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      Strategies to Reduce Heart Failure Hospitalizations and Readmissions: How Low Can We Go?

      , 1

      Cardiovascular Innovations and Applications

      Compuscript

      heart failure, readmissions, strategies

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          Abstract

          It is estimated that more than one million heart failure hospitalizations occur each year. Systolic heart failure and heart failure with preserved ejection fraction contribute equally to heart failure hospitalizations. Heart failure readmission rates continue to be about 25%. Strategies to reduce heart failure readmission are key to reducing hospitalization rates. The strategies to reduce heart failure hospitalization are as follows: (1) During hospitalization, diuresis to the euvolemic state is essential. Fifty percent of discharged heart failure patients have minimal weight loss during the hospitalization, representing minimal diuresis, but still fluid overload. (2) During hospitalization, interrogate the defibrillator or biventricular pacemaker (if applicable) to ensure that there is no right ventricular pacing and there is appropriate biventricular pacing. Interrogation of devices can identify arrhythmia or suboptimal biventricular pacing, which can contribute to decompensation. (3) Before discharge, identify the reason for decompensation, such as atrial fibrillation, infection, pulmonary embolism, or noncompliance. (4) Before discharge a multidisciplinary team is needed to educate the patient on diet, medications, fluid weight surveillance, and exercise. (5) A postdischarge visit should occur within 10 days and with emphasis on uptitration of neurohormonal blockers and continued congestion management. Such interventions conducted by a multidisciplinary team have the potential to reduce heart failure hospitalization rates.

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          Most cited references 43

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          Congestive renal failure: the pathophysiology and treatment of renal venous hypertension.

          Longstanding experimental evidence supports the role of renal venous hypertension in causing kidney dysfunction and "congestive renal failure." A focus has been heart failure, in which the cardiorenal syndrome may partly be due to high venous pressure, rather than traditional mechanisms involving low cardiac output. Analogous diseases are intra-abdominal hypertension and renal vein thrombosis. Proposed pathophysiologic mechanisms include reduced transglomerular pressure, elevated renal interstitial pressure, myogenic and neural reflexes, baroreceptor stimulation, activation of sympathetic nervous and renin angiotensin aldosterone systems, and enhanced proinflammatory pathways. Most clinical trials have addressed the underlying condition rather than venous hypertension per se. Interpreting the effects of therapeutic interventions on renal venous congestion are therefore problematic because of such confounders as changes in left ventricular function, cardiac output, and blood pressure. Nevertheless, there is preliminary evidence from small studies of intense medical therapy or extracorporeal ultrafiltration for heart failure that there can be changes to central venous pressure that correlate inversely with renal function, independently from the cardiac index. Larger more rigorous trials are needed to definitively establish under what circumstances conventional pharmacologic or ultrafiltration goals might best be directed toward central venous pressures rather than left ventricular or cardiac output parameters.
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            Impact of a Novel Adaptive Optimization Algorithm on 30-Day Readmissions: Evidence From the Adaptive CRT Trial.

            This study investigated the impact of the Medtronic AdaptivCRT (aCRT) (Medtronic, Mounds View, Minnesota) algorithm on 30-day readmissions after heart failure (HF) and all-cause index hospitalizations.
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              Overview of randomised trials of angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure

               R. GARG,  S YUSUF,  R Garg (1995)
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                Author and article information

                Journal
                CVIA
                Cardiovascular Innovations and Applications
                CVIA
                Compuscript (Ireland )
                2009-8618
                2009-8618
                October 2015
                October 2015
                : 1
                : 1
                : 5-12
                Affiliations
                1University of Florida, Gainesville, FL, USA
                Author notes
                Correspondence: Juan M. Aranda, Jr., MD, FACC, Shands Hospital, 1600 SW Archer Road, P.O. Box 100277, Gainesville, FL 32610, USA, Tel.: +352-273-9078, Fax: +352-846-0314, E-mail: arandjm@ 123456medicine.ufl.edu
                Article
                cvia20150004
                10.15212/CVIA.2015.0004
                Copyright © 2015 Cardiovascular Innovations and Applications

                This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 Unported License (CC BY-NC 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. See https://creativecommons.org/licenses/by-nc/4.0/.

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