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AIMS: Sex differences in long-term outcomes following hospitalization for heart failure (HF) across ejection fraction (EF) subtypes are not well described. In this study, we evaluated the risk of mortality and rehospitalization among males and females across the spectrum of EF over 5 years of follow-up following an index HF hospitalization event. METHODS AND RESULTS: Patients hospitalized with HF between 1 January 2006 and 31 December 2014 from the American Heart Associations Get With The Guidelines-Heart Failure registry with available 5-year follow-up using Medicare Part A claims data were included. The association between sex and risk of mortality and readmission over a 5-year follow-up period for each HF subtype (HF with reduced EF [HFrEF, EF ≤40%], HF with mildly reduced EF [HFmrEF, EF 41-49%], and HF with preserved EF [HFpEF, EF >50%]) was assessed using adjusted Cox models. The effect modification by the HF subtype for the association between sex and outcomes was assessed by including multiplicative interaction terms in the models. A total of 155 670 patients (median age: 81 years, 53.4% female) were included. Over 5-year follow-up, males and females had comparably poor survival post-discharge; however, females (vs. males) had greater years of survival lost to HF compared with the median age- and sex-matched US population (HFpEF: 17.0 vs. 14.6 years; HFrEF: 17.3 vs. 15.1 years; HFmrEF: 17.7 vs. 14.6 years for age group 65-69 years). In adjusted analysis, females (vs. males) had a lower risk of 5-year mortality (adjusted hazard ratio [aHR] 0.89, 95% confidence interval [CI] 0.87-0.90, p

AIMS: Although atrial fibrillation (AF) frequently coexists with heart failure with preserved ejection fraction (HFpEF), few data are available evaluating AF-specific care patterns and post-discharge outcomes in patients hospitalized for HFpEF. We evaluated AF-specific medical therapies and post-discharge outcomes among patients hospitalized for heart failure with mildly reduced ejection fraction (HFmrEF) or HFpEF by AF history. METHODS AND RESULTS: Trends in AF prevalence were evaluated among patients hospitalized for HFmrEF or HFpEF in the Get With The Guidelines-Heart Failure Registry from 2014 to 2020. Among those with linked Centers for Medicare & Medicaid Services post-discharge data, we assessed associations of AF with 12-month outcomes and determined trends in post-discharge prescriptions. Among 429 464 patients (median age 76 years [interquartile range 65-85], 57% women), 216 486 (50%) had a history of AF. Over time, the proportion of patients with AF increased slightly. Among the 79 895 patients with post-discharge data, AF was independently associated with higher risk of mortality and all-cause readmissions at 12 months, with stronger associations in HFpEF than in HFmrEF (mortality hazard ratio [HR] 1.13, 95% confidence interval [CI] 1.09-1.16 vs. HR 1.03, 95% CI 0.97-1.10; pinteraction  = 0.009). Anti-arrhythmic drug use after heart failure hospitalization was low (18%) and increased modestly over time. Amiodarone accounted for 71% of total anti-arrhythmic drug prescriptions. Overall use of anticoagulants after heart failure hospitalization has significantly increased from 52% in 2014 to 61% in 2019, but remained modest. CONCLUSION: Prevalence of AF is rising among patients hospitalized with HFpEF. Those with comorbid AF face elevated post-discharge risks of death and rehospitalization. Current use of pharmacological rhythm control is low.

AimsTo assess heart failure (HF) in-hospital quality of care and outcomes before and during the COVID-19 pandemic.Methods and resultsPatients hospitalized for HF with ejection fraction (EF)

AimsCommunity-based data on the association between cardiac autonomic neuropathy (CAN) and incident heart failure (HF) in type 2 diabetes are limited. We evaluated the association of CAN with incident HF in adults with type 2 diabetes.Methods and resultsThis analysis included participants from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study without HF at baseline. CAN was assessed by electrocardiogram-based measures of heart rate variability (HRV) and QT interval index (QTI). HRV was measured using standard deviation of all normal-to-normal intervals (SDNN) and root mean square of successive differences between normal-to-normal intervals (rMSSD). CAN was defined using composite measures of the lowest quartile of SDNN and highest quartiles of QTI and heart rate. Multivariable Cox regression models were used to generate adjusted hazard ratios (aHR) for HF in relation to various CAN measures. A total of 7160 participants (mean age 62.3 [standard deviation 6.4] years, 40.8% women, 61.9% white) were included. Over a median follow-up of 4.9 years (interquartile range 4.0-5.7), 222 participants developed incident HF. After multivariable adjustment for relevant confounders, lower HRV as assessed by SDNN was associated with a higher risk of HF (aHR for the lowest vs highest quartile of SDNN: 1.70, 95% confidence interval [CI] 1.14-2.54). Participants with CAN (defined as lowest quartile of SDNN and highest quartiles of QTI and heart rate) had a 2.7-fold greater risk of HF (aHR 2.65, 95% CI 1.57-4.48).ConclusionsIn a large cohort of adults with type 2 diabetes, CAN was independently associated with higher risk of incident HF.

Sodium-glucose co-transporter 2 (SGLT2) inhibitors have recently been recommended as a foundational therapy for patients with heart failure (HF) and reduced ejection fraction (HFrEF) because of their favourable effects on mortality, clinical events and quality of life. While clinical practice guidelines have recommended dapagliflozin or empagliflozin in all patients with HFrEF, or sotagliflozin in those with HFrEF and concomitant diabetes, the timing and practical integration of these drugs in clinical practice is less well defined. We propose that these drugs are candidates for early, upfront administration to patients with newly diagnosed HFrEF and for patients hospitalized with HF. Growing evidence has established early benefits, with clinically meaningful reductions in clinical events that reach statistical significance within days to weeks, following dapagliflozin, empagliflozin or, in diabetic patients, sotagliflozin initiation. Secondly, although major clinical trials have tested these drugs in patients already receiving background HF therapy, secondary analyses showed that their efficacy is independent of that. Third, SGLT2 inhibitors are generally safe and well tolerated, with clinical trial data reporting minimal effects on blood pressure, glycaemia-related adverse events, and no excess in acute kidney injury. Rather, they exert renal protective effects and reduce risk of hyperkalaemia, properties that favour initiation, tolerance and persistence of renin-angiotensin system inhibitors and mineralocorticoid receptor antagonists. This review supports the early initiation of dapagliflozin and empagliflozin (or sotagliflozin limited to patients with diabetes) to rapidly improve clinical outcome and quality of life of HFrEF patients.

AIMS: To evaluate the performance of the WATCH-DM risk score, a clinical risk score for heart failure (HF), in patients with dysglycaemia and in combination with natriuretic peptides (NPs). METHODS AND RESULTS: Adults with diabetes/pre-diabetes free of HF at baseline from four cohort studies (ARIC, CHS, FHS, and MESA) were included. The machine learning- [WATCH-DM(ml)] and integer-based [WATCH-DM(i)] scores were used to estimate the 5-year risk of incident HF. Discrimination was assessed by Harrells concordance index (C-index) and calibration by the Greenwood-Nam-DAgostino (GND) statistic. Improvement in model performance with the addition of NP levels was assessed by C-index and continuous net reclassification improvement (NRI). Of the 8938 participants included, 3554 (39.8%) had diabetes and 432 (4.8%) developed HF within 5 years. The WATCH-DM(ml) and WATCH-DM(i) scores demonstrated high discrimination for predicting HF risk among individuals with dysglycaemia (C-indices = 0.80 and 0.71, respectively), with no evidence of miscalibration (GND P ≥0.10). The C-index of elevated NP levels alone for predicting incident HF among individuals with dysglycaemia was significantly higher among participants with low/intermediate (

AimsThe primary objective of this systematic review was to estimate the prevalence and temporal changes in chronic comorbid conditions reported in heart failure (HF) clinical trials.Methods and resultsWe searched MEDLINE for HF trials enrolling more than 400 patients published between 2001 and 2016.Trials were divided into HF with reduced ejection fraction (HFrEF), HF with preserved ejection fraction (HFpEF), or trials enrolling regardless of ejection fraction. The prevalence of baseline chronic comorbid conditions was categorized according to the algorithm proposed by the Chronic Conditions Data Warehouse, which is used to analyse Medicare data. To test for a trend in the prevalence of comorbid conditions, linear regression models were used to evaluate temporal trends in prevalence of comorbidities. Overall, 118 clinical trials enrolling a cumulative total of 215 508 patients were included. Across all comorbidities examined, data were reported in a mean of 35% of trials, without significant improvement during the study period. Reporting of comorbidities was more common in HFrEF trials (51%) compared with HFpEF trials (27%). Among trials reporting data, hypertension (63%), ischaemic heart disease (44%), hyperlipidaemia (48%), diabetes (33%), chronic kidney disease (25%) and atrial fibrillation (25%) were the major comorbidities. The prevalence of comorbidities including hypertension, atrial fibrillation and chronic kidney disease increased over time while the prevalence of smoking decreased in HFrEF trials.ConclusionMany HF trials do not report baseline comorbidities. A more rigorous, systematic, and standardized framework needs to be adopted for future clinical trials to ensure adequate comorbidity reporting and improve recruitment of multi-morbid HF patients.

Multiple drug classes have shown incremental benefits in heart failure with reduced ejection fraction. Most of these trials were designed to achieve specific doses of the investigational agent. Clinical practice guidelines recommend using the same target dosing of therapies, as tolerated. However, with the increasing number of available therapies, clinicians face the challenge of simultaneously using several drugs, achieving target doses, and managing side effects that are often overlapping. Blood pressure, renal function, hyperkalaemia, and other factors may impede achieving target doses of all medications, leaving clinicians with dilemmas as to how to sequence and dose these various classes of drugs. The guideline-directed eligibility for certain drugs and devices requires stability on maximally tolerated doses of background therapies. However, significant variability exists in dosing achieved in clinical practice. We discuss the existing background data regarding the doses of heart failure medications in clinical trials and in practice, and provide recommendations on how to navigate this complex therapeutic decision-making.

Heart failure is the leading cause of readmissions in patients aged ≥65 years with high associated societal and economic costs. The utilization metric of 30-day risk standardized readmission rates (RSRRs) has therefore become a target to reduce healthcare costs. In this review, we discuss in detail the implementation, effectiveness, and unintended consequences of the Hospital Readmissions Reduction Program (HRRP)-the major healthcare policy approach in the U.S. to reduce readmissions by financially penalizing hospitals with higher than average 30-day RSRRs. The HRRP was enacted by the Patient Protection and Affordable Care Act of 2010 (popularly known as 'Obamacare'). The public reporting of RSRRs began in June 2009 and the HRRP readmission penalties went into effect starting fiscal year 2013. The policy had limited success in achieving its primary objective of reducing readmissions as the achieved reduction in heart failure readmissions was much smaller (∼9%) than anticipated (∼25%) with some of the reduction in RSRRs attributable to the artifact of administrative upcoding post-HRRP rather than an actual decline in readmissions. From the time of passage of this law, there have been significant concerns regarding gaming of the system such as increase in observation stays, delaying readmissions beyond discharge day 30, and inappropriate triage strategies in emergency departments in order to achieve lower readmission rates to avoid penalties. A series of independent reports have now suggested that implementation of the HRRP was associated with an increase in 30-day, 90-day, and 1-year risk-adjusted heart failure mortality in the U.S. with reversal in decade long trend of declining heart failure mortality. We review the evidence behind effect of the HRRP on readmissions and mortality outcomes as well as discuss various lessons to be learned from the design, implementation, and consequences of this policy.

Acute heart failure (HF) is a global pandemic with more than one million admissions to hospital annually in the US and millions more worldwide. Post-discharge mortality and readmission rates remain unchanged and unacceptably high. Although recent drug development programmes have failed to deliver novel therapies capable of reducing cardiovascular morbidity and mortality in patients hospitalized for worsening chronic HF, hospitalized HF registries and clinical trial databases have generated a wealth of information improving our collective understanding of the HF syndrome. This review will summarize key insights from clinical trials in acute HF and hospitalized HF registries over the last several decades, focusing on improving the management of patients with HF and reduced ejection fraction.

AimsThe direct renin inhibitor, aliskiren, is known to reduce plasma renin activity (PRA), but whether the efficacy of aliskiren varies based on an individual's baseline PRA in patients hospitalized for heart failure (HF) is presently unknown. We characterized the prognostic value of PRA and determined if this risk is modifiable with use of aliskiren.Methods and resultsThis pre-specified neurohormonal substudy of ASTRONAUT analysed all patients hospitalized for HF with ejection fraction (EF) ≤40% with available baseline PRA data (n = 1306, 80.9%). Risk associated with baseline PRA and short-term changes in PRA from baseline to 1 month was modelled with respect to 12-month clinical events. Median baseline PRA was 3.0 (interquartile range 0.6-16.4) ng/mL/h. Aliskiren significantly reduced PRA early after treatment initiation through 12-month follow-up compared with placebo (P

AimsTroponin levels are commonly elevated among patients hospitalized for heart failure (HF), but the prevalence and prognostic significance of early post-discharge troponin elevation are unclear. This study sought to describe the frequency and prognostic value of pre-discharge and post-discharge troponin elevation, including persistent troponin elevation from the inpatient to outpatient settings.Methods and resultsThe ASTRONAUT trial (NCT00894387; http://www.clinicaltrials.gov) enrolled hospitalized HF patients with ejection fraction ≤40% and measured troponin I prior to discharge (i.e. study baseline) and at 1-month follow-up in a core laboratory (elevation defined as >0.04 ng/mL). This analysis included 1469 (91.0%) patients with pre-discharge troponin data. Overall, 41.5% and 29.9% of patients had elevated pre-discharge [median: 0.09 ng/mL; interquartile range (IQR): 0.06-0.19 ng/mL] and 1-month (median: 0.09 ng/mL; IQR: 0.06-0.15 ng/mL) troponin levels, respectively. Among patients with pre-discharge troponin elevation, 60.4% had persistent elevation at 1 month. After adjustment, pre-discharge troponin elevation was not associated with 12-month clinical outcomes. In contrast, 1-month troponin elevation was independently predictive of increased all-cause mortality [hazard ratio (HR) 1.59, 95% confidence interval (CI) 1.18-2.13] and cardiovascular mortality or HF hospitalization (HR 1.28, 95% CI 1.03-1.58) at 12 months. Associations between 1-month troponin elevation and outcomes were similar among patients with newly elevated (i.e. normal pre-discharge) and persistently elevated levels (interaction P ≥ 0.16). The prognostic value of 1-month troponin elevation for 12-month mortality was driven by a pronounced association among patients with coronary artery disease (interaction P = 0.009).ConclusionsIn this hospitalized HF population, troponin I elevation was common during index hospitalization and at 1-month follow-up. Elevated troponin I level at 1 month, but not pre-discharge, was independently predictive of increased clinical events at 12 months. Early post-discharge troponin I measurement may offer a practical means of risk stratification and should be investigated as a therapeutic target.

AimsTo examine associations of below-target and target dose of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, with outcomes in patients with heart failure and reduced ejection fraction (HFrEF) in the Studies of Left Ventricular Dysfunction (SOLVD) Treatment trial.Methods and resultsTwo thousand five hundred and sixty-nine patients with HFrEF (ejection fraction ≤35%) were randomized to below-target (5-10 mg/day) dose placebo (n = 1284) or enalapril (n = 1285). One month post-randomization, blind up-titration to target (20 mg/day) dose was attempted for both study drugs in 2458 patients. Among the 1444 patients who achieved dose up-titration (placebo, n = 748; enalapril, n = 696; mean dose for both groups, 20.0 mg/day), target dose enalapril (vs. target dose placebo) was associated with a 9% absolute lower risk of the combined endpoint of heart failure hospitalization or all-cause mortality [adjusted hazard ratio (HR) 0.70; 95% confidence interval (CI) 0.60-0.81; P < 0.001] during 4 years of follow-up. Among the 1014 patients who could not achieve target dose (placebo, n = 486; enalapril, n = 528; mean dose for both groups, 8.8 mg/day), below-target dose enalapril (vs. below-target dose placebo) was associated with a 12% absolute lower risk of the combined endpoint of heart failure hospitalization or all-cause mortality (adjusted HR 0.68; 95% CI 0.57-0.81; P < 0.001). Among the 1224 patients receiving enalapril, target (vs. below-target) dose had no association with the combined endpoint of heart failure hospitalization or all-cause mortality (adjusted HR 1.04; 95% CI 0.87-1.23; P = 0.695).ConclusionIn patients with HFrEF, the clinical benefits of ACE inhibitors appear to be similar at both below-target and target doses.

AimsHeart failure (HF) patients show significant lateralized neural injury, accompanied by autonomic, mood and cognitive deficits. Both gray and white matter damage occurs and probably develops from altered cerebral blood flow (CBF), a consequence of impaired cardiac output. However, the distribution of regional CBF changes in HF patients is unknown, but is an issue in determining mechanisms of neural injury. Our aim was to compare regional CBF changes in HF with CBF in control subjects using non-invasive pseudo-continuous arterial spin labelling (ASL) procedures.Methods and resultsWe collected pseudo-continuous ASL data from 19 HF patients [mean age 55.5 ± 9.1 years; mean body mass index 27.7 ± 5.3 kg/m2 ; 13 male) and 29 control subjects (mean age 51.4 ± 5.3 years; mean body mass index 25.7 ± 3.6 kg/m2 ; 18 male), using a 3.0-Tesla magnetic resonance imaging (MRI) scanner. Whole-brain CBF maps were calculated, normalized to a common space, smoothed and compared between groups using ANCOVA (covariates; age, gender and gray matter volume). Reduced CBF appeared in multiple sites in HF patients in comparison with controls, with principally lateralized lower flow in temporal, parietal and occipital regions. Areas with decreased CBF included the bilateral prefrontal, frontal, temporal and occipital cortex, thalamus, cerebellum, corona radiate, corpus callosum, hippocampus and amygdala.ConclusionsHeart failure patients showed lower, and largely lateralized, CBF in multiple autonomic, mood and cognitive regulatory sites. The reduced CBF is likely to contribute to the lateralized brain injury, leading to the autonomic and neuropsychological deficits found in the condition.

AimsChange in NT-proBNP level is a common surrogate endpoint in early phase heart failure (HF) trials, but whether this endpoint is influenced by atrial fibrillation/flutter (AFF) is unclear.Methods and resultsThis analysis included 1358 patients from the ASTRONAUT trial, which randomized patients hospitalized for HF with EF ≤40% to aliskiren or placebo in addition to standard care. Patients were stratified by presence of AFF on baseline ECG. NT-proBNP was measured longitudinally by a core laboratory at baseline, 1 month, 6 months, and 12 months. Compared with non-AFF patients, AFF patients experienced greater reduction from baseline in log-transformed NT-proBNP (interaction P < 0.001), but this difference was not significant after adjustment (interaction P = 0.726). The ability of aliskiren to lower NT-proBNP during follow-up differed by AFF status (interaction P = 0.001), with aliskiren lowering NT-proBNP more than placebo among non-AFF patients only. After adjustment, baseline AFF was not associated with mortality or HF hospitalization at 12 months (all P ≥ 0.152).ConclusionIn this hospitalized HF cohort, AFF status did not influence post-discharge NT-proBNP trajectory or clinical outcomes after adjustment for patient characteristics. Aliskiren lowered follow-up NT-proBNP levels in patients without AFF, but had no influence among patients with AFF. This study generates the hypothesis that the ability of a HF trial to meet an NT-proBNP defined endpoint may be influenced by the prevalence of AFF in the population. Because aliskiren did not improve outcomes in patients without AFF, this analysis suggests changes in NT-proBNP induced by investigational therapies may be dissociated from clinical effects.

AimsHeart failure (HF) patients show cognitive and mood impairments, including short-term memory loss and depression, that have an adverse impacting on quality of life and self-care management. Brain regions, including the hippocampus, a structure significantly involved in memory and mood, show injury in HF, but the integrity of specific hippocampal subregions is unclear.Methods and resultsTo assess regional hippocampal volume loss, we evaluated 17 HF patients (mean age ± SD, 54.4 ± 2.0 years; 12 male, left ventricular ejection fraction 28.3 ± 6.8%; New York Heart Association class II/III 94%/6%) and 34 healthy control subjects (52.3 ± 1.3 years; 24 male) using high-resolution T1-weighted magnetic resonance imaging and evaluated localized surface changes with morphometric procedures. Hippocampi were manually outlined, and volumes calculated from normalized tracings. Volume differences between groups were assessed by two-sample t-tests, and regional differences were assessed by surface morphometry. Patients with HF exhibited smaller hippocampal volumes than controls (right 3060 ± 146 mm(3) vs. 3478 ± 94 mm(3), P = 0.02; left 3021 ± 145 mm(3) vs. 3352 ± 98 mm(3), P = 0.06). Volume reductions were detected principally in CA1, an area integral to an array of learning and memory functions, as well as in mid to posterior CA3 and subiculum.ConclusionThe hippocampus shows regional volume reduction in HF, which may contribute to short-term memory loss and depression associated with the condition.

AimsThe contribution of heart failure (HF) unrelated to vascular disease to the overall HF burden in older adults is not well characterized. This was investigated in this study.Methods and resultsWe assessed HF incidence and outcomes in 2895 participants of the Health ABC Study (age 74 ± 3 years, 48.4% men, 41.4% black) in relation to vascular disease (coronary, peripheral, or cerebrovascular disease) either present at baseline or developed prior to HF. During 11.4 years follow-up, 493 participants developed HF; 134 (27.2%) in participants without any prior vascular disease and 177 (36.8%) without coronary disease. Both baseline [hazard ratio (HR) 2.4, 95% confidence interval (CI) 1.9-2.8] and incident vascular disease (HR 4.3, 95% CI 3.6-5.2) were associated with HF. During a median follow-up of 2.1 years after HF onset, 67.5% participants died. Annual mortality after HF development was 21.3% in those with compared with 24.6% in those without vascular disease (HR 1.11, 95% CI 0.87-1.43; P = 0.399). There were 658 all-cause (436.3/1000 person-years) and 523 HF-related (346.4/1000 person-years) hospitalizations after HF development. There was no significant difference in hospitalizations between those with and without vascular disease [rate ratio (RR) 1.04, 95% CI 0.86-1.24 for all-cause, and RR 0.84 95% CI 0.69-1.02 for HF hospitalization]. HF with preserved EF was more common in participants without vascular disease (67.0% vs. 55.0%, P = 0.040).ConclusionA significant proportion of HF in older adults develops without prior vascular disease. Outcomes for these patients are poor compared with those with preceding vascular disease. These data suggest the need for more targeted HF prediction and prevention efforts.

Aims: According to the Kidney Disease: Improving Global Outcomes (KDIGO) guideline, the definition of chronic kidney disease (CKD) requires the presence of abnormal kidney structure or function for >3 months with implications for health. CKD in patients with heart failure (HF) has not been defined using this definition, and less is known about the true health implications of CKD in these patients. The objective of the current study was to identify patients with HF who met KDIGO criteria for CKD and examine their outcomes. Methods and results: Of the 1 419 729 Veterans with HF not receiving kidney replacement therapy, 828 744 had data on ≥2 ambulatory serum creatinine >90 days apart. CKD was defined as estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 (n = 185 821) or urinary albumin‐to‐creatinine ratio (uACR) >30 mg/g (n = 32 730) present twice >3 months apart. Normal kidney function (NKF) was defined as eGFR ≥60 ml/min/1.73 m2, present for >3 months, without any uACR >30 mg/g (n = 365 963). Patients with eGFR <60 ml/min/1.73 m2 were categorized into four stages: 45–59 (n = 72 606), 30–44 (n = 74 812), 15–29 (n = 32 077), and <15 (n = 6326) ml/min/1.73 m2. Five‐year all‐cause mortality occurred in 40.4%, 57.8%, 65.6%, 73.3%, 69.7%, and 47.5% of patients with NKF, four eGFR stages, and uACR >30mg/g (albuminuria), respectively. Compared with NKF, hazard ratios (HR) (95% confidence intervals [CI]) for all‐cause mortality associated with the four eGFR stages and albuminuria were 1.63 (1.62–1.65), 2.00 (1.98–2.02), 2.49 (2.45–2.52), 2.28 (2.21–2.35), and 1.22 (1.20–1.24), respectively. Respective age‐adjusted HRs (95% CIs) were 1.13 (1.12–1.14), 1.36 (1.34–1.37), 1.87 (1.84–1.89), 2.24 (2.18–2.31) and 1.19 (1.17–1.21), and multivariable‐adjusted HRs (95% CIs) were 1.11 (1.10–1.12), 1.24 (1.22–1.25), 1.46 (1.43–1.48), 1.42 (1.38–1.47), and 1.13 (1.11–1.16). Similar patterns were observed for associations with hospitalizations. Conclusion: Data needed to define CKD using KDIGO criteria were available in six out of ten patients, and CKD could be defined in seven out of ten patients with data. HF patients with KDIGO‐defined CKD had higher risks for poor outcomes, most of which was not explained by abnormal kidney structure or function. Future studies need to examine whether CKD defined using a single eGFR is characteristically and prognostically different from CKD defined using KDIGO criteria. [ABSTRACT FROM AUTHOR]

This article discusses the challenges and effectiveness of early post-discharge follow-up for patients hospitalized with heart failure (HF). While guidelines recommend early follow-up visits after discharge, the evidence supporting their effectiveness is limited. A study from France found that combined follow-up with a general practitioner and cardiologist was associated with a lower risk of death or rehospitalization, but a higher risk of HF readmission. The article emphasizes the importance of optimizing guideline-directed medical therapy (GDMT) during these visits and initiating GDMT prior to discharge to improve outcomes for HF patients. However, the article acknowledges the limitations of the study and the need for further research in this area. [Extracted from the article]

BackgroundThe effect of obesity on health related quality of life (HRQOL) and depression in a number of disease states is well documented, but its impact in heart failure (HF) patients remains speculative. We therefore examined the relationship between obesity, HRQOL, and depression in 358 patients with HF.Methods and resultsComparative analyses were conducted to determine if body mass index (BMI) was associated with HRQOL and depression in three groups of patients with HF-normal weight (BMI 18.5-24.9 kg/m2, n = 100), overweight (BMI 25-29.9 kg/m2, n = 141), and obese (BMI > or = 30 kg/m2, n = 117). Obese patients were younger than normal and overweight participants; all other demographic and clinical characteristics were similar. HRQOL and depression scores were significantly higher (worse) for obese patients. Body mass index was significantly correlated with all 3 scales of HRQOL (overall, r2 = .160; physical, r2 = .162; and mental, r2 = .217) as well as with depression (r2 = .166).ConclusionObese patients with HF are more likely to have poorer HRQOL, physical health, emotional well-being and depressive symptoms. Poorer HRQOL is predictive of worse outcomes in patients with HF; however, given the apparent obesity paradox in HF, further investigation of the impact of obesity in HF is urgently required.