Objectives Cardiopulmonary Exercise Testing (CPET) is a key diagnostic and prognostic for patients with HF. With exercise, peak VO2 is dependent on the ability to augment SV (inotropic response) and HR (chronotropic response). We sought to study blunted chronotropic response (chronotropic incompetence (CI) in patients undergoing diagnostic CPET. We further sought to explore the relationship of CI with other prognostic metrics obtained with CPET in an ambulatory heart failure cohort. Methods Fifty-seven patients, 37 men and 20 women, met our inclusion criteria for CI. Ages range from 27-81 years old, with a mean of 58.6 years. This population included HFrEF and HFpEF and ischemic and non-ischemic etiologies. LVEF ranged from 10-71%, with a mean of 35.2%. Patients with a peak RER < 1.0 were excluded. Results 610 CPETs were performed between 8/2020 and 1/2024; 420 patients met our inclusion criteria and 57 (13.6%) demonstrated CI. Percent predicted HR was calculated using a standard formula (220-Age). Our analysis defined CI as an observed peak HR less than 60% of the predicted peak HR. Patients were stratified by CI status and Welch’s or two-sample independent t-tests, adjusted for multiple comparisons, evaluated differences in prognostic measures across strata. The CI cohort had a significantly lower peak VO2 (p<0.001) and oxygen consumption at anaerobic threshold (p=0.005) compared to the cohort without CI. The CI group had a significantly steeper slope of VE/VCO2 (p=0.003) compared to the group without CI. The RER (p=0.33) and peak VO2/HR at peak exercise (p=0.83) were similar between the two groups. Conclusions We found CI in 13.6% of patients undergoing CPET with strong correlations to attained peak VO2, peak AT and slope of VE/VCO2 despite no differences similar RER and VO2/HR suggesting that inotropic responsive was not impacted by the CI. Early investigators have suggested that chronotropic responsiveness has a primordial impact of chronotropic responsiveness on attainment of peak VO2.Since our patients were predominantly paced, but most were on beta blockers and some in sinus rhythm. We need to find strategies to identify and ameliorate CI in patients with advanced heart failure.

Background Derangements of intravascular blood volumes (IBV) (total blood volume (TBV), Red blood volume (RBCV) and Plasma volume (PV)) are common and early biomarkers in patients with heart failure. Indeed, guideline recommendations and current therapies stress evaluation of these derangements and target normalization. In an ambulatory cohort of HF patients who underwent measurement of IBVs as part of their advanced heart failure evaluation, we hypothesized that baseline normal IBV’s would be beneficial, connote better patient outcomes including lower risk for hospitalization, improved NYHA, better ability to up titrate GDMT (GDMT score*) and better CPET metrics. Methods Of 202 pts who underwent baseline BVAs (Daxor, Oak Ridge, TN) 76 (37%) had a normal TBV (expressed as -10% to +10%). 48 of these patients had follow up data between 7-12 months. Of these, 45 fell into 1 of 3 phenotypes: Group I, normal TBV and normal RBCV and normal PV, Group II, normal TBV, increased or decreased RBCV and normal PV, and Grp III normal TBV, decreased RBCV, and increased PV. Results The blood volumes for each group are expressed in the figure. Both groups I and II had a 36% improvement in NYHA, but group III had a 52% decline on follow up. Similarly, groups I and I had an improvement in GDMT score on follow up whereas group III had a decline in GDMT score. We also examined baseline CPET variables (figure) with Group I having the best peak exercise VO2/HR (surrogate for stroke volume.) Additionally there were no hospital admission for group I, 8 (57%) unplanned admissions for group II and 10 (77%) admissions for group III, including 1 patient who underwent heart transplant, 1 LVAD and 3 (23%) deaths. Conclusions These finding suggest: normal TBV is important in caring for patients with heart failure as well as the TBV constituents which are also drive key HF targets including functional status, ability to tolerate GDMT up titration and exercise performance. We are overdue for a re-calibration of the topic of “volume” in heart failure which needs to include IBV as well as measurement and treatment of the IBV components.

BACKGROUND:Duchenne muscular dystrophy (DMD) is an X-linked neuromuscular disorder characterized by the absence of dystrophin, leading to progressive skeletal and cardiac muscle degeneration. Cardiomyopathy is a leading cause of morbidity and mortality in patients with DMD, often manifesting as a dilated cardiomyopathy with myocardial fibrosis and arrhythmia. Mineralocorticoid receptor antagonists, including the nonsteroidal agent finerenone, have emerged as disease-modifying therapies because of their antifibrotic, anti-inflammatory, and cardioprotective properties. CASE SUMMARY:A 45-year-old man with DMD and progressive nonischemic cardiomyopathy was initiated on finerenone in addition to guideline-directed medical therapy. Over 16 months, he demonstrated improvement in left ventricular ejection fraction and ventricular remodeling without adverse effects. DISCUSSION:Finerenone is a nonsteroidal mineralocorticoid receptor antagonist with potent antifibrotic and anti-inflammatory properties. This case highlights its potential role in DMD cardiomyopathy, where fibrosis is central to disease progression. TAKE-HOME MESSAGE:Finerenone may represent a novel therapy in DMD-associated cardiomyopathy and warrants further investigation for use in this population.

Background Variations in body mass indices (BMIs) occur in patients with heart failure and often limit therapeutic options. High BMI (h-BMI) impacts post heart transplant outcomes, and low BMI (l-BMI) has been associated with increased mortality while waiting for transplantation. There are conflicting beliefs about BMI variances ranging from the benefit of obesity (obesity paradox) to risk (cardiac cachexia). We evaluated the BMIs on new referrals for advanced heart failure care. Methods The range and distribution of BMIs of 620 patients referred over 2023-2024 are shown in Figure 1. We divided the patients into 6 BMI categories: I (60.4-81.7kg), II (40.4-55.7kg), III (30-30.9 kg), IV (25-29.9kg), V (18.7-24.9 kg) and VI (16.2-18.2 kg). Each group had 8 randomly selected patients (group I =6). We collected baseline and follow up data for each group. Results Forty-six patients were included (32 men/14 women), aged 19-81 years. All were ACC/AHA Stage C with an average NYHA Class of 2.85. Baseline 6MW was 325 meters. Baseline LVEF ranged from 24-49% (mean 37%). Diabetes was present in 21% and did not vary by BMI group. At 6- and 12-months average echo EF (%) did not vary significantly except in group VI which has the lowest baseline (24.3%), 6-month (25.3%) and 12-month (29.3%) EF. We collected GDMT scores (ESC HF 2023,10:3252-3363) at baseline and follow-up (Figure 2). In all BMI groups, GDMT score rose between baseline, 3 and 6 months (p< 0.0136 and p< 0.05, respectively). Group VI had the lowest GDMT score at baseline, 3 and 6 months (2.4, 2.9 and 3.4 respectively.) All patients were alive at 1 year except 1 patient each in groups I and III. Conclusions Several observations have emerged. First, all patients across the BMI spectrum can tolerate some degree of GDMT and can be titrated up over the initial 6 months with statistically significant increases at 3 and 6 months. The lowest GDMT scores over that period was in group VI. In months 7-12 GDMT scores fell mostly in Groups IV-VI. Second, GDMT can be an impactful “stabilizer” for patients with higher BMI (Groups I-III) while other cardiometabolic therapies are pursued. Thirdly, patients in Groups IV-VI appear be at higher risk (EF and sequential GDMT) and require more urgent nutritional/cardiometabolic strategies. Patients with advanced heart failure across the cardiometabolic spectrum require personalized care as they behave heterogeneously, related in part to their BMI.

Intravascular hypervolemia with polycythemia is a blood volume phenotype in patients with heart failure that portends additional risks including thrombotic events. This paper presents 4 patients with heart failure with this blood volume phenotype and focuses on its identification and the role of therapeutic phlebotomy including patient selection and outcomes.

Intravascular hypervolemia with polycythemia is a blood volume phenotype in patients with heart failure that portends additional risks including thrombotic events. This paper presents 4 patients with heart failure with this blood volume phenotype and focuses on its identification and the role of therapeutic phlebotomy including patient selection and outcomes.

Patients with cardiomyopathy and aortic dissection presents significant challenges. Some patients are too ill to go directly to transplantation and require a bridge strategy to address the cardiomyopathy and dissection. This case combines a total artificial heart with a frozen elephant trunk procedure to increase the likelihood of survival. The patient underwent transposition of the left subclavian artery to the left carotid artery prior to frozen elephant trunk combined with implantation of a total artificial heart, bridge to transplantation. The patient remained inpatient, and underwent heart transplantation, with discharge from the hospital. Bridge to transplantation in patients with dissection is feasible in selected patients.

Blood volume analysis provides a quantitative volume assessment in patients with equivocal or discordant clinical findings. Reports on its use in mechanical circulatory support are limited and it has never been described in patients with a total artificial heart. Our series demonstrates that patients supported with total artificial heart as a bridge to transplant have significant reductions in red blood cell volume and heterogeneous adaptations in their total blood volume and plasma volume. Pathologic derangements in our patient’s total blood volume were targeted to restore euvolemia.

Background The effects of exercise in patients with breast cancer (BC), has shown some profit, but consistency and magnitude of benefit remains unclear. We aimed to conduct a meta-analysis to assess the benefits of varying types of exercises in patients with BC. Methods Literature search was conducted across five electronic databases (MEDLINE, Web of Science, Scopus, Google Scholar and Cochrane) from 1st January 2000 through 19th January 2024. Randomized controlled trials (RCTs) assessing the impact of different types of exercise on outcomes related to fitness and quality of life (QOL) in patients with BC were considered for inclusion. Outcomes of interest included cardiorespiratory fitness (CRF), health-related quality of life (HRQOL), muscle strength, fatigue and physical function. Evaluations were reported as mean differences (MDs) with 95% confidence intervals (CIs) and pooled using random effects model. A p value < 0.05 was considered significant. Results Thirty-one relevant articles were included in the final analysis. Exercise intervention did not significantly improved the CRF in patients with BC when compared with control according to treadmill ergometer scale (MD: 4.96; 95%Cl [-2.79, 12.70]; P = 0.21), however exercise significantly improved CRF according to cycle ergometer scales (MD 2.07; 95% Cl [1.03, 3.11]; P = 0.0001). Physical function was significantly improved as well in exercise group reported by 6-MWT scale (MD 80.72; 95% Cl [55.67, 105.77]; P < 0.00001). However, exercise did not significantly improve muscle strength assessed using the hand grip dynamometer (MD 0.55; 95% CI [-1.61, 2.71]; P = 0.62), and fatigue assessed using the MFI-20 (MD -0.09; 95% CI [-5.92, 5.74]; P = 0.98) and Revised Piper scales (MD -0.26; 95% CI [-1.06, 0.55] P = 0.53). Interestingly, exercise was found to improve HRQOL when assessed using the FACT-B scale (MD 8.57; 95% CI [4.53, 12.61]; P < 0.0001) but no significant improvements were noted with the EORTIC QLQ-C30 scale (MD 1.98; 95% CI [-1.43, 5.40]; P = 0.25). Conclusion Overall exercise significantly improves the HRQOL, CRF and physical function in patients with BC. HRQOL was improved with all exercise types but the effects on CRF vary with cycle versus treadmill ergometer. Exercise failed to improve fatigue-related symptoms and muscle strength. Large RCTs are required to evaluate the effects of exercise in patients with BC in more detail.

BACKGROUND:This review delves into the intricate landscape of cardiorenal syndrome (CRS) and highlights the pivotal role of Blood Volume Analysis (BVA) in improving patient care and outcomes. SUMMARY:BVA offers a direct and highly accurate quantification of intravascular volume, red blood cell volume, and plasma volume, complete with patient-specific norms. This diagnostic tool enhances the precision of diuretic and red cell therapies, significantly elevating the effectiveness of conventional care. KEY MESSAGES:· Comprehensive Understanding: Our objectives encompass a comprehensive understanding of how BVA informs the evaluation and treatment of CRS, including its subtypes, pathophysiology, and clinical significance. · BVA Principles and Advantages: We delve into BVA principles, techniques, and measurements, elucidating its diagnostic potential and advantages compared to commonly used surrogate measures. · Clinical Relevance: We dissect the clinical relevance of BVA in various CRS scenarios, emphasizing its unique contributions to each subtype. · Improving patient outcomes: By assessing the tangible impact of BVA on patient outcomes through meticulous analysis of relevant clinical studies, we unveil its potential to enhance health outcomes and optimize resource utilization. · Multidisciplinary Collaboration: Acknowledging the challenges and limitations associated with BVA's clinical implementation, we underscore the importance of multidisciplinary collaboration among cardiologists, nephrologists, and other clinicians. · Future Directions: Finally, we identify research gaps and propose future directions for BVA and CRS, contributing to ongoing advancements in this field and patients affected by this complicated clinical syndrome.

Introduction The current landscape for patients referred to Advanced Heart Failure Clinics is dominated by patients with recent admissions for decompensated heart failure, advanced functional class, significant co-morbidities and underutilization of GDMT. Also, managing diuretics remains one of the most difficult problems clinicians encounter. Recognizing that most signs and symptoms and exam findings reflect volume status in the interstitial space, we sought to add direct blood volume measurements of the intravascular compartment to the diagnostic approach for these patients. Hypothesis Measuring personalized blood volume analyses (BVAs) (including total blood volume (TBV), plasma volume (PV) and red cell volume (RBCV)) for patients with advanced heart failure would provide additional information not otherwise obtainable to guide treatment decisions. Methods Between January 12, 2023, and March 31, 2023, 29 patients (18 men and 11 women) aged 19-81 years (mean 62) attending the Banner University Medical Center Advanced Heart Failure Clinic underwent BVA as part of a quality improvement process. The results were integrated with all other imaging, laboratory and clinical assessment to guide and inform treatment decisions. We focused on patients with 5 key clinical scenarios; prior to BVA the team made intravascular blood volume predictions. Results The BVAs were performed to help guide the following clinical questions (most patients had >1 indication): 1) volume assessment/inform diuretic plan (28), 2) optimize GDMT (7), 3) potential for inotrope wean (5), 4) transplant evaluation (4), and 5) assessment of anemia (2). Pre-BVA all patients except 3 were predicted to be hypervolemic based upon signs, symptoms, exercise capacity, biomarkers and examination. Of these 3, only 1 had hypovolemia, yet all 3 had anemia. Overall, the common BVA phenotypes (TBV/RBCV) were: • Hypervolemic/anemic 7(24%) • Hypovolemic/anemic 6(21%) • Hypervolemic/normocythemic 3(10%) • Hypervolemic/polycythemic 4(14%) • Normovolemic/anemic 2(7%) • Normovolemic/polycythemic 1(3%) • Normovolemic/normocythemic 6(21%). (See Figure 1.) The range of deviation in TBV for Hypervolemic patients was from +10.7 to +49.4% and in Hypovolemic patients was from -12.1 to -25.5%.The range of deviation in RBCV for Anemic patients was from -16 to -48.4% and in Polycythemic patients was from + 15 to + 38.7%. Conclusions In an advanced heart failure clinic, incorporating BVA into the patient care model yielded unexpected and profound dysregulation in TBV and RBCV. Both dysregulations became immediate targets for adjustment in therapeutics and guiding improvements in intravascular circulatory physiology not otherwise available. We plan to continue BVA use to improve patient therapeutics and outcomes.

AbstractAimsQuantitative methods have shown clinically significant heterogeneity in blood volume (BV) profiles across heart failure (HF) phenotypes. These profiles extend from hypovolaemia to normal BV and to variable degrees of BV hypervolaemia, frequently with similar clinical presentations. However, a comprehensive survey of BV profiles providing practical clinical guidance for the interpretation and management of quantitative plasma volume (PV) and red blood cell (RBC) mass findings has not been reported. The intent of this study is to advance this concept through a multicentre analysis.Methods and resultsA retrospective analysis of clinical and BV data was undertaken in stable NYHA class II–III HF patients (N = 546). BV was quantitated using established nuclear medicine indicator‐dilution methodology. Differing combinations of PV and RBC mass were identified contributing to marked heterogeneity in overall BV profiles. A quantitatively normal BV was identified in 32% of the cohort but of these only ~1/3 demonstrated a true normal BV (i.e., normal PV + normal RBC mass). The remaining portion of normal BV profiles reflected balanced combinations of compensatory PV expansion with RBC mass deficit (anaemia) (14% of cohort) and PV contraction with RBC mass excess (erythrocythemia) (6% of cohort). Main contributors to BV hypervolaemia were PV excess with a normal RBC mass (21% of cohort; 23% female) and PV excess with erythrocythemia (24% of cohort; 26% female). Hypovolaemia was predominately defined by RBC mass deficit with a normal PV (6% of cohort; 57% female) or RBC mass deficit with PV contraction (5% of cohort; 48% female).ConclusionsFindings support the clinical relevance of identifying and accurately interpreting the varying combinations of PV and RBC mass in patients with chronic HF. This in turn helps guide appropriate individualized patient management strategies. A practical volume‐based guideline is provided in an effort to aid clinician interpretation.

Introduction Viral causes of myocarditis and cardiomyopathy are well established with known agents such as parvoviruses, enteroviruses, and adenoviruses. Human metapneumovirus (hMPV), belonging to the Pneumovirdiae family, was first discovered in 2001 primarily resulting in upper and lower respiratory tract infections - most common in children, older individuals, and those with a weakened or compromised immune system. Once infected, it has been reported to cause pneumonia, croup, otitis media, and conjunctivitis. However, hMPV is a rare causing agent of myocarditis. Case Description History. A 27-year-old male with a significant past medical history of pleural effusions requiring thoracentesis, chronic kidney disease type III, nephrotic syndrome, and type 2 diabetes mellitus presented to the emergency room (ER) on multiple occasions in a 6-month duration experiencing tachycardia, coughing, shortness of breath with exertion and bi-lateral edema. Denied symptomatology of chills, nausea, emesis, and angina. Unknown family history due to poor relationship. Labs. Initially, the patients presenting symptoms were considered as possible recurrent pleural effusions, pneumonia, sepsis, and/or secondary to the known history of nephrotic syndrome. A nasopharyngeal swab sample was performed ruling out pneumonia, however, hMPV was detected. Estimated glomerular filtrate rate (eGFRcr CKD-EPI, 38 mL/min/1.73m2) was insignificantly low while levels of Pro-B type natriuretic peptide (pro-BNP, 12.029 pg/mL) and creatinine (2.36 mg/dL) were elevated. Cardiac Work. An Echocardiogram (ECHO) was performed indicating a normal left ventricular ejection fraction (LVEF) of 54% with trivial anterior and apical pericardial effusion with normal diastolic and systolic function. A second ECHO was completed within a 2-month period revealing a reduced LVEF of 37%, trace mitral valve and tricuspid valve regurgitation, and a dilated inferior vena cava. A cardiac MRI was performed 5 days later revealing an LVEF of 33% with pericardial and bilateral pleural effusions, cardiac output of 5.5 L/min, diffuse myocardial edema and no findings c/w infiltrative cardiomyopathy (Fig. 1). A cardiac pyrophosphate (PYP) scan was negative for cardiac amyloidosis. Conclusion Human metapneumovirus should be considered as an etiology, among other viruses, of cardiomyopathy as it has demonstrated its ability of being a causative agent of myocarditis and subsequent LV dysfunction.

The prognostic implications of intravascular volume status assessed by blood volume analysis (BVA) in ambulatory heart failure (HF) remain uncertain. The incremental benefits of assessing volume status, beyond the well-established filling pressures, in predicting HF outcomes are unknown.

Impairment to left ventricular (LV) filling may result from left-sided cardiovascular conditions proximal to the left ventricle (mitral stenosis, cor triatriatum, pulmonary venous obstruction),1 from LV myocardial conditions (including hypertrophic cardiomyopathy,2 amyloidosis3 and hemosiderosis4), from pericardial constriction (of several causes),5 and from LV endomyocardial fibrosis with or without eosinophilia.6 The last condition, which occurs mainly in Africa, causes extensive LV endocardial fibrosis located primarily in the LV inflow tract and is associated with little or no mural endocardial calcific deposits. The common denominator of all of these conditions is a normal-sized or small LV cavity. This report describes a hitherto unreported cause of impairment to LV filling: massive LV endocardial calcific deposits associated with LV hypertrophy of undetermined origin.

PurposeAnemia is a common coexisting condition in patients with heart failure (HF). In addition to true anemia from decreased red blood cell volume (RBCV), HF often results in congestion and increase in plasma volume (PV) which could lead to hemodilution as a cause of anemia. Anemia is associated with decreased cardiopulmonary exercise testing (CPET) performance in HF but the difference between true anemia and hemodilution in CPET performance is unknown.MethodsThis is a prospective two-center study enrolling patients with advanced HF who underwent invasive CPET and blood volume analysis (BVA). The BVA measures total blood volume (TBV), RBCV and PV using the indicator dilution technique with an I131-tagged albumin tracer. Anemia was defined using hematocrit cut-off of 41% in men and 36% in women. In anemia group, patients had true anemia if RBCV was < 95% of ideal RBCV. Patients with anemia and normal RBCV were categorized as hemodilution. One-way ANOVA was used to compare between 3 groups. If a significant difference was noted, pairwise comparison was subsequently performed.ResultsTotal of 43 patients were included. Of those, 42% were anemia (61% true anemia and 39% hemodilution). There was no significant difference in demographics or LVEF between groups. We observed a significant difference in the minute ventilation/carbon dioxide production (VE/VCO2) slope between groups (no anemia: 34.1 ± 7.8 vs. true anemia: 32.4 ± 7.6 vs. hemodilution: 43.4 ± 14.3, p=0.03). A pairwise comparison only showed a significant difference between true anemia and hemodilution (p=0.04). There were no between-group differences in mean peak oxygen consumption (VO2), % predicted maximal VO2 or respiratory exchange ratio (RER).ConclusionCompared to true anemia, hemodilution appears to have worse cardiopulmonary performance as evidenced by higher VE/VCO2. The underlying mechanisms of this finding as well as its clinical implications need to be further investigated. Anemia is a common coexisting condition in patients with heart failure (HF). In addition to true anemia from decreased red blood cell volume (RBCV), HF often results in congestion and increase in plasma volume (PV) which could lead to hemodilution as a cause of anemia. Anemia is associated with decreased cardiopulmonary exercise testing (CPET) performance in HF but the difference between true anemia and hemodilution in CPET performance is unknown. This is a prospective two-center study enrolling patients with advanced HF who underwent invasive CPET and blood volume analysis (BVA). The BVA measures total blood volume (TBV), RBCV and PV using the indicator dilution technique with an I131-tagged albumin tracer. Anemia was defined using hematocrit cut-off of 41% in men and 36% in women. In anemia group, patients had true anemia if RBCV was < 95% of ideal RBCV. Patients with anemia and normal RBCV were categorized as hemodilution. One-way ANOVA was used to compare between 3 groups. If a significant difference was noted, pairwise comparison was subsequently performed. Total of 43 patients were included. Of those, 42% were anemia (61% true anemia and 39% hemodilution). There was no significant difference in demographics or LVEF between groups. We observed a significant difference in the minute ventilation/carbon dioxide production (VE/VCO2) slope between groups (no anemia: 34.1 ± 7.8 vs. true anemia: 32.4 ± 7.6 vs. hemodilution: 43.4 ± 14.3, p=0.03). A pairwise comparison only showed a significant difference between true anemia and hemodilution (p=0.04). There were no between-group differences in mean peak oxygen consumption (VO2), % predicted maximal VO2 or respiratory exchange ratio (RER). Compared to true anemia, hemodilution appears to have worse cardiopulmonary performance as evidenced by higher VE/VCO2. The underlying mechanisms of this finding as well as its clinical implications need to be further investigated.

Among patients with chronic heart failure (HF) intravascular volume profiles vary significantly despite similar clinical compensation. However, little is known regarding changes in blood volume (BV) profiles over time. The objective of this analysis was to identify the extent and character of changes in volume profiles over time. A prospective analysis was undertaken in patients who were hospitalized and treated for fluid overload. Quantitative BV analyses were obtained in a compensated state at hospital discharge (baseline) and follow-up at 1, 3, and 6 mo. Data were available on 10 patients who remained stable without rehospitalization or medication change over a 6-mo period. Baseline BV profiles were highly variable at hospital discharge with an average deviation of +28% above normal in 6 patients and normal BV in 4 patients. Over the follow-up period, the median change in BV was -201 mL [-3% (-6, +3%)] from baseline with profiles remaining in the same volume category in 9 out of 10 patients. Crossover from normal BV to mild contraction (-13% of normal) occurred in one patient. Red blood cell mass demonstrated the largest change over 6 mo [median -275 (-410, +175) mL] with a deviation from normal of -14 (-20, +8) % (reflecting mild anemia). These findings suggest that BV profiles in clinically compensated patients with HF do not change substantially over a 6-mo period regardless of baseline expanded or normal BV. This lack of change in volume profiles particularly from an expanded BV has implications for long-term volume management, clinical outcomes, and also our understanding of volume homeostasis in HF.NEW & NOTEWORTHY The novel findings of this study demonstrate that blood volume profiles while highly variable in clinically compensated patients with HF on stable medical therapy do not change substantially over a 6-mo period regardless of baseline expanded or normal blood volumes. This lack of change in volume profiles particularly from an expanded blood volume has implications for long-term volume management and also for how we understand the pathophysiology of volume homeostasis in chronic HF.