Disorders of Extracellular Volume

Author(s):  
Elwaleed A. Elhassan ◽  
Robert W. Schrier
Keyword(s):  
1970 ◽  
Vol 64 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Lars Runeberg ◽  
B.-A. Lamberg ◽  
P. Reissell ◽  
H. Adlercreutz

ABSTRACT The time course of the renal excretion of calcium, magnesium, sodium, and potassium during sodium depletion and the rapid correction of the extracellular volume deficit was studied in normal subjects and in patients with Addison's disease (AD). The decrease in body weight was similar in the two groups, but the haematocrit value increased more in the patients with AD. Sodium depletion suppressed sodium excretion much more efficiently in normal controls than in the AD patients. Calcium excretion was roughly equally depressed in two groups. During sodium loading there was an immediate increase in renal sodium excretion in the patients with AD, whereas the sodium-retaining state generally continued for about one day in the normal controls. Urinary potassium decreased gradually during the first day of sodium loading in the normal controls but not in the AD patients. In the normal subjects calcium excretion remained low during the first day and increased on the second day of sodium loading. In the AD patients there was a gradual increase in urinary calcium during the first day of sodium loading, which did not, however, parallel the changes in urinary sodium content in individual urine samples. Urinary magnesium did not change significantly. It is concluded that the effect of adrenal steroids on renal calcium excretion is of minor importance. They may, however, to some extent induce calcium retention.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Atsushi Tanaka ◽  
Michio Shimabukuro ◽  
Hiroki Teragawa ◽  
Yosuke Okada ◽  
Toshinari Takamura ◽  
...  

Abstract Backgrounds/Aim Sodium glucose co-transporter 2 inhibitors promote osmotic/natriuretic diuresis and reduce excess fluid volume, and this improves cardiovascular outcomes, including hospitalization for heart failure. We sought to assess the effect of empagliflozin on estimated fluid volumes in patients with type 2 diabetes and cardiovascular disease (CVD). Methods The study was a post-hoc analysis of the EMBLEM trial (UMIN000024502), an investigator-initiated, multi-center, placebo-controlled, double-blinded, randomized-controlled trial designed primarily to evaluate the effect of 24 weeks of empagliflozin treatment on vascular endothelial function in patients with type 2 diabetes and established CVD. The analysis compared serial changes between empagliflozin (10 mg once daily, n = 52) and placebo (n = 53) in estimated plasma volume (ePV), calculated by the Straus formula and estimated the extracellular volume (eEV), determined by the body surface area, measured at baseline and 4, 12, and 24 weeks after initiation of treatment. Correlations were examined between the changes from baseline to week 24 in each estimated fluid volume parameter and several clinical variables of interest, including N-terminal pro-brain natriuretic peptide (NT-proBNP) concentration. Results In an analysis using mixed-effects models for repeated measures, relative to placebo empagliflozin reduced ePV by − 2.23% (95% CI − 5.72 to 1.25) at week 4, − 8.07% (− 12.76 to − 3.37) at week 12, and − 5.60% (− 9.87 to − 1.32) at week 24; eEV by − 70.3 mL (95% CI − 136.8 to − 3.8) at week 4, − 135.9 mL (− 209.6 to − 62.3) at week 12, and − 144.4 mL (− 226.3 to − 62.4) at week 24. The effect of empagliflozin on these parameters was mostly consistent across various patient clinical characteristics. The change in log-transformed NT-proBNP was positively correlated with change in ePV (r = 0.351, p = 0.015), but not with change in eEV. Conclusions Our data demonstrated that initiation of empagliflozin treatment substantially reduced estimated fluid volume parameters in patients with type 2 diabetes and CVD, and that this effect was maintained for 24 weeks. Given the early beneficial effect of empagliflozin on cardiovascular outcomes seen in similar patient populations, our findings provide an important insight into the key mechanisms underlying the clinical benefit of the drug. Trial registration University Medical Information Network Clinical Trial Registry, number 000024502


2021 ◽  
Vol 77 (18) ◽  
pp. 1312
Author(s):  
Tom Kai Ming Wang ◽  
Maria Vega Brizneda ◽  
Deborah Kwon ◽  
Zoran Popovic ◽  
Scott Flamm ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thiago Ferreira de Souza ◽  
Thiago Quinaglia Silva ◽  
Lígia Antunes-Correa ◽  
Zsofia D. Drobni ◽  
Felipe Osório Costa ◽  
...  

AbstractThere are limited data on the effects of anthracyclines on right ventricular (RV) structure, function, and tissue characteristics. The goal of this study was to investigate the effects of anthracyclines on the RV using cardiac magnetic resonance (CMR). This was a post-hoc analysis of a prospective study of 27 breast cancer (BC) patients (51.8 ± 8.9 years) using CMR prior, and up to 3-times after anthracyclines (240 mg/m2) to measure RV volumes and mass, RV extracellular volume (ECV) and cardiomyocyte mass (CM). Before anthracyclines, LVEF (69.4 ± 3.6%) and RVEF (55.6 ± 9%) were normal. The median follow-up after anthracyclines was 399 days (IQR 310–517). The RVEF reached its nadir (46.3 ± 6.8%) after 9-months (P < 0.001). RV mass-index and RV CM decreased to 13 ± 2.8 g/m2 and 8.13 ± 2 g/m2, respectively, at 16-months after anthracyclines. The RV ECV expanded from 0.26 ± 0.07 by 0.14 (53%) to 0.40 ± 0.1 (P < 0.001). The RV ECV expansion correlated with a decrease in RV mass-index (r = −0.46; P < 0.001) and the increase in CK-MB. An RV ESV index at baseline above its median predicted an increased risk of LV dysfunction post-anthracyclines. In BC patients treated with anthracyclines, RV atrophy, systolic dysfunction, and a parallel increase of diffuse interstitial fibrosis indicate a cardiotoxic response on a similar scale as previously seen in the systemic left ventricle.


2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
K Fischer ◽  
C Riecker ◽  
S Overney ◽  
M Stucki ◽  
H Tanner ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): European Association of Cardiothoracic Anaesthesiologists Research Grant Background Despite everyday use of electrical interventions in cardiovascular care, the extent and type of concomitant myocardial injury is not fully understood. Current literature disagrees about the question whether and how cardioversion or defibrillation damage the myocardium, especially when serologic markers are used. Such markers are not always cardiac-specific, nor diagnostic for type and region of myocardial injury. These limitations may be overcome by parametric T1 and T2 mapping. We aimed to investigate whether the acute and long-term impact of electrical cardioversion on myocardial structure and function is detectable using CMR imaging. Methods Patients scheduled for elective cardioversion were enrolled to undergo three CMR exams (3 Tesla): on the morning prior to cardioversion to assess pre-existing injury; two to five hours after cardioversion to assess the acute response; and six to ten weeks later to investigate chronic injury. The CMR exam studied left ventricular (LV) function, T2 mapping to measure edema, and extracellular volume (ECV) from T1 maps to measure diffuse fibrosis. Both the degree of injury and proportion (%) of myocardial area affected were analysed. Results Eight patients completed the study, requiring 1-2 shocks (totalling 120-300 J biphasic energy) to achieve sinus rhythm. LV ejection fraction increased after cardioversion from 47 ± 13% to 55 ± 15% (p = 0.020), and was 52 ± 16% at the third exam (p = 0.199). Even prior to intervention, some patients showed edema (baseline T2 &gt; 40ms) afflicting 49 ± 23% of their LV myocardium. Area affected by edema expanded to 72 ± 18% after cardioversion (p = 0.002) and returned to 54 ± 24% by the third exam. T2 rose from baseline (40.4 ± 1.8ms) after cardioversion acutely to 44.1 ± 5.2ms (p = 0.028) and normalized until the late exam (40.8 ± 3.1ms). Myocardial area affected by diffuse fibrosis (ECV &gt; 30%) was 28.3 ± 9.4% at baseline and 38.8 ± 18.9% late after cardioversion (p = 0.018). Pathologic T2 increases (indicative of edema) were not observed in all patients, but individuals with higher baseline ECV also experienced greater T2 increase after cardioversion (r = 0.840, p = 0.036). Conclusion Elective cardioversion improves LV systolic function, but also aggravates myocardial edema and possibly adds to diffuse fibrosis during several weeks thereafter. Such sequelae of cardioversion were observed mainly in patients with a greater burden of pre-existing myocardial injury. More data is needed to corroborate these preliminary findings and to study whether this type of myocardial injury predicts worse outcome. Moreover, changes in CMR markers caused by electrical interventions including defibrillation, may have the potential to confound diagnostic assessments of the underlying cardiac injury. Abstract Figure


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 699.1-699
Author(s):  
A. Gil-Vila ◽  
G. Burcet ◽  
A. Anton-Vicente ◽  
D. Gonzalez-Sans ◽  
A. Nuñez-Conde ◽  
...  

Background:Antisynthetase syndrome (ASS) is characterized by inflammatory myopathy, interstitial lung disease, arthritis, mechanical hands and Raynaud phenomenon, among other features. Recent studies have shown that idiopathic inflammatory myopathies (IIM) may develop cardiac involvement, either ischemic (coronary artery disease) or inflammatory (myocarditis). We wonder if characteristic lung interstitial involvement (interstitial lung disease) that appears in patients with the ASS may also affect the myocardial interstitial tissue. New magnetic resonance mapping techniques could detect subclinical myocardial involvement, mainly as edema (increase extracellular volume in interstitium and extracellular matrix), even in the absence of visible late Gadolinium enhancement (LGE).Objectives:Our aim was to describe the presence of interstitial myocarditis in a group of patients with ASS.Methods:Cross-sectional, observational study performed in a tertiary care center. We included 13 patients diagnosed with ASS (7 male, 53%, mean (SD) age at diagnosis 56,8 years (±11,8)). The patients were consecutively selected from our outpatient myositis clinic. Myositis specific and associated antibodies were performed by means of line immunoblot (EUROIMMUN©). Cardiac magnetic resonance (CMR) was performed on all patients. The study protocol includes functional cine magnetic resonance and standard late gadolinium enhancement (LGE), as well as novel parametric T1 and T2 mapping sequences (modified look locker inversion recovery sequences - MOLLI) with extracellular volume (ECV) calculation 20 minutes after the injection of a gadolinium-based contrast material.Results:CMR could not be performed in one patient due to anxiety. All patients studied (12) had a normal biventricular function, without alteration of segmental contraction. A third (4 out of 12, 33%) of the studied patients showed elevated T2 myocardial values without focal LGE, half of them (2/4) with an elevated ECV, consistent with myocardial edema. Two patients with normal T2 values showed unspecific LGE focal patterns, one in the right ventricle union points and another with mild interventricular septum enhancement (Figure 1). None of the patients studied refer any cardiac symptomatology. All the four patients with T2 mapping alterations (100%) had interstitial lung involvement, but only 4 out of 8 (50%) of the rest ASS patients without T2 mapping positivity. The autoimmune profile was as follows: 10 anti-Jo1/Ro52, 1 anti-EJ/Ro52, 2 anti-PL12.Conclusion:Myocarditis, although subclinical, appears to be a feature in ASS patients. T1 and T2 mapping sequences might be valuable to detect and monitor subclinical cardiac involvement in these patients. The possibility that the same etiopathogenic mechanism may be involved in the interstitial tissue in lung and myocardium is raised. More studies must be done in order to assert the prevalence of myocarditis in ASS.References:[1]Dieval C et al. Myocarditis in Patients With Antisynthetase Syndrome: Prevalence, Presentation, and Outcomes. Medicine (Baltimore). 2015 Jul;94(26):e798.[2]Myhr KA, Pecini R. Management of Myocarditis in Myositis: Diagnosis and Treatment. Curr Rheumatol Rep. 2020 Jul 22; 22:49.[3]Sharma K, Orbai AM, Desai D, Cingolani OH, Halushka MK, Christopher-Stine L, Mammen AL, Wu KC, Zakaria S. Brief report: antisynthetase syndrome-associated myocarditis. J Card Fail. 2014 Dec;20(12):939-45.Figure 1.Cardiac magnetic resonance images from ASS patients.Disclosure of Interests:None declared


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