an antioxidant effect with carvedilol in rat brain homogenates, 11 there has been no clinical demonstration of this selective effect in heart failure patients.…”

Section: Discussionmentioning

confidence: 99%

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Prospective, Randomized Comparison of Effect of Long-Term Treatment With Metoprolol or Carvedilol on Symptoms, Exercise, Ejection Fraction, and Oxidative Stress in Heart Failure

et al. 1999

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Background-With ␤-blocker use becoming more prevalent in treating chronic heart failure (CHF), the choice of drugs raises important theoretical and practical questions. Although the second-generation compound metoprolol is ␤ 1 -selective, the third-generation compound carvedilol is ␤-nonselective, with ancillary pharmacological properties including ␣-blockade and antioxidant effects. A prospective comparison of these 2 agents can address the issue of optimal adrenergic blockade in selecting agents for therapy in CHF. Methods and Results-Sixty-seven patients with symptomatic stable heart failure were randomly assigned to receive either carvedilol or metoprolol in addition to standard therapy for CHF. Measured variables included symptoms, exercise, ejection fraction, and thiobarbituric acid-reactive substances (TBARS) as an indirect marker of free radical activity. Metoprolol and carvedilol were well tolerated, and both patient groups showed beneficial effects of ␤-blocker therapy in each of the measured parameters, with no between-group differences. Ejection fraction increased over 6 months from 18Ϯ6.3% to 23Ϯ8.7% (PϽ0.005) with metoprolol and from 19Ϯ8.5% to 25Ϯ9.9% (PϽ0.0005) with carvedilol (PϭNS between groups). With metoprolol, TBARS values decreased from 4.7Ϯ0.9 nmol/mL at baseline to 4.2Ϯ1.5 nmol/mL at month 4 to 3.9Ϯ1.0 nmol/mL at month 6 (PϽ0.0001). With carvedilol, there was a parallel decline from 4.7Ϯ1.4 to 4.2Ϯ1.3 to 4.1Ϯ1.2 nmol/mL over the same time frame (PϽ0.025), with no between-group difference in these changes. Conclusions-Carvedilol and metoprolol showed parallel beneficial effects in the measured parameters over 6 months, with no relevant between-group differences in this heart failure population. (Circulation. 1999;99:2645-2651.)

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Section: Discussionmentioning

confidence: 99%

“…[17][18][19] Plasma for TBARS was collected twice at baseline before any exercise tests on that day in sodium heparin tubes and placed on ice (week Ϫ2 and week 0). Both baseline values were averaged.…”

mentioning

confidence: 99%

Prospective, Randomized Comparison of Effect of Long-Term Treatment With Metoprolol or Carvedilol on Symptoms, Exercise, Ejection Fraction, and Oxidative Stress in Heart Failure

et al. 1999

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“…The plasma and pericardial fluid of patients with heart failure contain elevated levels of thiobarbituric acid-reactive substances, which are markers of ROS activity. 5,6 Ellis et al 7 have also recently shown, by electron paramagnetic resonance spectroscopy, that lipid-derived ROS were significantly higher in patients with chronic heart failure than in control subjects. ROS may contribute in an important manner to the pathophysiology of heart failure by initiating myocyte apoptosis through nuclear factor (NF)-B and exerting direct negatively inotropic effects through depressed calcium uptake and reduced calcium-stimulated magnesiumdependent adenosine triphosphate activity of the cardiac sarcoplasmic reticulum.…”

Section: Oxidants and Antioxidants In The Myocardiummentioning

confidence: 94%

Heart Failure, Redox Alterations, and Endothelial Dysfunction

2001

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Abstract-Heart failure is characterized by neurohumoral alterations, such as activation of the sympathetic nervous system, stimulation of the renin-angiotensin system, increased activity of the endothelin system, increased production of norepinephrine, and increased circulating levels of cytokines. Oxidative stress is associated with the formation of reactive oxygen species (ROS). The myocardium has enzymes that stimulate ROS generation and enzymes with antioxidant effects. Several studies have suggested that ROS are increased in the failing heart. ROS may contribute to the pathophysiology of heart failure by initiating myocyte apoptosis and exerting direct negatively inotropic effects through the reduction of cytosolic intracellular free calcium. However, mechanisms such as endothelial dysfunction and inflammation have also been involved in the progression of heart failure. Antioxidants (eg, vitamin C) seem to improve endothelial functionality and reduce the inflammatory response in patients with heart failure. Therefore, in this review, we analyzed the involvement of ROS in the cellular and molecular mechanisms associated with endothelial dysfunction in heart failure.

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“…3,4) In the majority of hypertension animal models, the arterial internal diameter was generally reduced and the wall : lumen ratio was increased in the small arteries if they are compared under equivalent biophysical conditions. [1][2][3] On the other hand, free radicals and oxidative stress have been reported to play an important role in the pathogenesis of a variety of heart disease conditions, 5) ischemia-reperfusion injury, 6) congestive heart failure, 7) coronary artery disease, 8) and hypertension. 9,10) Some antioxidant compounds and diets have been shown to be effective in reducing oxidative damage in rats, especially in heart disease.…”

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confidence: 99%

Antihypertensive Potential and Mechanism of Action of Astaxanthin: III. Antioxidant and Histopathological Effects in Spontaneously Hypertensive Rats

Hussein

Goto

Oda

et al. 2006

Biological & Pharmaceutical Bulletin

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Evidence for enhanced free radical activity in chronic congestive heart failure secondary to coronary artery disease

Cited by 128 publications

References 15 publications

Prospective, Randomized Comparison of Effect of Long-Term Treatment With Metoprolol or Carvedilol on Symptoms, Exercise, Ejection Fraction, and Oxidative Stress in Heart Failure

Prospective, Randomized Comparison of Effect of Long-Term Treatment With Metoprolol or Carvedilol on Symptoms, Exercise, Ejection Fraction, and Oxidative Stress in Heart Failure

Heart Failure, Redox Alterations, and Endothelial Dysfunction

Antihypertensive Potential and Mechanism of Action of Astaxanthin: III. Antioxidant and Histopathological Effects in Spontaneously Hypertensive Rats

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