1,721,064 research outputs found

    Energetic myocardial metabolism and oxidative stress: let's make them our friends in the fight against heart failure

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    Heart failure (HF) is a syndrome causing a huge burden in morbidity and mortality worldwide. Current medical therapies for HF are aimed at suppressing the neurohormonal activation. However, novel therapies are needed for HF, independent of the neurohormonal axis, that can improve cardiac performance and prevent the progression of heart dysfunction. The modulation of cardiac metabolism may represent a new approach to the treatment of HF. The healthy heart converts chemical energy stored in fatty acids (FA) and glucose. Utilization of FA costs more oxygen per unit of ATP generated than glucose, and the heart gets 60-90% of its energy for oxidative phosphorylation from FA oxidation. The failing heart has been demonstrated to be metabolically abnormal, in both animal models and in patients, showing a shift toward an increased glucose uptake and utilization. The manipulation of myocardial substrate oxidation toward greater carbohydrate oxidation and less FA oxidation may improve ventricular performance and slow the progression of heart dysfunction. Impaired mitochondrial function and oxidative phosphorylation can reduce cardiac function by providing an insufficient supply of ATP to cardiomyocytes and by increasing myocardial oxidative stress. Although there are no effective stimulators of oxidative phosphorylation, several classes of drugs have been shown to open mitochondrial KATP channels and, indirectly, to improve cardiac protection against oxidative stress. This article focuses on the energetic myocardial metabolism and oxidative status in the normal and failing heart, and briefly, it overviews the therapeutic potential strategies to improve cardiac energy and oxidative status in HF patients. © 2009 Elsevier Masson SAS. All rights reserved

    Cardiac output monitoring by pressure recording analytical method in cardiac surgery

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    OBJECTIVE: A less-invasive method has been developed that may provide an alternative to monitor cardiac output from arterial pressure: beat-to-beat values of cardiac output can be obtained by pressure recording analytical method (PRAM). The purpose of this study was to assess the reliability of cardiac output determination by PRAM in cardiac surgery. METHODS: Cardiac output was measured in 28 patients undergoing coronary artery bypass grafting at 15 min after anaesthesia induction, 30 min after extracorporeal circulation, 1 and 3 h after arrival in the intensive care unit using thermodilution (ThD) method through a pulmonary artery catheter and PRAM. ThD cardiac output was calculated as the mean of five separate measurements. PRAM provided beat-by-beat cardiac output data continuously throughout the study and the cardiac output values displayed on a dedicated personal computer at each time point were recorded. Correlations were calculated and differences were compared by Bland-Altman analysis. RESULTS: A total of 112 measurements were obtained. Cardiac output ranged from 2.3 to 7.4 l/min, and a good linear correlation (R2=0.78, P<0.0001) was found between ThD and PRAM. The highest degree of correlation (R2=0.86) was obtained at 3 h after arrival in the intensive care unit. The lower degree of correlation (R2=0.70) was obtained 30 min after extracorporeal circulation. At Bland-Altman analysis, the overall estimates of cardiac output measured by PRAM closely agreed with ThD (mean difference, 0.027; standard deviation, 0.43; limits of agreement, -0.83 and +0.89). CONCLUSIONS: Under the studied conditions, our results demonstrate good agreement between PRAM data and ThD measurements, and this new method has shown to be accurate for real-time monitoring of cardiac output in cardiac surgery. Further studies will be required to assess this method in higher-risk patients and in the setting of haemodynamic instability or arrhythmias. This is the first study designed to assess the accuracy of PRAM in cardiac surgery

    PRAM: A non-invasive method to monitor cardiac output from arterial pressure during cardiac surgery

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    IDS Number: 728ZC Subject Category: Critical Care Medicine Document Type: Meeting Abstract 52
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