Mechanistic insights into chloride‐related heart failure progression according to the plasma volume status
Aims Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration. The applicability of this concept to real‐world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF pro...
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| Published in | ESC Heart Failure Vol. 9; no. 3; pp. 2044 - 2048 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.06.2022
John Wiley and Sons Inc Wiley |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2055-5822 2055-5822 |
| DOI | 10.1002/ehf2.13927 |
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| Abstract | Aims
Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration. The applicability of this concept to real‐world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF progression to a different type according to changes in the estimated plasma volume status (ePVS).
Methods and results
Data from 47 patients (32% men; 78.2 ± 9.7 years of age) with stable to worsening HF (37.5 ± 16 days) were analysed. Physical examination, standard blood tests, and b‐type natriuretic peptide (BNP) measurements were conducted. The ePVS was calculated as follows: ePVS (dL/g) = [100 − haematocrit (%)]/[haemoglobin (g/dL)]. For the study subjects as a whole (n = 47), changes in the ePVS correlated positively with changes in the serum chloride concentration from stable to worsening HF (r = 0.398, P = 0.0056). When divided into two groups of worsening HF with an increased (n = 31) vs. non‐increased serum chloride concentration (n = 16), no significant baseline differences in body weight, serum logBNP, or ePVS were detected between groups. Under worsening HF, the increase in body weight (2.34 ± 1.12 vs. 2.59 ± 1.56 kg, P = 0.57) and logBNP (0.39 ± 0.30 vs. 0.54 ± 0.31 pg/mL, P = 0.13) did not differ between groups, but the increase in the ePVS was smaller in the group with a non‐increased serum chloride concentration compared with that with an increased serum chloride concentration (0.292 ± 0.49 vs. 0.653 ± 0.60 dL/g, P = 0.044). An increase in the %change in ePVS ≥ 10% was less common in patients with a non‐increased chloride concentration (37% vs. 71%, P = 0.03). Patients with a non‐increased serum chloride concentration had more HF signs (3.31 ± 0.79 vs. 2.65 ± 0.71, P = 0.005) and a higher incidence of pulmonary rales (63% vs. 16%, P = 0.0024) than those with an increased serum chloride concentration.
Conclusions
According to the changes in the ePVS, HF progression may result from a difference between two HF types (i.e. increased vs. non‐increased serum chloride concentration) in the cardiac reserve in response to a given cardiac burden by modulating plasma volume status via the possible tonicity potential of chloride. |
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| AbstractList | Aims Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration. The applicability of this concept to real‐world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF progression to a different type according to changes in the estimated plasma volume status (ePVS). Methods and results Data from 47 patients (32% men; 78.2 ± 9.7 years of age) with stable to worsening HF (37.5 ± 16 days) were analysed. Physical examination, standard blood tests, and b‐type natriuretic peptide (BNP) measurements were conducted. The ePVS was calculated as follows: ePVS (dL/g) = [100 − haematocrit (%)]/[haemoglobin (g/dL)]. For the study subjects as a whole (n = 47), changes in the ePVS correlated positively with changes in the serum chloride concentration from stable to worsening HF (r = 0.398, P = 0.0056). When divided into two groups of worsening HF with an increased (n = 31) vs. non‐increased serum chloride concentration (n = 16), no significant baseline differences in body weight, serum logBNP, or ePVS were detected between groups. Under worsening HF, the increase in body weight (2.34 ± 1.12 vs. 2.59 ± 1.56 kg, P = 0.57) and logBNP (0.39 ± 0.30 vs. 0.54 ± 0.31 pg/mL, P = 0.13) did not differ between groups, but the increase in the ePVS was smaller in the group with a non‐increased serum chloride concentration compared with that with an increased serum chloride concentration (0.292 ± 0.49 vs. 0.653 ± 0.60 dL/g, P = 0.044). An increase in the %change in ePVS ≥ 10% was less common in patients with a non‐increased chloride concentration (37% vs. 71%, P = 0.03). Patients with a non‐increased serum chloride concentration had more HF signs (3.31 ± 0.79 vs. 2.65 ± 0.71, P = 0.005) and a higher incidence of pulmonary rales (63% vs. 16%, P = 0.0024) than those with an increased serum chloride concentration. Conclusions According to the changes in the ePVS, HF progression may result from a difference between two HF types (i.e. increased vs. non‐increased serum chloride concentration) in the cardiac reserve in response to a given cardiac burden by modulating plasma volume status via the possible tonicity potential of chloride. Aims Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration. The applicability of this concept to real‐world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF progression to a different type according to changes in the estimated plasma volume status (ePVS). Methods and results Data from 47 patients (32% men; 78.2 ± 9.7 years of age) with stable to worsening HF (37.5 ± 16 days) were analysed. Physical examination, standard blood tests, and b‐type natriuretic peptide (BNP) measurements were conducted. The ePVS was calculated as follows: ePVS (dL/g) = [100 − haematocrit (%)]/[haemoglobin (g/dL)]. For the study subjects as a whole (n = 47), changes in the ePVS correlated positively with changes in the serum chloride concentration from stable to worsening HF (r = 0.398, P = 0.0056). When divided into two groups of worsening HF with an increased (n = 31) vs. non‐increased serum chloride concentration (n = 16), no significant baseline differences in body weight, serum logBNP, or ePVS were detected between groups. Under worsening HF, the increase in body weight (2.34 ± 1.12 vs. 2.59 ± 1.56 kg, P = 0.57) and logBNP (0.39 ± 0.30 vs. 0.54 ± 0.31 pg/mL, P = 0.13) did not differ between groups, but the increase in the ePVS was smaller in the group with a non‐increased serum chloride concentration compared with that with an increased serum chloride concentration (0.292 ± 0.49 vs. 0.653 ± 0.60 dL/g, P = 0.044). An increase in the %change in ePVS ≥ 10% was less common in patients with a non‐increased chloride concentration (37% vs. 71%, P = 0.03). Patients with a non‐increased serum chloride concentration had more HF signs (3.31 ± 0.79 vs. 2.65 ± 0.71, P = 0.005) and a higher incidence of pulmonary rales (63% vs. 16%, P = 0.0024) than those with an increased serum chloride concentration. Conclusions According to the changes in the ePVS, HF progression may result from a difference between two HF types (i.e. increased vs. non‐increased serum chloride concentration) in the cardiac reserve in response to a given cardiac burden by modulating plasma volume status via the possible tonicity potential of chloride. Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non-increased serum chloride concentration. The applicability of this concept to real-world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF progression to a different type according to changes in the estimated plasma volume status (ePVS). Data from 47 patients (32% men; 78.2 ± 9.7 years of age) with stable to worsening HF (37.5 ± 16 days) were analysed. Physical examination, standard blood tests, and b-type natriuretic peptide (BNP) measurements were conducted. The ePVS was calculated as follows: ePVS (dL/g) = [100 - haematocrit (%)]/[haemoglobin (g/dL)]. For the study subjects as a whole (n = 47), changes in the ePVS correlated positively with changes in the serum chloride concentration from stable to worsening HF (r = 0.398, P = 0.0056). When divided into two groups of worsening HF with an increased (n = 31) vs. non-increased serum chloride concentration (n = 16), no significant baseline differences in body weight, serum logBNP, or ePVS were detected between groups. Under worsening HF, the increase in body weight (2.34 ± 1.12 vs. 2.59 ± 1.56 kg, P = 0.57) and logBNP (0.39 ± 0.30 vs. 0.54 ± 0.31 pg/mL, P = 0.13) did not differ between groups, but the increase in the ePVS was smaller in the group with a non-increased serum chloride concentration compared with that with an increased serum chloride concentration (0.292 ± 0.49 vs. 0.653 ± 0.60 dL/g, P = 0.044). An increase in the %change in ePVS ≥ 10% was less common in patients with a non-increased chloride concentration (37% vs. 71%, P = 0.03). Patients with a non-increased serum chloride concentration had more HF signs (3.31 ± 0.79 vs. 2.65 ± 0.71, P = 0.005) and a higher incidence of pulmonary rales (63% vs. 16%, P = 0.0024) than those with an increased serum chloride concentration. According to the changes in the ePVS, HF progression may result from a difference between two HF types (i.e. increased vs. non-increased serum chloride concentration) in the cardiac reserve in response to a given cardiac burden by modulating plasma volume status via the possible tonicity potential of chloride. Abstract Aims Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration. The applicability of this concept to real‐world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF progression to a different type according to changes in the estimated plasma volume status (ePVS). Methods and results Data from 47 patients (32% men; 78.2 ± 9.7 years of age) with stable to worsening HF (37.5 ± 16 days) were analysed. Physical examination, standard blood tests, and b‐type natriuretic peptide (BNP) measurements were conducted. The ePVS was calculated as follows: ePVS (dL/g) = [100 − haematocrit (%)]/[haemoglobin (g/dL)]. For the study subjects as a whole (n = 47), changes in the ePVS correlated positively with changes in the serum chloride concentration from stable to worsening HF (r = 0.398, P = 0.0056). When divided into two groups of worsening HF with an increased (n = 31) vs. non‐increased serum chloride concentration (n = 16), no significant baseline differences in body weight, serum logBNP, or ePVS were detected between groups. Under worsening HF, the increase in body weight (2.34 ± 1.12 vs. 2.59 ± 1.56 kg, P = 0.57) and logBNP (0.39 ± 0.30 vs. 0.54 ± 0.31 pg/mL, P = 0.13) did not differ between groups, but the increase in the ePVS was smaller in the group with a non‐increased serum chloride concentration compared with that with an increased serum chloride concentration (0.292 ± 0.49 vs. 0.653 ± 0.60 dL/g, P = 0.044). An increase in the %change in ePVS ≥ 10% was less common in patients with a non‐increased chloride concentration (37% vs. 71%, P = 0.03). Patients with a non‐increased serum chloride concentration had more HF signs (3.31 ± 0.79 vs. 2.65 ± 0.71, P = 0.005) and a higher incidence of pulmonary rales (63% vs. 16%, P = 0.0024) than those with an increased serum chloride concentration. Conclusions According to the changes in the ePVS, HF progression may result from a difference between two HF types (i.e. increased vs. non‐increased serum chloride concentration) in the cardiac reserve in response to a given cardiac burden by modulating plasma volume status via the possible tonicity potential of chloride. Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non-increased serum chloride concentration. The applicability of this concept to real-world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF progression to a different type according to changes in the estimated plasma volume status (ePVS).AIMSTwo types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non-increased serum chloride concentration. The applicability of this concept to real-world HF pathophysiology requires further investigation. The present study evaluated the mechanisms of HF progression to a different type according to changes in the estimated plasma volume status (ePVS).Data from 47 patients (32% men; 78.2 ± 9.7 years of age) with stable to worsening HF (37.5 ± 16 days) were analysed. Physical examination, standard blood tests, and b-type natriuretic peptide (BNP) measurements were conducted. The ePVS was calculated as follows: ePVS (dL/g) = [100 - haematocrit (%)]/[haemoglobin (g/dL)]. For the study subjects as a whole (n = 47), changes in the ePVS correlated positively with changes in the serum chloride concentration from stable to worsening HF (r = 0.398, P = 0.0056). When divided into two groups of worsening HF with an increased (n = 31) vs. non-increased serum chloride concentration (n = 16), no significant baseline differences in body weight, serum logBNP, or ePVS were detected between groups. Under worsening HF, the increase in body weight (2.34 ± 1.12 vs. 2.59 ± 1.56 kg, P = 0.57) and logBNP (0.39 ± 0.30 vs. 0.54 ± 0.31 pg/mL, P = 0.13) did not differ between groups, but the increase in the ePVS was smaller in the group with a non-increased serum chloride concentration compared with that with an increased serum chloride concentration (0.292 ± 0.49 vs. 0.653 ± 0.60 dL/g, P = 0.044). An increase in the %change in ePVS ≥ 10% was less common in patients with a non-increased chloride concentration (37% vs. 71%, P = 0.03). Patients with a non-increased serum chloride concentration had more HF signs (3.31 ± 0.79 vs. 2.65 ± 0.71, P = 0.005) and a higher incidence of pulmonary rales (63% vs. 16%, P = 0.0024) than those with an increased serum chloride concentration.METHODS AND RESULTSData from 47 patients (32% men; 78.2 ± 9.7 years of age) with stable to worsening HF (37.5 ± 16 days) were analysed. Physical examination, standard blood tests, and b-type natriuretic peptide (BNP) measurements were conducted. The ePVS was calculated as follows: ePVS (dL/g) = [100 - haematocrit (%)]/[haemoglobin (g/dL)]. For the study subjects as a whole (n = 47), changes in the ePVS correlated positively with changes in the serum chloride concentration from stable to worsening HF (r = 0.398, P = 0.0056). When divided into two groups of worsening HF with an increased (n = 31) vs. non-increased serum chloride concentration (n = 16), no significant baseline differences in body weight, serum logBNP, or ePVS were detected between groups. Under worsening HF, the increase in body weight (2.34 ± 1.12 vs. 2.59 ± 1.56 kg, P = 0.57) and logBNP (0.39 ± 0.30 vs. 0.54 ± 0.31 pg/mL, P = 0.13) did not differ between groups, but the increase in the ePVS was smaller in the group with a non-increased serum chloride concentration compared with that with an increased serum chloride concentration (0.292 ± 0.49 vs. 0.653 ± 0.60 dL/g, P = 0.044). An increase in the %change in ePVS ≥ 10% was less common in patients with a non-increased chloride concentration (37% vs. 71%, P = 0.03). Patients with a non-increased serum chloride concentration had more HF signs (3.31 ± 0.79 vs. 2.65 ± 0.71, P = 0.005) and a higher incidence of pulmonary rales (63% vs. 16%, P = 0.0024) than those with an increased serum chloride concentration.According to the changes in the ePVS, HF progression may result from a difference between two HF types (i.e. increased vs. non-increased serum chloride concentration) in the cardiac reserve in response to a given cardiac burden by modulating plasma volume status via the possible tonicity potential of chloride.CONCLUSIONSAccording to the changes in the ePVS, HF progression may result from a difference between two HF types (i.e. increased vs. non-increased serum chloride concentration) in the cardiac reserve in response to a given cardiac burden by modulating plasma volume status via the possible tonicity potential of chloride. |
| Author | Kataoka, Hajime |
| AuthorAffiliation | 1 Department of Internal Medicine Nishida Hospital Tsuruoka‐Nishi‐Machi 2‐266 Saiki Oita 876‐0047 Japan |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35384366$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1002_ehf2_14434 crossref_primary_10_3390_biomedicines12112473 crossref_primary_10_1002_ehf2_15054 crossref_primary_10_1038_s41598_024_64747_5 |
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| Copyright | 2022 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology. 2022. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | Heart failure Body fluid Vascular volume Chloride Pathophysiology |
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| References_xml | – volume: 2 start-page: 106 year: 2015 end-page: 115 article-title: Clinical significance of bilateral leg edema and added value of monitoring weight gain during follow‐up of patients with established heart failure publication-title: ESC Heart Fail – volume: 4 start-page: 623 year: 2017 end-page: 631 article-title: Proposal for heart failure progression based on the ‘chloride theory’: worsening heart failure with increased vs. non‐increased serum chloride concentration publication-title: ESC Heart Fail – volume: 108 start-page: 563 year: 2019 end-page: 573 article-title: Diagnostic and prognostic value of plasma volume status at emergency department admission in dyspneic patients: results from the PARADISE cohort publication-title: Clin Res Cardiol – volume: 20 start-page: 1426 year: 2018 end-page: 1435 article-title: Low serum chloride in patients with chronic heart failure: clinical associations and prognostic significance publication-title: Eur J Heart Fail – volume: 3 start-page: 886 year: 2015 end-page: 893 article-title: Prognostic value of estimated plasma volume in heart failure publication-title: JACC Heart Fail – volume: 230 start-page: 556 year: 2017 end-page: 561 article-title: Vascular expansion during worsening of heart failure: effects on clinical features and its determinants publication-title: Int J Cardiol – volume: 6 start-page: 123 year: 2021 end-page: 131 article-title: Clinical significance of spot urinary chloride concentration measurements in patients with acute heart failure: investigation on the basis of the ‘tubulo‐glomerular feedback’ mechanism publication-title: Cardio Open – volume: 16 start-page: 133 year: 2014 end-page: 142 article-title: The kidney in congestive heart failure: ‘are natriuresis, sodium, and diuretics really the good, the bad and the ugly?’ publication-title: Eur J Heart Fail – volume: 25 start-page: 213 year: 2019 end-page: 217 article-title: Biochemical determinants of changes in plasma volume after decongestion therapy for worsening heart failure publication-title: J Card Fail – volume: 10 start-page: 407 year: 2021 end-page: 428 article-title: Chloride in heart failure syndrome: its pathophysiologic role and therapeutic implication publication-title: Cardiol Ther – volume: 9 start-page: 706 year: 1954 end-page: 718 article-title: Ventricular function: Starling's law of the heart studied by means of simultaneous right and left ventricular function curves in the dog publication-title: Circulation – volume: 18 start-page: 2028 year: 2007 end-page: 2031 article-title: Decreased effective blood volume in edematous disorders: what does this mean? publication-title: J Am Soc Nephrol – volume: 25 start-page: 240 year: 2019 end-page: 248 article-title: The optimal plasma volume status in heart failure in relation to clinical outcome publication-title: J Card Fail – volume: 62 start-page: 516 year: 2013 end-page: 524 article-title: Timing of hemoconcentration during treatment of acute decompensated heart failure and subsequent survival: importance of sustained decongestion publication-title: J Am Coll Cardiol – volume: 19 start-page: 226 year: 2017 end-page: 236 article-title: Impact of haemoconcentration during acute heart failure therapy on mortality and its relationship with worsening renal function publication-title: Eur J Heart Fail – volume: 9 start-page: 333 year: 2020 end-page: 347 article-title: Hypochloremia in patients with heart failure: causes and consequences publication-title: Cardiol Ther – volume: 17 start-page: 689 year: 2015 end-page: 696 article-title: Prognostic role of cardiac power index in ambulatory patients with advanced heart failure publication-title: Eur J Heart Fail – volume: 9 start-page: 227 year: 2020 end-page: 244 article-title: Proposal for new classification and practical use of diuretics according to their effects on the serum chloride concentration: rationale based on the “chloride theory” publication-title: Cardiol Ther – volume: 104 start-page: 170 year: 2017 end-page: 173 article-title: The “chloride theory”, a unifying hypothesis for renal handling and body fluid distribution in heart failure pathophysiology publication-title: Med Hypotheses – ident: e_1_2_7_5_1 doi: 10.1016/j.jchf.2015.06.014 – ident: e_1_2_7_10_1 doi: 10.1681/ASN.2006111302 – ident: e_1_2_7_11_1 doi: 10.1002/ejhf.268 – ident: e_1_2_7_8_1 doi: 10.1002/ehf2.12043 – ident: e_1_2_7_13_1 doi: 10.1007/s40119-020-00194-3 – volume: 6 start-page: 123 year: 2021 ident: e_1_2_7_14_1 article-title: Clinical significance of spot urinary chloride concentration measurements in patients with acute heart failure: investigation on the basis of the ‘tubulo‐glomerular feedback’ mechanism publication-title: Cardio Open – ident: e_1_2_7_2_1 doi: 10.1016/j.ijcard.2016.12.059 – ident: e_1_2_7_9_1 doi: 10.1161/01.CIR.9.5.706 – ident: e_1_2_7_20_1 doi: 10.1002/ejhf.667 – ident: e_1_2_7_15_1 doi: 10.1002/ejhf.35 – ident: e_1_2_7_17_1 doi: 10.1007/s40119-021-00238-2 – ident: e_1_2_7_6_1 doi: 10.1007/s00392-018-1388-y – ident: e_1_2_7_3_1 doi: 10.1016/j.cardfail.2018.09.014 – ident: e_1_2_7_16_1 doi: 10.1007/s40119-020-00172-9 – ident: e_1_2_7_4_1 doi: 10.1016/j.mehy.2017.06.005 – ident: e_1_2_7_12_1 doi: 10.1002/ejhf.1247 – ident: e_1_2_7_7_1 doi: 10.1002/ehf2.12191 – ident: e_1_2_7_18_1 doi: 10.1016/j.cardfail.2018.11.019 – ident: e_1_2_7_19_1 doi: 10.1016/j.jacc.2013.05.027 |
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Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration. The... Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non-increased serum chloride concentration. The... Aims Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration. The... Abstract Aims Two types of heart failure (HF) progression were recently proposed on the basis of an increased vs. non‐increased serum chloride concentration.... |
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| SubjectTerms | Blood Body fluid Body Weight Chloride Chlorides Diuretics Electrolytes Female Heart Failure Hemoglobin Hemoglobins Humans Male Pathophysiology Patients Peptides Plasma Plasma Volume - physiology Pleural effusion Short Communication Short Communications Ultrasonic imaging Vascular volume |
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| Title | Mechanistic insights into chloride‐related heart failure progression according to the plasma volume status |
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