RESUMEN
BACKGROUND: Mixed venous saturation (MVS) obtained from the distal pulmonary artery (PA) during Swan-Ganz catheterization is the criterion standard for calculating cardiac output (CO) and cardiac index (CI) with the use of the Fick method. We think that calculating CI with the use of central venous saturation (CVS) instead of PA-MVS is both feasible and accurate. Earlier studies were small, enrolled heterogeneous patient populations, and resulted in inconsistent findings. METHODS: All patients undergoing right heart catheterization from January 2011 to January 2012 in our catheterization lab with simultaneous measurements of MVS obtained from the distal PA and CVS obtained from the superior vena cava (SVC) or right atrium (RA) were included. Out of the 902 patients enrolled, we excluded patients (n = 50) who had known cardiac shunt or dialysis fistula, had duplicate medical records, or were septic. We calculated the CI with the use of the assumed Fick method using both MVS (criterion standard) and CVS (SVC or RA saturations) in the remaining 852 patients. We measured the correlation and the agreement between the 2 methods with the use of the Pearson correlation coefficient and Bland-Altman analysis. RESULTS: Totals of 112 patients with simultaneous PA and RA saturation measurements (group I) and 740 patients with simultaneous PA and SVC saturation measurements (group II) were included. We found an excellent linear correlation between SVC and PA saturation (r = 0.928) and between RA and PA saturation (r = 0.95). There was also an excellent correlation between CI calculated with the use of PA saturation and CI calculated with the use of SVC (r = 0.87) or RA (r = 0.93) saturation. The mean bias of CVS-derived CI compared with MVS-derived CI (criterion standard) was -0.1 (95% limits of agreement [LOA] -1 to +0.77) in the SVC group and -0.006 (LOA -0.68 to +0.69) in the RA group. Patients with low CI had stronger correlation and smaller bias between the 2 methods compared with those with normal or high CI. The presence of baseline hypoxemia, valvular heart disease, or acute coronary syndrome had no significant effect on the correlation or the bias between the 2 methods. CONCLUSIONS: In cardiac patients, CVS can be used as a surrogate to true MVS in the calculation of CI. This method is readily available in patients who have central venous access, and may aid in early goal-directed treatment when cardiogenic shock is suspected.
Asunto(s)
Cateterismo Cardíaco/métodos , Cateterismo Venoso Central/métodos , Oxígeno/sangre , Anciano , Gasto Cardíaco , Femenino , Cardiopatías/sangre , Cardiopatías/fisiopatología , Humanos , Masculino , Persona de Mediana Edad , Arteria Pulmonar , Vena Cava SuperiorRESUMEN
BACKGROUND: Coenzyme Q10, or ubiquinone, is a non-prescription nutritional supplement. It is a fat-soluble molecule that acts as an electron carrier in mitochondria and as a coenzyme for mitochondrial enzymes. Coenzyme Q10 deficiency may be associated with a multitude of diseases including heart failure. The severity of heart failure correlates with the severity of coenzyme Q10 deficiency. Emerging data suggest that the harmful effects of reactive oxygen species are increased in patients with heart failure and coenzyme Q10 may help to reduce these toxic effects because of its antioxidant activity. Coenzyme Q10 may also have a role in stabilising myocardial calcium-dependent ion channels and preventing the consumption of metabolites essential for adenosine-5'-triphosphate (ATP) synthesis. Coenzyme Q10, although not a primary recommended treatment, could be beneficial to patients with heart failure. Several randomised controlled trials have compared coenzyme Q10 to other therapeutic modalities, but no systematic review of existing randomised trials has been conducted. OBJECTIVES: To review the safety and efficacy of coenzyme Q10 in heart failure. SEARCH METHODS: We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (2012, Issue 12); MEDLINE OVID (1950 to January Week 3 2013) and EMBASE OVID (1980 to 2013 Week 03) on 24 January 2013; Web of Science with Conference Proceedings (1970 to January 2013) and CINAHL Plus (1981 to January 2013) on 25 January 2013; and AMED (Allied and Complementary Medicine) (1985 to January 2013) on 28 January 2013. We applied no language restrictions. SELECTION CRITERIA: We included randomised controlled trials of either parallel or cross-over design that assessed the beneficial and harmful effects of coenzyme Q10 in patients with heart failure. When cross-over studies were identified, we considered data only from the first phase. DATA COLLECTION AND ANALYSIS: Two authors independently extracted data from the included studies onto a pre-designed data extraction form. We then entered the data into Review Manager 5.2 for analysis. We assessed study risk of bias using the Cochrane 'Risk of bias' tool. For dichotomous data, we calculated the risk ratio and for continuous data the mean difference (MD). Where appropriate data were available, we performed meta-analysis. For this review we prioritised data from pooled analyses only. Where meta-analysis was not possible, we wrote a narrative synthesis. We provided a QUOROM flow chart to show the flow of papers. MAIN RESULTS: We included seven studies with 914 participants comparing conenzyme Q10 versus placebo. There were no data on clinical events from published randomised trials. The included studies had small sample sizes. Meta-analysis was only possible for a few physiological measures and there was substantial heterogeneity.Only one study reported on total mortality, major cardiovascular events and hospitalisation. Five trials reported on the New York Heart Association (NYHA) classification of clinical status, but it was impossible to pool data due to heterogeneity. None of the included trials considered quality of life, exercise variables, adverse events or cost-effectiveness as outcome measures. Pooled analysis suggests that the use of coenzyme Q10 has no clear effect on left ventricular ejection fraction (MD -2.26; 95% confidence interval (CI) -15.49 to 10.97, n = 60) or exercise capacity (MD 12.79; 95% CI -140.12 to 165.70, n = 85). Pooled data did indicate that supplementation increased blood levels of coenzyme Q10 (MD 1.46; 95% CI 1.19 to 1.72, n = 112). However, there are only a small number of small studies with a risk of bias, so these results should be interpreted with caution. AUTHORS' CONCLUSIONS: No conclusions can be drawn on the benefits or harms of coenzyme Q10 in heart failure at this time as trials published to date lack information on clinically relevant endpoints. Furthermore, the existing data are derived from small, heterogeneous trials that concentrate on physiological measures: their results are inconclusive. Until further evidence emerges to support the use of coenzyme Q10 in heart failure, there might be a need to re-evaluate whether further trials testing coenzyme Q10 in heart failure are desirable.