Literature DB >> 30167551

The Affordable Care Act's Hospital Readmissions Reduction Program: Has the Biology Had Time to Catch Up With the Regulation?

Douglas L Mann1, Gordon F Tomaselli2.   

Abstract

Entities:  

Year:  2016        PMID: 30167551      PMCID: PMC6113532          DOI: 10.1016/j.jacbts.2016.10.004

Source DB:  PubMed          Journal:  JACC Basic Transl Sci        ISSN: 2452-302X


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The Hospital Readmissions Reduction Program (HRRP), which was established by the Affordable Care Act in 2012, requires that the Centers for Medicare & Medicaid Services reduce Medicare fee-for-service hospital readmission rates for conditions that account for expensive, high-volume admissions and frequent readmissions. The goal of HRRP is to improve the quality of health care and to lower health care costs by imposing penalties on hospitals deemed to have “excess readmissions.” Two of the 5 areas that were targeted for initial evaluation include cardiovascular diseases that affect millions of Americans, namely acute myocardial infarction and heart failure. Coronary artery bypass grafting is expected to be added to HRRP in FY 2017. In 2016, only 799 (24%) of more than 3,400 hospitals that are subject to the HRRP performed well enough on the Center for Medicare Services 30-day readmission program to avoid a penalty. Thus, HRRP will clearly have a significant negative financial impact on health care systems in this country. Although few people would dispute that reducing readmissions is an important way to lower health care spending, the critical question is whether HRRP will improve the quality of cardiovascular care for patients. As will be discussed below, it is not at all clear at this time that hospital readmissions are a valid surrogate measure for the quality of patient care in hospital. First, not all readmissions can or should be prevented; some readmissions are required as part of high-quality, good clinical care. Second, several recent studies have highlighted that hospitals with greater adherence to recommended care processes did not achieve meaningfully better 30-day hospital readmission rates compared with those with lower levels of performance 1, 2, 3. Moreover, in some instances, decreased 30-day rehospitalization rates have been associated with a trend toward paradoxically higher 1-year mortality (3). Finally, there are many other sociodemographic factors that are beyond a hospitals’ control, such as poverty and lack of access to community support services, that can also lead to increased risk of readmission. In addition to these social determinants of health, there is another fundamentally important issue that is seldom discussed in health care economics, which is that concept of impaired biological cardiovascular reserve in patients with heart disease. Here, we share several thoughts on this important issue. Any discussion of impaired biological reserve in Medicare patients must begin with a brief mention of the biology of aging and frailty. Aging has been defined as the time-dependent decline and deterioration of functional properties at the molecular, cellular, tissue, and organ levels that lead to a loss of homeostasis, which in turn is accompanied by decreased adaptability to stress and a concomitant increased vulnerability to disease (4). One extremely important phenotypic expression of biological aging is frailty, wherein small deficits accumulate, which may be insignificant individually, but in aggregate lead to increased susceptibility to disease. As noted by Fried et al. (5): “frailty can be defined as a physiologic state of increased vulnerability to stressors that results from decreased physiologic reserves, and even dysregulation, of multiple physiologic systems. This decreased reserve results in difficulty maintaining homeostasis in the face of perturbations.” Thus, aging and frailty lead to impaired biological reserve in the patient population that is most affected by HRRPs penalty plan for excessive readmissions. Above and beyond the biological issues of aging and frailty, the extant basic and clinical published reports suggests that the way in which the heart responds to stress may also contribute to impaired biological reserve. Experimental studies have shown that the myocardial response to injury is accompanied by a coordinated down-regulation of metabolic pathways, signaling pathways, and pathways that are critical to cardiac performance 6, 7. Although resolution of myocardial injury and recovery of cardiac function are often accompanied by a reversal of some of the abnormalities in cardiac transcriptional programs (e.g., calcium signaling and mitogen-activated protein kinases), the extant experimental and clinical literature suggests that many of the gene programs that become perturbed following cardiac injury remain persistently dysregulated and further perpetuate their effects by post-transcriptional mechanisms (8), which has been associated with increased vulnerability to a subsequent hemodynamic stress (7). Importantly, this vulnerability diminishes over time as more complete normalization of abnormal myocardial biology occurs (7). Although direct correlations between relatively short-term experimental studies in mice and long-term observations in the humans are not appropriate, these types of experimental observations combined with the current knowledge with respect to the biology of aging/frailty, do raise the important question of whether one can place an arbitrary time limit on how long it will take patients with impaired biological reserve to recover following an episode of decompensation requiring a hospitalization. Importantly, loss of biological reserve does not lend itself readily to statistical risk adjustment models, because unlike known demographic factors that can modeled statistically, impaired biological reserve and its recovery are poorly understood and hence less quantifiable. If recurrent hospitalizations are not a function of inadequate care and are driven, at least in part, by impaired biological cardiovascular reserve, one needs to ask whether it is reasonable to penalize health care systems for readmitting patients, particularly when recurrent hospitalization may be the only means to stabilize certain patients, as suggested by several clinical studies 9, 10. As with most things in health care, it is far easier to be critical than it is to be constructive, and it is not our intent to be critical of the Affordable Care Act, which has led to many positive changes in overall health care coverage for Americans. However, on the basis of the arguments raised in the preceding paragraphs, we believe that it is time to critically revaluate HRRP’s policy on excess readmissions in an effort to develop programs focused on short-term readmissions that are cost effective and that lead to improved clinical outcomes. This does not necessarily mandate the need for longer acute care hospitalizations; instead, we should focus on more intensive care in the ambulatory setting such as a bridge clinic or day hospital to monitor and support the recovery of sufficient biological reserve. Further, we believe that more research is critically needed to characterize the mechanistic underpinnings of impaired biological reserve, including optimal ways to measure it and its importance in determining functional outcomes and survival following hospitalization As always, we welcome your thoughts, and would ask you to share your opinions on the issue of impaired myocardial biological reserve and HRRP’s 30-day readmission program, either through social media (#JACCBTS) or by e-mail (JACCBTS@acc.org).
  10 in total

Review 1.  Untangling the concepts of disability, frailty, and comorbidity: implications for improved targeting and care.

Authors:  Linda P Fried; Luigi Ferrucci; Jonathan Darer; Jeff D Williamson; Gerard Anderson
Journal:  J Gerontol A Biol Sci Med Sci       Date:  2004-03       Impact factor: 6.053

2.  Is rehospitalization after heart failure admission a marker of poor quality? Time for re-evaluation.

Authors:  Christopher M O'Connor; Mona Fiuzat
Journal:  J Am Coll Cardiol       Date:  2010-07-27       Impact factor: 24.094

Review 3.  A systematic review and meta-analysis on the association between quality of hospital care and readmission rates in patients with heart failure.

Authors:  Claudia Fischer; Ewout W Steyerberg; Gregg C Fonarow; Theodore G Ganiats; Hester F Lingsma
Journal:  Am Heart J       Date:  2015-07-18       Impact factor: 4.749

4.  The biology of aging and frailty.

Authors:  Neal S Fedarko
Journal:  Clin Geriatr Med       Date:  2011-02       Impact factor: 3.076

5.  Dynamic gene expression patterns in animal models of early and late heart failure reveal biphasic-bidirectional transcriptional activation of signaling pathways.

Authors:  Janelle Rowell; Norimichi Koitabashi; David A Kass; Andreas S Barth
Journal:  Physiol Genomics       Date:  2014-08-26       Impact factor: 3.107

6.  Functional significance of the discordance between transcriptional profile and left ventricular structure/function during reverse remodeling.

Authors:  Veli K Topkara; Kari T Chambers; Kai-Chien Yang; Huei-Ping Tzeng; Sarah Evans; Carla Weinheimer; Attila Kovacs; Jeffrey Robbins; Philip Barger; Douglas L Mann
Journal:  JCI Insight       Date:  2016-04-06

7.  Association of 30-Day Readmission Metric for Heart Failure Under the Hospital Readmissions Reduction Program With Quality of Care and Outcomes.

Authors:  Ambarish Pandey; Harsh Golwala; Haolin Xu; Adam D DeVore; Roland Matsouaka; Michael Pencina; Dharam J Kumbhani; Adrian F Hernandez; Deepak L Bhatt; Paul A Heidenreich; Clyde W Yancy; James A de Lemos; Gregg C Fonarow
Journal:  JACC Heart Fail       Date:  2016-12       Impact factor: 12.035

8.  Divergent trends in survival and readmission following a hospitalization for heart failure in the Veterans Affairs health care system 2002 to 2006.

Authors:  Paul A Heidenreich; Anju Sahay; John R Kapoor; Michael X Pham; Barry Massie
Journal:  J Am Coll Cardiol       Date:  2010-07-27       Impact factor: 24.094

9.  Hospital performance measures and 30-day readmission rates.

Authors:  Mihaela S Stefan; Penelope S Pekow; Wato Nsa; Aruna Priya; Lauren E Miller; Dale W Bratzler; Michael B Rothberg; Robert J Goldberg; Kristie Baus; Peter K Lindenauer
Journal:  J Gen Intern Med       Date:  2012-10-16       Impact factor: 5.128

10.  Key pathways associated with heart failure development revealed by gene networks correlated with cardiac remodeling.

Authors:  Zhong Gao; Andreas S Barth; Deborah DiSilvestre; Fadi G Akar; Yanli Tian; Antti Tanskanen; David A Kass; Raimond L Winslow; Gordon F Tomaselli
Journal:  Physiol Genomics       Date:  2008-09-09       Impact factor: 3.107

  10 in total

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