United Healthcare Update: Bundled Payments

Beginning January 1, 2020, Duke Heart, in partnership with United Healthcare, will begin bundled payments for two episodes of care, CABG and outpatient PCI procedures. This payment model will tie both physician and hospital payments to the quality and cost of services provided under one episode. The episode length will include the anchor stay or anchor procedure plus 90 days beginning the day of discharge. Clinical episodes are designed to include all services that occur within the episode and are covered under one payment.

We have an internal team currently working to plan next steps. Details regarding the bundled payments and any new processes required will be sent directly to physicians who have performed these procedures.

We have done care redesign in the past and look forward to continuing to work on innovating ways to deliver high quality care to our patients with precision payment mechanisms.

Retirement Party Held for Mary Walton

Mary L. Walton, BSN, RN, Cardiothoracic OR schedule manager, formally retired from Duke University Hospital on Friday, Dec. 6. The Duke Heart leadership team hosted a retirement party on Dec. 11 in the Searle Center to celebrate Mary’s 42 years with Duke. Thanks to all who were able to join us!

After completing nursing school, Walton worked briefly at several hospitals including the Medical College of Virginia, University of Tennessee Hospital and Baptist Memorial Hospital in Memphis. She chose to come to Duke University Hospital in September, 1977. Mary started as a staff nurse in the Acute Cardiac Unit (ACU) and was promoted to Assistant Nurse Manager on 3200. Mary remained on 3200 in the Asst. NM role, and later as a staff nurse, until she transitioned to the CTOR scheduling office in 2001.

“Duke has been a good place for me, always. I’ve enjoyed my time here and a lot has changed in 42 years,” Walton remarked. “I can honestly say it has been a privilege, an honor to work here at Duke with the cardiovascular and thoracic surgery team.”

During her years with Duke, she was able to take two trips to Nicaragua with the pediatric heart team and received the Heart Center Award for Excellence in Cardiovascular Nursing in 2000. Walton has been present for the launch of Duke’s Ventricular Assist Device (VAD) program as well as the start of the Duke Lung and Heart Transplant programs. She has even seen the heart transplant team reach a historic milestone just recently when they became the first U.S. team to perform a DCD adult heart transplant.

Originally from Memphis, Tenn., Mary will continue to live in Durham and is looking forward to traveling, visiting with friends, relaxing at her home and eventually participating in volunteer work at Duke. We are grateful for the many years she has worked to care for our patients and to support our surgical teams. Please join us in wishing her the very best!

Journal Club Held

Kevin Friede did a fantastic job presenting data from the recent NEJM publication “A Genotype-Guided Strategy for Oral P2Y12 Inhibitors in Primary PCI.

Many thanks to Deepak Voora for facilitating the discussion and hosting our fellows at his home.

 

 

 

 

 

Duke Heart Virtual Food Drive

Please consider contributing to the Duke Heart Virtual Food Drive to support the Food Bank of Central & Eastern North Carolina. We know it has been a challenging year for many people throughout our region. In the vein of gratitude and community spirit, we thought we’d offer an opportunity to collectively give back to the greater Durham community. For each dollar contributed this month, the Food Bank can purchase $10 worth of food for a family in need. The Duke Heart VFD will run until mid-January. Please help us help the Food Bank!

To contribute, please visit: http://secure.foodbankcenc.org/goto/dukeheart.

CVRC Mandel Scholar & Seed Awards Announced

We are excited to share with you that Robert McGarrah is this year’s Duke Cardiovascular Research Center’s Mandel Scholar awardee. Congratulations, Rob!

McGarrah’s winning proposal:

With the rate of obesity increasing each year, obesity-related diseases have come to the forefront of our nation’s health concerns. One such disease, that has no reliable treatment other than weight loss, is nonalcoholic fatty liver disease (NAFLD). NAFLD is the most common liver disease in the country and has been linked to abnormal heart function. However, how a disease in the liver can affect a distant organ like the heart is unknown. Over the past five years, our lab has made strides in answering this question.  We have found that obesity turns off a certain metabolism pathway in the liver, leading to NAFLD and also increasing the levels of specific amino acids (building blocks of proteins) in the blood. When these amino acids are delivered to the heart, they cause the heart to store more fat, which is unhealthy, and to make more protein, which can cause unhealthy heart muscle thickening. We believe that this liver-heart cross talk might explain why NAFLD causes abnormal heart function. This Mandel Research Scholar Award will be used to test this hypothesis.

Congratulations to the following researchers who have recently been named Mandel Seed Award recipients!

Neil J. Freedman and Christopher L. Holley for their project, Atherogenic Mechanisms of Small Nucleolar RNAs

Atherosclerosis fundamentally involves oxidation, a chemical process that occurs normally in healthy cells but, in excess, can derange the chemical structure of lipids and proteins and thereby adversely affect their function. The pathogenesis of atherosclerosis initiates with oxidation of the cholesterol-rich low-density lipoprotein particles, and perpetuates with excessive oxidative cell signaling— termed “oxidative stress”—in the inner layers of the artery.

This project aims to attenuate excessive oxidative signaling through a novel regulatory mechanism involving particular RNA molecules known as small nucleolar RNAs, or “snoRNAs”, which are expressed throughout the body’s cells. We have found a group of snoRNAs that augment cellular oxidative stress, and we hypothesize that by interfering with the function of these snoRNAs we can mitigate atherosclerosis. For this purpose we will use mice that lack these particular snoRNAs, or “sno-knockout” mice, to build on findings from the first year of Mandel Foundation support for this project. We will compare aortic and brachiocephalic artery atherosclerosis between atherogenic Apoe-/- mice that are either sno-knockout or control (which express normal levels of the snoRNAs).

We recently found that these snoRNAs promote chemical modification (methylation) of specific messenger RNAs. For this reason, we will determine which messenger RNAs are modified by our snoRNAs in smooth muscle cells and macrophages, to discern possible molecular mechanisms by which these snoRNAs exacerbate oxidative stress in cells and thereby aggravate atherosclerosis. Novel results from these studies may ultimately have therapeutic implications for patients with atherosclerosis.

Ravi Karra, collaborating with Christopher Kontos for their project, Modeling the myovascular niche using human induced pluripotent stem cells:

The heart is made up multiple cell types including muscle cells, called cardiomyocytes, and cells that line the blood vessels, called endothelial cells. Cardiomyocytes and endothelial cells are tightly coupled and make up myovascular niches within the heart. Interactions between cardiomyocytes and endothelial cells are critical to heart development, heart function, and the progression of heart failure. Thus, a better understanding of how cardiomyocytes and endothelial cells interact can lead to new treatments for cardiovascular disease. Here, we present work to develop an in vitro model of the myovascular niche and to identify novel mechanisms for regulating cardiac growth and regeneration.

Sudha Shenoy collaborating with Jonathan Campbell for their project, The role of ubiquitination in glucagon-induced signaling bias and insulin secretion:

Type 2 diabetes (T2D) and associated insulin resistance contribute to the etiology of atherosclerosis and constitute major risk factors leading to morbidity and mortality from cardiovascular disease. The peptide hormone glucagon and the class B seven-transmembrane G protein-coupled receptors that are activated by glucagon play a fundamental role in regulating blood glucose levels. These receptors, namely the glucagon receptor (GCGR) and the glucagon-like peptide 1 receptor (GLP-1R) also regulate insulin release from pancreatic beta cells and are currently major targets for developing new treatments and drugs for T2D.

Glucagon binding elevates the second messenger cAMP through the activation of G proteins, and furthermore, the activated receptors are subjected to desensitization and internalization through recruitment of additional proteins, namely, GPCR kinases, ꞵ-arrestin and RAMPs. GLP-1R agonists enhance insulin secretion and reduce food intake, which promotes glucose lowering and reductions in body weight in patients with T2D. Glucagon agonists also increase satiety and induce energy expenditure, suggesting the combination of GCGR and GLP-1R agonism could have additive effects on weight reduction and further improve glycemia. Consequently, the GCGR is an emerging target in anti-diabetic therapy, particularly in the development of GCGR/GLP-1R co-agonists. However, there still remains an incomplete understanding of the signaling mechanisms invoked by either the GCGR or the GLP-1R, which limits the drug discovery to tackle T2D and associated morbidity.

In this context, we have now identified that GCGR is subjected to ubiquitin-dependent regulation. Ubiquitin is a small protein that acts as a signaling code when appended to active protein complexes. Our data suggests that ubiquitination of the GCGR increases signaling through G proteins, whereas ligand binding causes de-ubiquitination, leading to decreased G protein coupling and increased ꞵ-arrestin binding and activity. There is limited information on the regulation of GLP-1R by ubiquitination. Thus, our studies will test the role of GCGR and GLP-1R ubiquitination in the propagation of signaling via these transducers and identify the molecular mechanism(s) that link ubiquitin-dependent signaling to cellular function.

Duke Heart Holiday Gathering Held

Thanks to those of you who were able to join us at the Washington Duke Inn on Dec. 6 for our annual holiday gathering!

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Upcoming Opportunities/Save the Date:

Cardiology Grand Rounds

This week we are holding our final faculty meeting of the year. Please join us!

Upcoming Grand Rounds:

• December 24: No Grand Rounds. Happy Holidays!
• December 31: No Grand Rounds. Happy Holidays!

 

Have news to share?

If you have news to share with the Pulse readership, please contact Tracey Koepke, director of communications for Duke Heart at tracey.koepke@duke.edu. We would love to hear about your latest accomplishments, professional news, cool happenings, and any events or opportunities that may be of interest to our Duke Heart family. Please call with any questions: 919-681-2868. Feedback on Pulse is welcome and encouraged.

 

Duke Heart in the News:

 

December 6 — Manesh Patel

Pharmacy Times

Causes of Drug Shortages in the United States

https://www.pharmacytimes.com/insights/implications-of-potential-heparin-shortage/causes-of-drug-shortages-in-the-united-states

 

December 9 – Duke mention

The Columbus Dispatch

Ohioan’s adult heart becomes first in US history donated after circulatory death

https://www.dispatch.com/news/20191209/ohioanrsquos-adult-heart-becomes-first-in-us-history-donated-after-circulatory-death

 

December 10 — John Alexander

Medpage Today

FDA Panel Shoots Down Afib Cardioversion Drug Over Safety

medpagetoday.com/cardiology/arrhythmias/83816

 

December 11 — Albert Sun

Washington Post

A genetic mutation is associated with increased risk of heart failure in black people, study finds

https://www.washingtonpost.com/health/2019/12/11/genetic-mutation-is-associated-with-increased-risk-heart-failure-black-people-study-finds/

 

December 11 — Ann Marie Navar

Healthcare Finance News

Ensuring that new health tech doesn’t widen health inequity gaps

https://www.healthcarefinancenews.com/video/ensuring-new-health-tech-doesnt-widen-health-inequity-gaps

 

December 11 — Chiara Melloni

Healio/Cardiology Today

Type 2 MI confers elevated risk for death within 1-year follow-up

https://www.healio.com/cardiology/vascular-medicine/news/online/%7B9cc19f33-d5dc-481f-b586-cb108b423b64%7D/type-2-mi-confers-elevated-risk-for-death-within-1-year-follow-up

 

December 11 — Jessica Lunsford-Avery (psychiatry)

Medpage Today

Long Naps, Lots of Sleep Tied to Higher Stroke Risk

https://www.medpagetoday.com/neurology/strokes/83836

 

December 11 — Haider Warraich (alum)

ABC News

More Americans are dying at home rather than in hospitals

https://abcnews.go.com/Health/wireStory/americans-dying-home-hospitals-67672995

 

December 12 — Chetan Patel

Medscape

Duke Doctors Successfully Transplant ‘Resuscitated’ Heart

https://www.medscape.com/viewarticle/922558

 

December 12 — Adam DeVore

Medpage Today

Entresto Holds Up in the Real World … But Not for Everyone

https://www.medpagetoday.com/cardiology/chf/83862

 

December 13 — Dan Mark

TCTMD/the heart beat

EXCEL Investigators Respond to Data Suppression Claims as Debate Erupts Online

https://www.tctmd.com/news/excel-investigators-respond-data-suppression-claims-debate-erupts-online