scholarly journals Effects of Metolazone Administration on Congestion, Diuretic Response and Renal Function in Patients with Advanced Heart Failure

2021 ◽  
Vol 10 (18) ◽  
pp. 4207
Author(s):  
Alberto Palazzuoli ◽  
Gaetano Ruocco ◽  
Paolo Severino ◽  
Luigi Gennari ◽  
Filippo Pirrotta ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Function ◽  
Acute Decompensated Heart Failure ◽  
Nyha Class ◽  
Decompensated Heart Failure ◽  
Advanced Heart Failure ◽  
Loop Diuretics ◽  
Reduced Ejection Fraction ◽  
Diuretic Response

Background: Advanced heart failure (HF) is a condition often requiring elevated doses of loop diuretics. Therefore, these patients often experience poor diuretic response. Both conditions have a detrimental impact on prognosis and hospitalization. Aims: This retrospective, multicenter study evaluates the effect of the addition of oral metolazone on diuretic response (DR), clinical congestion, NTproBNP values, and renal function over hospitalization phase. Follow-up analysis for a 6-month follow-up period was performed. Methods: We enrolled 132 patients with acute decompensated heart failure (ADHF) in advanced NYHA class with reduced ejection fraction (EF < 40%) taking a mean furosemide amount of 250 ± 120 mg/day. Sixty-five patients received traditional loop diuretic treatment plus metolazone (Group M). The mean dose ranged from 7.5 to 15 mg for one week. Sixty-seven patients continued the furosemide (Group F). Congestion score was evaluated according to the ESC recommendations. DR was assessed by the formula diuresis/40 mg of furosemide. Results: Patients in Group M and patients in Group F showed a similar prevalence of baseline clinical congestion (3.1 ± 0.7 in Group F vs. 3 ± 0.8 in Group M) and chronic kidney disease (CKD) (51% in Group M vs. 57% in Group F; p = 0.38). Patients in Group M experienced a better congestion score at discharge compared to patients in Group F (C score: 1 ± 1 in Group M vs. 3 ± 1 in Group F p > 0.05). Clinical congestion resolution was also associated with weight reduction (−6 ± 2 in Group M vs. −3 ± 1 kg in Group F, p < 0.05). Better DR response was observed in Group M compared to F (940 ± 149 mL/40 mgFUROSEMIDE/die vs. 541 ± 314 mL/40 mgFUROSEMIDE/die; p < 0.01), whereas median ΔNTproBNP remained similar between the two groups (−4819 ± 8718 in Group M vs. −3954 ± 5560 pg/mL in Group F NS). These data were associated with better daily diuresis during hospitalization in Group M (2820 ± 900 vs. 2050 ± 1120 mL p < 0.05). No differences were found in terms of WRF development and electrolyte unbalance at discharge, although Group M had a significant saline solution administration during hospitalization. Follow-up analysis did not differ between the group but a reduced trend for recurrent hospitalization was observed in the M group (26% vs. 38%). Conclusions: Metolazone administration could be helpful in patients taking an elevated loop diuretics dose. Use of thiazide therapy is associated with better decongestion and DR. Current findings could suggest positive insights due to the reduced amount of loop diuretics in patients with advanced HF.

scholarly journals Oral Metolazone Versus Intravenous Chlorothiazide as an Adjunct to Loop Diuretics for Diuresis in Acute Decompensated Heart Failure With Reduced Ejection Fraction

2018 ◽  
Vol 54 (6) ◽  
pp. 351-357 ◽  
Author(s):  
Brian C. Bohn ◽  
Rim M. Hadgu ◽  
Hannah E. Pope ◽  
Jerrica E. Shuster
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Oral Formulation ◽  
Loop Diuretics ◽  
Reduced Ejection Fraction ◽  
Significant Difference ◽  
Patients With Heart Failure ◽  
Total Urine

Background: Thiazide diuretics are often utilized to overcome loop diuretic resistance when treating acute decompensated heart failure (ADHF). In addition to a large cost advantage, several pharmacokinetic advantages exist when administering oral metolazone (MTZ) compared with intravenous (IV) chlorothiazide (CTZ), yet many providers are reluctant to utilize an oral formulation to treat ADHF. The purpose of this study was to compare the increase in 24-hour total urine output (UOP) after adding MTZ or CTZ to IV loop diuretics (LD) in patients with heart failure with reduced ejection fraction (HFrEF). Methods and Results: From September 2013 to August 2016, 1002 patients admitted for ADHF received either MTZ or CTZ in addition to LD. Patients were excluded for heart failure with preserved ejection fraction (HFpEF) (n = 469), <24-hour LD or UOP data prior to drug initiation (n = 129), or low dose MTZ/CTZ (n = 91). A total of 168 patients were included with 64% receiving CTZ. No significant difference was observed between the increase in 24-hour total UOP after MTZ or CTZ initiation (1458 [514, 2401] mL vs 1820 [890, 2750] mL, P = .251). Conclusions: Both MTZ and CTZ similarly increased UOP when utilized as an adjunct to IV LD. These results suggest that while thiazide agents can substantially increase UOP in ADHF patients with HFrEF, MTZ and CTZ have comparable effects.

P773Initiation of sacubitril/valsartan and optimisation of evidence-based heart failure therapies after hospitalisation for acute decompensated heart failure: An analysis of the TRANSITION study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R Wachter ◽  
D Pascual-Figal ◽  
J Belohlavek ◽  
E Straburzynska-Migaj ◽  
K K Witte ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Target Dose ◽  
Open Label ◽  
Post Discharge ◽  
Reduced Ejection Fraction ◽  
Disease Modifying ◽  
Transition Study

Abstract Background Optimisation of chronic heart failure (HF) therapy remains the key strategy to improve outcomes after hospitalisation for acute decompensated HF (ADHF) with reduced ejection fraction (HFrEF). Initiation and uptitration of disease-modifying therapies is challenging in this vulnerable patient population. We aimed to describe the patterns of treatment optimisation including sacubitril/valsartan (S/V) in the TRANSITION study. Methods TRANSITION (NCT02661217) was a randomised, open-label study comparing S/V initiation pre- vs. post-discharge (1–14 days) in patients admitted for ADHF after haemodynamic stabilisation. The primary endpoint was the proportion of patients achieving 97/103 mg S/V twice daily (bid) at 10 weeks post-randomisation. Up-titration of S/V was as per label. Information on dose of S/V and on the use of concomitant HF medication was collected at each study visit up to week 26. Results A total of 493 patients received at least one dose of S/V in the pre-discharge arm and 489 patients in the post-discharge arm. One month after randomisation, 45% of patients in the pre-d/c arm vs. 44% in the post-discharge arm used 24/26 mg bid starting dose and 42% vs. 40% were on 49/51 mg S/V bid, respectively. At week 10, 47% of patients had achieved the target dose in the pre-discharge arm vs. 51% in the post-discharge arm. At the end of the follow-up at 26 weeks, the proportion of patients on S/V target dose further increased to 53% in the pre-discharge and 61% in the post-discharge arm (Figure 1). At week 10, the mean dose of S/V was 132 mg in the pre-discharge arm and 136 mg in the post-discharge arm, and at week 26, it was 140 mg and 147 mg, respectively. Before hospital admission, 52% and 54% of the patients received a beta-blocker (BB) in the pre-discharge and post-discharge group, respectively, and 42% in both arms received a mineralcorticoid receptor antagonist (MRA). At time of discharge, 68% and 71%% of the patients received a BB and 68% and 65% an MRA, in the pre-discharge and post-discharge groups, respectively. These proportions remained stable to week 10 and week 26. Uptitration of sacubitril/valsartan Conclusions In the vulnerable post-ADHF population, initiation of S/V and up-titration to target dose was feasible within 10 weeks in half of the patients alongside with a 20% increase in the use of other disease-modifying medications that remained stable through the end of the 6-month follow-up. Acknowledgement/Funding The TRANSITION study was funded by Novartis

scholarly journals ALTERATION IN RENAL FUNCTION FOLLOWING LOOP DIURETICS IN PATIENTS WITH ACUTE DECOMPENSATED HEART FAILURE

2019 ◽  
pp. 61-63
Author(s):  
PRUDENCE A RODRIGUES ◽  
SOUMYA GK ◽  
NADIA GRACE BUNSHAW ◽  
SARANYA N ◽  
SUJITH K ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Function ◽  
Renal Injury ◽  
Loop Diuretic ◽  
Acute Decompensated Heart Failure ◽  
Diuretic Therapy ◽  
Decompensated Heart Failure ◽  
Loop Diuretics ◽  
Contributing Factors ◽  
The Impact

Objective: The objective of the study was to monitor the impact of loop diuretic therapy in patients with acute decompensated heart failure (ADHF) and to assess other predictors of renal dysfunction in patients with ADHF. Methods: An observational study over a period of 6 months from January 2018 to June 2018 in the Department of Cardiology, in a Tertiary Care Teaching Hospital, Coimbatore, Tamil Nadu. Patients on diuretic therapy (loop diuretic) were enrolled. Patients with prior chronic kidney disease were excluded from the study. The patients were evaluated based on change in serum creatinine (SCr) and other contributing factors were assessed by acute kidney injury network and worsening of renal function criteria. Results: A total of 135 patients were enrolled, of which 73% were males and 27% were females. The mean age of the subjects was 61.55±13 years. The baseline means SCr was 1.62±0.92 mg/dl. On evaluation, 41% were really affected and 59% remain unaffected. Factors such as hypertension (p=0.047) and angiotensin-converting enzyme inhibitors (ACE-I) (p=0.023) were found to be significant predictors of renal injury. Conclusion: Variation in renal function in ADHF patients was multifactorial. The direct influence of loop diuretics on renal function was present but was not well established. Hypertension and ACE-I have found to show influence in the development of renal injury as contributing factors. There exists both positive and negative consequence of loop diuretics on renal function.

scholarly journals Renal Function during Hospitalization and Outcome in Chinese Patients with Acute Decompensated Heart Failure

2021 ◽  
Author(s):  
Hao-Wei Lee ◽  
Chin-Chou Huang ◽  
Chih-Yu Yang ◽  
Hsin-Bang Leu ◽  
Po-Hsun Huang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Function ◽  
Clinical Outcomes ◽  
Acute Decompensated Heart Failure ◽  
Significant Risk ◽  
Decompensated Heart Failure ◽  
Chinese Patients ◽  
Cox Regression Analysis ◽  
The Impact

Abstract It is well known that the heart and kidney have a bi-directional correlation, in which organ dysfunction results in maladaptive changes in the other. We aimed to investigate the impact of renal function and its decline during hospitalization on clinical outcomes in patients with acute decompensated heart failure (ADHF). A total of 119 consecutive Chinese patients admitted for ADHF were prospectively enrolled. The course of renal function was presented with estimated glomerular filtration rate (eGFR), calculated by the four-variable equation proposed by the Modification of Diet in Renal Disease (MDRD) Study. Worsening renal function (WRF), defined as eGFR decline between admission (eGFRadmission) and pre-discharge (eGFRpredischarge), occurred in 41 patients. Clinical outcomes during the follow-up period were defined as 4P-major adverse cardiovascular events (4P-MACE), including the composition of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, and nonfatal HF hospitalization. During an average follow-up period of 2.6±3.2 years, 66 patients experienced 4P-MACE. Cox regression analysis revealed that impaired eGFRpredischarge, but not eGFRadmission or WRF, was significantly correlated with the development of 4P-MACE (HR, 2.003; 95% CI, 1.072–3.744; P=0.029). In conclusion, impaired renal function before discharge, but not WRF, is a significant risk factor for poor outcomes in patients with ADHF.

Heart Failure

2020 ◽  
Author(s):  
Sachin P Shah ◽  
Mandeep R. Mehra
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Acute Decompensated Heart Failure ◽  
Heart Association ◽  
Decompensated Heart Failure ◽  
Advanced Heart Failure ◽  
Circulatory Support ◽  
Preserved Ejection Fraction ◽  
Reduced Ejection Fraction

Heart failure is a syndrome related to abnormal cardiac performance with a consequence of impaired cardiac output at rest or with exertion and/or congestion, which usually leads to symptoms of fatigue, dyspnea, and edema. The syndrome is characterized by various phenotypes related to a vast array of etiologies with diverse management targets. The current broad categorization of heart failure separates patients based on ejection fraction. Further description of the phenotype beyond ejection fraction is imperative to correctly identify the etiology of heart failure and, ultimately, to choose medical, device, and surgical therapies appropriately. This review covers the epidemiology of heart failure, defining the phenotype and etiology of heart failure, recognition and management of acute decompensated heart failure, management of chronic heart failure with a reduced ejection fraction, implantable cardioverter-defibrillators in heart failure with a reduced ejection fraction, management of heart failure with a preserved ejection fraction, and advanced heart failure. Figures show the evolution of therapy in chronic heart failure from the symptom-directed model, the complex pathophysiology and principal aberrations underlying heart failure with preserved ejection fraction, and concepts underlying surgical therapy in advanced heart failure using Laplace’s law. Tables list various etiologies of heart failure; sensitivity and specificity of clinical, biomarker, and radiographic data in the diagnosis of acute decompensated heart failure; drugs and devices with a demonstrated survival benefit in heart failure with a reduced ejection fraction; neurohormonal antagonist dosing in heart failure with a reduced ejection fraction; randomized, placebo-controlled trials in heart failure with a preserved ejection fraction; categorization of heart failure according to American Heart Association/American College of Cardiology heart failure stage, New York Heart Association functional class, and Interagency Registry for Mechanically Assisted Circulatory Support level; and poor prognostic indicators in heart failure. This review contains 4 highly rendered figures, 8 tables, and 114 references.

Heart Failure

2018 ◽  
Author(s):  
Sachin P Shah ◽  
Mandeep R. Mehra
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Acute Decompensated Heart Failure ◽  
Heart Association ◽  
Decompensated Heart Failure ◽  
Advanced Heart Failure ◽  
Circulatory Support ◽  
Preserved Ejection Fraction ◽  
Reduced Ejection Fraction

Heart failure is a syndrome related to abnormal cardiac performance with a consequence of impaired cardiac output at rest or with exertion and/or congestion, which usually leads to symptoms of fatigue, dyspnea, and edema. The syndrome is characterized by various phenotypes related to a vast array of etiologies with diverse management targets. The current broad categorization of heart failure separates patients based on ejection fraction. Further description of the phenotype beyond ejection fraction is imperative to correctly identify the etiology of heart failure and, ultimately, to choose medical, device, and surgical therapies appropriately. This review covers the epidemiology of heart failure, defining the phenotype and etiology of heart failure, recognition and management of acute decompensated heart failure, management of chronic heart failure with a reduced ejection fraction, implantable cardioverter-defibrillators in heart failure with a reduced ejection fraction, management of heart failure with a preserved ejection fraction, and advanced heart failure. Figures show the evolution of therapy in chronic heart failure from the symptom-directed model, the complex pathophysiology and principal aberrations underlying heart failure with preserved ejection fraction, and concepts underlying surgical therapy in advanced heart failure using Laplace’s law. Tables list various etiologies of heart failure; sensitivity and specificity of clinical, biomarker, and radiographic data in the diagnosis of acute decompensated heart failure; drugs and devices with a demonstrated survival benefit in heart failure with a reduced ejection fraction; neurohormonal antagonist dosing in heart failure with a reduced ejection fraction; randomized, placebo-controlled trials in heart failure with a preserved ejection fraction; categorization of heart failure according to American Heart Association/American College of Cardiology heart failure stage, New York Heart Association functional class, and Interagency Registry for Mechanically Assisted Circulatory Support level; and poor prognostic indicators in heart failure. This review contains 3 highly rendered figures, 7 tables, and 113 references.

Incidence and Outcomes of Acute Heart Failure With Preserved Versus Reduced Ejection Fraction in SPRINT

2021 ◽  
Author(s):  
Bharathi Upadhya ◽  
James J. Willard ◽  
Laura C. Lovato ◽  
Michael V. Rocco ◽  
Cora E. Lewis ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Hospital Readmission ◽  
Statistical Power ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Unique Identifier ◽  
Black Race ◽  
Reduced Ejection Fraction

Background: In the SPRINT (Systolic Blood Pressure Intervention Trial), intensive BP treatment reduced acute decompensated heart failure (ADHF) events. Here, we report the effect on HF with preserved ejection fraction (HFpEF) and HF with reduced EF (HFrEF) and their subsequent outcomes. Methods: Incident ADHF was defined as hospitalization or emergency department visit, confirmed, and formally adjudicated by a blinded events committee using standardized protocols. HFpEF was defined as EF ≥45%, and HFrEF was EF <45%. Results: Among the 133 participants with incident ADHF who had EF assessment, 69 (52%) had HFpEF and 64 (48%) had HFrEF ( P value: 0.73). During average 3.3 years follow-up in those who developed incident ADHF, rates of subsequent all-cause and HF hospital readmission and mortality were high, but there were no significant differences between those who developed HFpEF versus HFrEF. Randomization to the intensive arm had no effect on subsequent mortality or readmissions after the initial ADHF event, irrespective of EF subtype. During follow-up among participants who developed HFpEF, although relatively modest number of events limited statistical power, age was an independent predictor of all-cause mortality, and Black race independently predicted all-cause and HF hospital readmission. Conclusions: In SPRINT, intensive BP reduction decreased both acute decompensated HFpEF and HFrEF events. After initial incident ADHF, rates of subsequent hospital admission and mortality were high and were similar for those who developed HFpEF or HFrEF. Randomization to the intensive arm did not alter the risks for subsequent all-cause, or HF events in either HFpEF or HFrEF. Among those who developed HFpEF, age and Black race were independent predictors of clinical outcomes. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01206062.

Heart Failure

2020 ◽  
Author(s):  
Sachin P Shah ◽  
Mandeep R. Mehra
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Acute Decompensated Heart Failure ◽  
Heart Association ◽  
Decompensated Heart Failure ◽  
Advanced Heart Failure ◽  
Circulatory Support ◽  
Preserved Ejection Fraction ◽  
Reduced Ejection Fraction

Heart failure is a syndrome related to abnormal cardiac performance with a consequence of impaired cardiac output at rest or with exertion and/or congestion, which usually leads to symptoms of fatigue, dyspnea, and edema. The syndrome is characterized by various phenotypes related to a vast array of etiologies with diverse management targets. The current broad categorization of heart failure separates patients based on ejection fraction. Further description of the phenotype beyond ejection fraction is imperative to correctly identify the etiology of heart failure and, ultimately, to choose medical, device, and surgical therapies appropriately. This review covers the epidemiology of heart failure, defining the phenotype and etiology of heart failure, recognition and management of acute decompensated heart failure, management of chronic heart failure with a reduced ejection fraction, implantable cardioverter-defibrillators in heart failure with a reduced ejection fraction, management of heart failure with a preserved ejection fraction, and advanced heart failure. Figures show the evolution of therapy in chronic heart failure from the symptom-directed model, the complex pathophysiology and principal aberrations underlying heart failure with preserved ejection fraction, and concepts underlying surgical therapy in advanced heart failure using Laplace’s law. Tables list various etiologies of heart failure; sensitivity and specificity of clinical, biomarker, and radiographic data in the diagnosis of acute decompensated heart failure; drugs and devices with a demonstrated survival benefit in heart failure with a reduced ejection fraction; neurohormonal antagonist dosing in heart failure with a reduced ejection fraction; randomized, placebo-controlled trials in heart failure with a preserved ejection fraction; categorization of heart failure according to American Heart Association/American College of Cardiology heart failure stage, New York Heart Association functional class, and Interagency Registry for Mechanically Assisted Circulatory Support level; and poor prognostic indicators in heart failure. This review contains 4 highly rendered figures, 8 tables, and 114 references.

P1637Rehospitalisations during 26 weeks of follow up from initiation of sacubitril/valsartan after acute decompensated heart failure: An analysis of the TRANSITION study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D Pascual-Figal ◽  
K K Witte ◽  
R Wachter ◽  
J Belohlavek ◽  
E Straburzynska-Migaj ◽  
...  
Keyword(s):  
Heart Failure ◽  
Emergency Room ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Open Label ◽  
Post Discharge ◽  
Open Label Study ◽  
Reduced Ejection Fraction ◽  
Transition Study

Abstract Background Patients with acute decompensated heart failure (ADHF) are at high risk of recurrent hospitalisations and death. In-hospital initiation of sacubitril/valsartan (S/V) reduced the risk for HF re-hospitalisation by 44% compared to enalapril in the PIONEER-HF study during the 8-week follow-up period. We aimed to describe the pattern of readmissions and their causes in the TRANSITION study, which randomised participants to pre-discharge or post-discharge initation of S/V. Methods TRANSITION (NCT02661217) was a randomised, open-label study comparing S/V initiation pre- vs. post-discharge (1–14 days) in haemodynamically stabilised patients with HF with reduced ejection fraction, admitted for ADHF. The primary endpoint was the proportion of patients achieving 97/103 mg S/V twice daily at 10 weeks post-randomisation. Information on rehospitalisation was collected throughout the study up to 26 weeks. Results A total of 493 patients received S/V in the pre-discharge arm and 489 patients in the post-discharge arm. Readmissions due to any cause were reported in 9.7% and 18.1% in the pre-discharge arm vs. 10.6% and 21.3% in the post-discharge arm within 30 days, and 10 weeks respectively. During the 26-weeks follow-up, all-cause readmission was reported in 34.5% of patients in the pre-discharge arm vs. 34.6% in the post-discharge arm. Median time to first rehospitalisation was 67 days in the pre-discharge arm (IQR: 26–110 days) and 50 days (IQR: 23–108 days) in the post-discharge arm. At least one HF hospitalisation was reported in 7.5% of patients in the pre-discharge arm and 7.4% in the post-discharge arm during 10 weeks and in 11.8% and 12.3% of patients, respectively, during 26 weeks of follow-up. Median duration of HF readmission was 7 days (IQR: 4–11 days) in the pre-discharge group and 6.5 days (IQR: 6.5–10 days) in the post-discharge arm. In total 2.6% and 5.5% patients in pre-discharge arm and 3.9% and 7% in the post-discharge arm visited an emergency room during 10 weeks and 26 weeks, respectively. Conclusions Initiation of S/V in patients hospitalised for ADHF either before or shortly after discharge, results in comparable rates of all cause and HF rehospitalisations, as well as emergency room visits without hospital admission over the 26 week follow-up period. HF re-hospitalisations rates at 10 weeks in TRANSITION are in line with the 8% in S/V arm reported in PIONEER-HF during the 8-weeks follow-up. Acknowledgement/Funding The TRANSITION study was funded by Novartis

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