Reliability of bioreactance and pulse-power analysis in measuring cardiac index in patients undergoing cardiac surgery with cardiopulmonary bypass

Abstract Objectives: Less-invasive and continuous cardiac output monitors recently have been developed to monitor patient hemodynamics. The aim of this study was to compare the accuracy, precision, and trending ability of noninvasive bioreactance-based Starling SV and miniinvasive pulse-power device LiDCOrapid to bolus thermodilution technique with a pulmonary artery catheter (TDCO) when measuring cardiac index in the setting of cardiac surgery with cardiopulmonary bypass (CPB). Design: A prospective method-comparison study. Setting: Oulu University Hospital, Finland. Participants: Twenty patients undergoing cardiac surgery with CPB. Interventions: Cardiac index measurements were obtained simultaneously with TDCO intraoperatively and postoperatively, resulting in 498 measurements with Starling SV and 444 with LiDCOrapid. Measurements and Main Results: The authors used the Bland-Altman method to investigate the agreement between the devices and four-quadrant plots with error grids to assess the trending ability. The agreement between TDCO and Starling SV was qualified with a bias of 0.43 L/min/m² (95% confidence interval [CI], 0.37‐0.50), wide limits of agreement (LOA, –1.07 to 1.94 L/min/m²), and a percentage error (PE) of 66.3%. The agreement between TDCO and LiDCOrapid was qualified, with a bias of 0.22 L/min/m² (95% CI 0.16‐0.27), wide LOA (–0.93 to 1.43), and a PE of 53.2%. With both devices, trending ability was insufficient. Conclusions: The reliability of bioreactance-based Starling SV and pulse-power analyzer LiDCOrapid was not interchangeable with TDCO, thus limiting their usefulness in cardiac surgery with CPB

Genome scan for loci regulating HDL cholesterol levels in Finnish extended pedigrees with early coronary heart disease

Coronary heart disease (CHD) is the leading cause of mortality in Western societies. Its risk is inversely correlated with plasma high-density lipoprotein cholesterol (HDL-C) levels, and approximately 50% of the variability in these levels is genetically determined. In this study, the aim was to carry out a whole-genome scan for the loci regulating plasma HDL-C levels in 35 well-defined Finnish extended pedigrees (375 members genotyped) with probands having low HDL-C levels and premature CHD. The additive genetic heritability of HDL-C was 43%. A variance component analysis revealed four suggestive quantitative trait loci (QTLs) for HDL-C levels, with the highest LOD score, 3.1, at the chromosomal locus 4p12. Other suggestive LOD scores were 2.1 at 2q33, 2.1 at 6p24 and 2.0 at 17q25. Three suggestive loci for the qualitative low HDL-C trait were found, with a nonparametric multipoint score of 2.6 at the chromosomal locus 10p15.3, 2.5 at 22q11 and 2.1 at 6p12. After correction for statin use, the strongest evidence of linkage was shown on chromosomes 4p12, 6p24, 6p12, 15q22 and 22q11. To search for the underlying gene on chromosome 6, we analyzed two functional and positional candidate genes (peroxisome proliferator-activated receptor-delta (PPARD), and retinoid X receptor beta, (RXRB)), but found no significant evidence of association. In conclusion, we identified seven chromosomal regions for HDL-C regulation exceeding the level for suggestive evidence of linkage