Oxidative Stress and Cardiac Failure
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Although there have been important advances in the treatment of chronic cardiac insufficiency CCI , the morbidity and mortality rates continue to be high. The ischemia-reperfusion, increased neurohumoral activity, cytokine stimulation, and the presence of inflammatory cells are stimuli that generate free radicals and modifiers of the state of oxidative stress in CCI.
Under normal conditions there is a balance between the production of oxygen free radicals and the defensive antioxidant systems. Any change in this balance in favor the free radicals produces oxidative stress.. Experiments in mice with acute myocardial infection have suggested a slight relationship between the appearance of cardiac insufficiency and oxidative stress. Different therapeutic interventions have been used to decrease oxidative stress in patients with CCI.
On the experimental level, using models of ischemia and reperfusion, it has been shown that the administration of antioxidants prevents or delays the transition from a state of compensated cardiac insufficiency to one of decompensated cardiac insufficiency. Nevertheless, animal studies have demonstrated greater metabolism of oxygen free radicals with a consequent increase in oxidative stress. The purpose of this study was to analyze the state of post cardiac transplant oxidative stress by measuring MDA levels in plasma and the activity of different enzyme antioxidant systems. The measurements were obtained in patients with CCI and in a group of healthy controls, and were then compared..
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This study included 11 patients with cardiac transplants 8 men, 3 women , with an average age of 48 years range 16 years to 62 years. The average amount of time post transplant was 20 months range 12 months to 26 months. The immunosupressive protocol consisted of cyclosporin A, azatioprin, and steroids. Endomyocardial biopsies were performed on all patients within 2 weeks of the measurement of the oxidative stress parameters. The biopsies were performed by jugular puncture according to the classic technique and disposable biotopes, from which at least 4 samples were obtained for diagnostic study under the microscope.
Patients with cardiac insufficiency. Nineteen patients, all male, with cardiac insufficiency were studied, with an average age of 61 years range 44 to 75 years of age , NYHA FC III, stable, and following the usual treatment regimen diuretics, digitalis, angiotensive enzyme conversion inhibitors [AECI], and without beta-blockers at the time of the study. For ethical reasons a control group of patients receiving immunsuppressive medication could not be used. The control group was composed of 14 healthy subjects who were age- and sex-paired. All control subjects were asymptomatic, without significant morbid antecedents, and with a normal physical examination.
We excluded subjects with known coronary risk factors, or who had been treated with any medication, vitamin supplements, antioxidants, or who regularly ingested alcohol.. The parameters for oxidative stress were determined in peripheral blood. The hemolyzate was extracted using the method described by McCord et al. The oxidation level was determined by photocolorimetry at nm. The activity was expressed as units U per mg of hemoglobin Hb.. CAT was determined by the method described by Beers et al. Table 1 shows the clinical characteristics of the transplant patients and of the patients with cardiac insufficiency.
There was no significant age difference.
Oxidative stress in cardiovascular diseases Goswami SK, Maulik SK - J Pract Cardiovasc Sci
Of the group with CCI, 5 were hypertensive, 3 diabetic, 4 dyslipidemic, and 6 had suffered an acute myocardial infarction AMI. None of the patients was a smoker at the time of the study. Figure 1 shows the results of the measurements of plasma MDA. The MDA values were found to be significantly increased in patients with CCI and cardiac transplant with respect to the control group 3.
On the other hand, the GSH-Px activity was greater in the transplant group with respect to the control group 0. The principal finding of this study was that patients who underwent cardiac transplant had an increase in oxidative stress, as evinced by an increase in the concentration of plasma MDA.
SOD activity was found to be decreased in transplant patients with respect to the control group, while GSH-Px activity was found to be increased post-cardiac transplant with respect to the control group. On the other hand, no significant changes were observed in CAT activity between the CCI group and the transplant group. These results show that there is a change in the enzyme antioxidant systems in patients with CCI and transplant patients that causes an overall increase in oxidative stress..
The lipoperoxidation of the membranes is a relatively slow process. Nevertheless, recurrent cycles of ischemic reperfusion in the heart and the skeletal muscle and the auto-oxidation of catecholamines may increase lipoperoxidation of the membranes. The resulting increase in oxidative stress favors transition to a state characterized by depression of the cardiac function. This increase in oxidative stress has been demonstrated in patients with CCI through an increase in plasma MDA values. They observed an increase in MDA during the first 3 months post-transplant, a fall in the MDA level, and a later increase after the first year.
The increase in oxidative stress during the first period was attributed to the transplant procedure itself ischemia of the donor heart, ischemia and reperfusion time, viral or bacterial infections. Based on animal studies, Kirshenbaum and Singal 36 postulated that when an increase in the generation of oxygen free radicals is produced, the heart, in an adaptive response, increases the enzyme defense systems.
Oxidative Stress and Heart Failure
Therefore, oxidative stress may serve to prevent or minimize this. Nevertheless, the adaptive response is limited, occurring in very advanced stages, as for example in the case of CCI, a deficit in the antioxidant enzyme systems. The principal damage caused by the accumulation of H 2 O 2 is the production of the highly reactive hydroxyl radical, against which no physiological defense systems exist. Additionally, exhaustion of the enzyme antioxidant systems can be produced by direct damage caused by free radicals, as it has been shown that H 2 O 2 inactivates SOD, 39 and decreased values of SOD in plasma have been found in mice post cardiac transplant.
Nevertheless, after the first year, SOD activity tended to fall off, which coincided with the increase in oxidative stress. This increased state of oxidative stress has been demonstrated in patients with CCI by an elevation in MDA plasma values. Nevertheless, CAT allows the cell to decompose H 2 O 2 independently of the intracellular glutation concentration, given that it has been shown that the content of plasma thiols, an indicator of the oxidative state of the extracellular medium, is reduced in patients with CCI.
Among the limitations of our study is the small number of patients studied. This was a comparative study and not a follow-up study, so that there is no demonstration of the changes attributable to cardiac transplant. Oxidative stress was not evaluated in the myocardium but in the plasma, with the limitations of extrapolating the results to what happens in the myocardium or to reflect on what may have occurred in other organs; although blood can reflect the capacity of the entire organism to react against oxidative stress, and its values and enzyme activities may express multiple sources of oxidative stress, among them the striated muscle of cardiac insufficiency..
Departamento de Enfermedades Cardiovasculares. Marcoleta, E-mail: pcastro med. Home Articles in press Current Issue Archive. ISSN: Previous article Next article. Issue 8. Pages August Download PDF. Universidad de Chile. This item has received. Article information.
TABLE 1. Characteristics of the study population. Show more Show less. Introduction and objective.
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Chronic heart failure CHF is associated with oxidative stress. Heart transplantation, an important therapeutic alternative in these patients, could reduce oxidative stress by improving cardiac function. Our aim was to evaluate post-heart transplantation oxidative stress. Patients and method. The demographic characteristics of the three groups were similar.
Mean time from transplantation was GSH-Px activity increased after transplantation compared to control subjects 0. A significant decrease in SOD activity was found in the heart transplant vs.
CHF group 0. These findings demonstrated the presence of permanent oxidative stress in patients who have undergone heart transplantation, characterized by an increase in MDA and a decrease in SOD activity, despite an increase in GSH-Px activity.. Palabras clave:. Any change in this balance in favor the free radicals produces oxidative stress. The measurements were obtained in patients with CCI and in a group of healthy controls, and were then compared.
Patients with cardiac insufficiency Nineteen patients, all male, with cardiac insufficiency were studied, with an average age of 61 years range 44 to 75 years of age , NYHA FC III, stable, and following the usual treatment regimen diuretics, digitalis, angiotensive enzyme conversion inhibitors [AECI], and without beta-blockers at the time of the study. Healthy control subjects For ethical reasons a control group of patients receiving immunsuppressive medication could not be used.
We excluded subjects with known coronary risk factors, or who had been treated with any medication, vitamin supplements, antioxidants, or who regularly ingested alcohol. Markers for oxidative stress The parameters for oxidative stress were determined in peripheral blood. The activity was expressed as units U per mg of hemoglobin Hb. The epidemiology of heart failure: the Framingham study.. J Am Coll Cardiol, 22 , pp.
A Nature Research Journal. The results of the Q-SYMBIO trial showing a reduction in mortality in patients with heart failure treated with coenzyme Q 10 have substantial limitations. Nevertheless, they highlight the need to identify effective new therapies targeted at mitochondrial dysfunction and oxidative stress in heart failure. Yancy, C. Mortensen, S. The effect of coenzyme Q 10 on morbidity and mortality in chronic heart failure.
Burgoyne, J. Redox signaling in cardiac physiology and pathology. Oka, T.
Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure. Nature , — Lygate, C. Metabolic flux as a predictor of heart failure prognosis. Hare, J. Impact of oxypurinol in patients with symptomatic heart failure. Ernster, L. Biochemical, physiological and medical aspects of ubiquinone function. Acta , — McMurray, J. Coenzyme Q 10 , rosuvastatin, and clinical outcomes in heart failure: a pre-specified substudy of CORONA controlled rosuvastatin multinational study in heart failure. O'Connor, C. JAMA , — Dai, D.
Mitochondrial targeted antioxidant peptide ameliorates hypertensive cardiomyopathy. Download references. Correspondence to Ajay M.