Medicare Hospital Readmission Penalties: as Important as Life Itself

The 20th Annual Scientific Meeting

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HFSA

S15

037 Chronic Administration with Cenderitide Goes Beyond Enalapril in Cardiorenal Function and Anti-Remodeling Through Reverse Activation of Gene Pathways in Experimental Heart Failure Tomoko Ichiki, S. Jeson Sangaralingham, Gail J. Harty, Brenda K. Huntley, Gerald E. Harders, Denise M. Heublein, John C. Burnett; Mayo Clinic, Rochester, MN

036 Sacubitril/Valsartan Reduces Serum Uric Acid Level, an Independent Predictor of Adverse Outcomes in HFrEF: Results From PARADIGM-HF Ulrik M. Mogensen1, Pardeep S. Jhund1, Lars Køber2, Margaret F. Prescott3, Martin P. Lefkowitz3, Jean-Lucien Rouleau4, Scott D. Solomon5, Karl Swedberg6, Michael R. Zile7, Milton Packer8, John J.V. McMurray1; 1University of Glasgow, Glasgow, United Kingdom; 2Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; 3Novartis Pharmaceuticals Corporation, East Hanover, NJ; 4Montreal Heart Institute, Montreal, QC, Canada; 5Brigham and Women’s Hospital, Boston, MA; 6University of Gothenburg, Gothenburg, Sweden; 7Medical University of South Carolina, Charleston, SC; 8Baylor University Medical Center, Dallas, TX Purpose: Serum uric acid/urate (UA) levels reflect purine production, metabolism and excretion. UA is produced in the final step of purine nucleotide metabolism by xanthine oxidase and increased levels may reflect oxidative stress. UA has proinflammatory and other potentially harmful effects. We examined the association between UA level and outcomes in patients with HFrEF and the effect of sacubitril/ valsartan on UA concentrations in patients in PARADIGM-HF. Methods: The association between UA and the primary composite outcome of cardiovascular (CV) death or HF hospitalization, its components and all-cause mortality was examined among 8213 patients using quintiles of UA (Q1: < 5.3, Q2: 5.3–6.2, Q3: 6.3–7.2, Q4: 7.3–8.5, Q5: 8.6–17.1 mg/dL), adjusted for baseline prognostic variables: age, sex, race, region, systolic blood pressure, heart rate, ejection fraction, NYHA class, history of HF hospitalization, duration of HF, atrial fibrillation, diabetes, BMI, prior myocardial infarction, prior stroke, eGFR, hemoglobin, sodium, albumin, randomized treatment, diuretic dose, and log NT-proBNP. Results: Patients in Q5 compared with Q1 were younger (62.8 vs 64.2 years), more often male (88.7% vs 63.1%), had lower blood pressure (119 vs 123 mmHg), lower eGFR (57.4 vs 76.6 ml/min/ 1.73 m2), and greater diuretic use. Higher UA was associated with a higher risk of the primary composite outcome (adjusted HR compared with Q1, Q5 = 1.30 [95%CI 1.11–1.53], P = .001), CV death (1.45 [1.18–1.78], P < .001), HF hospitalization (1.41 [1.14–1.74], P = .002), and all-cause mortality (1.38 [1.15–1.66], P = .001). Analysis of UA as a continuous variable gave similar results. Sacubitril/valsartan reduced serum UA compared with enalapril, treatment difference −0.25 [0.18–0.33] mg/dL, P < .001, at 12 months (Figure). Conclusion: Serum UA was an independent predictor of worse outcomes after multivariable adjustment in patients with HFrEF. Sacubitril/valsartan reduced UA more than enalapril.

Fig. Serum uric acid geometric means with 95% CI according to randomized treatment. *P < .001.

Introduction: The cardiac natriuretic peptides (NPs) have cardiorenal protective properties which play important roles in heart failure (HF) through the activation of their receptor, GC-A or GC-B. The designer natriuretic peptide, cenderitide, is the only dual GC-A/GC-B agonist and has superior effects than native NPs in preclinical studies. We have reported the acute effects of cenderitide in normal humans, however the chronic effects of cenderitide therapy on cardiorenal function and remodeling in HF are unknown. We sought to determine the actions of chronic administration of cenderitide in comparison to the ACE inhibitor, enalapril, on cardiorenal function and remodeling in experimental HF. Hypothesis: We hypothesized that cenderitide mediates cardiorenal and anti-remodeling actions which are superior ACE inhibition in HF. Methods: Canine experimental HF was induced by rapid ventricular pacing at 240 bpm for 10 days. Canines were divided into 3 groups (n = 5 of each), untreated, cenderitide with continuous SQ pump (5 ng/kg/min) or oral enalapril (ACEi, 0.5 mg/kg/day) for 10 days from the beginning of pacing. We measured hemodynamics, echo parameters, circulating neurohumoral factors at day 11. We also examined 182 gene profiles using RTPCR microarrays related to the NP system, fibrosis, growth factors, and inflammation in left atrium (LA) and kidney cortex (KC). Gene network, pathway, bio-function and comparison analysis were performed using Ingenuity Pathway Analysis (IPA) System. Results: The cenderitide group showed significantly less atrial and renal weights, higher cardiac output, glomerular filtration rate, and ejection fraction, and lower systemic vascular resistance and plasma renin activity without lowering mean arterial pressure (MAP) compared to untreated while the ACEi group lacked these effects with lower MAP. Gene profile analyses in LA and KC showed significant reverse effects on modulated genes in HF such as TNF-alpha, IL-1 beta, ROCK-2, caspase 7, Fas ligand, C-Myc and TP53 in the cenderitide group compared to untreated, which was not observed with ACEi. Network and pathway analysis revealed improvements with cenderitide in the LA and KC with improvements in global gene pathways specifically related to cell survival, cellular movement, and inflammatory/immune response, which were not observed or were less with ACEi. Conclusions: Continuous SQ infusion of the designer peptide cenderitide demonstrated superior beneficial effects on cardiorenal function and remodeling genes compared to ACE inhibition by reducing activated deleterious gene profiles in HF, suggesting key cardiorenal protective actions of cenderitide in the setting of HF.

038 Medicare Hospital Readmission Penalties: as Important as Life Itself Ahmad Abdul-Aziz1, Keith D. Aaronson1, Scott L. Hummel1,2; 1University of Michigan, Ann Arbor, MI; 2Ann Arbor Veterans Affairs Health System, Ann Arbor, MI Introduction: U.S. hospitals are penalized for excess 30-day readmissions in Medicare patients with heart failure (HF), pneumonia (PNA), and acute myocardial infarction (AMI). Readmission penalties, driven primarily by HF performance, are ten-fold greater than for excess mortality (≤3% vs. ≤0.3% of Medicare reimbursement). We investigated how penalties might change if the methodology equally weighted 30-day readmissions and mortality. Methods: We obtained publicly-reported hospital data for FY 2014: readmission penalties, Excess Readmission Ratio (ERR; ratio of riskadjusted predicted to expected 30-day readmissions), and 30-day mortality rates for HF, PNA, and AMI. An aggregate ERR for each hospital, weighted by number of cases, was calculated: ERRAGG = (#cases HF*ERRHF + #cases PNA*ERRPNA + #cases AMI*ERRAMI)/(total #cases). An Excess Mortality Ratio (EMR) was calculated for each condition/hospital by dividing the risk-adjusted predicted mortality by the national average mortality, with aggregate EMR (EMRAGG) analogous to ERRAGG. We created an “Excess Composite Outcome Ratio” (ECORAGG) by equally weighting readmission and mortality: ECOR AGG = (ERR AGG + EMR AGG )/2. We examined correlations between readmission penalties, ERRAGG, EMRAGG, and ECORAGG, and used analysis of variance to compare readmission penalties in hospitals with publicly reported “As, Worse than, or Better than Expected” 30-day mortality rates for HF, PNA, and AMI, and in hospitals with discordant performance by ERRAGG and ECORAGG. Results: In 1997 U.S. hospitals, readmission penalties closely tracked ERRAGG, but were minimally related to EMRAGG and modestly associated with ECORAGG (Figure A-C). As publicly reported HF mortality improved, readmission penalties increased in graded fashion (all inter-group comparisons P < .001; Figure D); there was no analogous relationship with PNA or AMI. 17% of hospitals had ERRAGG > 1 and were financially penalized for excess readmissions, yet had ECORAGG < 1, i.e. superior outcomes if mortality and readmissions were considered equally. Conversely, 16% of hospitals had ERRAGG < 1 and ECORAGG > 1, and received little or no financial penalty despite inferior combined mortality and readmissions. (Figure E–F, all intergroup P < .001) Conclusions: Risk-adjusted excess 30-day readmissions and deaths are weakly associated with each other and are differentially incentivized. Medicare penalties for one-third of U.S. hospitals would be substantially affected if readmissions and mortality were weighted equally. This appears to be a particularly important consideration for HF, the main driver of readmission penalties.

S16 Journal of Cardiac Failure Vol. 22 No. 8S August 2016 Patients with severe sepsis who have a prior history of heart failure receive less aggressive fluid resuscitation compared to those who do not.

040 Multi-Disciplinary Team Approach to Cardiogenic Shock Reduces in-Hospital Mortality Azam Hadi1, Sanjeeb Bhattacharya1, Irmina Gradus-Pizlo1, Holly Cook2; 1Indiana University, Indianapolis, IN; 2Indiana University Health, Indianapolis, IN

039 ICU Patients with Severe Sepsis Receive Less Aggressive Fluid Resuscitation if They Have a Prior History of Heart Failure Monique S. Tanna, Vincent Major, Simon Jones, Yin Aphinyanaphongs; NYU School of Medicine, New York, NY Introduction: Antimicrobials and aggressive fluid resuscitation are the mainstay of treatment of severe sepsis with current guidelines recommending early goal-directed therapy to target parameters of adequate perfusion. While the optimal fluid strategy in patients with sepsis-associated myocardial dysfunction or a pre-existing history of heart failure (HF) has not been defined, the current standard is to apply the same strategy to these patients. However, clinician bias may lead to less aggressive fluid resuscitation in practice and this may impact outcomes. Methods: This is a retrospective cohort study of adult ICU patients extracted from the Medical Information Mart for Intensive Care (MIMIC) III database. The inclusion criterion was patients with severe sepsis based on ICD-9 codes indicative of infection concurrent with new onset organ dysfunction who were admitted to an ICU within 24 hours of presentation, had an ICU stay of at least 24 hours and had a transthoracic echocardiogram performed during the hospitalization. Patients were divided into three cohorts: no history of HF and normal EF (No-HF), no history of HF and new systolic dysfunction (Sepsis-HF) and known prior systolic or diastolic HF (Pre-HF). Systolic dysfunction was categorized as mild (EF = 40– 50%), moderate (EF = 30–39%) or severe (EF < 30%). All statistical analyses were performed using R (Vienna, Austria). Results: From 2001–2012, there were 2765 patients who met inclusion criteria; 1604 in the No-HF cohort, 496 Sepsis-HF (216 mild, 134 moderate, 146 severe) and 665 Pre-HF (351 normal, 87 mild, 80 moderate, 147 severe).The Pre-HF cohort had a significantly higher OASIS severity of illness score (median score, 40 [IQR 33, 48]) compared to the No-HF group (39 [31, 47], P = .03), while OASIS scores in the Sepsis-HF cohort (42 [35, 49]) were significantly higher than both the No-HF (P < .001) and Pre-HF groups (P = .02). Compared to the NoHF cohort (13 [7, 19]), van Walraven Elixhauser comorbidity scores were significantly higher in both Sepsis-HF (15 [10, 22], P < .001) and Pre-HF (18 [13, 24], P < .001). Despite having higher severity of illness, total intravenous fluid administration over the first 24 hours of ICU admission was significantly lower in the Pre-HF group compared to the No-HF group (2914 [1364, 5381] mL vs. (4350 [2276, 7321] mL), P < .001). There was no difference among the Sepsis-HF (3873 [1989, 7060] mL) and No-HF groups (P = .09). In-hospital mortality was 21% and in a multivariable logistic regression model, was associated with the highest quintile of OASIS score (odds ratio (OR) 1.97 [95% CI 1.49–2.60]), Van Walraven Elixhauser score (OR 1.97 [95% CI 1.48– 2.61]) and total intravenous volume administered over the first 24 hours (OR 1.36 [95% CI 1.01–1.83]) after adjusting for age, sex and ejection fraction. Conclusions:

Introduction: Cardiogenic shock remains a high mortality condition with rates ranging between 40–50%. The aim of this study is to determine the effectiveness of a hospitalwide process improvement initiative labeled as Level One Cardiogenic Shock Rapid Response(analogous to an acute MI rapid response) that deploys a multi-disciplinary team enabling rapid mobilization of tertiary care institutional resources for the early recognition, coordination and treatment of patients with cardiogenic shock. The hypothesis was that this concerted approach results in decreased in-hospital mortality. Methods: Retrospective analysis of the pilot Level One Cardiogenic Shock Rapid Response program (protocol group) for patients (predominantly transfers from community hospitals to the tertiary center) from January 2014 to Dec 2015 comparing it to a similar but larger similar cardiogenic shock patient population that received standard response and therapy (control group) during the years prior i.e., Jan 2012 until Dec 2013. The program used a systems-based team approach that starts with activation of the pager for the on call Level One Cardiogenic Shock heart failure trained cardiologist who (when appropriate) advises activation of a burst page that alerts the ICU nurse, critical care physician, CV surgeon, level one shock coordinator, etc. This team immediately arrive at the patient’s bedside with the Level One Cardiogenic Shock cardiologist assuming primary responsibility and institutes rapid use of protocol-directed therapy; early support of ventilation and oxygenation; rapid institution of pharmacologic therapy i.e., inotropes and/or vasopressors; and disease specific triage to advanced mechanical interventions (when appropriate) including deployment of Impella, ECMO, VAD. The primary endpoint was in-hospital mortality. Secondary endpoint was utilization of advanced mechanical circulatory support i.e., Impella, ECMO, VAD. Results: 437 patients were in the control and 110 in the protocol group. Baseline characteristics were similar and etiology of cardiogenic shock (i.e., post MI, acute myocarditis, acute systolic heart failure, etc) were similar in both groups. The protocol group had significant reduction inhospital mortality i.e., 35% (38/110) vs. 45% (197/437) (P value < .05). The utilization of advanced mechanical support was significantly higher in the protocol group i.e., 30/ 110 vs. 55/437 in the control group (P value < .0003). Conclusion: Analogous to current practice in acute MI and Stroke, the activation of a coordinated rapid response team and early goal-directed therapy in an expedited appropriate manner for cardiogenic shock patients was associated with improved survival possibly reflecting appropriate/ aggressive utilization of resources including advanced mechanical circulatory therapy. The number needed to treat utilizing the protocol intervention was calculated at 10.