Addressing The Risk For Sudden Cardiac Death in Heart Failure (Printer-Friendly)

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CME/CE Information
CME/CE Released: 04/30/2013 ; Reviewed and Renewed: 06/16/2014 ; Valid for credit through 06/16/2015
Target Audience
This activity is intended for electrophysiologists, interventional cardiologists, cardiac surgeons, general cardiologists,
internists, critical care specialists, cardiology nurses, and other allied healthcare professionals.
Goal
The goal of this activity is to provide strategies with clinical tools and techniques to appropriately risk stratify and optimize
primary prevention strategies for patients at high risk of sudden cardiac death.
Learning Objectives
Upon completion of this activity, participants will be able to:
1. Identify persistent treatment gaps within the heart failure population
2. Evaluate potential mechanisms underlying the risk for sudden death and heart failure
3. Assess the role of implantable and wearable cardiac defibrillators to address the risk of sudden cardiac death in
patients with ischemic and nonischemic heart failure
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Faculty and Disclosures
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As an organization accredited by the ACCME, Medscape, LLC, requires everyone who is in a position to control the content of
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Moderator
Scott D. Solomon, MD
Professor of Medicine, Harvard Medical School; Director, Noninvasive Cardiology; Director, Cardiac Imaging Core Laboratory
and Clinical Trials Endpoints Center, Brigham and Womens Hospital, Boston, Massachusetts
Disclosure: Scott D. Solomon, MD, has disclosed the following relevant financial relationships:
Served as an advisor or consultant for: Novartis Pharmaceuticals Corporation; Sanofi; Zoll Medical Corporation; Amgen Inc.;
Abbott Laboratories; Theracos, Inc.; GlaxoSmithKline; Sandoz
Received grants for clinical research from: Sanofi; Amgen Inc.; Novartis Pharmaceuticals Corporation; Abbott Laboratories;
Boston Scientific
Dr Solomon 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 Solomon does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved by
Panelists
Philip B. Adamson, MD
Director, Heart Failure Institute at Oklahoma Heart Hospital; Director, Oklahoma Foundation for Cardiovascular Research;
Adjunct Associate Professor of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
Disclosure: Philip B. Adamson, MD, has disclosed the following relevant financial relationships:
Served as an advisor or consultant for: Medtronic, Inc.; St. Jude Medical; CardioMEMS; Cardiologic Innovations, CVRx, Inc.;
Sensible Medical Innovations
Served as a speaker or a member of a speakers bureau for: Medtronic, Inc.; St. Jude Medical; CardioMEMS; Cardiologic
Innovations; CVRx, Inc.; Sensible Medical Innovations; Actelion Pharmaceuticals, Ltd.
Dr Adamson does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by
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Dr Adamson does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved
by the FDA for use in the United States.
Paul Hauptman, MD
Professor of Internal Medicine, Division of Cardiology; Assistant Dean, Clinical and Translational Research, Saint Louis
University School of Medicine, St. Louis, Missouri
Disclosure: Paul Hauptman, MD, has disclosed the following relevant financial relationships:
Served as an advisor or consultant for: BioControl Medical; Otsuka Pharmaceutical Co., Ltd.
Served as a speaker or a member of a speakers bureau for: Otsuka Pharmaceutical Co., Ltd.
Received grants for clinical research from: Celladon
Dr Hauptman does not intend to discuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approved by
Dr Hauptman does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics not approved
by the FDA for use in the United States.
Editor
Ronald K. Miller, PhD
Scientific Director, Medscape, LLC

Disclosure: Ronald K. Miller, PhD, has disclosed no relevant financial relationships.
Acute MI 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:
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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
Nafeez Zawahir, MD
CME Clinical Director, Medscape, LLC

Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.
Nurse Planner
Laurie E. Scudder, DNP, NP
Nurse Planner, 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.
From Medscape Education Cardiology
Addressing the Risk for Sudden Cardiac Death in Heart

Failure CME/CE
Scott D. Solomon, MD; Philip B. Adamson, MD; Paul Hauptman, MD
CME/CE Released: 04/30/2013 ; Reviewed and Renewed: 06/16/2014 ; Valid for credit through 06/16/2015
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Slide 1.
Philip B. Adamson, MD: Hello, my name is Phil Adamson. I am from the Heart Failure Institute at the Oklahoma Heart
Hospital in Oklahoma City.
Paul Hauptman, MD: I am Paul Hauptman from St. Louis University School of Medicine in St. Louis, Missouri.
Scott D. Solomon, MD: And I am Scott Solomon from Harvard Medical School and Brigham and Womens Hospital in
Boston, Massachusetts. We are here today to discuss the very real risk for sudden cardiac death (SCD) in patients who have
heart failure (HF). Nearly 5 million patients in the United States have HF, and nearly 500,000 are diagnosed with HF for the first
time each year. These patients are particularly vulnerable to sudden cardiac arrest. Survival rates are very poor in these
patients.
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Slide 2.
Our objectives today are to identify persistent treatment gaps within the HF population; to evaluate the potential mechanisms
underlying the risk for SCD and HF; and to assess the role of implantable cardioverter-defibrillators (ICDs) and wearable
cardioverter-defibrillators (WCDs) to address the risk of SCD in patients with ischemic and nonischemic HF. Why dont we
begin. Phil, Paul, thanks for joining. Lets talk about the risk for sudden death in the patient with HF. Paul, who is at greatest
risk, and why?
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Slide 3.
Dr Hauptman: That is really the million dollar question. We know who is at risk in a global sense. We know that ejection
fraction (EF), for example, will predict SCD risk. We know a family history of SCD is a strong predictor. Aside from that, it gets
more difficult, which is the clinical challenge. We do not have a good way to divide patients who are, let us say, at very high
risk, from high risk, to moderate risk, to lower risk. If you are on the higher end of the low EF group, you are probably at lower
risk. That is about the extent of our ability to navigate the prognostic waters.
Dr Solomon: The risk of SCD is certainly higher if your EF is very low. What about HF with preserved EF? Are those people
also at increased risk?
Dr Hauptman: That is less clear. My feeling is that those patients at risk are largely mediated through hypokalemia and
metabolic abnormalities. I do not think that risk is anywhere near what it is for the low EF group. I should also add that the
degree to which patients are symptomatic with HF is very important. The more symptomatic the patient is, the less likely they
will have a sudden death event.
Dr Adamson: That is a problem with how we come up with risk stratification. We study populations and assess a relative risk
but then when we apply that to an individual, it is very difficult to hone in on that individuals risk, to gain insight into the decisionmaking process for an ICD, focusing on those at highest risk, the post-myocardial infarction (MI) patient with left ventricular
systolic dysfunction. Identifying those subsets of the HF population may help us guide patients with advice, and help us with
our judgment as well.
Dr Solomon: I agree that when we try to figure out what factors influence the risk for sudden death in a post-MI population, we
cannot at present do a very good job.
Slide 4.
Looking at the VALIANT trial, where there were approximately 14,600 patients, nearly 1100 had an event, and more than 900
people died suddenly.[1] We tried very hard to identify which factors predicted sudden death. Unfortunately, all the factors that
predict sudden death in that population are also the factors that predict death of any sort. We did not have very sophisticated
electrocardiographic measures but even if we did, I am not sure that we could have discovered the factors. Certainly there are
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no biomarkers that predict SCD.
Slide 5.
Dr Adamson: For transparency, we need to indicate that when we say sudden death we mean preventable sudden death.
That would mean the population of patients in whom lethal arrhythmias cause an abrupt problem that can be treated. Other
things cause sudden death: cerebrovascular accidents, pulmonary embolism, myocardial rupture, and aneurysms. We have to
clarify which group of patients who die suddenly can be helped. We need to identify the arrhythmic group, because we have
ways to treat them.
Dr Hauptman: We should also clarify that we are talking about a primary prevention strategy. We know that if you have had a
primary event, you are at high risk. Sustained ventricular tachycardia (VT), symptomatic VT with presyncope and syncope, and
an actual SCD event puts you at the highest risk. We know that there are certain periods of time, like early post-MI, when you
are at higher risk than later, following your MI when the patient is at risk.
We know that a wider QRS probably portends a poor overall prognosis, including SCD. Those patients are most concerning.
New-onset cardiomyopathy is a very mixed heterogeneous population. They can include some patients at high risk, but they
can also include some patients at low risk. Depending on presentation, up to 50% of those patients will improve their EF with
aggressive medical therapy.
Dr Solomon: The issue of timing is incredibly important. We looked at the timing of sudden death relative to an MI in the
VALIANT trial.[1] We found that the risk of SCD was dramatically highest in the first 30 days, then declined fairly rapidly. Even if
your EF was > 40% in the first 30 days, your risk of dying was > 1% per month. These were people who were discharged from
the hospital, not expected to die, not expected to have SCD, went home, and then were found dead. The other point that you
made, Phil, is that we want to consider those SCDs we can prevent. In the post-MI patient population they are not all due to
arrhythmia.
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Slide 6.
We looked at this again in the VALIANT trial where we had autopsies on a subset of patients. We saw that in about 50% of
patients who died suddenly, we could not identify either a new MI, a rupture, or any other clear reason for death. We assume
that those are the arrhythmic deaths. Whether we could prevent all of those, we do not know.[2] In the chronic HF population,
we see the same thing. When they are hospitalized with HF, then get discharged, their risk is extremely high early and then
comes down gradually with time. Is this a window of opportunity?
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Slide 7.
Dr Adamson: I think it is. It is difficult. Clinical trials applying therapies like ICDs, in that vulnerable period, the highest risk
period, do not reduce mortality. That is a paradox. It is difficult to understand. Why, for example in DINAMIT was there no
overall reduction in the risk for death with early application of an ICD?[3] There are many possible answers, or at least
speculations. That vulnerable period from MI and left ventricular dysfunction until 30 to 40 days is a very high-risk period, but is
not best treated by an implantable device. This presents the opportunity to use alternative therapies that we have not had
before.
Dr Solomon: There was another trial besides DINAMIT. It was called IRIS and it showed essentially the same thing.[4] Early
post-MI ICD did not benefit these patients.
Dr Hauptman: If you want to extend it, although it is an old trial and we do not practice this way, the CABG Patch Trial
suggested that there is no benefit from early ICD placement post-revascularization.[5] Obviously this was in the
pre-transvenous defibrillator age.
Slide 8.
Dr Adamson: That leads to the concept that there are retrievable arrhythmias, or treatable arrhythmias. Then there are other
causes of SCD that may not be best thought of as an arrhythmic process. That leads us to make recommendations for all
post-MI medical therapies such as -blockers and angiotensin-converting enzyme (ACE) inhibitors, to affect the remodeling
process that could lead to another MI or vascular remodeling that leads to SCD. When we get into the technocratic stage of
devices that do wonderful things, we forget that the medicines we have used after MI are very effective at lowering mortality.
We should focus on using those medicines and encouraging people to focus on them as well. True application of an
antiarrhythmic intervention is where the conundrum comes. How do we choose which patient should get an ICD? How do we
choose which patient should go home with a WCD? Now that we have WCDs, where does that fit in with the processing of our
clinical judgment?
Dr Solomon: We have come a long way with medications. In the VALIANT trial, the majority of patients were on -blockers,
statins, aspirin, and, by definition, getting an inhibitor of the renin-angiotensin system; yet we had an 11% sudden death rate.[1]
Granted, we cannot necessarily affect the outcome in all of those patients, but are there strategies we should think about in
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these high-risk patients, and then move to the broader HF population?

Dr Hauptman: VALIANT as a clinical trial is not indicative of a real world clinical practice. In 2010 we published a paper in
Circulation: Cardiovascular Quality and Outcomes that described -blocker use in a generic HF population; < 40% of
patients had a -blocker prescription covering at least 80% of the 90 days leading up to defibrillator placement.[6] - blocker
compliance/adherence was high in VALIANT because it was a clinical study; in the real world it is much lower. There is clearly
an opportunity to maximize medical therapy post-MI and in new-onset HF. That is the lowest tech way to prevent SCD: put a
patient on a -blocker, maybe also an aldosterone antagonist following MI. EPEHESUS showed similar findings to
VALIANT.[7]
Dr Adamson: If we have an ischemic patient in that vulnerable period where ICDs do not seem to reduce mortality, but we
have high risk, what do you recommend in that group?
Dr Solomon: I would first note that these studies tended to implant devices relatively late post-MI. The average time of
implantation in DINAMIT was 17 days.[3] What we found in the VALIANT trial was that the risk started very early. We are
discharging patients now -- I do not know about Oklahoma or St. Louis, but in Boston, we are discharging patients within 3 or 4
days post-MI. That policy rarely changes, even if their EF is reduced post-MI. That puts them in an extremely vulnerable
period. For each individual patient we need to consider whether they would benefit from some type of temporary treatment
before we can make a determination of whether they might need an ICD long-term.
Dr Hauptman: Do you think these electrical events post-MI, when they do occur, are all VT or ventricular fibrillation (VF)? Do
you have any idea what the incidence of bradycardic arrest, pulseless electrical activity (PEA) arrest, is? Neither the WCDs nor
ICDs are going to save the patient. Could that explain the failure of these trials to show a benefit?
Slide 9.
Dr Adamson: That is hard to say. It seems that of the arrhythmic or electrical events that lead to sudden death, it is thought
that around 85% to 90% are tachyarrhythmias. Sustained bradyarrhythmias account for maybe 10%. Then the
electromechanical disassociation PEA-type arrhythmias, in which there is no treatment really, is a small percentage. I think 2%
to 5% are probably unrecoverable.
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Dr Hauptman: Scott, you mentioned the autopsy study in VALIANT. There was an autopsy study in ATLAS.[8] In
nonischemics in ATLAS a fair percentage - - I do not recall the exact number, died of acute MI even though they were
nonischemics. They went on to develop plaque rupture. We have seen that as well. Not all sudden death events in the
nonischemic population are electrical.
Dr Adamson: We do not have time to talk about whether it is an ischemic cardiomyopathy, or cardiomyopathy in the presence
of ischemic heart disease, and what risks that portrays. It becomes very difficult to sort out outcomes from clinical trials based
on those definitions. What group of patients are we even studying? Then, when you put it into practice it becomes quite a
conundrum.
Dr Solomon: Paul, we have been talking a fair amount about the post-MI patient. Obviously the chronic HF patient is at risk as
well. In your practice treating chronic HF patients, do you see windows of opportunity for shorter term therapies than
implantable devices?
Slide 10.
Dr Hauptman: You are talking about the de novo HF presentation. These patients are challenging. By the Centers for
Medicare and Medicaid Services (CMS), the national coverage determination, you have to wait 9 months before you can put an
ICD.[9] I have always argued that there are 2 types of patients who present de novo. There are those who have truly de novo
cardiomyopathy and HF. Then there are those who have established cardiomyopathy but a de novo presentation of HF. How
do you distinguish those two? That is a challenge. For the group that you think has established cardiomyopathy, to wait 9
months is asking a lot. It is also asking a lot from medical therapy. I do not know about you Phil, but I would say if you were to
see a left bundle branch block pattern, an end-diastolic dimension of 7.5 cm to 8 cm -- that did not just occur in the last 30
days. That person has established cardiomyopathy, especially if you throw in a family history of cardiomyopathy. Those
patients are especially concerning. In general, those patients are not going to be among the 50% that improves their EF. A
few of them might but most will not.
Dr Adamson: The 9-month wait period is a real risk. When you look at the DEFINITE trial,[10] looking back at the people who
had de novo -- as close as they could call de novo HF -- in that trial, there was still a benefit of an ICD within the first 3 months
of implantation. There are data, albeit retrospective, that an ICD reduces SCD in nonischemic patients requiring a shorter
waiting period from the time of their diagnosis or closer to their diagnosis. It is a conundrum. Our risks are critical, possibly a
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SCD that could have been prevented. Yet, the alternative is 9 months of wearing a WCD. That sometimes is difficult to
recommend to a patient.
Fortunately, patients with prolonged QRS durations have to wait a shorter period of time for resynchronization therapy. We
have a general consensus that there should be a 3-month waiting period for a cardiac resynchronization therapy (CRT) device.
These are not inconsequential questions because of the potential financial liability if we put ICDs in wrong, at the wrong time,
and have to pay back the money plus penalties. These are issues we all have to face in this country. Timing is not just a
consensus question, is a regulatory question, as well as a financial reimbursement question.
Slide 11.
Dr Hauptman: Phil, that is really a great point. As a clinician you have a challenge. You have American College of Cardiology
(ACC)/ American Heart Association (AHA) guidelines.[11] You have the recently published ACC appropriateness paper across
369 different indications.[10] You have the national coverage determination,[9] you have clinical judgment, you have patient
preference, and then you must synthesize these and not expose yourself to risk. Yet ultimately the issue is about the patient.
Making sure that the patient is not put at risk is the real clinical challenge.
Dr Adamson: It is a challenge.
Dr Solomon: Many of these guidelines are based on EF, which we know is variable. It can change in the course of a patients
illness. It is also a measurement, and I am an echocardiographer, but it is a measurement that has an error around it of
probably 7 points either way. Can we be completely sure that we know what category a patient fits into when we try to assess
the risk?
Dr Hauptman: I love this point because, unfortunately, we paint by numbers now. We act as if something magical happens.
At 36%, you are not at risk. At 34%, put in a defibrillator. That presents two completely different approaches to the patient. Is
36 really 36? Is the 34 really 34? Is the 36 going to stay 36? Is the 34 going to stay 34? We act as if there are these cutoffs
that are meaningful for the patient. The patient does not know what the EF is. The patient just does not want to have a SCD.
That is a true surrogate. Scott, I am sure you have never had a patient who shows up in the office and says, Hey doc, my EF
is 29%. I think I need a defibrillator.
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Dr Solomon: The problem is that we focus on that number. We ignore other things that we know about the patient. I can tell
you that from large clinical trials we can see that a patient with diabetes and an EF of 40% is at risk for sudden death just as
much as a patient without diabetes and an EF of 25%. Renal function is another incredibly important modifier of risk that we
are not paying attention to. What about the data for the use of WCDs? There have not been the type of trials we saw with the
ICDs. We assume that if you are wearing one and you have an arrhythmia that they are effective. That depends on many
things, including the patients adherence. Do patients like to wear these, or should I say are they comfortable wearing them
enough so that they leave them on when they are at rest?
Dr Adamson: That is a big deal, both of those questions. Number one, do we know that it is effective? As Paul mentioned, it
is not effective against bradyarrhythmias.
It is not effective if it is sitting on the bedside while the patient is sleeping. Your data, and others, have demonstrated that many
SCDs, if not the majority of true out-of-the-hospital/at-home sudden deaths, occur while patients are sleeping. If they do not
feel comfortable enough to wear it to bed while sleeping, which is one of the most vulnerable times, they could die suddenly.
The post-MI period to me seems to be a no-brainer. Patients really buy into the WCD because they know in 30 days, or 40
days, or whatever their waiting period might be, they see the light at the end of the tunnel. It is the nonischemic patients who
are at risk where you are compelled to wait 9 months.
Dr Solomon: You mention sleeping. It is apropos that you alluded to many of the patients who had SCD during sleep.
Obviously people ask all the time if they should buy an automated external defibrillator (AED). Well, you need 2 things then:
that the patient is having an arrhythmia, and that there is a spouse who wants to resuscitate them.
Dr Adamson: And who is awake?
Dr Solomon: Right.
Slide 12.
Dr Hauptman: We know that that approach does not work from the HAT study.[12]
In fact, it was a failure. The number of events was relatively small. The number of events for which the external defibrillator was
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actually applied was small. You need an educated caregiver, who is at home at the time, who can recognize when it happens.
It should not be upstairs and the patient downstairs. That is often lacking. The early implant will not work. The home defibrillator
will not work. In the WCD registry, the compliance was remarkably high. It was nearly 22 hours a day in something like 900
patients.[13]
Slide 13.
I was actually surprised when I saw those data. We are concerned if patients say, Well, I will not wear it today. Obviously we
tell them when they take a shower they can take it off. I think 22 hours is really a positive finding. The duration of use, in
general, is not 9 months. It is somewhere between 1 to 2 months when you consider the post-MI population.[14] Clinically there
is hardly anything more rewarding than to be able to say to a patient, You know what, you can take the WCD off occasionally,
and, we do not have to put in a transvenous device.
Dr Adamson: Or the one who had a shock.
Dr Hauptman: Good point.
Dr Adamson: Now you have a secondary prevention strategy for an implantable device. That is also very gratifying. Those
anecdotes, I think, drive the utilization of the WCD.
Dr Solomon: Is it fair to say, in summing up, that for these very high risk patients there are options other than implanting an
expensive device, and perhaps we need to grow awareness of these alternative options, emphasizing the risk to these
patients.
Dr Adamson: Pressure comes from matching quality markers and mortality post MI, and the high risk in that 30-day period for
sudden death, using the WCD is a grand opportunity for institutions to recognize the opportunity to reduce mortality post-MI. I
think that is a great starting point, and how we apply the WCD to the longer term chronic HF patients in a primary prevention
strategy will evolve over time. It is a great opportunity for us to improve quality and reduce mortality after MI.
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Slide 14.
Dr Solomon: Paul and Phil, this has been a great discussion. Thank you for participating in this activity. To proceed to the
CME posttest click the earned CME credit link on this page.
This transcript has been edited for style and clarity.
Abbreviations
ACC = American College of Cardiology
ACE = angiotensin-converting enzyme
AED = automated external defibrillator
AHA = American Heart Association
ATLAS = assessment of treatment with lisinopril and survival
CABG = coronary artery bypass graft
CMS = Centers for Medicare and Medicaid Services
CRT = cardiac resynchronization therapy
DEFINITE = Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation
DINAMIT = Defibrillator in Acute Myocardial Infarction Trial
EF = ejection fraction
EPHESUS = Eplerenone Post-AMI Heart Failure Efficacy and Survival Study
HAT = Home Automated External Defibrillator Trial
HF = heart failure
ICD = implantable cardioverter-defibrillator
IRIS = Immediate Risk Stratification Improves Survival
MI = myocardial infarction
PEA = pulseless electrical activity
SCD = sudden cardiac death
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VALIANT = VALsartan In Acute myocardial infarction

VF = ventricular fibrillation
VT = ventricular tachycardia
WCD = wearable cardioverter-defibrillator
References
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2. Pouleur AC, Barkoudah E, Uno H, et al. Pathogenesis of sudden unexpected death in a clinical trial of patients with
myocardial infarction and left ventricular dysfunction, heart failure, or both.Circulation. 2010; 122:597-602.
3. Dorian P, Hohnloser SH, Thorpe KE, et al. Mechanisms underlying the lack of effect of implantable cardioverterdefibrillator therapy on mortality in high-risk patients with recent myocardial infarction: insights from the Defibrillation in
Acute Myocardial Infarction Trial (DINAMIT).Circulation. 2010;122:2645-2652.
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5. Bigger JT Jr. Prophylactic use of implanted cardiac defibrillators in patients at high risk for ventricular arrhythmias after
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From Medscape Education Cardiology

Addressing the Risk for Sudden Cardiac Death in Heart

no biomarkers that predict SCD.

these high-risk patients, and then move to the broader HF population?

VALIANT = VALsartan In Acute myocardial infarction

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