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Heart Failure: Interventions to Reduce Morbidity, Mortality, and Hospitalizations

  • Authors: Clyde W. Yancy, MD; William T. Abraham, MD; Anne B. Curtis, MD
  • CME/CE Released: 10/1/2013; Reviewed and Renewed: 10/9/2014
  • Valid for credit through: 10/9/2015
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Target Audience and Goal Statement

This activity is intended for heart failure specialists, electrophysiologists, general cardiologists, internists, critical care specialists, nurses, nurse practitioners, and physician assistants who care for patients at risk for sudden cardiac death.

The goal of this activity is to update clinicians' awareness of management techniques to address the risks of decompensation and sudden cardiac arrest in patients with heart failure.

Upon completion of this activity, participants will be able to:

  1. Analyze how decompensation and/or sudden cardiac arrest affect heart failure morbidity and mortality
  2. Review management techniques aimed at preventing decompensation and sudden cardiac arrest in patients with heart failure


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  • Clyde W. Yancy, MD

    Magerstadt Professor of Medicine, Chief of Cardiology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois


    Disclosure: Clyde W. Yancy, MD, has disclosed no relevant financial relationships.

    Dr Yancy does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States.

    Dr Yancy does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

  • William T. Abraham, MD

    Professor of Internal Medicine; Director, Division of Cardiovascular Medicine; Deputy Director, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio


    Disclosure: William T. Abraham, MD, has disclosed the following relevant financial relationships:
    Served as an advisor or consultant for: Abbott Laboratories; BIOTRONIK; Medtronic, Inc.; Novartis Pharmaceuticals Corporation; Respicardia, Inc.; St. Jude Medical; Sunshine Heart, Inc.; Zoll Medical Corporation

    Dr Abraham does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States.

    Dr Abraham does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.

  • Anne B. Curtis, MD

    Charles and Mary Bauer Professor and Chair, Department of Medicine, University at Buffalo, Buffalo, New York; President and CEO, UBMD Internal Medicine, Amherst, New York


    Disclosure: Anne B. Curtis, MD, has disclosed the following relevant financial relationships:
    Served as an advisor or consultant for: Biosense Webster, Inc.; Bristol-Myers Squibb Company; Daiichi Sankyo, Inc.; Medtronic, Inc.; Ortho-McNeil-Janssen Pharmaceuticals, Inc.; Sanofi; St. Jude Medical; Pfizer Inc
    Served as a speaker or a member of a speakers bureau for: Medtronic, Inc.; St. Jude Medical

    Dr Curtis does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by the FDA for use in the United States.

    Dr Curtis does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by the FDA for use in the United States.


  • Ronald K. Miller, PhD

    Scientific Director, Medscape, LLC


    Disclosure: Ronald K. Miller, PhD, has disclosed no relevant financial relationships.

Steering Committee

  • Deepak L. Bhatt, MD, MPH

    Chief of Cardiology, VA Boston Healthcare System; Senior Physician, Brigham and Women's Hospital; Professor of Medicine, Harvard Medical School; Senior Investigator, TIMI Study Group, Boston, Massachusetts


    Disclosure: Deepak L. Bhatt, MD, MPH, has disclosed the following relevant financial relationships:
    Received grants for clinical research from: AstraZeneca Pharmaceuticals LP; Bristol-Myers Squibb Company; Eisai Inc.; Ethicon, Inc.; Medtronic, Inc.; sanofi-aventis; The Medicines Company; Medtronic, Inc.

  • Roberta C. Bogaev, MD

    Assistant Professor of Medicine, Baylor College of Medicine, Houston, Texas; Private Practice Cardiologist, Schnitzler Cardiovascular Consultants, San Antonio, Texas


    Disclosure: Roberta C. Bogaev, MD Roberta C. Bogaev, MD, has disclosed no relevant financial relationships.

  • Ted E. Feldman, MD

    Professor of Medicine, Northwestern University School of Medicine, Evanston, Illinois


    Disclosure: Ted E. Feldman, MD, has disclosed the following relevant financial relationships:
    Served as an advisor or consultant for: Abbott Laboratories; Boston Scientific; Coherex Medical, Inc.; Edwards Lifesciences; Intervalve; Daiichi Sankyo, Inc.; Eli Lilly and Company; W.L. Gore & Associates, Inc.
    Served as a speaker or a member of a speakers bureau for: Boston Scientific Received grants for clinical research from: Abbott Laboratories; Boston Scientific; Edwards Lifesciences; St. Jude Medical; W.L. Gore & Associates, Inc.

  • Jagmeet P. Singh, MD, PhD

    Associate Professor of Medicine, Cardiac Arrhythmia Service, Massachusetts General Hospital Heart Center, Harvard Medical School, Boston, Massachusetts


    Disclosure: Jagmeet P. Singh, MD, PhD, has disclosed the following relevant financial relationships:
    Served as an advisor or consultant for: BIOTRONIK; Boston Scientific; Medtronic, Inc.; St. Jude Medical; Sorin Group; CardioInsight Technologies Inc.; Thoratec Corporation
    Served as a speaker or a member of a speakers bureau for: BIOTRONIK; Boston Scientific; St. Jude Medical; Sorin Group
    Received grants for clinical research from: BIOTRONIK; Boston Scientific; St. Jude Medical; Sorin Group; Medtronic, Inc.

CME Reviewer(s)

  • Nafeez Zawahir, MD

    CME Clinical Director, Medscape, LLC


    Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

  • Laurie E. Scudder, DNP, NP

    Clinical Editor, Continuing Professional Education Department, Medscape, LLC; Clinical Assistant Professor, School of Nursing and Allied Health, George Washington University, Washington, DC


    Disclosure: Laurie E. Scudder, DNP, NP, has disclosed no relevant financial relationships.

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Heart Failure: Interventions to Reduce Morbidity, Mortality, and Hospitalizations

Authors: Clyde W. Yancy, MD; William T. Abraham, MD; Anne B. Curtis, MDFaculty and Disclosures

CME/CE Released: 10/1/2013; Reviewed and Renewed: 10/9/2014

Valid for credit through: 10/9/2015


  • Clyde W. Yancy, MD: Hello, welcome. My name is Dr Clyde Yancy, chief of cardiology, Northwestern University in Chicago, Illinois, and I am delighted to be the host for today's program titled "Heart Failure: Interventions to Reduce Morbidity, Mortality, and Hospitalizations." I am absolutely thrilled to share this information with you today because I am joined by two of my close friends and colleagues with whom I have collaborated over the years, and for whom I have tremendous respect. First is Dr Bill Abraham, chief of cardiology at The Ohio State University in Columbus, and the second is Dr Anne Curtis, who is the chair of medicine at the University of Buffalo, State University of New York. Guys, it is a delight to be able to have this conversation with you.

    We are talking about heart failure (HF) -- or left ventricle (LV) dysfunction -- and we will paint a portrait of the factors that can reduce the burden of disease, morbidity, mortality, and hospitalizations in these patient. It is interesting that one of our guests represents electrophysiology and the other device therapies in HF, and let's say I represent medical therapy.

    To start, let's summarize what is considered state-of-the-art treatment to reduce morbidity and mortality in patients who have HF and have recently been hospitalized. Bill, why don't you start, and tell us where device therapies fall in this construct.

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  • William T. Abraham, MD: The foundation for any device-based therapy in HF is optimal medical therapy. We first want to optimize neural hormonal inhibitors and antagonists. There are angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), β-blockers, and now, included in the new American College of Cardiology Foundation/American Heart Association guidelines, an increased mandate for aldosterone antagonists.[1] The guidelines re-evaluate patients and consider the appropriateness and timing for device therapies such as implantable cardiac defibrillators (ICDs) or cardiac resynchronization (CRT) devices.

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  • Dr Yancy: Sudden cardiac death (SCD) continues to be a nagging concern, despite better use of medical therapies. We can attenuate the risk of death due to pump failure, but SCD is still our nemesis in this disease process. How do we assess SCD risk and how do we modify that risk for patients hospitalized with HF?

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  • Anne B. Curtis, MD: The cornerstone of HF is always the ejection fraction (EF), and with systolic HF we always measure the EF so we have a benchmark. The key questions when a patient is hospitalized with HF are: Have they been on optimal medical therapy already? Can the therapy be optimized? The answers can give you a sense of whether this is a new diagnosis of HF or the patient has been diagnosed with chronic HF, and what your expectation can be of improvement of the EF. If it is a recent diagnosis, we are obliged, for good reasons, to optimize medical therapy, to see how much recovery there might be over the next few months. If patients have been treated before or if we know they have a long history of HF, we might think about device therapy, and whether an ICD is appropriate.

    The risk for any individual patient in the short term is low, but it is real. We do not want to lose a patient while we are treating them, and we try to ensure that they have the best possible functional capacity and quality of life.

    Dr Yancy: We have a robust armamentarium from which we can make wise choices that can dramatically modify the natural history of patients with HF. Bill, you made reference to the new ACCF/AHA guidelines. I had the privilege of chairing the committee that wrote those guidelines. We established the nomenclature of guideline-directed medical therapy, with an emphasis on the importance of exercising the right decision at the right time for each individual patient because it makes a substantial difference in outcomes.[1] All 3 of us are aware of the incredible progress made over the last decade and a half that has taken the prospects of better survival and better quality of life for the patient with HF to another level. But let's drill down a little further, because it sounds like we know exactly what to do now for patients with HF, and we can go home and start working on something else. In fact, there are real challenges in treating HF.

    Anne, let's start with you this time. You spoke about monitoring LV function and waiting for it to recover. Most electrophysiologists are anxious to implant an ICD device in the patient. I would appreciate your thoughts on this issue. One of the sticking points we face right now is timing. When have we given medical therapy enough time to work? When are we comfortable that the EF has improved? How clear is it that the EF really is the signal, or is there something else that ought to be part of the decision-making process? Let's address 2 important issues, the first of which is timing.

  • Slide 4.

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  • Dr Curtis: The guidelines recommend at least 3 months of optimal medical therapy for a patient with HF. This is especially true for a newly-diagnosed patient, because some patients can improve with this treatment.[1,2]

    Dr Yancy: Dr Curtis, you do a consult on a patient who has an EF of 29%? The patient has had a recent MI. What do you do? How do you instruct your house staff? The patient is on a small dose of an evidenced-based β-blocker, ACE, or ARB, and aldosterone antagonist.

  • Slide 5.

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  • Dr Curtis: When you have a patient who has had an acute MI -- and of course, heart failure and MIs go together -- but if you are specifically talking about a new patient who has a large transmural MI with an EF of 29%, you need to start therapy. You cannot keep them in the hospital while they are hopefully recovering, so you need to consider a wearable cardioverter-defibrillator (WCD) because the patient is at high risk early on after an MI. The guidelines say not to implant an ICD right away in those patients because there are clinical trials that show ICDs do not provide benefit.[3]

  • Slide 6.

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  • We have to do something temporarily while optimizing medical therapy and we see how much recovery there is actually going to be.

    Dr Yancy: That is an interesting possibility. We are dealing with LV dysfunction treated medically where there is some anxiety about the risk of SCD. One option is a WCD. Bill, what are the options from a medical standpoint? Here is someone who is in that, if you will, blinking period, where we know that ICDs do not save lives, even though they reduce SCD events. Overall there is no reduction in mortality. ICDs are not an indicated therapy for the first 40 days after an MI. What are the indicated medical therapies in this scenario?

  • Slide 7.

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  • Dr Abraham: The indicated medical therapies are evidence-based and quite clear. The mainstays are the neural hormonal inhibitors. You mentioned this patient was on a low dose of a β-blocker. I would certainly work aggressively to optimize the β-blocker dose to a target level proven to be effective in randomized controlled trials, or at least get as close to that dose as the patient can tolerate. Also make sure the patient is on an evidence-based dose of an ACE inhibitor or an ARB, and add an aldosterone antagonist to that regimen.

  • Slide 8.

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  • We know that there is a reasonably good chance that 2 things will happen; first, the ventricle may recover or undergo reverse remodeling, and a few months later the EF might be 35% or 40%. There may no longer be an indication for an implantable device. Second, during that vulnerable period these drugs reduce the risk of SCD and the risk of overall mortality.

    Dr Yancy: This is a great conversation. Every practitioner in our field has encountered patients with residual LV dysfunction after an MI, and we are concerned about the real risks, the most tragic of which would be SCD. I agree with your message: adhere to the medical therapies and constantly monitor changes in LV function. But we still have a patient who has an uncertain future. Bill, say you come to see the patient who is already on an effective dose of an evidence-based β-blocker, an aldosterone antagonist, and an ACE or ARB. EF is 29%. There are ambient ventricular rhythm disturbances, and it is early on after the patient's MI. Do the ambient ventricular rhythm disturbances influence your decision-making? Give me both your gut answer and your intellectual answer.

  • Slide 9.

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  • Dr Abraham: The intellectual answer is that ventricular rhythm disturbances are not necessarily predictive of future events or SCD. At a gut level, this scenario creates anxiety. I worry about these patients, especially young patients with young families who have had a recent event or are on good therapy but continue to exhibit quite a bit of ventricular ectopic activity. I worry about them, whether the data supports it or not. I would consider the option Anne already mentioned, a WCD, in these patients.

  • Slide 10.

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  • I look at that device as a bridge.

  • Slide 11.

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  • Recent data from Andrew Epstein and others suggest that WCDs can be effective during the 40-day or 3-month period following an MI or an MI with revascularization, although the need for them is relatively limited; only about 1.4% of patients will receive an appropriate shock.[5] The problem is I do not know who the 1.4% are.

    Dr Yancy: I want to get back to the issue of risk, because it is unquestionable. We all know which medical therapies to initiate in our patients with reduced EF, even in the setting of HF after a recent infarct. It is deciding how to modify the risk of SCD that causes great anxiety. It is more than just the EF that we are interested in -- it is the status of the coronary disease. There is new evidence about late enhancement on cardiac MRI. Are there ways we can be more confident about correctly assessing this risk, or is it just about the EF?

  • Slide 12.

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  • Dr Curtis: More people have made their careers in academic medicine trying to figure this one out. Many different kinds of risk stratifiers have been used: viability of tissue; T-wave alternans testing; and electrophysiologic studies, which went out of fashion years ago because they were not predictive. We always seem to come back to the EF as the key discriminator to determine whether a patient is at risk, and that method is not perfect. This is one of the key messages: If we could predict who was going to wind up in sudden cardiac arrest, we would implant a lot fewer ICDs. We have to protect patients. The numbers are small, but we want to save lives.

    Dr Yancy: It does drive you batty because you might have a patient with a 29% EF and think an ICD is indicated after you have optimized therapy. Then you have a patient with a 36% EF, and an ICD is not indicated. The difference between 29% and 36% on an echocardiogram is a function of how much coffee you had that morning when reading the echocardiogram. The point is that we have to exercise a lot of clinical judgment and bedside acumen because we do not have the confidence we would like in either our markers or our therapies.

    I am trying to make sure we have some great take-home messages for the clinicians who are seeing the type of patients we are talking about today. In patients with LV dysfunction in whom we are trying to address the risk of SCD, I restate that they need to be on guideline-directed medical therapy, evidence-based β-blockers, ACEs or ARBs, and aldosterone antagonists. We also need to provide the clinician with a summary of how to assess the risk and understand when an ICD is indicated.

    Dr Curtis: I want to bring up another point regarding guideline-based medical therapy. Too often I see physicians put patients on tiny doses of β-blockers and a whiff of an ACE inhibitor and think they are providing guideline-based therapy. I think you both agree that is not what is intended.

    Dr Yancy: The doses have to be appropriate, no question.

    Dr Curtis: Yes. Then, the guidelines for device therapy for MIs specify a waiting period of 40 days and 3 months for HF, and so we are obliged to wait out those time periods. The waiting periods are partly based on the guidelines and partly based on what is considered appropriate use.[6] We have to get patients through the waiting period. If your gut tells you the patient is at risk, you can use a WCD in the meantime.

  • Slide 13.

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  • In a patient with a long history of HF, or if the patient has had previous infarcts and we know their EF is low, it may be reasonable to think about an ICD sooner. Again, you have to assess the patient and consider your options carefully.

    Dr Yancy: Bill, I want you to take this one to another level. We have been talking about the combination of appropriate guideline-directed medical therapy, assessing the risk for SCD, being aware of the timing for an ICD if indicated, and the possible benefit of using a WCD. You have been involved in yet another aspect of managing a patient with LV dysfunction in an outpatient setting -- the ability to use device platforms to enhance our knowledge and understand how the disease is progressing. For the benefit of our audience, what is considered state-of-the-art in this scenario? The right medical therapy, the right assessment of SCD risk, or the correct device therapy? How do we improve patient care?

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  • Dr Abraham: I see a major role for remote telemonitoring of HF patients. That begs the question: With what technology? What types of inputs are most valuable? Historically, we have monitored patients' symptoms, changes in daily weight, perhaps some vital signs. This is clearly useful, particularly in the setting of an HF disease management program. There are technologies that go beyond that: device-based diagnostics; the ability to get information on heart rate variability and patient activity; and intrathoracic impedance from implantable cardioverters, cardioverter defibrillators, and CRT devices. There are also, of course, investigational implantable hemodynamic monitors that give us direct access to and insight into the patient's state of hemodynamic compensation or decompensation.

    Frankly, we are still learning about all of these modalities. The totality of the data for device-based diagnostics suggests that they are good tools for risk stratification. They can tell us which patients are most likely to be hospitalized in the next 30 days. To date, interventions based on that information have not reduced the likelihood of HF or hospitalization, and no trials have looked at mortality. There are data that suggest that implantable hemodynamic monitors may be valuable as well; this is a rapidly emerging field.

    Dr Yancy: The neat thing about this is that it is a dynamic field, meaning that there are some things that are set in stone, some that are moving quickly, and others to which we are still seeking answers. We have addressed a lot of these issues today, like what really is the risk for SCD as suggested by EF, and definitive statements that we have all made about medical therapy and getting support for that from electrophysiologists.

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  • Then there is also the important dynamic of understanding where we need to be. Perhaps, where we need to be is with WCDs, so that we can completely manage patient risk and our anxieties. But we need to remember that a patient is at the center of all this, and we must to understand how they might respond to wearing a vest, and whether we giving are them the best way to deal with their anxiety. We need to understand the technology, but we need to understand other new technologies that might improve outcomes. Then we have to come back full circle to good old device therapy, because we still implant ICDs. The majority of them are there just in case, thankfully, but they represent sophisticated insurance policies. Maybe we can improve their reliability and understand that a little bit better.

    Although I think all discussions about HF are fascinating, this discussion has been particularly fascinating because you two represent leading-edge information sources who can help us better understand HF. What is the take-home message about LV dysfunction and SCD risk?

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  • Dr Curtis: You need to measure LV function and you need to assess whether or not the event in question is acute or chronic. If the patient has chronic HF or a chronic low EF, it may be time to implant an ICD. We did not talk much about cardiac resynchronization therapy, but that is something that should be in the mix. In the appropriate patient, this would be the right way to go, and making that decision and implanting the device when it is appropriate can improve on medical therapy and be truly life-saving.

    Dr Yancy: Bill, in summary, what are the take-home messages for an HF cardiologist dealing with a patient who has a reduced EF, HF, or post-MI dysfunction, and SCD risk. What are the "must do's"?

    Dr Abraham: While we continue to search for better predictors of mortality risk in these patients, the EF continues to be primary in assessment of LV function and reassessment after optimizing medical therapies. As we discussed, the foundation of treatment is optimal medical therapy and re-evaluation of LV structure and function. If an indication for device therapy persists after optimizing medical therapy, patients should receive an ICD or CRT device. There may be a role for WCDs as a bridging strategy in the interim for some patients.

    Dr Yancy: The only thing I will add to the information that you have both shared is that we have to remember that, ultimately, there is a patient at the center of all of this. One of the major themes that we have all had to revisit is how to interface with the patient differently, better, and how to make the patient part of the team. The whole concept of patient-centeredness revolves around what outcomes the patient desires, how they perceive the information provided, how can we can deliver the information differently, how can we get patients to be more invested, and how can we be certain that we are not imposing upon a patient? For some patients, feeling better is the most important issue, for others living as long as possible is what is important, and for others, having as few encumbrances to their lifestyle or as little disruption in their own economics is what is important. In today's world, we have to come back to the bedside or the chairside and say: How can we help you feel better? We need to listen carefully and then implement the right compliment of all these strategies.

    It has been a delight to participate in this program. Thank you both so much.

    Dr Abraham: Thank you.

    Dr Yancy: I want to thank you for your time and attention today. It has been a fabulous discussion, with good friends and colleagues, about important issues. I hope that the information we have shared with you has been of benefit.

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  • There are opportunities for CME, if you will simply follow the prompts on the screen as we sign off. Thank you once again for attending today's program, "Heart Failure: Interventions to Reduce Morbidity, Mortality, and Hospitalizations." Thank you very much.

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This transcript has been edited for style and clarity.

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