1,721,019 research outputs found
Redefining Boundaries in Heart Failure Care The Potential and Pitfalls of Subcutaneous Furosemide
No full textResponse by Dauw and Mullens to Letters Regarding Article, "Protocolized Natriuresis-Guided Decongestion Improves Diuretic Response: The Multicenter ENACT-HF Study"
No full textIn Response: We thank all our colleagues for their interest in our study. 1 Dr Albulushi questions how patient selection might affect the generalizability of our results. A detailed description of the inclusion and exclusion criteria has been published previously. 2 Our study had a pragmatic design with the goal of mimicking real-life practice as much as possible. In essence, almost all patients with fluid overload on a daily loop diuretic dose of ≥40 mg of furosemide or equivalent with elevated natriuretic peptides could be included. Only patients in shock or impending shock and patients with a potential need for renal replacement therapy were excluded. As a result, the patient population in our study is comparable to that of recent registries of acute heart failure. 3 Of note, comor-bidities were highly prevalent, and almost half of the patients had chronic kidney disease (defined as an estimated glomerular filtration rate <60 mL/min/1.73 m 2). Regarding arrhythmias, 54% of patients had a history of atrial fibrillation, and 45% were in atrial fibrillation at the time of admission. Therefore, our study population seems generalizable to real-world patients. Dr Albulushi was also interested in long-term data on readmission rates or mortality, but we did not collect data beyond discharge. Shahriar et al request more information on the diuretic response assessments after the first loop diuretic dose. Indeed, there were more patients with an insufficient urine output (UO; 19.6%) than an insufficient urinary sodium concentration (UNa; 12.6%) in the protocol arm. We performed additional analyses to provide more in-depth information: 36 (25.2%) patients had any sign of insufficient diuretic response. Of those, 8 (5.6%) only had UNa <50 mmol/L; 18 (12.6%) only had UO <100 mL/h, and 10 (7.0%) had both UNa <50 mmol/L and UO <100 mL/h. Thus, both measures can be incongruent and have additive value. Recent observational data in a small group of acute heart failure patients have already suggested that UNa and UO may differ. 4 When a threshold of UNa <70 mmol/L is applied, 60 (24.5%) patients in the standard of care group and 26 (18.3%) patients in the protocol group had an insufficient diuretic response. Potentially, a cutoff value of UNa <70 mmol/L might identify a larger group of patients with an insufficient diuretic response. A cutoff value of UNa <70 mmol/K was also used in the recent Pragmatic Urinary Sodium-Based Treatment Algorithm in Acute Heart Failure randomized trial. 5 In addition, the trial used a higher UO threshold with UO <150 mL/h. Again, the natriuresis-guided protocol performed better than the standard of care, but UNa and UO were not always congruent. ARTICLE INFORMATION Affiliation
Unravelling Congestion in Heart Failure: Mechanisms, Diagnosis and Treatment
No full textHeart failure exerts a significant and growing burden on public health globally. It
currently afflicts approximately 2% of the adult Western population, impacting the
lives of an estimated 64.3 million individuals across the world 1. This alarming
prevalence is further underscored by the fact that heart failure ranks as the
primary cause for hospital admissions, accounting for 1-2% of all admissions and
representing the most prevalent reason for hospitalization among the elderly 1.
Despite a modest decline in the overall incidence of heart failure in Europe, its
prevalence continues to surge due to the improved treatment options, which has
substantially prolonged the life expectancy of patients with heart failure 2. This
perpetuates the significance of heart failure as a pressing public health concern.
Heart failure is a multifaceted syndrome characterized by diverse causes, disease
trajectories, and phenotypes. At its core, heart failure manifests when the heart
cannot supply sufficient cardiac output to meet the body's metabolic demands.
Various cardiac and non-cardiac conditions, including cardiomyopathy, coronary
artery disease, valvular heart disease, arrhythmias, and pericardial disease, can
either present as heart failure or progress to it when left untreated. While multiple
diagnostic criteria and classifications have been proposed 3–5, a recent universal
definition introduced by an expert panel aims to streamline and standardize heart
failure diagnosis and classification globally 6:
Congestion plays a pivotal role in this universal definition, representing one of the
hallmark signs of heart failure. It is the downstream effect of neurohormonal
activation that occurs in response to an insufficient cardiac output. Lower intraaortic
pressures lead to increased sympathetic activation, which in turn decreases
renal perfusion and directly stimulates renin release 7. Simultaneously, heart
failure directly impacts renal perfusion, further stimulating renin secretion and
intensifying the renin-angiotensin-aldosterone system.7. This neurohormonal
activation results in renal sodium and water retention, expanding both
intravascular and extravascular volumes and culminating in congestion.
Beyond its diagnostic relevance, congestion significantly impacts patients' quality
of life 8 and stands as the primary reason for hospitalization among heart failure
patients 9. Furthermore, congestion can impair target organ function, which is
associated with increased mortality 10.
Despite its ubiquitous presence in heart failure, the methods for diagnosing,
monitoring, and treating congestion have seen limited advancements in recent
decades. Physicians still often rely solely on clinical examinations to detect and
monitor congestion. However, the most common clinical signs lack sufficient
sensitivity and specificity11. Echocardiography can definitely aid in early detection
of congestion, but it is technically challenging and not readily available.
Furthermore, serial assessment with echocardiography to monitor congestion
remains impractical on a large scale. Thus, alternative methods are imperative for
the timely detection and monitoring of congestion, enabling early intervention to
prevent patient deterioration and hospitalization. Recently, the use of ultrasound
to detect organ congestion, such as lung ultrasound for detecting and monitoring
lung congestion, has gained interest 12. These relatively simple techniques might
improve the monitoring of congestion and help to guide decongestive therapies.
However, these ultrasound techniques require further investigation before large
scale implementation can be suggested.
Additionally, the implantation of sensors in the pulmonary artery tree allows for
wireless monitoring of pulmonary artery pressures as an indicator of congestion
13. Trial data support its use, but real-world data, especially from Europe are
needed to further define their role in heart failure care.
The most important advances in the treatment of congestion have been the
introduction of neurohormonal blockers at the end of the previous century14–16.
These agents prevent congestion upstream and reduce heart failure
hospitalizations and mortality in patients with heart failure and reduced ejection
fraction. In the last years, therapy was further improved with the use of
angiotensin receptor – neprilysin inhibitors (ARNI) 17 and sodium-glucose
cotransporter-2 inhibitors (SGLT2i) 18,19. However, there has been a relative lack
of breakthroughs in the specific treatment of congestion. Furthermore, for patients
with heart failure with preserved ejection fraction, SGLT2i are currently the only
agents that reduce the risk of heart failure hospitalization 20,21.
Loop diuretics remain the cornerstone treatment for congestion, yet their use
relies primarily on clinical experience and expert opinion. 22. Moreover, a
significant knowledge gap existed regarding the use of diuretics until recently.
Several trials, including the Cardiorenal Rescue Study in Acute Decompensated
Heart Failure (CARRESS-HF) 23, Diuretic Optimization Strategies Evaluation
(DOSE) 24, and Aldosterone Targeted Neurohormonal Combined with Natriuresis
Therapy in Heart Failure (ATHENA) 25 trials, have explored diuretic strategies in
acute heart failure. However, none of these trials has provided conclusive evidence
for an optimal diuretic approach. Consequently, many patients are discharged
while still experiencing congestion, which has been associated with worse
prognosis 26–28 , emphasizing the urgent need to enhance decongestion strategies.
Loop diuretics are also commonly used in ambulatory heart failure patients to
prevent or treat congestion. However, their use has not consistently improved
outcomes 29. The decision to continue loop diuretics as maintenance therapy likely
depends on the control of the underlying heart failure. Determining which patients
can safely discontinue loop diuretics remains a challenge, as current data are
insufficient to guide selection criteria. Similarly, sodium restriction is advised for
most heart failure patients to prevent congestion 3,4, but recent studies have failed
to demonstrate significant benefits on outcomes 30. With neurohormonal blockers
reducing renal sodium avidity and congestion episodes, the role of routine sodium
restriction in heart failure management is unclear. Apparently, selected patients
with heart failure with reduced ejection fraction can tolerate high sodium intake
(up to 4.7 g per day) 31, but the mechanisms behind this remain unelucidated.
A specific population of interest is patients with post-myocardial infarction left
ventricular dysfunction. Despite the proven benefits of neurohormonal blockers,
recent trials such as the Prospective ARNI vs. ACE inhibitor trial to Determine
Superiority in reducing heart failure Events after Myocardial Infarction
(PARADISE-MI) have shown no advantage of ARNI over angiotensin-converting
enzyme inhibitors in these patients 32. This may be attributed to changes in
myocardial infarction treatment practices over the years, with early reperfusion
and left ventricular function recovery 33. However, most data on left ventricular
dysfunction predate these advancements, necessitating updated information to
better understand the development of heart failure and congestion in the current
era.
The trajectory of heart failure and congestion prevention is not solely dependent
on pharmacological approaches; cardiac implantable electronic devices,
particularly cardiac resynchronization therapy, play a pivotal role. However, there
remains underutilization of these devices, primarily due to inadequate referrals
from primary and secondary care providers 34. Enhancing our understanding of
device functionality and patient selection criteria could facilitate better
implementation.
This doctoral thesis aims to address the aforementioned challenges. It seeks to
provide insights into congestion pathophysiology, detection, monitoring, and
optimization of treatment strategies. Additionally, it will focus on post-infarction
left ventricular dysfunction, providing much-needed contemporary data. Finally,
the thesis will explore ways to enhance the utilization of cardiac implantable
electronic devices in heart failure management. By delving into these critical
areas, this thesis endeavors to contribute to the advancement of heart failure
management and the improvement of patient outcomes
Unravelling Congestion in Heart Failure: Mechanisms, Diagnosis and Treatment
No full textHeart failure exerts a significant and growing burden on public health globally. It
currently afflicts approximately 2% of the adult Western population, impacting the
lives of an estimated 64.3 million individuals across the world 1. This alarming
prevalence is further underscored by the fact that heart failure ranks as the
primary cause for hospital admissions, accounting for 1-2% of all admissions and
representing the most prevalent reason for hospitalization among the elderly 1.
Despite a modest decline in the overall incidence of heart failure in Europe, its
prevalence continues to surge due to the improved treatment options, which has
substantially prolonged the life expectancy of patients with heart failure 2. This
perpetuates the significance of heart failure as a pressing public health concern.
Heart failure is a multifaceted syndrome characterized by diverse causes, disease
trajectories, and phenotypes. At its core, heart failure manifests when the heart
cannot supply sufficient cardiac output to meet the body's metabolic demands.
Various cardiac and non-cardiac conditions, including cardiomyopathy, coronary
artery disease, valvular heart disease, arrhythmias, and pericardial disease, can
either present as heart failure or progress to it when left untreated. While multiple
diagnostic criteria and classifications have been proposed 3–5, a recent universal
definition introduced by an expert panel aims to streamline and standardize heart
failure diagnosis and classification globally 6:
Congestion plays a pivotal role in this universal definition, representing one of the
hallmark signs of heart failure. It is the downstream effect of neurohormonal
activation that occurs in response to an insufficient cardiac output. Lower intraaortic
pressures lead to increased sympathetic activation, which in turn decreases
renal perfusion and directly stimulates renin release 7. Simultaneously, heart
failure directly impacts renal perfusion, further stimulating renin secretion and
intensifying the renin-angiotensin-aldosterone system.7. This neurohormonal
activation results in renal sodium and water retention, expanding both
intravascular and extravascular volumes and culminating in congestion.
Beyond its diagnostic relevance, congestion significantly impacts patients' quality
of life 8 and stands as the primary reason for hospitalization among heart failure
patients 9. Furthermore, congestion can impair target organ function, which is
associated with increased mortality 10.
Despite its ubiquitous presence in heart failure, the methods for diagnosing,
monitoring, and treating congestion have seen limited advancements in recent
decades. Physicians still often rely solely on clinical examinations to detect and
monitor congestion. However, the most common clinical signs lack sufficient
sensitivity and specificity11. Echocardiography can definitely aid in early detection
of congestion, but it is technically challenging and not readily available.
Furthermore, serial assessment with echocardiography to monitor congestion
remains impractical on a large scale. Thus, alternative methods are imperative for
the timely detection and monitoring of congestion, enabling early intervention to
prevent patient deterioration and hospitalization. Recently, the use of ultrasound
to detect organ congestion, such as lung ultrasound for detecting and monitoring
lung congestion, has gained interest 12. These relatively simple techniques might
improve the monitoring of congestion and help to guide decongestive therapies.
However, these ultrasound techniques require further investigation before large
scale implementation can be suggested.
Additionally, the implantation of sensors in the pulmonary artery tree allows for
wireless monitoring of pulmonary artery pressures as an indicator of congestion
13. Trial data support its use, but real-world data, especially from Europe are
needed to further define their role in heart failure care.
The most important advances in the treatment of congestion have been the
introduction of neurohormonal blockers at the end of the previous century14–16.
These agents prevent congestion upstream and reduce heart failure
hospitalizations and mortality in patients with heart failure and reduced ejection
fraction. In the last years, therapy was further improved with the use of
angiotensin receptor – neprilysin inhibitors (ARNI) 17 and sodium-glucose
cotransporter-2 inhibitors (SGLT2i) 18,19. However, there has been a relative lack
of breakthroughs in the specific treatment of congestion. Furthermore, for patients
with heart failure with preserved ejection fraction, SGLT2i are currently the only
agents that reduce the risk of heart failure hospitalization 20,21.
Loop diuretics remain the cornerstone treatment for congestion, yet their use
relies primarily on clinical experience and expert opinion. 22. Moreover, a
significant knowledge gap existed regarding the use of diuretics until recently.
Several trials, including the Cardiorenal Rescue Study in Acute Decompensated
Heart Failure (CARRESS-HF) 23, Diuretic Optimization Strategies Evaluation
(DOSE) 24, and Aldosterone Targeted Neurohormonal Combined with Natriuresis
Therapy in Heart Failure (ATHENA) 25 trials, have explored diuretic strategies in
acute heart failure. However, none of these trials has provided conclusive evidence
for an optimal diuretic approach. Consequently, many patients are discharged
while still experiencing congestion, which has been associated with worse
prognosis 26–28 , emphasizing the urgent need to enhance decongestion strategies.
Loop diuretics are also commonly used in ambulatory heart failure patients to
prevent or treat congestion. However, their use has not consistently improved
outcomes 29. The decision to continue loop diuretics as maintenance therapy likely
depends on the control of the underlying heart failure. Determining which patients
can safely discontinue loop diuretics remains a challenge, as current data are
insufficient to guide selection criteria. Similarly, sodium restriction is advised for
most heart failure patients to prevent congestion 3,4, but recent studies have failed
to demonstrate significant benefits on outcomes 30. With neurohormonal blockers
reducing renal sodium avidity and congestion episodes, the role of routine sodium
restriction in heart failure management is unclear. Apparently, selected patients
with heart failure with reduced ejection fraction can tolerate high sodium intake
(up to 4.7 g per day) 31, but the mechanisms behind this remain unelucidated.
A specific population of interest is patients with post-myocardial infarction left
ventricular dysfunction. Despite the proven benefits of neurohormonal blockers,
recent trials such as the Prospective ARNI vs. ACE inhibitor trial to Determine
Superiority in reducing heart failure Events after Myocardial Infarction
(PARADISE-MI) have shown no advantage of ARNI over angiotensin-converting
enzyme inhibitors in these patients 32. This may be attributed to changes in
myocardial infarction treatment practices over the years, with early reperfusion
and left ventricular function recovery 33. However, most data on left ventricular
dysfunction predate these advancements, necessitating updated information to
better understand the development of heart failure and congestion in the current
era.
The trajectory of heart failure and congestion prevention is not solely dependent
on pharmacological approaches; cardiac implantable electronic devices,
particularly cardiac resynchronization therapy, play a pivotal role. However, there
remains underutilization of these devices, primarily due to inadequate referrals
from primary and secondary care providers 34. Enhancing our understanding of
device functionality and patient selection criteria could facilitate better
implementation.
This doctoral thesis aims to address the aforementioned challenges. It seeks to
provide insights into congestion pathophysiology, detection, monitoring, and
optimization of treatment strategies. Additionally, it will focus on post-infarction
left ventricular dysfunction, providing much-needed contemporary data. Finally,
the thesis will explore ways to enhance the utilization of cardiac implantable
electronic devices in heart failure management. By delving into these critical
areas, this thesis endeavors to contribute to the advancement of heart failure
management and the improvement of patient outcomes
Cardiac device troubleshooting in the intensive care unit: an educational review
No full textNumerous patients with a cardiac implantable electronic device are admitted to the cardiac intensive care unit (ICU). When taking care of these patients, it is essential to have basic knowledge of potential device problems and how they could be tackled. This review summarizes common issues with pacemakers, implantable cardioverter-defibrillators, and cardiac resynchronization devices and provides a framework for troubleshooting in the ICU. In addition, specific aspects of intensive care that might interfere with cardiac devices are discussed. [GRAPHICS] .J.D. andW.M. are researchers for the Limburg Clinical Research Center (LCRC) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), province of Limburg, Flemish government, Hasselt University, ZiekenhuisOost-Limburg, and Jessa Hospital
The importance of developing hyperkalaemia in heart failure during long-term follow-up
No full textBackground:Hyperkalaemia is a potentially life-threatening condition. Furthermore, it is one of the main reasons for discontinuation and dose reduction of renin-angiotensin-aldosterone system inhibitors (RAASi) in clinical practice. However, exact data on the prevalence and consequences of occurrence of hyperkalaemia when taking RAASi in a dedicated heart failure care setting are scarce. Methods:Consecutive patients diagnosed with heart failure from a single tertiary hospital between August 2000 and May 2017 were retrospectively evaluated. Primary endpoint was the development of hyperkalaemia (>= 5.5 mmol/L) at any moment during follow-up. Results:About 396 patients were included in the current analysis (mean follow-up 6.9 years). 26% (n = 104) and 12% (n = 46) of patients developed hyperkalaemia (>= 5.5 mmol/L and >= 6.0 mmol/L, respectively). Diabetes mellitus (OR = 1.80, 95% CI = 1.03-3.19) and baseline creatinine (mg/dL) (OR = 2.37, 95% CI = 2.37-3.85) were independent risk factors for hyperkalaemia. Development of hyperkalaemia was associated with 6.5 higher odds for recurrence. Only 10% developed hyperkalaemia during up-titration of RAASi, while 90% developed during later follow-up on stable doses of RAASi. hyperkalaemia was not associated with worse outcome after multivariate adjustment for baseline co-morbidities. However, hyperkalaemia was associated with discontinuation and lower doses of MRAs during follow-up (p = 0.007). Discontinuation of MRA due to hyperkalaemia was associated with an increase in all-cause mortality in HFrEF patients (HR = 1.77, 95% CI = 1.05-2.99). Conclusions:Approximately, one-fourth of patients developed hyperkalaemia during follow-up which was associated with a lower MRA dose during follow-up. Discontinuation of MRA, but not hyperkalaemia itself, was associated with an increased risk of all-cause mortality and heart failure admission in HFrEF patients.Pieter Martens is supported by a doctoral fellowship by the Research Foundation - Flanders (FWO, grant-number: 1127917N). Pieter Martens, Petra Nijst, and Wilfried Mullens are researchers for the Limburg Clinical Research Program (LCRP) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), Hasselt University, Ziekenhuis Oost-Limburg and Jessa Hospital. Pieter Martens has received consultancy fees from and an unrestricted research grant from Vifor Pharma.Martens, P (corresponding author), Ziekenhuis Oost Limburg, Dept Cardiol, Schiepse Bos 6, B-3600 Genk, Belgium.
[email protected]
Determinants of maximal dose titration of sacubitril/valsartan in clinical practice
No full textBackground: Little information is available about the tolerability of uptitration to the maximal dose of sacubitril/valsartan and the predictors and clinical correlates of achieving such a dose. Methods: All consecutive heart failure patients with reduced ejection fraction (HFrEF) who received sacubitril/valsartan for a class-IB indication in a tertiary heart failure clinic were retrospectively analysed. Predictors of maximal uptitration including associated changes in clinical parameters were assessed in patients with at least 1 follow-up. Results: A total of 401 HFrEF-patients received sacubitril/valsartan. Uptitration was possible in 41% and up to 32% of patients tolerated the maximal dose of sacubitril/valsartan. Younger age (HR = 0.862; CI = 0.751-0.989), higher systolic-blood-pressure (HR = 1.077; CI = 1.014-1.137), lower serum creatinine (HR = 0.064; CI = 0.005-0.822), and higher previous dose of renin-angiotensin-system-inhibitors (RASi [HR = 1.065; CI = 1.016-1.115]) independently predicted a higher odds of tolerating a maximal dose of sacubitril/valsartan. Patients who were seen more frequently in a structured heart failure clinic were also more likely to receive a maximal dose (p = .038). Patient assigned to the maximal dose, were more often able to reduce their loop diuretic dose (p = .001) and more often had an increase in serum creatinine (p = .011), without a higher risk for hyperkalemia (p = .524). An improvement in New York Heart Association class and the rate of heart failure hospitalisations was observed in all patients, independent of the sacubitril/valsartan dose. Conclusion: Uptitration to the maximal dose of sacubitril/valsartan is possible in up to 32% of real-world HFrEF-patients in our cohort, which relates to both patient characteristics' as well as heart failure care-related factors.Pieter Martens is supported by a doctoral fellowship by the Research Foundation-Flanders (FWO, grant-number: 1127917N). Pieter Martens and Wilfried Mullens are researchers for the Limburg Clinical Research Centre (LCRC) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), Hasselt University, Ziekenhuis OostLimburg, and Jessa Hospital.Martens, P (reprint author), Ziekenhuis Oost Limburg, Dept Cardiol, Schiepse Bos 6, B-3600 Genk, Belgium
[email protected]
Ambulatory haemodynamic-guided management reduces heart failure hospitalisations in a multicentre European heart failure cohort
No full textAims To investigate the outcomes and associated costs of haemodynamic-guided heart failure (HF) management with a pulmonary artery pressure (PAP) sensor in a multicentre European cohort. Methods and results Data from all consecutive patients receiving a PAP sensor in Ziekenhuis Oost-Limburg, University Hospital Zurich and Sheffield Teaching Hospitals NHS Foundation Trust before January 2021 were collected. Medication changes, total number of HF hospitalizations and HF related health care costs (composed of HF hospitalizations, outpatient cardiology visits and monitoring costs) were compared between the pre-implantation and post-implantation period at 3, 6, and 12 months. PAP evolution post-implantation were grouped according to baseline mPAP ≥25 mmHg versus <25 mmHg and changes from baseline were analyzed via an area under the curve (AUC) analysis. A total of 48 patients received a PAP sensor (29 CardioMEMS and 19 Cordella devices) with a median follow-up of 19 (13-30) months. Mean age was 71 ± 10 years, 25.0% were female, 68.8% had a left ventricular ejection fraction < 50%, median NT-proBNP was 1801 (827-4503) pg/mL, and 89.6% were in NYHA class III. The number of diuretic therapy changes were non-significantly increased after 3 months (49 vs. 82; P = 0.284) and 6 months (82 vs. 127; P = 0.093) with a significant increase noted after 12 months (118 vs. 195; P = 0.005). The mPAP AUC decreased by À1418 mmHg-days for patients with a baseline mean PAP ≥ 25 mmHg. The number of HF hospitalizations was reduced for all patients after 6 (34 vs. 17; P = 0.014) and 12 months (48 vs. 29; P = 0.032). HF related health care costs were reduced from € 6286 to € 3761 at 6 months (P = 0.012) and from € 8960 to € 6167 at 12 months (P = 0.032). Conclusion Haemodynamic-guided HF management reduces HF hospitalizations and HF related health care costs in selected HF patients amongst different European health care systems
Renal and cardiac effects of salt loading in ambulatory heart failure patients
No full text73 p < 0.01) and, moreover, we also documented a higher sacubitril/valsartan prescription (67% vs 55%; p = 0.06) instead of lower loop diuretics use (47% vs 35%, p = 0.05). Mineralocorticoid receptor antagonist (77% vs 83%; p = 0.19) and beta blockers (94% in both groups) therapy did not change. With a total median follow-up of 19 months (Q1-Q3: 9-36), Kaplan-Meier mortality analysis was represented in Figure 1. Conclusions: In our centers, since SGLT2-i approval for HFrEF, there exists a fast joining of SGLT2-i to HFrEF therapy. It could help us to accomplish lower rates of loop diuretics prescription enabling a better titration of drugs with proven positive impact in remodelling and morbimortality. These results support in real-world the provider role of SGLT2-i, explaining a higher increase of left ventricular ejection fraction in post SGLT2-i group, with a non-statistically significant trend to lower mortality probably due to a small follow-up. Follow-up clinical visit Figure 1. Funding Acknowledgements: Type of funding sources: None. Background: Patients with hypotension have consistently been excluded from heart failure (HF) randomized controlled trials. This group of HF patients is largely unstudied. We aimed to characterize HF patients with hypotension. Methods: We retrospectively studied adult outpatients with systolic dysfunction followed in our HF clinic from January 2012 to December 2020. Patients without blood pressure measurement on the index visit (first medical visit) were excluded. We defined hypotension as systolic blood pressure (SBP) of less than 100 mmHg. The endpoint under analysis was all-cause mortality. Patients were followed until January 2023. Patients with hypotension were compared with the remaining. A Cox-regression analysis was used to assess the prognostic impact of hypotension and to study the prognostic impact of evidence-based therapy separately in HF patients with SPB < 100mmHg and those with SPB ≥ 100mmHg. Adjustments were made considering potential confounders. Results: We studied 1206 chronic ambulatory HF patients, 64.9% male, mean age 71 years, 47.4% with severe systolic dysfunction. Regarding the medication in use, 91.4% were on beta blockers (BB), 82.8% were on renin angiotensin system inhibitors (RASi), including angiotensin converting enzyme inhibitors, angiotensin receptor blockers or angiotensin receptor neprilysin inhibitors; 29.6% were on min-eralocorticoid receptor antagonists (MRA). A total of 157 patients (13.0%) presented SBP < 100mmHg on the index visit. Hypotensive patients more often presented atrial fibrillation and severe systolic dysfunction; they had lower haemoglobin values and higher brain natriuretic peptide (BNP) levels. Patients with hypotension were less medicated with RASi (70.7% vs 84.6%, p < 0.001) but more with MRA (39.6% vs 28.1%, p = 0.004) and diuretics (86.6% vs 78.6%, p = 0.02). There were no differences regarding BB use between both groups. During a median follow-up of 47 (27-85) months 645 (53.5%) patients died, 61.1% in those with hypotension and 52.3% in the remaining, p = 0.04. The use of RASi in hypotensive patients was associated with better survival (HR = 0.42 (0.26-0.69)) as in those with SPB ≥ 100mmHg (HR = 0.64 (0.51-0.80)). Contrarily to patients with SPB ≥ 100mmHg, in those with hypotension, BB use was not associated with survival benefit (HR = 0.61 (0.46-0.81) and 0.98 (0.48-1.97), respectively). MRA use showed no prognostic impact in either group. Conclusions: Hypotension was associated with poor prognosis in HF patients. In HF patients with SBP < 100mmHg, BB and MRA use did not impact prognosis, however, RASi use portended a survival benefit. Despite their exclusion from most HF therapy trials, hypotensive patients might benefit from RASi drugs. Renal and cardiac effects of salt loading in ambulatory heart failure patients Funding Acknowledgements: Type of funding sources: Public grant(s)-National budget only. Main funding source(s): Hartfalenfonds ZOL-UHasselt Limburg Sterk Merk Background: Current guidelines recommend to limit sodium intake in heart failure (HF) patients. However, stringent sodium restriction can increase neurohormonal activation, decrease quality of life and was not advantageous in recent trials. In addition, recent studies suggest that the skin can function as a sodium buffer. Purpose: To study effects and handling of an increased salt load in patients with HF and reduced ejection fraction. Methods: Eighteen patients with HF and left ventricular ejection fraction < 40% and 10 age-and sex-matched healthy volunteers without cardiovascular disease were included. HF patients with severe right ventricular dysfunction, eGFR < 30 mL/min/1.73 m 2 or severe valvular dysfunction were excluded. After 2 weeks of run-in, all study participants received 3 grams of sodium chloride (capsules of 1 g three times daily) on top of their usual diet for 4 weeks. Patients were evaluated at inclusion, at 2 weeks (end of run-in), 4 weeks (2 weeks of sodium chloride intake) and 6 weeks (4 weeks of sodium chloride intake). At each evaluation, clinical parameters, Everest congestion score, lab, echocardiography, 24-hour urine collection and bio-impedance measurements of total body water were performed. Blood volume and plasma volume were assessed using a radio-labeled red blood cells dilution technique before salt loading (at 2 weeks) and and the end of the study (at 6 weeks). At the same time points, a skin biopsy was taken at the lower leg to assess skin sodium content and glycosaminoglycan content. Results: Mean age was 66 ± 8 years, 2 (11.1%) were female, median LVEF was 35 (31-39) %, median eGFR was 68 (51-74) mL/min/1.73 m 2 and median NT-proBNP was 431 (275-961) ng/L at baseline and all patients were optimally treated medically. Salt loading did not influence weight, blood pressure, congestion score or NT-proBNP (Figure 1). There was no significant change in total body water (from 46.87 L to 44.41 L; p = 0.780), plasma volume (2735 mL vs. 2904 mL; p = 0.231) and total blood volume (4748 mL vs. 4885 mL; p = 0.327). Renal sodium excretion increased from 150 ± 55 mmol/24h to 173 ± 58 mmol/24h (p = 0.024), while plasma renin decreased from 286 (25-550) í µí¼ U/L to 88 (19-362) í µí¼ U/L (p = 0.002) (Figure 2). Salt loading did not significantly influence LVEF (from 35% to 35%; p = 0.801), leftType of funding sources: Public grant(s) – Nationalbudget only. Main funding source(s): Hartfalenfonds ZOL-UHasselt Limburg SterkMer
The value of urinary sodium assessment in acute heart failure
No full textAcute heart failure (AHF) is a frequent medical condition that needs immediate evaluation and appropriate treatment. Patients with signs and symptoms of volume overload mostly require intravenous loop diuretics in the first hours of hospitalization. Some patients may develop diuretic resistance, resulting in insufficient and delayed decongestion, with increased mortality and morbidity. Urinary sodium measurement at baseline and/or during treatment has been proposed as a useful parameter to tailor diuretic therapy in these patients. This systematic review discusses the current sum of evidence regarding urinary sodium assessment to evaluate diuretic efficacy in AHF. We searched Medline, Embase, and Cochrane Clinical Trials Register for published studies that tested urinary sodium assessment in patients with AHF..D. and W.M. are researchers for the Limburg Clinical Research Center (LCRC) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), province of Limburg, Flemish government, Hasselt University, Ziekenhuis Oost-Limburg, and Jessa Hospital
- …
