The Association Between Intra-abdominal Pressure and Diuretic Response in Heart Failure.

PURPOSE OF THE REVIEW: An efficient diuretic response is vital during cardiac decompensation in heart failure (HF) patients. The increase in intra-abdominal pressure (IAP) could be one of the keys for understanding cardiorenal syndrome and guiding diuretic treatment during hospitalization. In this review, we analyze the relationship between IAP and diuretic response in HF patients. RECENT FINDINGS: Increased IAP is associated with worsening renal function (WRF) in patients with advanced HF. Furthermore, the persistence of a rise in IAP after the first 72 h of intravenous diuretic treatment has been correlated with a worse diuretic response, a higher degree of congestion, and an impaired prognosis. The rise in IAP in HF patients has been associated with impaired renal function and a lower diuretic response. Nonetheless, more studies are needed to elucidate the actual role of IAP in congestive nephropathy and whether it may help guide diuretic therapy during acute decompensations.

Intra-abdominal pressure and its relationship with markers of congestion in patients admitted for acute decompensated heart failure.

Systemic congestion is one of the mechanisms involved in acute decompensated heart failure (ADHF). Increased intra-abdominal pressure (IAP), elicited by abdominal congestion, has been related to acute kidney injury and prognosis. Nonetheless, the link between diuretic response, surrogate markers of congestion and renal function remains poorly understood. We measured IAP in 43 patients from a non-interventional, exploratory, prospective, single center study carried out in patients admitted for ADHF. IAP was measured with a calibrated electronic manometer through a catheter inserted in the bladder. Normal IAP was defined as < 12 mmHg. At baseline, median IAP was 15 mmHg, with a reduction over the next 72 h to a median of 12 mmHg. A higher IAP at admission was associated with higher baseline blood urea (83 mg/dL [62-138] vs. 50 mg/dL [35-65]; p = 0.007) and creatinine (1.30 mg/dL vs. 0.95 mg/dL; p = 0.027), and with poorer diuretic response 72 h after admission, either measured by diuresis (14.4 mL/mg vs. 21.6 mL/mg; [p = 0.005]) or natriuresis (1.2 mEqNa/mg vs. 2.0 mEqNa/mg; [p = 0.008]). A higher incidence for 1-year all-cause mortality (45.0% vs. 16.7%; log-rank test = 0.041) was observed among those patients with IAP > 12 mmHg at 72 h. In patients with ADHF, higher IAP at admission is associated with poorer baseline renal function and impaired diuretic response. The persistence of IAP at 72 h above 12 mmHg associates to longer length of hospital stay and higher 1-year all-cause mortality.

Prognostic significance of acute kidney injury and small increases in creatinine concentration during acute decompensation of heart failure. / Importancia pronóstica del daño renal agudo y de los pequeños aumentos de la concentración de creatinina durante la descompensación aguda de la insuficiencia cardiaca.

BACKGROUND: Diagnosis of acute kidney injury (AKI) during acute decompensations of heart failure (ADHF) remain challenging. We analysed the incidence and prognosis of AKI, and the significance of small increases of creatinine, during ADHF and after stabilization. PATIENTS AND METHODS: Patients admitted for ADHF were prospectively included. Creatinine was measured at admission, 48h thereafter and 24h before discharge. AKI was diagnosed when creatinine increased≥50% in 7 days (RIFLE criteria) or≥0.3mg/dL in 48h (AKIN criteria) during admission. Changes between baseline creatinine (measured within 3-month before admission) and one month after discharge were assessed, to seek for residual impairment of renal function and its significance. RESULTS: Two hundred and four patients were included. Incidence of AKI was 28.4% (n=58). Creatinine peaked by day 5 in patients with AKI vs. non-AKI (1.9 vs. 1.1mg/dL; P<.000) and remained significantly higher among patients with AKI 3 months after discharge (increase of 20 vs. 4%; P=.013). Twelve-months mortality was associated with increases in cystatin C, NT-proBNP and AKI (15.5 vs. 44.8%, P<.000), being the latter the most powerful independent predictor of death ?Exp(B)=5.34; P=.009?. Minor increases in creatinine (20% or 0.2mg/dL) during admission associated lesser 12-months survival (P=.033 and P=.019, respectively). Increases in creatinine≥10% between baseline and one month after discharge are associated with higher mortality (12.6 vs. 22.5%, P=.044). CONCLUSIONS: AKI is a strong predictor of mortality after ADHF. Minor increments in creatinine concentrations, below the accepted threshold for AKI definition, are prognostically meaningful.

Prognostic value of multimodal assessment of congestion in acute heart failure. / Valor pronóstico de la valoración multimodal de la congestión en la insuficiencia cardiaca aguda.

Systemic venous congestion is present in most cases of acute decompensated heart failure (ADHF). An accurate assessment of congestion is key to improve outcomes and avoid residual congestion. Physical examination has limitations for grading congestion; hence, new methods for assessing congestion have been developed. A multimodal approach, combining surrogate markers of congestion, may be a suitable strategy. The aim of this study was to compare the prognostic value of Amino terminal fragment of pro-Brain Natriuretic Peptide (NT-proBNP), Carbohydrate cancer antigen 125 (CA125), lung ultrasound, relative plasma volume status (rPVS) and urea/Creatinine ratio (U/C ratio), to predict one-year all-cause mortality. MATERIAL AND METHODS: Retrospective, observational analysis of 203 patients admitted at the Internal Medicine ward of a tertiary teaching Hospital due to ADHF, followed in monographic outclinic. Clinical data were obtained from hospital records. Therapeutic interventions followed exclusively the clinical judgement of the physician responsible for each patient. RESULTS: 203 patients were included for the final analysis between 2013 and 2018. Chronic heart failure (CHF) was present in 130 patients (65%); 51 patients (26.2%) had class III-IV of New York Heart Association (NYHA); 116 patients (60%) had HF with preserved ejection fraction (HFpEF). Forty-two patients (21.6%) died during follow-up. NT-proBNP≥3804 pg/mL (HR 2.78 [1.27 - 6.08]; P=.010) and rPVS≥-4.54% (HR 2.74 [1.18 - 6.38]; P=.019), were independent predictors for 1-year all-cause mortality on top of CA125, lung ultrasound and U/C ratio. CONCLUSIONS: NT-proBNP and rPVS are independent predictors of one-year mortality among patients admitted for ADHF.

Variation in intraabdominal pressure in patients with acute heart failure according to left ventricular ejection fraction. Results of an intraabdominal pressure study. / Variación de la presión intraabdominal en los pacientes con insuficiencia cardíaca aguda según la fracción de eyección ventricular izquierda. Resultados del estudio PIA.

BACKGROUND: The increase in intraabdominal pressure (IAP) has been correlated with increased creatinine levels in patients with heart failure with severely reduced left ventricular ejection fraction (HFrEF). However, IAP has not been examined in more stable patients or those with heart failure with preserved ejection fraction (HFpEF). PATIENTS AND METHOD: We conducted an observational, prospective descriptive study that measured the IAP of patients hospitalised for decompensated heart failure (HF). The sample was stratified according to left ventricular ejection fraction (LVEF), with a cut-off of 50%. The objective was to analyse the IAP, the baseline characteristics and degree of congestion using clinical ultrasonography and impedance audiometry. RESULTS: The study included 56 patients, 22 with HFrEF and 34 with HFpEF. The patients with HFrEF presented a higher prevalence of ischaemic heart disease (11% vs. 6%; p = 0.010) and chronic obstructive pulmonary disease/asthma (6% vs. 2%; p = 0.025). The IAP was higher in the patients with HFrEF (17.2 vs. 13.3 mmHg; p = 0.004), with no differences in renal function at admission according to the LVEF (CKD-EPI creatinine) (HFrEF 55.0 mL/min/1.73 m2 [32.6-83.6] vs. HFpEF 55.0 mL/min/1.73 m2 [44.0-74.9]; p = 0.485). The patients with HFrEF presented a more congestive profile determined through ultrasonography (inferior vena cava collapse [26% vs. 50%; p = 0.001]), impedance audiometry (total body water at admission, 46 L vs. 41 L; p = 0.052; and at 72 h, 50.2 L vs. 39.1 L; p = 0.038) and CA125 concentration (68 U/mL vs. 39 U/mL; p = 0.037). CONCLUSIONS: During the decompensation episodes, the patients with HFrEF had a greater increase in IAP and a higher degree of systemic congestion.

Design and baseline characteristics of SALT-HF trial: hypertonic saline therapy in ambulatory heart failure.

AIMS: Hypertonic saline solution (HSS) plus intravenous (IV) loop diuretic appears to enhance the diuretic response in patients hospitalized for heart failure (HF). The efficacy and safety of this therapy in the ambulatory setting have not been evaluated. We aimed to describe the design and baseline characteristics of the SALT-HF trial participants. METHODS AND RESULTS: 'Efficacy of Saline Hypertonic Therapy in Ambulatory Patients with HF' (SALT-HF) trial was a multicenter, double-blinded, and randomized study involving ambulatory patients who experienced worsening heart failure (WHF) without criteria for hospitalization. Enrolled patients had to present at least two signs of volume overload, use ≥ 80 mg of oral furosemide daily, and have elevated natriuretic peptides. Patients were randomized 1:1 to treatment with a 1-h infusion of IV furosemide plus HSS (2.6-3.4% NaCl depending on plasmatic sodium levels) versus a 1-h infusion of IV furosemide at the same dose (125-250 mg, depending on basal loop diuretic dose). Clinical, laboratory, and imaging parameters were collected at baseline and after 7 days, and a telephone visit was planned after 30 days. The primary endpoint was 3-h diuresis after treatment started. Secondary endpoints included (a) 7-day changes in congestion data, (b) 7-day changes in kidney function and electrolytes, (c) 30-day clinical events (need of IV diuretic, HF hospitalization, cardiovascular mortality, all-cause mortality or HF-hospitalization). RESULTS: A total of 167 participants [median age, 81 years; interquartile range (IQR), 73-87, 30.5% females] were randomized across 13 sites between December 2020 and March 2023. Half of the participants (n = 82) had an ejection fraction >50%. Most patients showed a high burden of comorbidities, with a median Charlson index of 3 (IQR: 2-4). Common co-morbidities included diabetes mellitus (41%, n = 69), atrial fibrillation (80%, n = 134), and chronic kidney disease (64%, n = 107). Patients exhibited a poor functional NYHA class (69% presenting NYHA III) and several signs of congestion. The mean composite congestion score was 4.3 (standard deviation: 1.7). Ninety per cent of the patients (n = 151) presented oedema and jugular engorgement, and 71% (n = 118) showed lung B lines assessed by ultrasound. Median inferior vena cava diameter was 23 mm, (IQR: 21-25), and plasmatic levels of N-terminal-pro-B-type natriuretic peptide (NTproBNP) and antigen carbohydrate 125 (CA125) were increased (median NT-proBNP 4969 pg/mL, IQR: 2508-9328; median CA125 46 U/L, IQR: 20-114). CONCLUSIONS: SALT-HF trial randomized 167 ambulatory patients with WHF and will determine whether an infusion of hypertonic saline therapy plus furosemide increases diuresis and improves decongestion compared to equivalent furosemide administration alone.

Prognostic value of multimodal assessment of congestion in acute heart failure.

BACKGROUND: A physical examination has limited performance in estimating systemic venous congestion and predicting mortality in patients with heart failure. We have evaluated the usefulness of the N-terminal prohormone of brain natriuretic peptide (NT-proBNP), cancer antigen 125 (CA125), lung ultrasound findings, relative plasma volume (rPV) estimation, and the urea/creatinine ratio as surrogate parameters of venous congestion and predictors of mortality. METHODS: This work is a retrospective study of 203 patients admitted for acute heart failure in a tertiary hospital's internal medicine department with follow-up in a specialized outpatient clinic between 2013 and 2018. Clinical data were collected from hospital records. Treatment was decided upon according to the clinical judgment of each patient's attending physician. The main outcome measure was all-cause mortality at one year of follow-up. RESULTS: Patients' mean age was 78.8 years and 47% were male. A total of 130 (65%) patients had chronic heart failure, 51 (26.2%) patients were in New York Heart Association class III-IV, and 116 (60%) patients had preserved left ventricular ejection fraction. During follow-up, 42 (22%) patients died. Values of NT-proBNP≥3804pg/mL (HR 2.78 [1.27-6.08]; p=.010) and rPV≥-4.54% (HR 2.74 [1.18-6.38]; p=.019) were independent predictors of all-cause mortality after one year of follow-up. CONCLUSIONS: NT-proBNP and rPV are independent predictors of one-year mortality among patients hospitalized for decompensated heart failure.

Variation in intraabdominal pressure in patients with acute heart failure according to left ventricular ejection fraction. Results of an intraabdominal pressure study.

BACKGROUND: The increase in intraabdominal pressure (IAP) has been correlated with increased creatinine levels in patients with heart failure with severely reduced left ventricular ejection fraction (HFrEF). However, IAP has not been examined in more stable patients or those with heart failure with preserved ejection fraction (HFpEF). PATIENTS AND METHOD: We conducted an observational, prospective descriptive study that measured the IAP of patients hospitalised for decompensated heart failure (HF). The sample was stratified according to left ventricular ejection fraction (LVEF), with a cut-off of 50%. The objective was to analyse the IAP, the baseline characteristics and degree of congestion using clinical ultrasonography and impedance audiometry. RESULTS: The study included 56 patients, 22 with HFrEF and 34 with HFpEF. The patients with HFrEF presented a higher prevalence of ischaemic heart disease (11% vs. 6%; p = 0.010) and chronic obstructive pulmonary disease/asthma (6% vs. 2%; p = 0.025). The IAP was higher in the patients with HFrEF (17.2 vs. 13.3 mmHg; p = 0.004), with no differences in renal function at admission according to the LVEF (CKD-EPI creatinine) (HFrEF 55.0 mL/min/1.73 m2 [32.6-83.6] vs. HFpEF 55.0 mL/min/1.73 m2 [44.0-74.9]; p = 0.485). The patients with HFrEF presented a more congestive profile determined through ultrasonography (inferior vena cava collapse [26% vs. 50%; p = 0.001]), impedance audiometry (total body water at admission, 46 L vs. 41 L; p = 0.052; and at 72 h, 50.2 L vs. 39.1 L; p = 0.038) and CA125 concentration (68 U/mL vs. 39 U/mL; p = 0.037). CONCLUSIONS: During the decompensation episodes, the patients with HFrEF had a greater increase in IAP and a higher degree of systemic congestion.

Follow-up results in a specialised consultation after discharge for heart failure. / Resultados del seguimiento en una consulta monográfica tras el alta por insuficiencia cardiaca.

BACKGROUND: Despite advances in the diagnosis and treatment of heart failure (HF), the condition still has high morbidity and mortality. Health education and the treatment of comorbidities have been shown to be effective, as has multidisciplinary care in specialised units, although this involves organisational and structural efforts that are not always feasible. We present the results of a simple outpatient consultation, focused on the specialised care of HF. PATIENTS AND METHODS: The consultation included patients discharged after hospitalisation (index hospitalisation) for decompensated HF from an internal medicine department. The follow-up was conducted by internists especially dedicated (not exclusively) to HF and a nurse partially dedicated to HF. The follow-up consisted of fixed visits 1, 3, 6 and 12 months after the discharge, with more visits on demand if needed. RESULTS: A total of 250 patients were included with a minimum follow-up of 1 year. The reduction in hospitalisations and emergency department visits was 56% and 61% (P<.05), respectively, for HF and 46% and 40% (P<.05), respectively, for any cause. Treatment optimisation was also achieved, with a significant increase in the evidence-based drug prescription rate and the reduction of other drugs, such as calcium antagonists. CONCLUSION: A simple model based on a specialised care consultation for HF is effective in reducing readmissions and optimising the treatment. The lack of healthcare resources should not be an obstacle for specialised care for patients with HF.

Intraabdominal pressure and worsening renal function during decompensations of heart failure. A preliminary report from the PIA study. / Presión intraabdominal y empeoramiento de la función renal durante las descompensaciones de la insuficiencia cardiaca. Un informe preliminar del estudio PIA.

BACKGROUND: An increase in intraabdominal pressure (IAP) during acute heart failure, seems to be directly related to worsening renal function, which leads to worse clinical outcomes. We aimed to analyze the relationship between IAP and determinants of renal function during admission for acute decompensation of heart failure (ADHF) in a conventional Internal Medicine Ward. PATIENTS AND METHODS: Descriptive and prospective study. Patients admitted for ADHF with an estimated glomerular filtration rate > 30mL/min/1.73 m2, willing to participate and who gave their informed consent were included. Ethics Committee of Aragon approved the protocol (PI 15 0227). RESULTS: We hereby report the results of an interim analysis of the first 28 patients included. Patients were divided in 2groups according to the median of IAP measured during the first 24h after admission for ADHF, namely high IAP (IAP>15mmHg) and low (IAP< 15mmHg). Fourteen patients were included in each group. No differences were found in baseline clinical characteristics, comorbidities or treatment between both groups. Patients with IAP above 15mmHg, showed a significant lower baseline estimated glomerular filtration rate (70.7 vs. 44.4mL/min/1.73 m2 with p=0.004], blood urea 36 vs. 83mg/dL with p=0.002]; serum creatinine 0.87 vs. 1.3mg/dL with p=0.004 and cystatin C 1.2 vs. 1.94mg/dL with p= 0.002. Additionally, these patients had higher uric acid (5.7 vs. 8.0, p=0.046), lower hemoglobin concentrations (11.7 vs. 10.5g/L, p=0.04) and longer length of hospital stay (6.5 vs. 9.6 days, p=0.017). CONCLUSIONS: The increase in IAP seems to be a frequent finding in patients admitted for ADHF. Patients share similar clinical profile irrespective of IAP, although the increase in IAP is associated with a significant baseline impairment of renal function.

Residual congestion and clinical intuition in decompensated heart failure. / La congestión residual y la intuición clínica en la insuficiencia cardiaca descompensada.

Congestive symptoms are the key to recognising decompensated heart failure, whose treatment is based on reducing the congestion until a clinical situation has been reached that allows the patient to be discharged to continue outpatient treatment. The important aspect is not the degree of congestion at admission but rather the congestion that persists after energetic diuretic therapy. The persistence of congestive signs following an apparently correct and effective therapy has been called residual congestion and is associated with a poor prognosis. The tools for determining this condition are still rudimentary. Methods therefore need to be developed that enable a more accurate assessment.

Prognostic value of the urea:creatinine ratio in decompensated heart failure and its relationship with acute kidney damage. / Valor pronóstico de la ratio urea / creatinina en la insuficiencia cardiaca descompensada y su relación con el daño renal agudo.

BACKGROUND: Worsening renal function is associated with an adverse prognosis for patients with acute heart failure (AHF). Urea-creatinine ratio (U:C ratio) might be useful for measuring renal function and could help stratify patients with AHF. MATERIAL AND METHODS: An observational and prospective study was conducted to analyse the prognostic value of the U:C ratio, measured during the first 24-28 hours of admission, for patients hospitalised for decompensated Heart failure, and its relationship with estimated glomerular filtration rate (eGFR) and acute kidney injury (AKI). RESULTS: The study included 204 patients, with a mean age of 79.3 years, and a median eGFR of 55 mL/min/1.73m2. In the multivariate analysis, an U:C ratio above the median (50) was related to the development of AKI (36.5% vs. 21.9%) and to increased mortality, both overall (OR 2.75) and by HF (OR 3.50) in long term. In combination with eGFR, the U:C ratio showed prognostic value in patients with normal eGFR (mortality of 4.4% for an U:C ratio ≤ 50 vs. 22% for U:C ratio > 50; p=0.01), as well as a better predictive capacity for AKI than each of them separately (AUC, 0.718; 95% CI 0.643-0.793; p>.000). CONCLUSIONS: An U:C ratio > 50 is a predictor of increased long-term mortality for patients hospitalised for decompensated HF and with normal eGFR. Given the simplicity of this biomarker, its use in clinical practice should be more systematic.

Involvement of systemic venous congestion in heart failure. / Implicación de la congestión venosa sistémica en la insuficiencia cardíaca.

Systemic venous congestion has gained significant importance in the interpretation of the pathophysiology of acute heart failure, especially in the development of renal function impairment during exacerbations. In this study, we review the concept, clinical characterisation and identification of venous congestion. We update current knowledge on its importance in the pathophysiology of acute heart failure and its involvement in the prognosis. We pay special attention to the relationship between abdominal congestion, the pulmonary interstitium as filtering membrane, inflammatory phenomena and renal function impairment in acute heart failure. Lastly, we review decongestion as a new therapeutic objective and the measures available for its assessment.

Pathophysiology of acute heart failure: a world to know.

Our understanding of the pathophysiological mechanisms of heart failure (HF) has changed considerably in recent years, progressing from a merely haemodynamic viewpoint to a concept of systemic and multifactorial involvement in which numerous mechanisms interact and concatenate. The effects of these mechanisms go beyond the heart itself, to other organs of vital importance such as the kidneys, liver and lungs. Despite this, the pathophysiology of acute HF still has aspects that elude our deeper understanding. Haemodynamic overload, venous congestion, neurohormonal systems, natriuretic peptides, inflammation, oxidative stress and its repercussion on cardiac and vascular remodelling are currently considered the main players in acute HF. Starting with the concept of acute HF, this review provides updates on the various mechanisms involved in this disease.

[Prognostic value of measuring the diameter and inspiratory collapse of the inferior vena cava in acute heart failure]. / Valor pronóstico de la medición del diámetro y colapso inspiratorio de la vena cava inferior en la insuficiencia cardiaca aguda.

OBJECTIVES: To assess the utility of measuring the diameter and collapse of the inferior vena cava (IVC) in acute heart failure (AHF), its relationship with the prognosis and serum biomarkers of congestion. PATIENTS AND METHODS: An observational prospective study was conducted that included 85 patients with AHF, classifying them into 4 groups according to IVC diameter (≤ or >20mm) and inspiratory collapse (< or ≥50%) at admission. The endpoints were mortality due to HF and the combined event of mortality and readmission for HF at 180 days. RESULTS: Some 24.7% of the patients had an undilated IVC and ≥50% collapse (group 1); 20% had an undilated IVC and <50% collapse (group 2), 5.9% had a dilated IVC and ≥50% collapse (group 3); and 49.4% had a dilated IVC and <50% collapse (group 4). The lack of inspiratory collapse but not IVC dilation was related to higher concentrations of urea (P=.007), creatinine (P=.004), uric acid (P=.008), NT-proBNP (P=.009) and CA125 (P=.005). Survival free of the combined event at 180 days was lower in those patients with no IVC collapse. CONCLUSIONS: Dilation and the absence of the inspiratory collapse of the IVC are common in the context of AHF. The lack of inspiratory collapse of the IVC during the decompensation phase identifies a subgroup of patients with poorer prognosis at 6 months.

[Microvascular pulmonary tumor embolism in a patient with urothelial tumor]. / Embolismo tumoral pulmonar microvascular en paciente con tumor urotelial.

Pulmonary tumor embolisms (PTE) are an infrequent cause of dyspnea in oncological patients. The majority are diagnosed in patients with advanced tumors, above all localized in the breast, lung or stomach. There are few published cases involving patients with urothelial tumors. We present the case of a 69 year-old male, without a previous diagnosis of cancer, who was admitted due to subacute dyspnea, with clinical suspicion of pulmonary thromboembolism (PT). The patient died on the fifth day of admission. The autopsy confirmed the existence of a tumor in the left renal pelvis with hepatic and lymphoganglionary metastasis and an extensive microvascular pulmonary embolism that affected a large part of the capillaries and medium-caliber blood vessels of both lungs. PTE were considered responsible for the progressive respiratory failure and as the final cause of death. The most frequent clinical presentation of PTE is dyspnea. They are often mistaken for PT and diagnosis is not easy. Their prognosis is very bad, with extremely high mortality and confirmation is usually post-mortem.