Vulnerability to functional decline is associated with noncardiovascular cause of 90-day readmission in hospitalized patients with heart failure.

BACKGROUND: Hospital readmission is common among patients with heart failure. Vulnerability to decline in physical function may increase the risk of noncardiovascular readmission for these patients, but the association between vulnerability and the cause of unplanned readmission is poorly understood, inhibiting the development of effective interventions. OBJECTIVES: We examined the association of vulnerability with the cause of readmission (cardiovascular vs. noncardiovascular) among hospitalized patients with acute decompensated heart failure. DESIGNS, SETTINGS, AND PARTICIPANTS: This prospective longitudinal study is part of the Vanderbilt Inpatient Cohort Study. MAIN OUTCOME AND MEASURES: The primary outcome was the cause of unplanned readmission (cardiovascular vs. noncardiovascular). The primary independent variable was vulnerability, measured using the Vulnerable Elders Survey (VES-13). RESULTS: Among 804 hospitalized patients with acute decompensated heart failure, 315 (39.2%) experienced an unplanned readmission within 90 days of discharge. In a multinomial logistic model with no readmission as the reference category, higher vulnerability was associated with readmission for noncardiovascular causes (relative risk ratio [RRR] = 1.36, 95% confidence interval [CI]: 1.06-1.75) in the first 90 days after discharge. The VES-13 score was not associated with readmission for cardiovascular causes (RRR = 0.94, 95% CI: 0.75-1.17). CONCLUSIONS: Vulnerability to functional decline predicted noncardiovascular readmission risk among hospitalized patients with heart failure. The VES-13 is a brief, validated, and freely available tool that should be considered in planning care transitions. Additional work is needed to examine the efficacy of interventions to monitor and mitigate noncardiovascular concerns among vulnerable patients with heart failure being discharged from the hospital.

Co-occurrence of Myocardial Sarcoidosis and Left Ventricular Non-compaction in a Patient with Advanced Heart Failure.

A 46-year-old man with systolic heart failure, end-stage renal disease on dialysis, ventricular tachycardia and pulmonary sarcoidosis presented with decompensated heart failure and cardiogenic shock of unknown aetiology. The hospital course was complicated by worsening shock requiring inotropic and mechanical circulatory support, as well as eventual dual heart and kidney transplantation. Cardiac imaging was used to assess the aetiology of the patient's non-ischaemic cardiomyopathy, including a PET scan and cardiac MRI. Imaging demonstrated findings consistent with left ventricular non-compaction, but was inconclusive for cardiac sarcoidosis. After eventual heart transplantation, histopathology of the patient's explanted heart showed evidence of both non-compaction and cardiac sarcoidosis. In this case report, the authors review the pathophysiology of both cardiac sarcoidosis and left ventricular non-compaction, and highlight a multimodality approach to the diagnosis of non-ischaemic cardiomyopathy.

Increased Dephospho-uncarboxylated Matrix Gla-Protein Is Associated With Lower Axial Skeletal Muscle Mass in Patients With Hypertension.

BACKGROUND: Matrix Gla-protein (MGP) is a well-established inhibitor of vascular calcification that is activated by vitamin K-dependent carboxylation. In the setting of vitamin K2 deficiency, dephospho-uncarboxylated MGP (dpucMGP) levels increase, and have been associated with large artery stiffening. Vitamin K2 is also a mitochondrial electron carrier in muscle, but the relationship of vitamin K2 deficiency and dpucMGP with muscle mass is not well understood. We therefore aimed to examine the association of vitamin K2 deficiency and dpucMGP with skeletal muscle mass in patients with hypertension. METHODS: We studied 155 hypertensive adults without heart failure. Axial skeletal muscle mass was measured using magnetic resonance imaging from axial steady-state free precession images. DpucMGP was measured with ELISA. Carotid-femoral pulse wave velocity (CF-PWV) was measured from high-fidelity arterial tonometry recordings. RESULTS: We found an inverse relationship between dpucMGP levels and axial muscle mass, with progressively rising dpucMGP levels correlating with decreasing axial muscle mass. In an unadjusted linear regression model, correlates of dpucMGP included axial skeletal muscle area factor (ß = -0.32; P < 0.0001) and CF-PWV (ß = 0.31; P = 0.0008). In adjusted analyses, independent correlates of dpucMGP included axial skeletal muscle area factor (ß = -0.30; P = 0.0003) and CF-PWV (ß = 0.20; P = 0.019). CONCLUSIONS: In hypertensive adults, dpucMGP is independently associated with lower axial muscle mass, in addition to increased large artery stiffness. Further studies are required to investigate the role of vitamin K supplementation in this population.

Use of Tissue Plasminogen Activator Alteplase Purge Solution in an Impella 5.5 Heart Pump.

Standardized Impella purge solutions have traditionally consisted of 5-40% dextrose with or without unfractionated heparin as a means of anticoagulation. Such a solution serves to create a pressure barrier preventing entry of blood into the pump's motor housing with heparin providing adequate purge pathway patency in the event of this occurring. We present a case of tissue plasminogen activator (tPA, Activase) utilization in lieu of the recommended purge solution due to concern for thrombus formation of the purge pathway in a 51-year-old male with cardiogenic shock status-post Impella 5.5 heart pump placement for hemodynamic support while awaiting heart transplantation. The purge solution was successfully administered for 48 hours without complication and a reduction in average purge pressure with increase in purge flow rate was observed.

Body Composition, Natriuretic Peptides, and Adverse Outcomes in Heart Failure With Preserved and Reduced Ejection Fraction.

OBJECTIVES: The purpose of this study was to determine the relationship between body composition, N-terminal B-type natriuretic peptide (NT-proBNP) levels, and heart failure (HF) phenotypes and outcomes. BACKGROUND: Abnormalities in body composition can influence metabolic dysfunction and HF severity; however, data assessing fat distribution and skeletal muscle (SM) size in HF with reduced (HFrEF) and preserved EF (HFpEF) are limited. Further, whether NPs relate more closely to axial muscle mass than measures of adiposity is not well studied. METHODS: We studied 572 adults without HF (n = 367), with HFrEF (n = 113), or with HFpEF (n = 92). Cardiac magnetic resonance was used to assess subcutaneous and visceral abdominal fat, paracardial fat, and axial SM size. We measured NT-proBNP in 334 participants. We used Cox regression to analyze the relationship between body composition and mortality. RESULTS: Compared with controls, pericardial and subcutaneous fat thickness were significantly increased in HFpEF, whereas patients with HFrEF had reduced axial SM size after adjusting for age, sex, race, and body height (p < 0.05 for comparisons). Lower axial SM size, but not fat, was significantly predictive of death in unadjusted (standardized hazard ratio: 0.63; p < 0.0001) and multivariable-adjusted analyses (standardized hazard ratio = 0.72; p = 0.0007). NT-proBNP levels more closely related to lower axial SM rather than fat distribution or body mass index (BMI) in network analysis, and when simultaneously assessed, only SM (p = 0.0002) but not BMI (p = 0.18) was associated with NT-proBNP. However, both NT-proBNP and axial SM mass were independently predictive of death (p < 0.05). CONCLUSIONS: HFpEF and HFrEF have distinct abnormalities in body composition. Reduced axial SM, but not fat, independently predicts mortality. Greater axial SM more closely associates with lower NT-proBNP rather than adiposity. Lower NT-proBNP levels in HFpEF compared with HFrEF relate more closely to muscle mass rather than obesity.

Mitochondrial Dysfunction in Heart Failure With Preserved Ejection Fraction.

Heart failure with preserved ejection fraction (HFpEF) is a complex syndrome with an increasingly recognized heterogeneity in pathophysiology. Exercise intolerance is the hallmark of HFpEF and appears to be caused by both cardiac and peripheral abnormalities in the arterial tree and skeletal muscle. Mitochondrial abnormalities can significantly contribute to impaired oxygen utilization and the resulting exercise intolerance in HFpEF. We review key aspects of the complex biology of this organelle, the clinical relevance of mitochondrial function, the methods that are currently available to assess mitochondrial function in humans, and the evidence supporting a role for mitochondrial dysfunction in the pathophysiology of HFpEF. We also discuss the role of mitochondrial function as a therapeutic target, some key considerations for the design of early-phase clinical trials using agents that specifically target mitochondrial function to improve symptoms in patients with HFpEF, and ongoing trials with mitochondrial agents in HFpEF.

Creating a Culture of Wellness in Residency.

Despite increased awareness and recognition of the prevalence of physician burnout and the associated risks of depression and suicide, there is a paucity of actionable guidelines for residency programs to mitigate these risks for their residents. In this Invited Commentary, the authors acknowledge that, although there are inherent barriers to resident wellness, there are numerous modifiable barriers that present opportunities for programs to enable culture change and improve resident well-being. The authors frame the discussion with a personal narrative written by a resident in their internal medicine program who experienced burnout, depression, and suicidality during his intern year. They aim to inspire residency programs and hospital leadership to identify and intervene upon the modifiable barriers to wellness for residents in their programs in order to shape meaningful cultural change.