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BackgroundLeft ventricular outflow tract velocity time integral (LVOT VTI) is a measure of cardiac systolic function and cardiac output. Heart failure patients with low cardiac output are known to have poor cardiovascular outcomes. Thus, extremely low LVOT VTI may predict heart failure patients at highest risk for mortality.MethodsPatients with heart failure and extremely low LVOT VTI were identified from a single-center database. Baseline characteristics and heart failure related clinical outcomes (death, LVAD) were obtained at 12 months. Correlation between clinical endpoints and the following variables were analyzed: ejection fraction (EF), pulmonary artery systolic pressure (PASP), NYHA class, renal function, Doppler cardiac output (CO), and LVOT VTI.ResultsStudy cohort consisted of 100 patients. At the 12-month follow up period, 30 events (28 deaths, 2 LVADs) were identified. Occurrence of death and LVAD implantation was statistically associated with a lower LVOT VTI (p = 0.039) but not EF (p = 0.169) or CO (p = 0.217). In multivariate analysis, LVOT VTI (p = 0.003) remained statistically significant, other significant variables were age (p = 0.033) and PASP (p = 0.022). Survival analysis by LVOT VTI tertile demonstrated an unadjusted hazard ratio of 4.755 (CI 1.576-14.348, p = 0.006) for combined LVAD and mortality at one year.ConclusionsExtremely low LVOT VTI strongly predicts adverse outcomes and identifies patients who may benefit most from advanced heart failure therapies.

Aims In heart failure (HF) with preserved ejection fraction (HFpEF), excessive redistribution of blood volume into the central circulation leads to elevations of intracardiac pressures with exercise limitations. Splanchnic ablation for volume management (SAVM) has been proposed as a therapeutic intervention. Here we present preliminary safety and efficacy data from the initial roll‐in cohort of the REBALANCE‐HF trial. Methods and results The open‐label (roll‐in) arm of REBALANCE‐HF will enrol up to 30 patients, followed by the randomized, sham‐controlled portion of the trial (up to 80 additional patients). Patients with HF, left ventricular ejection fraction (LVEF) ≥50%, and invasive peak exercise pulmonary capillary wedge pressure (PCWP) ≥25 mmHg underwent SAVM. Baseline and follow‐up assessments included resting and exercise PCWP, New York Heart Association (NYHA) class, Kansas City Cardiomyopathy Questionnaire (KCCQ), 6‐min walk test, and N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP). Efficacy and safety were assessed at 1 and 3 months. Here we report on the first 18 patients with HFpEF that have been enrolled into the roll‐in, open‐label arm of the study across nine centres; 14 (78%) female; 16 (89%) in NYHA class III; and median (interquartile range) age 75.2 (68.4–81) years, LVEF 61.0 (56.0–63.2)%, and average (standard deviation) 20 W exercise PCWP 36.4 (±8.6) mmHg. All 18 patients were successfully treated. Three non‐serious moderate device/procedure‐related adverse events were reported. At 1‐month, the mean PCWP at 20 W exercise decreased from 36.4 (±8.6) to 28.9 (±7.8) mmHg (p < 0.01), NYHA class improved by at least one class in 33% of patients (p = 0.02) and KCCQ score improved by 22.1 points (95% confidence interval 9.4–34.2) (p < 0.01). Conclusion The preliminary open‐label results from the multicentre REBALANCE‐HF roll‐in cohort support the safety and efficacy of SAVM in HFpEF. The findings require confirmation in the ongoing randomized, sham‐controlled portion of the trial.

BackgroundWidespread use of angiotensin receptor blocker and neprilysin inhibitor (ARNI) remains low, and many patients are unable to tolerate the medication due to hypotension at the currently recommended starting dose.HypothesisThe aim of this study is to assess if lower than standard doses of ARNI, sacubitril/valsartan (S/V), significantly reduces NT‐proBNP and leads to any change in diuretic dose, serum potassium, or creatinine.MethodsIn a retrospective study of 278 patients who were started on a low dose S/V at a single medical center, 45 patients were selected for the study cohort. Patients were subcategorized to Group 1 (n = 10): very low dose S/V (half a tab of 24/26 mg BID), Group 2 (n = 10): very low dose titrated to low dose S/V, and Group 3 (n = 25): low dose S/V (24/26 mg BID). NT‐proBNP, diuretic dose, serum potassium, and creatinine were compared before and after initiation of S/V.ResultsAmong all groups, there was a significant reduction in NT‐proBNP level (Group 1: p < .01, Group 2: p < .01, and Group 3: p < .001). In addition, there was a significant reduction in diuretic dose across all groups combined (furosemide 53 mg/day vs. 73 mg/day; p = .03), with 17.8% (8/45) patients being able to discontinue their diuretic completely. There was no significant change in potassium or creatinine.ConclusionsLower than standard dose of S/V significantly reduces NT‐proBNP and diuretic requirement without change in potassium or creatinine, which provides hope that patients who cannot tolerate standard doses of S/V due to hypotension may be able to receive the benefits of S/V therapy.

The treatment of congestive heart failure is an expensive undertaking with much of this cost occurring as a result of hospitalization. It is not surprising that many remote monitoring strategies have been developed to help patients maintain clinical stability by avoiding congestion. Most of these have failed. It seems very unlikely that these failures were the result of any one underlying false assumption but rather from the fact that heart failure is a progressive, deadly disease and that human behavior is hard to modify. One lesson that does stand out from the myriad of methods to detect congestion is that surrogates of congestion, such as weight and impedance, are not reliable or actionable enough to influence outcomes. Too many factors influence these surrogates to successfully and confidently use them to affect HF hospitalization. Surrogates are often attractive because they can be inexpensively measured and followed. They are, however, indirect estimations of congestion, and due to the lack specificity, the time and expense expended affecting the surrogate do not provide enough benefit to warrant its use. We know that high filling pressures cause transudation of fluid into tissues and that pulmonary edema and peripheral edema drive patients to seek medical assistance. Direct measurement of these filling pressures appears to be the sole remote monitoring modality that shows a benefit in altering the course of the disease in these patients. Congestive heart failure is such a serious problem and the consequences of hospitalization so onerous in terms of patient well-being and costs to society that actual hemodynamic monitoring, despite its costs, is beneficial in carefully selected high-risk patients. Those patients who benefit are ones with a prior hospitalization and ongoing New York Heart Association (NYHA) class III symptoms. Patients with NYHA class I and II symptoms do not require hemodynamic monitoring because they largely have normal hemodynamics. Those with NYHA class IV symptoms do not benefit because their hemodynamics are so deranged that they cannot be substantially altered except by mechanical circulatory support or heart transplantation. Finally, hemodynamic monitoring offers substantial hope to those patients with normal ejection fraction (EF) heart failure, a large group for whom medical therapy has largely been a failure. These patients have not benefited from the neurohormonal revolution that improved the lives of their brothers and sisters with reduced ejection fractions. Hemodynamic stabilization improves the condition of both but more so of the normal EF cohort. This is an important observation that will help us design future trials for the 50% of heart failure patients with normal systolic function.

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The COVID-19 pandemic underscored our healthcare system's unpreparedness to manage an unprecedented pandemic. Heart failure (HF) physicians from 14 different academic and private practice centers share their systems' challenges and innovations to care for patients with HF, heart transplantation, and patients on LVAD support during the COVID-19 pandemic. We discuss measures implemented to alleviate the fear in seeking care, ensure continued optimization of guideline directed medical therapy (GDMT), manage the heart transplant waiting list, continue essential outpatient monitoring of anticoagulation in LVAD patients and surveillance testing post-heart transplant, and prevent physician burnout. This collaborative work can build a foundation for better preparation in the face of future challenges.

Angiotensin-converting enzyme activity in serum or bronchoalveolar lavage fluid does not reflect damage of endothelial cells or damage of alveolocapillary integrity in acute pulmonary disease.