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Percutaneous ventricular assist devices (pVADs) are indicated to provide hemodynamic support in high-risk percutaneous interventions and cardiogenic shock. However, there is a paucity of published data regarding the etiologies and predictors of 90-day readmissions following pVAD use. We studied the data from the US Nationwide Readmissions Database (NRD) for the years 2013 and 2014. Patients with a primary discharge diagnosis of pVAD use were collected by searching the database for International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) procedural code 37.68 (Impella and TandemHeart devices). Amongst this group, we examined 90-day readmission rates. Comorbidities as identified by "CM_" variables provided by the NRD were also extracted. The Charlson Comorbidity Index was calculated using appropriate ICD-9-CM codes, as a secondary diagnosis. A 2-level hierarchical logistic regression model was then used to identify predictors of 90-day readmission following pVAD use. Records from 7074 patients requiring pVAD support during hospitalization showed that 1562 (22%) patients were readmitted within 90 days. Acute decompensated heart failure (22.6%) and acute coronary syndromes (11.2%) were the most common etiologies and heart failure (odds ratio [OR]: 1.39, 95% confidence interval [CI]: 1.17-1.67), chronic obstructive pulmonary disease (OR: 1.26, 95% CI: 1.07-1.49), peripheral vascular disease (OR: 1.305, 95% CI: 1.09-1.56), and discharge into short- or long-term facility (OR: 1.28, 95% CI: 1.08-1.51) were independently associated with an increased risk of 90-day readmission following pVAD use. This study identifies important etiologies and predictors of short-term readmission in this high-risk patient group that can be used for risk stratification, optimizing discharge, and healthcare transition decisions.

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Background: Heart failure with preserved ejection fraction (HFpEF) is associated with pulmonary vascular dysfunction, particularly during exercise. Pulmonary vasodilators may favorably reduce pulmonary artery (PA) tone in HFpEF, but this could theoretically worsen left atrial hypertension and pulmonary congestion. Objective: To evaluate whether the inhaled b-adrenergic agonist albuterol would improve PA vascular function during exercise in HFpEF. Methods: We performed a randomized double blind placebo controlled trial testing the effects of inhaled albuterol on resting and exercise hemodynamics in HFpEF using high fidelity micromanometer catheters and expired gas analysis. The primary end point was pulmonary vascular resistance (PVR) during exercise. Results: Subjects with HFpEF (n=30) underwent resting and exercise hemodynamic assessment and were then randomized 1:1 to inhaled, nebulized albuterol or placebo, followed by repeat assessment of rest and exercise hemodynamics. Albuterol improved the primary endpoint of exercise PVR as compared to placebo (¡0.6 §0.5 vs +0.1 §0.7 Wood units, p=0.003). As compared to placebo, albuterol enhanced PA compliance with exercise, improved cardiac output reserve and RV-PA coupling, reduced right atrial and pulmonary artery pressures, and enhanced left ventricular transmural distending pressure during exercise (all p<0.01), with no untoward increase in pulmonary capillary hydrostatic pressures. Conclusions: Albuterol improves pulmonary vascular function and cardiac hemodynamics with exercise in patients with HFpEF. Further study is warranted to evaluate the chronic efficacy of b-agonists and other pulmonary vasoactive medicines in this population. Clinical Trial Registration: Inhaled Beta-adrenergic agonists to Treat Pulmonary Vascular Disease in Heart Failure with Preserved Ejection Fraction (BEAT HFpEF) -NCT02885636.