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Results for “extracellular volume fraction”

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At least 19 recordsLinked to original sources

PubMed2026

Enhanced risk stratification in hypertrophic cardiomyopathy through the integration of extracellular volume fraction on cardiovascular magnetic resonance.

AIMS: This study investigated the incremental prognostic value of cardiovascular magnetic resonance (CMR)-derived extracellular volume fraction (ECV), a marker of diffuse interstitial fibrosis, beyond late gadolinium enhancement (LGE) in hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: We analysed 990 consecutive HCM patients (median age 58 years, male 68.3%) who underwent CMR between 2012 and 2024. LGE and global ECV were quantified, and their associations with the primary endpoint of HCM-related events-a composite of sudden cardiac death (SCD) events, heart failure (HF) events, and HCM-related death-were assessed. During a median follow-up of 3.2 years, 64 (6.5%) patients experienced the primary endpoint. While LGE (median 7.1%, IQR 2.3-16.9%) and ECV (median 29.0%, IQR 26.6-32.0%) were moderately correlated (R = 0.604, P < 0.001), both were significantly associated with increased risk of the primary endpoint and individual outcomes of SCD and HF events, and optimal cutoffs were determined as LGE ≥ 27% and ECV ≥ 35%. Patients with ECV ≥ 35% had more symptoms, a more severe phenotype with greater systolic and diastolic dysfunction, and more pathogenic gene variants. Notably, ECV remained a significant predictor of the primary endpoint (adjusted HR 1.08, 95% CI 1.02-1.15, per 1%) after adjustment for key disease variables, including left ventricular ejection fraction and LGE. Elevated ECV effectively identified high-risk individuals even among lower-risk subgroups, including those with low LGE burden. CONCLUSION: Increased ECV is an independent predictor of HCM-related outcomes. ECV may serve as a novel imaging biomarker to refine risk stratification in HCM patients who do not meet traditional LGE-based high-risk criteria.

Humans↗

PubMed2026

Comprehensive assessment of vasospastic angina using coronary computed tomography angiography: synergistic value of the presence of myocardial bridge, perivascular inflammation, and myocardial extracellular volume fraction.

AIMS: Coronary computed tomography angiography (CCTA) has evolved beyond anatomical assessment to include sophisticated tissue characterization. While an elevated perivascular fat attenuation index around the right coronary artery (FAI-RCA) is known to reflect coronary inflammation in vasospastic angina (VSA), recurrent vasospasms may also induce chronic subclinical myocardial injury and subsequent remodelling, potentially associated with an increased myocardial extracellular volume fraction (ECV). However, the diagnostic integration of ECV and FAI-RCA for identifying VSA in patients with angina with non-obstructive coronary arteries (ANOCA) remains to be elucidated. METHODS AND RESULTS: This study included consecutive ANOCA patients who underwent CCTA with a dedicated ECV protocol, followed by an invasive spasm provocation test. Comprehensive CCTA analysis quantified both FAI-RCA and the transmural ECV gradient (the difference between endocardial and epicardial ECV: ECVEndo - ECVEpi). Of the 100 patients analysed (mean age: 65.3 ± 11.8 years; 55% male), 27 were diagnosed with VSA. Multivariable logistic regression analysis identified transmural ECV gradient [odds ratio (OR): 1.12, 95% confidence interval (CI): 1.01-1.25], presence of myocardial bridging (MB) (OR: 3.49, 95% CI: 1.25-9.74), and high FAI-RCA (> -70.95 Hounsfield units [HU]) (OR: 5.79, 95% CI: 2.06-16.30) as significant independent predictors of VSA (all P < 0.05). Notably, the integration of transmural ECV gradient provided incremental diagnostic value beyond FAI-RCA and MB, as assessed by the Net Reclassification Improvement and Integrated Discrimination Improvement. CONCLUSION: A multi-parametric CCTA approach potentially identifies patients at high risk for VSA. The significant association of the transmural ECV gradient with VSA suggests that myocardial remodelling imaging provides a novel diagnostic window into the cumulative myocardial impact of vasospasm, independent of active adipose tissue inflammation and the presence of MB.

Humans↗

PubMed2026

Human Immunodeficiency Virus-Associated Proteomic Signature of Myocardial Fibrosis and Incident Heart Failure.

BACKGROUND: People with human immunodeficiency virus (HIV) (PWH) are at higher risk of myocardial fibrosis and subsequent heart failure (HF) compared to people without HIV (PWOH). Mechanisms underlying this risk and its specificity to PWH are unclear. METHODS: We measured 2594 proteins in plasma obtained concurrently with cardiovascular magnetic resonance imaging among 342 PWH and PWOH. We estimated associations with HIV serostatus and myocardial fibrosis (elevated extracellular volume fraction [ECV] ≥30% among women, ≥28% among men) using multivariable regression. Among an independent community-based cohort, we estimated associations between the identified signature and time to incident HF. RESULTS: Mean age of participants was 55 (standard deviation [SD], 6) years, 25% were female, 61% were PWH (88% on antiretroviral therapy, 74% with undetectable HIV RNA), and 52% had elevated ECV. We identified 39 proteins and 1 cluster of 42 proteins that were higher among PWH versus PWOH and positively associated with elevated ECV, independent of risk factors (false discovery rate <0.05). Among an independent cohort of 3223 PWOH (mean age, 68 [SD, 9] years; 52% female; 118 incident HF cases over a mean of 9.8 [SD, 1.4] years), we found that this protein cluster and 34 of 39 individual proteins were associated with time to incident HF. This signature was statistically enriched for T-cell activation, tumor necrosis factor signaling, ephrin signaling, and tissue maintenance and repair. CONCLUSIONS: We identified an HIV-related proteomic signature associated with myocardial fibrosis regardless of HIV serostatus and that predicted incident HF among the general population. Our results identify several novel associations related to specific immune processes that may contribute to risk of myocardial fibrosis and subsequent HF among both PWH and PWOH.

Humans↗

PubMed1978

Third factor and edema formation.

Urine extracts as well as plasma and urine fractions from normal persons during extracellular volume expansion and from patients with edema of different origin were tested for natriuretic (rat bioassay) and antinatriferetic (frog skin) activity. Whereas the extracts and fractions from normal persons with extracellular volume expansion proved to have a distinct natriuretic and antinatriferetic effect, no such effect was observed with urine and plasma preparations from patients with sodium retention and edema. Whether or not edema formation is mediated by a loss of natriuretic activity remains still to be clarified.

Adult↗

PubMed1977

Volume composition of the lateral cervical nucleus in the cat. I. A stereological and electron microscopical study of normal and deafferentated animals.

The neuropil of the lateral cervical nucleus (LCN) has been studied by means of ultrastructural stereological methods. Estimates of the fractional volumes of axons, glial cells (three types), extracellular space, boutons, bouton mitochondria, dendrites, dendritic mitochondria, neuronal somata and blood vessels were calculated for four normal cats and eight cats which had been subjected to spinal deafferentation 2, 4, 9, and 14 days before perfusion. 14 days after operation the fractional volume of boutons and dendrites in the nucleus was considerably lower on the operated side, corresponding to a reduction of 67% and 64% respectively. The bouton reduction was higher than could have been expected from findings in earlier qualitative studies. The reduction in dendritic volume, which was already present after 4 days, had not been detected in earlier studies of the LCN. Dark dendrites were found both in normal animals and on the normal and operated sides in operated animals. The variation from animal to animal was great but the figures for the deafferented sides were significantly higher. The general value of the stereological technique in ultrastructural neuroanatomical research is discussed and it is concluded that quantitative methods are more sensive to small and gradual changes and should give a better estimation of transneuronal effects and of the amount of degeneration than purely qualitative methods.

Afferent Pathways↗

PubMed1979

Medullary collecting duct function in the remnant kidney before and after volume expansion.

The role of the medullary collecting ducts (CD) in the regulation of water and electrolyte excretion by the remnant kidney has not been determined. Medullary CD function was therefore studied by the microcatheterization technique during hydropenia and after volume expansion with an isotonic saline load in rats with sham-operated normal kidney (stage I), remnant kidney (stage II), remnant kidney after contralateral nephrectomy (stage III), and sham-operated normal kidney after contralateral nephrectomy (stage-III control). Sodium, potassium, water, and solute reabsorption along the medullary CD were not altered in stage II during hydropenia when compared to normal control (stage I), but water reabsorption proximal to the medullary CD was decreased. In stage III, where the uremia was mild (BUN, 41 mg/dl), the fractions of the filtered load of sodium (72%) and water (62%) which were reabsorbed along the medullary CD were reduced in comparison to stage II (94% and 83%, respectively), stage I, or stage-III control. The fraction of filtered potassium entering the medullary CD was increased to 53% in stage III, compared to 16% in stage II, and 10 or 11% in stage I or stage-III control. No change in the fraction of filtered potassium remaining along the collecting ducts was observed. After volume expansion, there was no significant change in the fraction of filtered sodium and water remaining along the medullary CD in stage I, II, or III. The greater fractional excretion in stage III resulted from decreased reabsorption in more proximal nephron segments. The results indicate that (a) during hydropenia, fractional reabsorption of sodium and water is decreased along the medullary CD of the stage-III remnant kidney in the presence of mild uremia, (b) the increased fractional excretion of potassium in the remnant kidney with uremia is not determined by altered potassium handling in the medullary CD but occurs proximal to this nephron segment, and (c) extracellular fluid volume expansion with isotonic saline results in similar inhibition of fractional sodium and water reabsorption in the collecting ducts of both remnant and normal kidneys.

Animals↗

PubMed1979

Extracellular fluid volume and renal indices in essential hypertension.

Extracellular fluid volume (EFV), total blood volume (TBV), and renal indices were determined in 53 permanent essential hypertensive patients with normal renal function and balanced sodium intake and urinary output. In comparison with normal subjects, hypertensives had normal EFV values while TBV and the TBV/EFV ratio were significantly reduced (p less than 0.001). In hypertensives, a significant negative relationship (r = -0.40; p less than 0.005) was observed between the TBV/EFV ratio and diastolic arterial pressure. No correlation existed between TBV and diastolic pressure, whereas EFV (and also interstitial fluid volume) was positively related to diastolic arterial pressure (r = +0.41; p less than 0.005). Extracellular fluid volume and interstitial fluid volume were both directly correlated to the renal filtration fraction (r = +0.45; p less than 0.005). The study suggests that, in the disturbed partition of the extracellular fluid of hypertensives, changes in the interstitial space are involved and are related to variations in the renal indices.

Adult↗

PubMed1978

Natriuretic effect of propranolol on dogs with chronic bile-duct ligation.

1. Chronic ligation of the bile duct in dogs is associated with salt retention and a blunted natriuretic response to extracellular volume expansion. The mechanism of this phenomenon has not been clarified. 2. We have examined the influence of chronic beta-adrenergic blockade on sodium excretion in dogs with bile-duct ligation during extracellular hypotonic volume expansion. 3. Urinary excretion of sodium and fractional excretion of sodium rose significantly after 5 days of oral DL-propranolol administration to dogs with bile-duct ligation. 4. The antinatriuresis after bile-duct ligation was not followed by a significant alteration in the mean peripheral plasma renin activity as compared with control values. 5. It is suggested that propranolol can partially reverse the antinatriuresis of chronic bile-duct ligation, and that this is mediated by an extrarenal effect of the beta-adrenergic blockade.

Animals↗

PubMed1978

Effect of chronic dietary saline loading on the fractional distribution of cardiac output and intrarenal circulation in the rat.

The effect of chronic saline loading for 3 weeks has been studied on the fractional distribution of cardiac output and intrarenal circulation in the rat. In response to the saline loading extracellular volume was slightly expanded and cardiac output moderately increased, the extent of which seemed to correlate with the fluid intake. Fractional organ flow distribution remained unaffected. Long-term saline loading resulted in a redistribution of intrarenal circulation characterized by an enhanced medullary blood flow, either isolated, or associated with an eventual dispropartional increase of cortical flow, while the renal fraction remained unaltered. On the basis of the results it is concluded that during long-term saline loading the augmentation of medullary circulation is a specific phenomenon characteristic of the kidney and is independent of the changes in cardiac output or other systemic haemodynamic effects. The isolated increase of medullary circulation is claimed to have a volume-regulatory function.

Animals↗

PubMed1979

Extracellular potassium accumulation in voltage-clamped frog ventricular muscle.

1. Application of voltage clamp pulses (1--10 sec) to frog ventricular strips causes temporary changes in the extracellular K concentration. 2. The changes in the extracellular K concentration can be estimated from (a) slowly decaying post-clamp after-potentials, (b) changes in the action potential duration, and (c) measurements with a K-selective micro-electrode. 3. The depolarization of the resting potential and the shortening of the action potential are present in approximately the same proportions during voltage-clamp induced extracellular K accumulation and during perfusion with a K-ricn Ringer solution but small consistent differences are noticed. 4. The measurements of the after-potential, the action potential shortening, and the K-electrode response were analysed as indicators of extracellular K+ activity and it was concluded that the after-potential provides the most convenient and reliable estimate of the absolute magnitude of the voltage-clamp induced extracellular K accumulation. 5. The depolarizing after-potentials decay more slowly than the hyperpolarizing after-potentials but it is found that this reflects the selectivity of the membrane to K+ concentrations as predicted by the Nernst or the Goldman equations. 6. Analysis of the redistribution of accumulated K+ from the decay of the after-potential suggests that the major part of the redistribution process can be described by a single time constant (2--4 sec). A much longer time constant is required for a smaller component of the 'tail' in order to bring [K]o to the normal resting state. 7. N-shaped relations similar to the 'steady state' current-voltage relation are obtained when the post-clamp after-potential, the action potential shortening, and the K-electrode response are plotted versus the clamped membrane potential. The maxima of these curves are located around -40 mV and the minima around -20 mV. 8. In spite of a significant outward membrane current (1--1.5 microamperemeter) in the minimum region (-20 mV), the post-clamp after-potential is often hyperpolarizing in nature suggesting extracellular K depletion. 9. These findings indicate that the K efflux is lower at -20 mV than at both higher and lower potentials and suggest that the N-shape 'steady state' current-voltage relation mainly reflects the voltage dependency of the K current. 10. A theory for K accumulation in a single compartment is presented which predicts that a simple linear RC-circuit may describe the electrical response of the preparation in a limited potential range around the resting potential. The extracellular accumulation space was estimated to be 13--16% of the total volume of the preparation. It is tentatively suggested that the accumulation space is equivalent to the subendothelial fraction of the extracellular space.

Action Potentials↗

PubMed1977

Phosphaturic effect of furosemide: role of PTH and carbonic anhydrase.

The first objective of this study was to examine the effects of furosemide on renal phosphate excretion in the presence and absence of a constant level of parathyroid hormone (PTH) while extracellular fluid volume was held constant. In the absence of PTH, furosemide did not significantly increase fractional phosphate excretion (FEP%, 4.2 +/- 2.7 to 6.2 +/- 1.9%; five dogs). In the presence of PTH, furosemide increased FEP% from 23.4 +/- 3.7 to 33.8 +/- 6.0% (P less .025; five dogs). Thus, the phosphaturia induced by furosemide was dependent on the presence of PTH. The second objective was to evaluate the hypothesis that furosemide exerts its phosphaturic effect through carbonic anhydrase inhibition, and therefore we tested for additivity of the phosphaturic effect of furosemide, and acetazolamide. In the presence of a constant level of PTH, acetazolamide increased FEP % from 24.5 +/- 1.8% to 40.7 +/- 5.1% P less than .025, five dogs. The subsequent administration of furosemide did not further increase FEP%, delta 3.3 +/- 8.9%; NS. Thus, the phosphaturic effect of furosemide was not additive to that of acetazolamide, indicating that acetazolamide and furosemide may share similar mechanisms for inhibiting phosphate reabsorption.

Acetazolamide↗

PubMed1977

Circulating inhibitor of sodium-potassium-activated adenosine triphosphatase after expansion of extracellular fluid volume in rats.

1. Serum was collected from normal rats and from rats volume-expanded with isotonic sodium chloride solution. 2. The serum was fractionated by gel filtration on Sephadex G-25 and each fraction was tested for inhibitory activity against sodium-potassium-activated adenosine triphosphatase prepared from rat kidney homogenate. 3. A single low-molecular-weight fraction, eluting after the salts and after exogenously added lysine-vasopressin, had significantly greater enzyme inhibitory activity when obtained from serum of volume-expanded animals than from control serum. 4. As this fraction has been shown in previous independent studies to contain a natriuretic factor, it may be concluded that one property of this factor is the ability to inhibit sodium-potassium-activated adenosine triphosphatase.

Adenosine Triphosphatases↗

PubMed1979

Diffusion from an iontophoretic point source in the brain: role of tortuosity and volume fraction.

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Animals↗

PubMed1979

Collecting duct sodium reabsorption in deoxycorticosterone-treated rats.

In vitro studies of isolated, perfused, cortical collecting tubules have demonstrated that prior chronic deoxycorticosterone acetate (DOCA) treatment increases sodium reabsorption in this nephron segment, yet sodium balance in vivo is maintained. To evaluate the effect of chronic DOCA treatment on collecting duct sodium reabsorption in vivo, we compared fractional sodium delivery (FD(Na)%) out of the superficial late distal tubule with the fraction of sodium remaining at the base and the tip of the papillary collecting duct during extracellular fluid volume expansion in untreated, salt-treated, and DOCA-salt-treated rats. In untreated rats, FD(Na)% to the distal tubule was 6.5+/-1.0%, and to the base was 8.7+/-1.6% (Delta2.2+/-0.9%, P < 0.05). FD(Na)% to the tip was 4.9+/-1.1%, significantly less than FD(Na)% to the base (Delta3.7+/-1.1%, P < 0.01). In salt-treated rats, FD(Na)% to the distal tubule was 8.3+/-0.8%, and to the base was 10.4+/-1.1%. FD(Na)% to the tip was 5.9+/-0.6%, significantly less than FD(Na)% to the base (Delta 4.6+/-1.0%, P < 0.005). In DOCA-salt-treated rats, FD(Na)% to the distal tubule was 16.1+/-2.6% and to the base was 9.5+/-1.9% (Delta 6.6+/-1.7%, P < 0.005). FD(Na)% to the tip was 5.9+/-1.2%, also significantly less than FD(Na)% to the base (Delta 3.6+/-1.1%, P < 0.01). We conclude that (a) in DOCA-salt-treated rats, sodium delivery to the end of the superficial distal tubule is greater than in untreated or salt-treated rats; (b) in DOCA-salt-treated rats, sodium delivery to the end of the superficial distal tubule is greater than to the base of the papillary collecting duct, suggesting stimulation of sodium reabsorption in the cortical and(or) outer medullary collecting duct; and (c) sodium reabsorption by the papillary collecting duct is unaffected by chronic DOCA-salt treatment in the volume-expanded rat.

Absorption↗

PubMed1978

Distribution and excretion of the mercury chelating agent sodium 2,3-dimercaptopropane-1-sulfonate in the rat.

The distribution and excretion of sodium 2,3-dimercapto-1,3 14C-propane-1-sulfonate as dependent on time has been studied in the rat. The highest concentration is found in the kidneys, the lowest in the brain. The excretion is very rapid (T1/2 = 19 min) and follows a monoexponential curve during the first hour after administration. This holds for plasma and most of the organs too. The apparent distribution volume of the radioactivity is equivalent to the volume of the extracellular water. After oral administration, 30-40% is absorbed from the gut. The results lead to the conclusion that a fraction of the drug is weakly bound to plasma- and membrane-proteins. They are discussed with respect to the treatment of heavy metal poisoning.

Animals↗

PubMed1976

Fasting urine excretion of magnesium, calcium, and sodium in patients with renal calcium stones.

Urine excretion of magnesium (Mg), calcium (Ca) and sodium(Na) was studied in patients with renal Ca stones having normal kidney function (n= 60), and in matched controls (n= 60), on a free diet following an overnight fasting period. In some formers, Mg was lower than in normals, whereas Ca was unusually high resulting in a significantly higher molar Ca/Mg ratio (p less than 0.001). 2. In 3 out of 4 stone groups Na excretion was significantly elevated because of reduced tubular reabsorption. In normals, fractional Na excretion varied between 0.44 and 0.54% of endogenous creatinine clearance, whereas it exceeded 1% in the stone patients. Conversely, the molar ratio Na/Ca was equal in all groups. 3. Fasting urinary cyclic AMP was comparable in both populations supporting the assumption that in the majority of patients Ca- or Mg- wasting via urine may not be responsible for secondary hyperparathyroidism. In small selected groups, losses of divalent cations may act in concert, leading to stimulation of the parathyroid glands. 4. Correlations between minerals and Na reveal a close relationship between Na, Ca and Mg in terms of clearance and excretion rate in patients and controls. Fractional Na and Ca excretion are correlated in patients but not in normals. This suggests that in the absence of phosphaturia, factors other than extracellular volume expansion and/or hyperparathyroidism are operative in stone disease. 5. The origin of fasting natriuresis and relative hypercalciuria may be ascribed to a change, as yet not causally identified, in distal tubular Na reabsorption.

Calcium↗

PubMed1979

Antiphosphaturic action of 25 (OH) vitamin D3 in experimental Fanconi syndrome.

Renal handling of phosphorus was studied in the following groups of parathyroidectomized rats with maleate-induced Fanconi syndrome: 1) 6 rats receiving intravenous parathyroid hormone, 2) 6 rats receiving intravenous dibutyryl cyclic AMP (DBcAMP), 3) 6 rats undergoing volume expansion with saline, 4) 12 rats receiving intravenous 25 (OH)vitamin D3, 5) 12 rats with acute hypercalcemia induced by intravenous CaCl2, 6) 6 rats with phosphate deprivation, and 7) 6 rats receiving intravenous calcitonin. Parathyroid hormone and calcitonin failed to increase the urinary excretion of both cAMP and phosphorus. Likewise, DBcAMP failed to increase the urinary excretion of phosphorus. Extracellular volume expansion and hypercalcemia (serum calcium 12.9 +/- 0.7 mg/100 ml) did not alter the tubular reabsorption of phosphorus. In phosphate-deprived animals, the fractional excretion 0.16 +/- 0.05 (mean +/- SE) was lower than that in the control animals (maleate-treated without phosphate depletion), 0.46 +/- 0.04 (P less than 0.001). 25 (OH)vitamin D3 decreased the fractional excretion of phosphorus from 0.39 +/- 0.03 in the control (maleate-treated not receiving 25 (OH)vitamin D3) to 0.23 +/- 0.02 (P less than 0.001) in the experimental animals. The present study demonstrated an antiphosphaturic effect of 25(OH)vitamin D3 in experimental Fanconi syndrome; the mechanism of this action is not well understood.

Animals↗

PubMed1979

Effect of renal vein ligation with or without suprarenal inferior vena cava ligation on sodium and phosphate excretions during acute extracellular volume expansion in the rat.

Right nephrectomy with or without inferior vena cava (IVC) ligation was performed in rats 1 week after left renal vein ligation. Left kidney function and sodium and phosphate excretions by volume expansion were investigated. Inulin (CIN) and para-aminohippuric acid (CPAH) clearances and fractional excretions of sodium (FENa) and phosphate (FEP) were examined before and after volume expansion was induced by normal saline. Kidney functions were well preserved with development of collateral venous channels; biochemical parameters returned to the normal ranges. However, CIN and CPAH were reduced to 33 to 25 per cent of control values and the filtration fraction was elevated. After volume expansion, a marked increment of FENa was observed in cases of IVC ligation but the increment in animals without IVC ligation was less than in the control group. FEP was also increased in experimental groups but the magnitude of phosphaturia was not so prominent compared to the control group. The increment of FEP was not comparable to that of FENa. Thus, from the aspect of kidney function, this experiment showed the rationality of left renal vein ligation with contralateral nephrectomy. From the pathophysiologic aspect, the magnitude of natriuresis and phosphaturia by volume expansion was not prominent and a reduced reabsorptive capacity for sodium and phosphate may exist in a solitary kidney with a ligated renal vein. When suprarenal IVC ligation was also done, prominent natriuresis was observed with saline infusion.

Animals↗