Actual Plasma Volume Research Articles

Can Plasma Volume Determination in Cirrhosis Be Replaced by an Algorithm Using Body Weight and Hematocrit?

Patients with cirrhosis often develop hyperdynamic circulation with increased cardiac output, heart rate, and redistribution of the circulating volume with expanded plasma volume (PV). PV determination is part of the evaluation of patients with cirrhosis, but gold-standard methods are invasive, expensive, and time-consuming. Therefore, other estimations of PV would be preferable, and the aim of this study was therefore to study if PV, as assessed by a simplified algorithm based on hematocrit and weight, can replace the gold-standard method. We included 328 patients with cirrhosis who had their PV assessed by the indicator dilution technique as the gold-standard method (PVI-125). Actual PV was estimated as PVa = (1 - hematocrit)·(a + (b·body weight)). Ideal PV was estimated as PVi = c · body weight, where a, b, and c are constants. PVI-125, PVa, and PVi were 3.99 ± 1.01, 3.09 ± 0.54, and 3.01 ± 0.65 (Mean ± SD), respectively. Although PVI-125 correlated significantly with PVa (r = 0.72, p < 0.001), a Bland-Altman plot revealed wide limits of confidence. The use of simplified algorithms does not sufficiently estimate PV and cannot replace the indicator dilution technique.

Removal of the influence of plasma volume fluctuations for the athlete biological passport and stability of haematological variables in active women taking oral contraception.

The haematological module of the athlete biological passport (ABP) monitors longitudinal haematological variations that could be indicative of blood manipulation. This study applied a multi‐parametric model previously validated in elite cyclists to compare inferred and actual PV variations, whereas the potential influence of the oral contraceptive pill (OCP) cycle on the ABP blood biomarkers and plasma volume (PV) in 14 physically active women taking OCPs was also investigated. Blood and serum samples were collected each week for 8 weeks, and the ABP haematological variables were determined according to the World Anti‐Doping Agency guidelines. Transferrin (sTFN), ferritin (FERR), albumin (ALB), calcium (Ca), creatinine (CRE), total protein (TP) and low‐density lipoprotein (LDL) were additionally computed as ‘volume‐sensitive’ variables in a multivariate analysis to determine individual estimations of PV variations. Actual PV variations were indirectly measured using a validated carbon monoxide rebreathing method. We hypothesised ABP markers to be stable during a standard OCP cycle and estimated PV variations similar to measured PV variations. Measured PV variations were in good agreement with the predictions and allowed to explain an atypical passport finding (ATPF). The ABP biomarkers, Hbmass and PV were stable over 8 weeks. Significant differences occurred only between Week 7 and Week 1, with lower levels of haemoglobin concentration ([Hb]), haematocrit (HCT) and red blood cell count (RBC)(−4.4%, p < 0.01; −5.1%, p < 0.01; −5.2%, p < 0.01) and higher levels of PV at week 7 (+9%, p = 0.05). We thus concluded that estimating PV variations may help interpret individual ABP haematological profiles in women.

Prognostic value of simple risk index and plasma volume status in patients with acute decompensated heart failure

Abstract Background Increased heart rate (HR) and low systolic blood pressure (SBP) are associated with adverse clinical outcomes in patients admitted for acute decompensated heart failure (ADHF), and simple risk index (SRI) based on easily assessed clinical characteristics (age, HR, and SBP) provides prognostic information. On the other hand, plasma volume (PV) expansion plays an essential role in heart failure, and PV status is has been reported to be associated with adverse outcomes in ADHF patients. However, there is no information available on the value of the combination of SRI and PV status in patients admitted for ADHF. Methods and results We studied 301 patients admitted for ADHF. At the admission, SRI was calculated as (HR x [age/10]2)/SBP. PV status was calculated as the following: Actual PV = (1 − hematocrit) x [a + (b x body weight)] (a=1530 in males and a=864 in females, b=41 in males and b=47.9 in females), Ideal PV = c x body weight (c=39 in males and c=40 in females), and PV status = [(actual PV − ideal PV)/ideal PV] x 100(%). During a follow-up period of 4.3±3.2 yrs, 95 patients had all-cause death (ACD) and 68 patients had cardiovascular death (CVD). At multivariate Cox analysis, SRI and PV status were significantly associated with ACD and CVD, independently of the prior history of heart failure hospitalization and serum creatinine and sodium levels, after the adjustment with serum albumin level and anemia. Patients with both greater SRI (≥35.1 by ROC analysis; AUC 0.599 [0.524–0.674]) and greater PV status (≥8.1% by ROC analysis; AUC 0.625 [0.550–0.700]) had a significantly higher risk of ACD and CVD than those with either or none of them (ACD: 49% vs 27% vs 24%, p&amp;lt;0.0001, CVD: 39% vs 18% vs 15%, p&amp;lt;0.0001,respectively). Conclusion The combination of SRI and PV status might be useful for stratifying patients at risk for the total mortality and cardiovascular death in patients with ADHF. Funding Acknowledgement Type of funding sources: None.

Calculated Plasma Volume Status Is Associated With Mortality in Acute Respiratory Distress Syndrome.

This is a retrospective cohort study of subjects enrolled in four previously completed National Heart Lung and Blood Institute-sponsored acute respiratory distress syndrome trials, using data from the National Institutes of Health Biologic Specimen and Data Repository Information Coordinating Center repository. Study subjects included 3,165 patients with acute respiratory distress syndrome previously enrolled in National Heart Lung and Blood Institute-sponsored acute respiratory distress syndrome trials. The exposure variable of interest was plasma volume status, calculated as the percentage alteration of actual plasma volume calculated on the basis of weight and hematocrit using sex-specific constants. We performed Kaplan-Meier survival analysis and univariable and adjusted Cox proportional hazard models to determine the association of plasma volume status with 60-day mortality. The median age of subjects was 52 years (interquartile range, 40-63 yr). Median plasma volume status was 5.9% (interquartile range, -2.4% to 13.6%), and overall, 68% of subjects had positive plasma volume status suggesting plasma volume higher than ideal plasma volume. In adjusted models, plasma volume status greater than median was associated with 38% greater risk for mortality (hazard ratio, 1.38; 95% CI, 1.20-1.59; p < 0.001). Each interquartile range increase in plasma volume status was associated with greater mortality in adjusted models (hazard ratio, 1.24 per interquartile range increase; 95% CI, 1.13-1.36; p < 0.001). Plasma volume status greater than median was associated with fewer ventilator-free days (18 vs 19 d; p = 0.0026) and ICU-free days (15 vs 17 d; p = 0.0001). Plasma volume status is independently associated with mortality, ICU-free days, and ventilator-free days among subjects with acute respiratory distress syndrome. Plasma volume status could be considered for risk-stratification and to direct therapy, particularly fluid management.

Effect of Empagliflozin Versus Placebo on Plasma Volume Status in Patients with Acute Myocardial Infarction and Type 2 Diabetes Mellitus.

IntroductionPlasma volume status (PVS), a parameter of the discrepancy between actual plasma volume (PV) and ideal PV, has been recently evaluated as a prognostic marker in patients with heart failure. This subgroup analysis of the EMBODY trial was designed to determine whether a sodium-glucose cotransporter 2 (SGLT2) inhibitor affects the alleviation of heart failure and improvement of PVS in patients after acute myocardial infarction (AMI) with congestive heart failure (CHF).MethodsThe EMBODY trial was a prospective, multicenter, randomized, double-blind, placebo-controlled trial to identify the effect of an SGLT2 inhibitor on cardiac sympathetic hyperactivity in patients with AMI and type 2 diabetes mellitus (T2DM) in Japan. In total, 105 patients were randomized (1:1) to receive 10 mg empagliflozin or a placebo (once daily), 2 weeks after the onset of AMI. In this subanalysis, we investigated the time-course of PVS at baseline and weeks 4, 12, and 24.ResultsOverall, 96 patients were included in the subgroup analysis set (age 64.3 ± 10.9 years, 80.2% men; 46 in the empagliflozin group and 50 in the placebo group). Body weight and PVS decreased in the empagliflozin group compared with the placebo group at 24 weeks (− 2.2 vs. + 0.1 kg, P < 0.001, and − 5.1 vs. − 0.3%, P < 0.001, respectively). Decreased PVS, defined as a change in PVS of < − 4.5%, was associated with the administration of empagliflozin (odds ratio 2.61, 95% confidence interval 1.11–6.15, P = 0.028). N-terminal pro b-type natriuretic peptide levels decreased in both the empagliflozin and placebo groups (1028.7–370.3 pg/mL, P < 0.001, and 1270.6–673.7 pg/mL, P < 0.01, respectively).ConclusionEmpagliflozin reduced the body weight and PVS. Early SGLT2 inhibitor administration in patients with AMI, CHF, and T2DM can therefore be effective in reducing the body weight and PVS.Trial RegistrationUMIN 000030158.

Abstract 13625: Effect of Empagliflozin versus Placebo on Plasma Volume Status in Patients With Acute Myocardial Infarction and Type 2 Diabetes Mellitus: Subgroup Analysis of the Embody Trial

Background: Plasma volume status (PVS), a parameter of the discrepancy between actual plasma volume (PV) and ideal PV, has been evaluated recently as a prognostic marker of patients with heart failure. This subgroup analysis of the EMBODY trial was designed to determine whether the sodium-glucose cotransporter 2 (SGLT2) inhibitor affect the improvement of heart failure and PVS in patients after acute myocardial infarction (AMI) with congestive heart failure (CHF). Methods: The EMBODY trial was a prospective, multicenter, randomized, double-blind, placebo-controlled trial to identify the effect of the SGLT2 inhibitor on cardiac sympathetic hyperactivity in patients with AMI and type 2 diabetes mellitus (T2DM) in Japan. A total of one hundred and five patients were randomized (1:1) to receive once-daily 10 mg empagliflozin or placebo 2 weeks after the onset of AMI. In this subanalysis, we investigated the time-course of PVS on baseline, weeks 4, 12 and 24. Results: Overall, 96 patients were included in the subgroup analysis set (64.3±10.9 years, male 80.2%, and 46 in the empagliflozin group and 50 in the placebo group). The empagliflozin group showed significant decreases in body weight, systolic blood pressure, and PVS compared with the placebo group at 24 weeks (-2.2 vs. +0.1 kg, P=0.0007; -6.6 vs. +3.5 mmHg, P=0.003; and -5.1 vs. -0.3%, P=0.0006; respectively). Decreased of PVS, defined as change of PVS &lt; -4.5 % was associated with received empagliflozin (odds ratio, 2.61; 95% confidence interval, 1.11 - 6.15; P=0.028). On the other hand, NT-Pro BNP levels significantly decreased in the empagliflozin group and placebo group (1028.7 to 370.3 pg/ml, P=0.0001 and 1270.6 to 673.7 pg/ml, P=0.006, respectively). Conclusion: Empagliflozin reduced not only body weight but also PVS. These results suggested that early SGLT2 inhibitor administration in patients with AMI, CHF and T2DM could be effective to reduce body weight and PVS.

Predictive value of plasma volume status for contrast-induced nephropathy in patients with heart failure undergoing elective percutaneous coronary intervention

Abstract Predictive value of plasma volume status for contrast-induced nephropathy in patients with heart failure undergoing elective percutaneous coronary intervention. Objective Contrast-induced nephropathy (CIN) remains a common complication of coronary procedure and increases poor outcomes, especially in patients with heart failure. Plasma volume expansion relates to worsening prognosis of heart failure. We hypothesised that calculated plasma volume status (PVS) might provide predictive utility for contrast-induced nephropathy in patients with heart failure undergoing elective percutaneous coronary intervention (PCI). Methods We enrolled 441 patients with heart failure undergoing PCI from 2012 to 2018. Pre-procedural PVS was calculated by comparing actual plasma volume (aPV) derived from the Hakim formula to ideal plasma volume (iPV). CIN was defined as an absolute SCr increase ≥0.5 mg/dl within 72h of contrast medium exposure. We assessed the association between PVS and risk of contrast-induced nephropathy in patients with heart failure undergoing elective PCI. Results In 441 patients, 28 (6.3%) patients developed CIN. The median pre-procedural PVS was −0.02 (−0.09–0.05). The best cutoff value of PVS for predicting CIN was 0.04 with 64.5% sensitivity and 75.5% specificity according to the ROC analysis (C statistic = 0.718; 95% CI: 0.674–0.760),of which predictive value is similar to NT-proBNP (C statistics 0.721 vs. 0.773, P=0.355). After adjusting for potential confounding risk factors, multivariable analysis demonstrated that PVS &amp;gt;0.04 (OR=3.142, 95% CI: 1.185–8.332, P&amp;lt;0.05) and NT-proBNP &amp;gt;4518pg/ml (OR=7.591, 95% CI: 2.886–19.968, P&amp;lt;0.05)were strong independent predictors of CIN. Conclusion Pre-procedural PVS is an independent risk factor for predicting CIN markedly, of which predictive value is comparable to BNP and also independent of BNP. The best cutoff point of PVS for predicting CIN was 0.04. ROC for PVS and NT-proBNP to predict CIN Funding Acknowledgement Type of funding source: None

The impact of subclinical congestion on the outcome of patients undergoing transcatheter aortic valve implantation.

BackgroundWe investigated the impact of an elevated plasma volume status (PVS) in patients undergoing TAVI on early clinical safety and mortality and assessed the prognostic utility of PVS for outcome prediction.Materials and methodsWe retrospectively calculated the PVS in 652 patients undergoing TAVI between 2009 and 2018 at two centres. They were then categorized into two groups depending on their preoperative PVS (PVS ≤−4; n = 257 vs PVS>−4; n = 379). Relative PVS was derived by subtracting calculated ideal (iPVS = c × weight) from actual plasma volume (aPVS = (1 − haematocrit) × (a + (b × weight in kg)).ResultsThe need for renal replacement therapy (1 (0.4%) vs 17 (4.5%); P = .001), re‐operation for noncardiac reasons (9 (3.5%) vs 32 (8.4%); P = .003), re‐operation for bleeding (9 (3.5%) vs 27 (7.1%); P = .037) and major bleeding (14 (5.4%) vs 37 (9.8%); P = .033) were significantly higher in patients with a PVS>−4. The composite 30‐day early safety endpoint (234 (91.1%) vs 314 (82.8%); P = .002) confirms that an increased preoperative PVS is associated with a worse overall outcome after TAVI.ConclusionsAn elevated PVS (>−4) as a marker for congestion is associated with significantly worse outcome after TAVI and therefore should be incorporated in preprocedural risk stratification.

P4552The prognostic impact of worsening and improved renal function in acute decompensated heart failure with and without plasma volume expansion

Abstract Background Recent studies showed that both worsening renal function (WRF) and improved renal function (IRF) during hospitalization are associated with poor prognosis in patients with acute decompensate heart failure (ADHF). On the other hand, plasma volume (PV) expansion plays an essential role in ADHF. However, there is little information about the difference of prognostic impact of WRF and IRF in ADHF patients, relating to PV status (PVS). Methods We prospectively studied 348 patients admitted for ADHF. PVS was defined as follows: actual PV = (1 - hematocrit) × [a + (b × body weight)] (a=1530 in males and a=864 in females, b=41.0 in males and b=47.9 in females); ideal PV = c × body weight (c=39 in males and c=40 in females); and PVS = [(actual PV - ideal PV)/ideal PV] × 100 (%). WRF and IRF were defined as an increase and a decrease in serum creatinine of ≥0.3 mg/dl from admission to discharge, respectively. The endpoint was readmission for worsening heart failure (WHF) within 1 year. Result Median PVS was 6.7% (IQR: −4.1%–16.7%). 43 and 21 patients had WHF in groups with high PVS (PVS ≥ median) and low PVS (PVS &gt; median), respectively. In high PVS group, multivariate Cox analysis showed that IRF was independently and significantly associated with WHF (p=0.016, HR: 2.4 [1.2–4.8]), but WRF was not (p=0.55, HR: 0.7 [0.3–2.1]). On the other hand, in low PVS group, WRF was independently associated with WHF (p=0.035, HR: 3.0 [1.1–8.1]), but IRF was not (p=0.27, HR: 2.1 [0.6–8.0]). Kaplan-Meier analysis revealed that only patients with IRF had a significantly higher risk of WHF than those with stable renal function (SRF) in high PVS group, while patients with WRF had a significantly higher risk of WHF than those with SRF in low PVS group. Worsening heart failure-free rate curves Conclusion In ADHF patients with PV expansion, IRF during hospitalization could predict poor outcomes, but WRF could not. On the other hand, in ADHF patients without PV expansion, not IRF but WRF could predict poor outcomes. PVS guided-therapy may be considered in secondary prevention for WHF.

P5409Plasma volume status provides the additional prognostic information to the Get With the Guidelines-Heart Failure risk score in acute decompensated heart failure patients

Abstract Background The Get with The Guidelines (GWTG) heart failure (HF) risk score was developed in the GWTG inpatient HF registry to predict in-hospital mortality and also reported to be associated with post-discharge long-term outcomes. Plasma volume (PV) expansion plays an essential role in HF. Recently, it has been reported that PV is estimated by a simple formula based on hematocrit and body weight, not using radioisotope assays, and PV status provides prognostic information in patients (pts) with acute decompensated heart failure (ADHF). However, there is no information available on the long-term prognostic value of the combination of PV status and GWTG-HF risk score in pts admitted for ADHF. Methods and results We studied 301 ADHF pts discharged with survival. Variables required for the GWTG-HF risk score were race, age, systolic blood pressure, heart rate, serum levels of blood urea nitrogen and sodium, and the presence of chronic obstructive pulmonary disease. PV status was calculated as the following: Actual PV = (1 − hematocrit) x [a + (b x body weight)] (a=1530 in males and a=864 in females, b=41 in males and b=47.9 in females), Ideal PV = c x body weight (c=39 in males and c=40 in females), and PV status = [(actual PV − ideal PV)/ideal PV] x 100(%). During a follow-up period of 4.3±3.2 yrs, 95 pts had all-cause death (ACD). At multivariate Cox analysis, GWTG-HF risk score and PV status were significantly associated with the total mortality, independently of eGFR and the prior history of heart failure hospitalization, after the adjustment with serum albumin level and anemia. Pts with both high GWTG-HF risk score (≥39 by ROC analysis; AUC 0.655 [0.586–0.724]) and greater PV status (≥8.1% by ROC analysis; AUC 0.624 [0.566–0.692]) had a significantly higher risk of ACD than those with either or none of them (58% vs 30% vs 21%, p&lt;0.0001, respectively). Conclusion PV status would provide the additional long-term prognostic information to GWTG-HF risk score in ADHF pts.

Plasma volume status predicts prognosis in patients with acute heart failure syndromes.

The intravascular compartment is known as the plasma volume, and the extravascular compartment represents fluid within the interstitial space. Plasma volume expansion is a major symptom of heart failure. The aim of the current study was to investigate the impact of plasma volume status on the prognosis of acute heart failure syndromes. We analyzed 1115 patients with acute heart failure syndromes who were admitted to our hospital. These patients were divided into three groups based on their plasma volume status at admission: first tertile (plasma volume status <41.9%, n = 371), second tertile (41.9%⩽ plasma volume status <49.0%, n = 372), and third tertile (49.0%⩽ plasma volume status, n = 372). Plasma volume status was defined as follows: actual plasma volume = (1 - hematocrit) × [ a + ( b × body weight)] ( a=1530 in males and a=864 in females, b=41.0 in males and b=47.9 in females); ideal plasma volume = c × body weight ( c=39 in males and c=40 in females); and plasma volume status = [(actual plasma volume - ideal plasma volume)/ideal plasma volume] × 100 (%). In the Kaplan-Meier analysis, all-cause mortality, cardiac mortality and cardiac events increased progressively from the first to third tertile ( p <0.001, respectively). In the Cox proportional hazard analysis, after adjusting for potential confounding factors, plasma volume status was an independent predictor of all-cause mortality (hazard ratio 1.429, p < 0.001), cardiac mortality (hazard ratio 1.416, p = 0.001) and cardiac events (hazard ratio 1.207, p = 0.004). Increased congestion is associated with increased morbidity and mortality in heart failure patients. Plasma volume status, which represents intravascular compartment and congestion, can identify poor prognosis in patients with acute heart failure syndromes.

Abstract 12177: Plasma Volume Status Predicts Mortality in Heart Failure Patients

Background: The intravascular compartment is known as the plasma volume (PV). PV expansion plays an essential role in heart failure (HF), and large degrees of congestion relate to morbidity and mortality. Recently, it has been reported that PV is estimated by a simple formula based on hematocrit and body weight, not using radioisotope assays. We aimed to investigate the impact of PV status on prognosis of HF. Methods and Results: We calculated PV status as the following: Actual PV=(1-hematocrit)х[a+(bхbody weight)] (a=1530 in males and a=864 in females, b=41 in males and b=47.9 in females), Ideal PV=cхbody weight (c=39 in males and c=40 in females), and PV status=[(actual PV-ideal PV)/ideal PV]х100(%). We analyzed 1115 patients with HF who admitted to our hospital. These patients were divided into 3 groups based on the PV status: 1 st (PV status&lt;41.9%, n=371), 2 nd (41.9%≤PV status&lt;49.1%, n=372) and 3 rd tertiles (49.1%≤PV status, n=372). In the multiple regression analysis to determine PV status, among considerable clinical variables, B-type natriuretic peptide (BNP), sodium and estimated glomerular filtration rate (eGFR) were predictors of PV status (BNP: ß=0.280, P&lt;0.001; sodium: ß=-0.197, P&lt;0.001; and eGFR: ß=-0.214, P&lt;0.001). In the average follow-up of 1007 days, 287 deaths (149 cardiac deaths and 138 non-cardiac deaths) occurred. In the Kaplan-Meier analysis, all-cause mortality progressively increased from 1 st to 2 nd and 3 rd groups (13.5%, 21.2% and 42.5%, P&lt;0.001). In the Cox proportional hazard analysis, after adjusting for potential confounding factors including age, NYHA class, ejection fraction, BNP, sodium, eGFR, co-morbidities and medications, PV status was an independent predictor of all-cause mortality in HF patients (hazard ratio 1.420, 95% confidence interval 1.227-1.625, P&lt;0.001). Conclusion: PV status, a marker of intravascular compartment and congestion, can identify high mortality in HF patients.

Calculated plasma volume status and prognosis in chronic heart failure.

Plasma volume (PV) expansion hallmarks worsening chronic heart failure (CHF) but no non-invasive means of quantifying volume status exists. Because weight and haematocrit are related to PV, they can be used to calculate relative PV status (PVS). We tested the validity and prognostic utility of calculated PVS in CHF patients. First, we evaluated the agreement between calculated actual PV (aPV) and aPV levels measured using (125)Iodine-human serum albumin. Second, we derived PVS as: [(calculated aPV - ideal PV)/ideal PV] × 100%. Third, we assessed the prognostic implications of PVS in 5002 patients from the Valsartan in Heart Failure Trial (Val-HeFT), and validated this in another 246 routine CHF outpatients. On analysis, calculated and measured aPV values correlated significantly in 119 normal subjects and 30 CHF patients. In the Val-HeFT cohort, mean (+SD) PVS was -9 ± 8% and related to volume biomarkers such as brain natriuretic peptide (BNP). Over 2 years, 977 (20%) patients died. Plasma volume status was associated with death and first morbid events in a 'J-shaped' fashion with the highest risk seen with a PVS > -4%. Stratification into PVS quartiles confirmed that a PVS > -4% was associated with increased mortality (unadjusted hazard ratio 1.65, 95% confidence interval 1.44-1.88, χ(2) = 54, P < 0.001) even after adjusting for 22 variables, including brain natriuretic peptide. These results were mirrored in the validation cohort. Relative PVS calculated from simple clinical indices reflects the degree to which patients have deviated from their ideal PV and independently relates to outcomes. The utility of PVS-driven CHF management needs further evaluation.

104 Prognostic utility of calculated plasma volume status in chronic heart failure

Background Plasma volume (PV) expansion is a hallmark feature of worsening heart failure that is notoriously underestimated by clinical examination. While radioisotope assays optimally quantify PV status, numerous haemodialysis-based equations also exist for its estimation. The prognostic utility of such formulas in chronic heart failure (CHF) is unknown. Methods We analysed the relation between estimated PV status and mortality in 246 outpatients with CHF (mean (±SD) age 67±13 years, NYHA class 2±1, LVEF 28±8%). PV status was calculated (Hakim RM, et al) by subtracting the patients actual PV ((1-haematocrit) × (a + (b × weight)); a and b are gender-specific constants) from their ideal PV ((c × weight); c=gender-specific constant). Results Median (±IQR) PV status was—261±550 ml with 78% and 21% of patients having PV contraction and expansion, respectively. Patients with PV excess had significantly higher creatinine and lower albumin levels. Over a median follow-up of 13±16 months, 36 (15%) patients died. PV status predicted mortality (HR 1.001, 95% CI 1.001 to 1.002, p=0.001) in a graded fashion (Abstract 104 figure 1A) and did so independently of NYHA class, LVEF, weight, haematocrit and creatinine. A PV status ≤−178 ml optimally predicted survival (ROC AUC 0.68, p=0.0007) and conferred a 75% reduced hazard for death (HR 0.16, 95% CI 0.07 to 0.37, p Conclusions Calculating plasma volume status in CHF patients appears prognostically useful and suggests that dehydration is better tolerated than volume excess in these individuals and that targeting therapy to achieve a plasma volume status ≤178 ml might increment survival.

Affinity-capture protease reactor for single-step production and purification of antiangiogenic plasminogen fragment from human plasma

Bait and Snip Affinity columns have been around for many years, as have immobilized protease reactor columns. The latter are used to cleave precursor molecules into an active form by passing over a column containing immobilized enzymes. Now, Shimizu and Hasumi (p. 590) have combined these two concepts to create a facile means to proteolytically remove and isolate an active cleavage product from its precursor. The advantage of this affinity capture reactor system is that it allows initial concentration on the column of the substrate from a crude mixture, followed by cleavage under conditions that are more favorable for maintaining substrate activity and preventing denaturation. Final purification of the cleaved product is also simplified. To demonstrate the application of the system, the authors covalently immobilized lysine, which binds to plasminogen, plus the metalloproteinase bacillolysin MA (BL-MA) on a sepharose column, over which was passed crude human plasma. Plasminogen in the plasma bound to the ...

Clinical signs of normal plasma volume expansion during pregnancy

A majority of cases of pregnancy complications are associated with a relative maternal hypovolemia. The records of 200 pregnant women who had plasma volume determinations were reviewed in hopes of finding indicators of relative maternal hypovolemia other than the pregnancy complication itself. The signs of relative hypovolemia in pregnant women include those of decreased uterine growth, absence of a maternal systolic flow murmur, and absence of significant dependent ankle edema. Laboratory tests indicative of maternal hypovolemia include failure to develop a decline in maternal hematocrit, serum blood urea nitrogen/creatinine ratio > 15, a decreased creatinine clearance, abnormal platelet function, elevated serum glutamic oxaloacetic transaminase, ultrasonic evidence of oligohydramnios and/or decreased maternal heart size, and absence of hypervolemia on chest x-ray film. These findings and tests are only relative indicators of maternal hypovolemia, and it is suggested that, for an accurate defining of pregnant women who are at risk, the actual plasma volume determination has to be performed frequently in the pregnant population.