Sublingual microvascular perfusion is reduced by UF and can be restored temporarily using autotransfusion by TP due to increased venous return. SDF imaging is able to detect these volume changes. SDF imaging and TP could become a useful bedside tool to evaluate the patient's (microvascular) volume status and response to therapy in dialysis or intradialytic hypotension.

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Objective: Sympathetic nerve activation is causally related to insulin resistance as both a cause and a consequence. Resting heart rate (RHR) reflects sympathetic nerve activity. We investigated the effect of RHR on the incidence of type 2 diabetes mellitus (T2DM) in patients with clinically manifest vascular diseases. Design: Data were used from the second manifestations of arterial disease (SMART) study: a prospective cohort study of patients with clinically manifest vascular diseases (nZ3646). Methods: RHR was obtained using an electrocardiogram. Patients were followed up for incident type 2 diabetes (nZ289) during a median period of 5.5 (interquartile range 3.2-8.4) years. The relation between RHR and incident T2DM was estimated by Cox proportional hazard analysis. As age was an effect modifier (PZ0.048), analyses were stratified for age. Results: Patients in quartile 4 (Q4) of RHR had a 65% increased risk of T2DM compared with those in Q1 (reference; hazard ratios (HR), 1.65; 95% confidence interval (95% CI), 1.15-2.36) adjusted for age, gender, smoking, estimated glomerular filtration rate, systolic blood pressure, location of vascular disease, and antihypertensive medication. Every 10 beats per minute (bpm) increase in RHR increased the risk for T2DM with 10% (HR, 1.10; 95% CI, 1.00-1.21) in the total population. This risk was particularly high in subjects aged 55-63 years (per 10 bpm: HR, 1.22; 95% CI, 1.04-1.43) and was independent of the location of vascular disease and beta-blocker use. Conclusions: Increased RHR, an indicator of sympathetic nerve activity, is associated with an increased risk for T2DM in patients with manifest vascular diseases, particularly in middle-aged patients.

The purpose of the study was to investigate microcirculation and vascular reactivity during experimental endotoxemia and endotoxin tolerance in humans by comparing different methods of approach. Endotoxin tolerance was induced in nine healthy volunteers by intravenous injection of 2 ng . kg(-1) . d(-1) LPS for 5 consecutive days. Microcirculation and vascular reactivity were monitored before and after LPS administrations on days 1 and 5 by near-infrared spectroscopy, sidestream dark-field imaging, and forearm blood flow by venous occlusion strain-gauge plethysmography during local intra-arterial infusion of endothelial-dependent vasodilator acetylcholine (0.5, 2, and 8 microg . min(-1) . dL(-1)). LPS administration induced a significant rise in all measured cytokines. During subsequent LPS administrations, the increase in cytokine levels was almost completely abolished, indicating the development of tolerance. Near-infrared spectroscopy showed 79% (interquartile range [IQR], 62%-92%) attenuation of recovery slope after ischemia 2 h after LPS administration on day 1 (P = 0.04), which was absent on day 5 (P = 0.72). Sidestream dark-field imaging showed 33% (IQR, 14%-40%) and 30% (IQR, 10%-33%) diminished flow in medium and large microvessels, respectively, 2 h after LPS administration on day 1 (P = 0.07 and 0.04, respectively), which was absent on day 5 (P = 0.47 for both vessels). Forearm blood flow measurements showed an attenuation of acetylcholine-induced vasodilatory response, with 67% (IQR, 45%-72%) 4 h after the first LPS administration (P = 0.01), but not when tolerance was present on day 5 (P = 0.61). Human endotoxemia results in endothelial dysfunction that can be adequately detected with different methods and was restored with development of LPS tolerance.

Objective: Presence of hypertensive target organ damage is related to increased vascular risk and mortality. Whether combined presence of hypertensive target organ damage confers higher vascular risk compared to single presence is unknown. This study evaluates the separate and combined effects of impaired renal function [estimated glomerular filtration rate (eGFR) 60 ml/min per 1.73 m 2 ], albuminuria (albumin/creatinine-ratio men !2.5 mg/mmol, women !3.5 mg/mmol) and left-ventricular hypertrophy (LVH) (Sokolow-Lyon and/or Cornell-voltage criterion) on the occurrence of vascular events and mortality in patients with vascular disease (coronary artery disease, cerebrovascular disease, and peripheral arterial disease).Methods and results: A cohort of patients with vascular diseases (n ¼ 4319) was followed (median 4.4 years) for the occurrence of vascular events (stroke, myocardial infarction, vascular death) and mortality. LVH was present in 11%, impaired renal function in 15%, and albuminuria in 18%. Presence of at least two hypertensive target organ damage was prevalent in 8%. The risk for vascular events was hazard ratio 1.5 [95% confidence interval (CI) 1.2-1.9] for presence of one hypertensive target organ damage and hazard ratio 3.8 (95% CI 2.3-6.3) for three manifestations of hypertensive target organ damage (adjusted for age, sex). For mortality this was hazard ratio 1.4 (95% CI 1.1-1.7) and hazard ratio 3.2 (95% CI 1.9-5.2). Hazard ratios for single presence of different types of organ damage were comparable and independent of the presence of hypertension.Conclusions: Impaired renal function, albuminuria, and LVH are prevalent in patients with vascular disease and confer independent and additive risk for vascular events and mortality. Measurement of hypertensive target organ damage in patients with vascular disease identifies patients at very high risk and may have treatment implications.

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on behalf of the SMART Study GroupAbdominal obesity is characterized by sympathetic nerve activation (SNA), probably mediated by elevated insulin and leptin levels. Resting heart rate (RHR) is a marker of sympathetic tone, and independently associated with cardiovascular events and death in various populations. We investigated and quantified the relation between visceral adipose tissue (VAT) and RHR in patients with vascular disease. In 3,723 patients with manifest vascular disease, visceral and subcutaneous fat tissue was measured with ultrasonography. RHR was obtained from an electrocardiogram (ECG). The association between quartiles of VAT and RHR was quantified using linear regression analysis with adjustments for potential confounding factors. Separate analyses were performed for men and women and for location of vascular disease. Visceral fat was categorized into sex-pooled quartiles (Q) ranging from 2.7-8.0 cm in Q1 (reference) to 9.4-20.6 cm in Q4. High visceral fat thickness was associated with increased RHR, in men (Q4 vs. Q1, β = 4.36; 95% confidence interval (CI) = 3.11-5.61) and women (β = 1.48; 95% CI = −0.70 to 3.66), after full adjustment. Waist circumference and BMI had a significant relation with RHR in men (β = 3.51; 95% CI = 2.21-4.81 and β = 2.80; 95% CI = 1.51-4.08, respectively) but these relations were smaller and not significant in women (β = 0.71; 95% CI = −1.44 to 2.85 and β = 0.24; 95% CI = −1.90 to 2.37, respectively). There was no relation between subcutaneous fat and RHR in men and women. The relation between visceral fat and RHR was similar in patients with different locations of vascular diseases. Increased visceral fat is associated with increased RHR in male and female patients with vascular disease, independent of the location.

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