In patients with HF, untreated OSA is associated with an increased risk of death independently of confounding factors.

TNF-alpha is present early in a model of large myocardial infarction and is sustained into the later stage within the myocardium. Expression of this cytokine is not only confined strictly to the infarct or peri-infarct zone but is expressed by cardiac myocytes within the myocardium contralateral to the infarct. Therefore TNF-alpha production forms a part of an important intrinsic myocardial stress response system to injury.

Patients with heart failure have less subjective daytime sleepiness compared with individuals from a community sample, despite significantly reduced sleep time, whether or not they have OSA. In patients with heart failure, the absence of subjective sleepiness is not a reliable means of ruling out OSA.

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Background-Obstructive sleep apnea (OSA) and central sleep apnea are common in patients with heart failure. We hypothesized that in such patients, severity of OSA is related to overnight rostral leg fluid displacement and increase in neck circumference, severity of central sleep apnea is related to overnight rostral fluid displacement and to sleep PCO 2 , and continuous positive airway pressure alleviates OSA in association with prevention of fluid accumulation in the neck. Methods and Results-In 57 patients with heart failure (ejection fraction Յ45%), we measured change in leg fluid volume and neck circumference before and after polysomnography, and we measured transcutaneous PCO 2 during polysomnography. Patients were divided into an obstructive-dominant group (Ն50% of apneas and hypopneas obstructive) and a central-dominant group (Ͼ50% of events central

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. Vitamin C prevents hyperoxia-mediated vasoconstriction and impairment of endothelium-dependent vasodilation. Am J Physiol Heart Circ Physiol 282: H2414-H2421, 2002. First published January 10, 2002 10.1152/ajpheart.00947.2001.-High arterial blood oxygen tension increases vascular resistance, possibly related to an interaction between reactive oxygen species and endothelium-derived vasoactive factors. Vitamin C is a potent antioxidant capable of reversing endothelial dysfunction due to increased oxidant stress. We tested the hypotheses that hyperoxic vasoconstriction would be prevented by vitamin C, and that acetylcholine-mediated vasodilation would be blunted by hyperoxia and restored by vitamin C. Venous occlusion strain gauge plethysmography was used to measure forearm blood flow (FBF) in 11 healthy subjects and 15 congestive heart failure (CHF) patients, a population characterized by endothelial dysfunction and oxidative stress. The effect of hyperoxia on FBF and derived forearm vascular resistance (FVR) at rest and in response to intra-arterial acetylcholine was recorded. In both healthy subjects and CHF patients, hyperoxia-mediated increases in basal FVR were prevented by the coinfusion of vitamin C. In healthy subjects, hyperoxia impaired the acetylcholine-mediated increase in FBF, an effect also prevented by vitamin C. In contrast, hyperoxia had no effect on verapamil-mediated increases in FBF. In CHF patients, hyperoxia did not affect FBF responses to acetylcholine or verapamil. The addition of vitamin C during hyperoxia augmented FBF responses to acetylcholine. These results suggest that hyperoxic vasoconstriction is mediated by oxidative stress. Moreover, hyperoxia impairs acetylcholine-mediated vasodilation in the setting of intact endothelial function. These effects of hyperoxia are prevented by vitamin C, providing evidence that hyperoxia-derived free radicals impair the activity of endotheliumderived vasoactive factors.oxygen; acetylcholine; heart failure; endothelium HIGH ARTERIAL BLOOD OXYGEN (O 2 tension) causes vasoconstriction in healthy humans (2,4,6,7,28). Although hyperoxic vasoconstriction was first reported at least 90 years ago (2), the mechanism(s) for this phenomenon in healthy humans is poorly understood. Several animal models of hyperoxic vasoconstriction suggest that O 2 tension may influence one or more of the endothelium-derived factors that contribute to the maintenance of vascular tone, such as NO, endothelin, and vasoactive prostaglandins (5,26,29,35). One potential mechanism by which hyperoxia may affect these vasoactive substances is the generation of reactive oxygen species (ROS) that occurs with increased O 2 tension. For example, it has been demonstrated in vitro that superoxide anions derived from hyperoxia react rapidly with NO (37), thereby, decreasing its bioavailability. However, in healthy humans, the hypothesis that hyperoxic vasoconstriction is related to ROS generation or that hyperoxia may impair the function of endothelium-derived vasoactive factors has not b...

Background: Right ventricular failure (RVF) is a cause of major morbidity and mortality after left ventricular assist device (LVAD) implantation. It is, therefore, integral to identify patients who may benefit from biventricular support early post-LVAD implantation. Our objective was to explore the performance of risk prediction models for RVF in adult patients undergoing LVAD implantation. Methods: A systematic search was performed on Medline, Embase, Cochrane Central Register of Controlled Trials, and Cochrane Database of Systematic Reviews from inception until August 2019 for all relevant studies. Performance was assessed by discrimination (via C statistic) and calibration if reported. Study quality was assessed using the Prediction Model Risk of Bias Assessment Tool criteria. Results: After reviewing 3878 citations, 25 studies were included, featuring 20 distinctly derived models. Five models were derived from large multicenter cohorts: the European Registry for Patients With Mechanical Circulatory Support, Interagency Registry for Mechanically Assisted Circulatory Support, Kormos, Pittsburgh Bayesian, and Mechanical Circulatory Support Research Network RVF models. Seventeen studies (68%) were conducted in cohorts implanted with continuous-flow LVADs exclusively. The definition of RVF as an outcome was heterogenous among models. Seven derived models (28%) were validated in at least 2 cohorts, reporting limited discrimination (C-statistic range, 0.53–0.65). Calibration was reported in only 3 studies and was variable. Conclusions: Existing RVF prediction models exhibit heterogeneous derivation and validation methodologies, varying definitions of RVF, and are mostly derived from single centers. Validation studies of these prediction models demonstrate poor-to-modest discrimination. Newer models are derived in cohorts implanted with continuous-flow LVADs exclusively and exhibit modest discrimination. Derivation of enhanced discriminatory models and their validations in multicenter cohorts is needed.