Objective: The accuracy of bioimpedance stroke volume index (SVI) is questionable as studies report inconsistent results. It remains unclear whether the algorithms alone are responsible for these findings. We analyzed the raw impedance data with three algorithms and compared bioimpedance SVI to transpulmonary thermodilution (SVI(TD)).
Design And Setting: Prospective observational clinical study in a university hospital.
Patients: Twenty adult patients scheduled for coronary artery bypass grafting (CABG).
Interventions: SVI(TD) and bioimpedance parameters were simultaneously obtained before surgery (t1), after bypass (t2), after sternal closure (t3), at the intensive care unit (t4), at normothermia (t5), after extubation (t6) and before discharge (t7). Bioimpedance data were analyzed off-line using cylinder (Kubicek: SVI(K); Wang: SVI(W)) and truncated cone based algorithms (Sramek-Bernstein: SVI(SB)).
Measurements And Results: Bias and precision between the SVI(TD) and SVI(K), SVI(SB), and SVI(W) was 1.0+/-10.8, 9.8+/-11.4, and -15.7+/-8.2 ml/m2 respectively, while the mean error was abundantly above 30%. Analysis of data per time moment resulted in a mean error above 30%, except for SVI(W) at t2 (28%).
Conclusions: Estimation of SVI by cylinder or truncated cone based algorithms is not reliable for clinical decision making in patients undergoing CABG surgery. A more robust approach for estimating bioimpedance based SVI may exclude inconsistencies in the underlying algorithms in existing thoracic bioimpedance cardiography devices.
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http://dx.doi.org/10.1007/s00134-007-0938-y | DOI Listing |
Transl Stroke Res
January 2025
Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
The role of chromatin biology and epigenetics in disease progression is gaining increasing recognition. Genes that escape X chromosome inactivation (XCI) can impact neuroinflammation through epigenetic mechanisms. Our previous study has suggested that the X escapee genes Kdm6a and Kdm5c are involved in microglial activation after stroke in aged mice.
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December 2024
Sunnybrook Health Sciences Centre, Toronto, ON, Canada.
Background: White matter hyperintensities (WMH) are commonly observed on MRI in Alzheimer's disease (AD), but the molecular pathways underlying their relationships with the ATN biomarkers remain unclear. The aim of this study was to identify genetic variants that may modify the relationship between WMH and the ATN biomarkers.
Method: This genome-wide interaction study (GWIS) included individuals with AD, MCI, and normal cognition from ADNI (n = 1012).
Alzheimers Dement
December 2024
Indiana University School of Medicine, Stark Neurosciences Research Institute, Department of Neurology, Indianapolis, IN, USA.
Background: Diagnosis of Alzheimer's disease (AD) via MRI is costly and can be limited by regional availability. With the recent advancements and discovery of amyloid in the retina, diagnosis of AD and the effect of AD pathology on the retina is becoming well characterized. However, the prevalence of vascular contributions to cognitive impairment and dementia (VCID) and its effects on the retina are less well known.
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December 2024
Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.
Background: Systemic Arterial Hypertension (SAH), distinguished by a persistent elevation of blood pressure, emerges as a risk factor for stroke and Alzheimer's Disease (AD). Additionally, recent evidence suggests that stroke may adversely affect memory, potentially playing a role in the development of AD. This study aimed to investigate the influence of permanent focal ischemic stroke on memory, as well as on sensorimotor function (asymmetry of the front paws) and cerebral infarct size in adult male spontaneously hypertensive rats (SHR), compared to normotensive Wistar Kyoto (WKY) rats.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Background: Ischemic stroke (IS) is a risk factor for developing Alzheimer's disease (AD). In this context, microglial activation is a shared cellular response to these two conditions that can be either beneficial or detrimental. Previous research has established that mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) treatment leads to enhanced functional recovery and reduced brain infarct volume in animal IS models.
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