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Circulation: Arrhythmia and Electrophysiology Topic Review
Circulation: Arrhythmia and Electrophysiology Editors’ Picks
Most Read Articles on the Topic of Ventricular Arrhythmias
The Editors
The following articles are being highlighted as part of Circulation: Arrhythmia and Electrophysiology’s Topic Review series. This series will
summarize the most important manuscripts, as selected by the editors, published in Circulation: Arrhythmia and Electrophysiology and the
rest of the Circulation portfolio. The studies included in this article represent the most read manuscripts published on the topic of atrial
fibrillation in 2009 and 2010. (Circ Arrhythm Electrophysiol. 2011;4:e76-e83.)
Sudden Deaths in Young Competitive Athletes:
Analysis of 1866 Deaths in the United States,
1980 to 2006
Fabio Coccolo, MD; N.A. Mark Estes, MD; Caterina S. Barillà, MD;
Elena Biagini, MD; Giovanni Quarta, MD; Maria Rosa Conte, MD;
Paolo Bruzzi, MD, PhD; Barry J. Maron, MD
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Summary: In patients with hypertrophic cardiomyopathy, syncope
can be neurally mediated or a warning of dangerous arrhythmias or
hemodynamic impairment, but its prognostic significance is not
clearly established. We assessed the relationship between syncope
and sudden death in 1511 consecutive hypertrophic cardiomyopathy
patients; 205 (14%) had a history of unexplained or neurally
mediated syncope. Over a 5.6-year mean follow-up, 74 patients died
suddenly. Unexplained syncope but not neurally mediated syncope
was associated with an increased risk of sudden death (hazard ratio,
1.78, P⫽0.08 compared with patients without syncope). Temporal
proximity of unexplained syncope to initial patient evaluation was
important. Patients with recent unexplained syncope (ⱕ6 months
before initial evaluation) showed a 5-fold increase in risk compared
with patients without syncope, a relationship that was maintained
throughout all age groups. In adolescents, unexplained syncope was
associated with a 60% cumulative risk at 5 years. Older patients
(ⱖ40 years) with remote syncope (⬎5 years before initial evaluation) showed no increased sudden death risk. Thus, unexplained
syncope is a marker for increased risk in hypertrophic cardiomyopathy, particularly when it occurs in close temporal proximity to
patient evaluation. Remote syncopal events are not a marker of
increased risk in older patients.
Barry J. Maron, MD; Joseph J. Doerer, BS; Tammy S. Haas, RN;
David M. Tierney, MD; Frederick O. Mueller, PhD
Summary: We have estimated the absolute number of sudden deaths
in US competitive athletes from a large registry assembled over a
27-year period, using systematic identification and tracking strategies. A total of 1866 athletes who died suddenly (or survived cardiac
arrest), 19⫾6 years of age, were identified throughout the United
States from 1980 to 2006 in 38 diverse sports. Sudden deaths were
predominantly due to cardiovascular disease (1049 [56%]) but also
included deaths due to blunt trauma that caused structural damage
(416 [22%]), commotio cordis (65 [4%]), and heat stroke (46 [2%]).
Among the 1049 cardiovascular deaths, the highest number of events
in a single year was 76 (2005 and 2006), with an average of 66 per
year (range, 50 –76) over the last 6 years, many of which could not
have been identified reliably by preparticipation screening (even
with an ECG); 29% of deaths were among blacks, 54% of victims
were in high school, 82% of the deaths occurred with physical
exertion during competition/training, and only 11% were female.
The most common cardiovascular causes were hypertrophic cardiomyopathy (36%) and congenital coronary artery anomalies (17%). In
this national registry, the absolute number of cardiovascular sudden
deaths in young US athletes was relatively low, with a rate of ⬍100
per year. These data are relevant to the current debate surrounding
preparticipation screening programs with ECGs and suggest the need
for systematic and mandatory reporting of sudden deaths in athletes
to a national registry.
Conclusions: In the present large cohort of patients with hypertrophic cardiomyopathy, unexplained syncope was a risk factor for
sudden death. Patients with syncopal events that occurred in close
temporal proximity to the initial evaluation showed a substantially
higher risk of sudden death than patients without syncope. Older
patients with remote syncopal events did not show an increased risk.2
Conclusions: In this national registry, the absolute number of cardiovascular sudden deaths in young US athletes was somewhat
higher than previous estimates but relatively low nevertheless, with
a rate of ⬍100 per year. These data are relevant to the current debate
surrounding preparticipation screening programs with ECGs and also
suggest the need for systematic and mandatory reporting of athlete
sudden deaths to a national registry.1
Propranolol Decreases Tachycardia and
Improves Symptoms in the Postural
Tachycardia Syndrome: Less Is More
Syncope and Risk of Sudden Death in
Hypertrophic Cardiomyopathy
Summary: Postural tachycardia syndrome (POTS) is a disorder of
chronic orthostatic intolerance that disproportionately affects women
of childbearing age. It is characterized by a constellation of symptoms that occur during standing but resolve with sitting or lying
down. A most striking feature of this disorder is the excessive
increase in heart rate that occurs on standing in the absence of
Satish R. Raj, MD, MSCI; Bonnie K. Black, RN, CNP; Italo Biaggioni, MD;
Sachin Y. Paranjape, BS; Maricelle Ramirez; William D. Dupont, PhD;
David Robertson, MD
Paolo Spirito, MD; Camillo Autore, MD; Claudio Rapezzi, MD; Paola Bernabò, MD;
Roberto Badagliacca, MD; Martin S. Maron, MD; Sergio Bongioanni, MD;
Correspondence to The Editors, Circulation: Arrhythmia and Electrophysiology Editorial Office, 560 Harrison Ave, Suite 502, Boston, MA 02118.
E-mail [email protected]
© 2011 American Heart Association, Inc.
Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org
e76
DOI: 10.1161/CIRCEP.111.968941
The Editors
Most Read in Ventricular Arrhythmias
e77
hypotension. Given the striking tachycardia, ␤-adrenergic blockers
would seem like ideal treatments, but prior anecdotal and experimental experience has been disappointing. We report the first
placebo-controlled trial of propranolol in POTS. A low dose of
propranolol (20 mg) immediately decreased heart rate and orthostatic
tachycardia and improved the orthostatic symptoms in patients with
POTS. A higher dose of propranolol (80 mg) elicited more complete
␤-blockade with a further lowering of heart rate but did not further
improve symptoms and may have made some symptoms worse.
These data suggest that although low doses of propranolol are of
benefit in POTS, higher doses might be counterproductive. These
data also offer a potential explanation for the conflicting prior results
of ␤-blockers in POTS.
Germany) Brugada syndrome registry. The registry included 1029
consecutive individuals (72% men). In the registry, 36% of the patients
were symptomatic and 64% were asymptomatic. The cardiac event rate
per year was 7.7% in patients with aborted sudden cardiac death, 1.9%
in patients with syncope, and 0.5% in asymptomatic patients. Symptoms
and spontaneous type 1 ECG were predictors of arrhythmic events,
whereas sex, familial history of sudden cardiac death, inducibility of
ventricular tachyarrhythmias during electrophysiological study, and the
presence of an SCN5A mutation were not predictive of arrhythmic
events. In the FINGER registry, the rate of cardiac events in the
asymptomatic Brugada syndrome patients was low, and the inducibility
of ventricular tachyarrhythmias during electrophysiological study did
not properly stratify the arrhythmic risk.
Conclusions: Low-dose oral propranolol significantly attenuated
tachycardia and improved symptoms in POTS. Higher-dose propranolol did not further improve, and may worsen, symptoms.3
Conclusions: In the largest series of Brugada syndrome patients thus
far, event rates in asymptomatic patients were low. Inducibility of
ventricular tachyarrhythmia and family history of SCD were not
predictors of cardiac events.5
Syncope While Driving Clinical
Characteristics, Causes, and Prognosis
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Dan Sorajja, MD; Gillian C. Nesbitt, MD; David O. Hodge, MS; Phillip A. Low, MD;
Stephen C. Hammill, MD; Bernard J. Gersh, MBChB, DPhil; Win-Kuang Shen, MD
Summary: In a large case-control study of 3877 patients with
syncope, 381 patients (9.8%) reported an episode of syncope while
driving. A peak of syncope while driving was observed among
elderly patients. This has potential public health implications because this peak corresponds to an age group with a higher frequency
of accidents per driver-year in the general public. The most common
cause of syncope while driving was neurally mediated syncope (37.3%).
The next most common identifiable causes were cardiac arrhythmias,
including bradyarrhythmias, ventricular tachyarrhythmias, and supraventricular tachyarrhythmias (11.8%). Long-term survival among
patients who had syncope while driving (driving group) was comparable
to that of an age- and sex-matched cohort from the Minnesota population (P⫽0.15). Among the driving group, syncope recurred in 72
patients, 35 of whom (48.6%) had recurrence ⬎6 months after the initial
evaluation. Syncope while driving recurred in 10 patients in the driving
group, 7 episodes of which (70%) occurred ⬎12 months after the initial
evaluation. The actuarial recurrence of syncope while driving was 0.7%
at 6 months and 1.1% at 12 months during follow-up. The causes of
syncope, the late recurrences of syncope (during ⬎6 months of
follow-up), and the overall low incidence of recurrent syncope while
driving provide useful information to supplement current recommendations on driving for these patients.
Conclusions: In our study, neurally mediated syncope was the most
common type of syncope while driving. The causes of syncope, the
late recurrences of syncope (during ⬎6 months of follow-up), and
the overall low incidence of recurrent syncope while driving provide
useful information to supplement current recommendations on driving for these patients.4
Long-Term Prognosis of Patients Diagnosed
With Brugada Syndrome: Results From the
FINGER Brugada Syndrome Registry
V. Probst, MD, PhD; C. Veltmann, MD; L. Eckardt, MD; P.G. Meregalli, MD;
F. Gaita, MD; H.L. Tan, MD, PhD; D. Babuty, MD, PhD; F. Sacher, MD;
C. Giustetto, MD; E. Schulze-Bahr, MD, PhD; M. Borggrefe, MD, PhD;
M. Haissaguerre, MD; P. Mabo, MD, PhD; H. Le Marec, MD, PhD;
C. Wolpert, MD, PhD; A.A.M. Wilde, MD, PhD
Summary: Brugada syndrome is characterized by ST-segment elevation in the right precordial leads and an increased risk of sudden
cardiac death. Fundamental questions remain on the best strategy for
assessing the real disease-associated arrhythmic risk, especially in
asymptomatic patients. The aim of the present study was to evaluate
the prognosis and risk factors of sudden cardiac death in Brugada
syndrome patients in the FINGER (France, Italy, Netherlands,
ECG Criteria to Identify Epicardial Ventricular
Tachycardia in Nonischemic Cardiomyopathy
Ermengol Vallès, MD; Victor Bazan, MD; Francis E. Marchlinski, MD
Summary: ECG criteria for identifying an epicardial origin of
ventricular tachycardia appear to be region and substrate specific.
This is an important consideration because many ventricular
tachycardias associated with nonischemic cardiomyopathy are epicardial in origin, and most of them originate from substrate-based
abnormalities near the superior and lateral mitral valve region. It is
imperative to identify which patients are likely to benefit from an
epicardial approach. Simple morphological criteria, including the
presence of a q wave in lead I, create a high degree of suspicion for
a probable epicardial location in the setting of nonischemic cardiomyopathy. A suggested 4-step algorithm that incorporates modified
interval criteria and well-defined morphological criteria enhances the
diagnostic sensitivity and specificity of ECG assessment for ventricular tachycardia localization and should facilitate the planning and
success of catheter ablation of ventricular tachycardia in this setting.
Conclusions: Morphological ECG features that describe the initial
QRS vector can help identify basal-superior/lateral epicardial ventricular tachycardias in nonischemic cardiomyopathy.6
Impact of Implantable CardioverterDefibrillator, Amiodarone, and Placebo on the
Mode of Death in Stable Patients With Heart
Failure: Analysis From the Sudden Cardiac
Death in Heart Failure Trial
Douglas L. Packer, MD; Jordan M. Prutkin, MD, MHS; Anne S. Hellkamp, MS;
L. Brent Mitchell, MD; Robert C. Bernstein, MD; Freda Wood, RN, MSN;
John P. Boehmer, MD; Mark D. Carlson, MD; Robert P. Frantz, MD;
Steve E. McNulty, MS; Joseph G. Rogers, MD; Jill Anderson, RN;
George W. Johnson, BSEE; Mary Norine Walsh, MD; Jeanne E. Poole, MD;
Daniel B. Mark, MD, MPH; Kerry L. Lee, PhD; Gust H. Bardy, MD
Summary: The Sudden Cardiac Death in Heart Failure Trial (SCDHeFT) demonstrated that implantable cardioverter-defibrillator therapy reduces all-cause mortality in patients with New York Heart
Association class II/III heart failure and a left ventricular ejection
fraction ⱕ35% on optimal medical therapy. This report examined the
mode of death in SCD-HeFT. A total of 2521 subjects were
randomly assigned to placebo, amiodarone, or shock-only, singlelead implantable cardioverter-defibrillator therapy. Over a median
follow-up of 45.5 months, 666 deaths were reviewed by an events
committee and categorized as sudden death presumed to be ventricular tachyarrhythmic, heart failure–related, bradyarrhythmic, nonarrhythmic non– heart failure–related, or noncardiac. Implantable
cardioverter-defibrillator therapy reduced cardiac and ventricular
tachyarrhythmic mortality and had no impact on mortality resulting
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Circ Arrhythm Electrophysiol
December 2011
from heart failure or noncardiac causes compared with placebo. The
cardiac and ventricular tachyarrhythmic mortality reductions were
evident in subjects with New York Heart Association class II but not
in subjects with class III heart failure. The reduction in ventricular
tachyarrhythmic mortality with implantable cardioverterdefibrillator therapy was similar in subjects with ischemic and
nonischemic disease. Amiodarone compared with placebo had no
significant effect on any mode of death, although there was an
increase in noncardiac mortality in those with New York Heart
Association class III heart failure who were receiving amiodarone.
Implantable cardioverter-defibrillator therapy has a beneficial effect
on reducing sudden death presumed to be due to ventricular
tachyarrhythmias without an effect on heart failure mortality.
Conclusions: Implantable cardioverter-defibrillator therapy reduced
cardiac mortality and sudden death presumed to be ventricular
tachyarrhythmic in SCD-HeFT and had no effect on heart failure
mortality. Amiodarone had no effect on all-cause mortality or its
cause-specific components, except for an increase in noncardiac
mortality in class III patients.7
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Systematic Assessment of Patients With
Unexplained Cardiac Arrest: Cardiac Arrest
Survivors With Preserved Ejection Fraction
Registry (CASPER)
Andrew D. Krahn, MD; Jeffrey S. Healey, MD; Vijay Chauhan, MD;
David H. Birnie, MD; Christopher S. Simpson, MD; Jean Champagne, MD;
Martin Gardner, MD; Shubhayan Sanatani, MD; Derek V. Exner, MD;
George J. Klein, MD; Raymond Yee, MD; Allan C. Skanes, MD; Lorne J. Gula, MD;
Michael H. Gollob, MD
Summary: Cardiac arrest without evident cardiac disease may be
caused by genetic conditions that are difficult to diagnose. Provocative
testing to unmask a phenotype is often necessary to detect primary
electric disease, direct genetic testing, and perform family screening.
Patients resuscitated from cardiac arrest that was unexplained after an
initial evaluation showed normal left ventricular function and an
absence of coronary artery disease underwent systematic testing that
included advanced imaging and drug challenge. A diagnosis was
obtained in 56% of patients. Key testing included MRI to detect
arrhythmogenic right ventricular cardiomyopathy and myocarditis, telemetry and ergonovine challenge to diagnose coronary spasm, and
adrenaline/procainamide infusion to diagnose long-QT syndrome, catecholaminergic polymorphic ventricular tachycardia, and Brugada syndrome. Targeted genetic testing demonstrated evidence of causative
mutations in 47% of patients tested, which resulted in detection of
disease in 24% of 64 family members screened. This systematic
approach to clinical testing unmasked the cause of apparently unexplained cardiac arrest in the majority of patients. This clinical approach
assists in directing genetic testing to confirm genetically mediated
arrhythmia syndromes and facilitates directed family screening to
identify at-risk family members.
Conclusions: Systematic clinical testing, including drug provocation
and advanced imaging, results in unmasking of the cause of apparently
unexplained cardiac arrest in ⬎50% of patients. This approach assists in
directing genetic testing to diagnose genetically mediated arrhythmia
syndromes, which results in successful family screening.8
Electrocardiographic Features of
Arrhythmogenic Right Ventricular Dysplasia
Rahul Jain, MD; Darshan Dalal, MD; Amy Daly, MS; Crystal Tichnell, MGC;
Cynthia James, PhD; Ariana Evenson, MHSA; Rohit Jain, MD;
Theodore Abraham, MD; Boon Yew Tan, MBChB; Hari Tandri, MD;
Stuart D. Russell, MD; Daniel Judge, MD; Hugh Calkins, MD
Summary: Diagnosis of arrhythmogenic right ventricular dysplasia
(ARVD) relies on results of diagnostic tests that screen for structural
abnormalities of the right ventricle, ventricular arrhythmias, a family
history of sudden death or ARVD, and ECG abnormalities that have
been linked to ARVD. Among the many diagnostic tests that are
used to screen patients for ARVD, the ECG is of particular
importance because of its widespread availability and low cost. In
this study, we performed a systematic analysis of the 12-lead ECG in
ARVD patients compared with controls. To our knowledge, this is
the first study to evaluate the ECG features of ARVD patients on the
basis of the presence or absence of a complete or incomplete right
bundle-branch block (RBBB). This is of particular importance
because incomplete RBBB or complete RBBB patterns are commonly observed in patients with ARVD. The results of this study
reveal that in the absence of a complete RBBB or incomplete RBBB,
T-wave inversion through V3 is the single ECG parameter that
demonstrates optimal sensitivity and specificity. Second, for patients
with an incomplete RBBB pattern, T-wave inversion through V3 is
also the single ECG parameter that demonstrates optimal sensitivity
and specificity. Third, for patients with a complete RBBB pattern, an
r⬘/s ratio of ⬍1 in V1 was the single ECG parameter that demonstrated optimal sensitivity and specificity. It is our hope that the
findings of our study will be confirmed in other populations of
ARVD patients and that in the future, the ECG can be relied on with
greater confidence as a screening tool for ARVD.
Conclusions: We comprehensively evaluated the diagnostic value of
ECG markers for ARVD. On the basis of the findings, we propose an
algorithm, with examination of QRS morphology being the first step,
for ECG evaluation of ARVD patients. Definite criteria are then
applied on the basis of the presence of no RBBB, incomplete RBBB,
and complete RBBB to obtain the best diagnostic utility of the ECG.9
Yield of Genetic Screening in Inherited
Cardiac Channelopathies: How to Prioritize
Access to Genetic Testing
Rong Bai, MD; Carlo Napolitano, MD, PhD; Raffaella Bloise, MD;
Nicola Monteforte, MD; Silvia G. Priori, MD, PhD
Summary: There is a rapid growth in the request of genetic screening
for long-QT syndrome, Brugada syndrome, and catecholaminergic
polymorphic ventricular tachycardia. Genetic testing is often offered
to all patients irrespective of whether they are “clearly” affected or
“possibly” affected by one of such diseases, and even family
members of unexplained sudden death victims and idiopathic ventricular fibrillation survivors are directed to genotyping in an attempt
to clarify the substrate of the arrhythmic event. To help clinicians
and third-party payers prioritize access to genotyping when resources
are limited, it becomes critical to draw some cost/benefit considerations. We retrospectively analyzed data of 1394 consecutive probands to determine the yield of genetic screening and cost per
positive genotyping in patients with either a conclusive or a possible
diagnosis of long-QT syndrome, Brugada syndrome, or catecholaminergic polymorphic ventricular tachycardia and in family members of unexplained sudden death victims and idiopathic ventricular
fibrillation survivors. We demonstrated that genotyping has the
highest cost efficacy in individuals with a clinical conclusive
diagnosis of long-QT syndrome or catecholaminergic polymorphic
ventricular tachycardia. The yield and cost of genotyping is also
reasonable in patients with type I Brugada syndrome ECG and
atrioventricular block. However, genotyping family members of
unexplained sudden death victims and idiopathic ventricular fibrillation survivors had low yield. Family history evaluation might be
useful to better target genetic screening.
Conclusions: Genotyping can be performed at reasonable cost in
individuals with conclusive diagnosis of long-QT syndrome and
catecholaminergic polymorphic ventricular tachycardia and in patients with type I Brugada syndrome ECG with atrioventricular
block. These patients should be given priority to access genetic
testing.10
The Editors
Atrial Fibrillation Ablation Strategies for
Paroxysmal Patients: Randomized Comparison
Between Different Techniques
Luigi Di Biase, MD; Claude S. Elayi, MD; Tamer S. Fahmy, MD;
David O. Martin, MD; Chi Keong Ching, MD; Conor Barrett, MD; Rong Bai, MD;
Dimpi Patel, DO; Yaariv Khaykin, MD; Richard Hongo, MD; Steven Hao, MD;
Salwa Beheiry, RN; Gemma Pelargonio, MD; Antonio Dello Russo, MD;
Michela Casella, MD; Pietro Santarelli, MD; Domenico Potenza, MD;
Raffaele Fanelli, MD; Raimondo Massaro, MD; Paul Wang, MD;
Amin Al-Ahmad, MD; Mauricio Arruda, MD; Sakis Themistoclakis, MD;
Aldo Bonso, MD; Antonio Rossillo, MD; Antonio Raviele, MD;
Robert A. Schweikert, MD; David J. Burkhardt, MD; Andrea Natale, MD
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Summary: Whether different ablation strategies affect paroxysmal
atrial fibrillation (AF) long-term freedom from AF/atrial
tachyarrhythmia (AT) is unclear. This study compared 3 different
ablation approaches on the long-term success rate in patients with
paroxysmal AF. This is the first prospective study comparing 3
ablation techniques in patients with paroxysmal AF. Complex
fractionated atrial electrogram (CFAE) ablation alone had the
smallest impact on the freedom from AF/AT at 1-year follow-up.
The hybrid strategy, which combines isolation of the pulmonary
vein antrum and ablation of CFAEs, was not associated with a
better success rate, defined as event freedom from AF or AT at
6-month and 1-year follow-up when compared with pulmonary
vein antrum isolation alone. This study reinforces the concept that
electric isolation of all the pulmonary veins remains a cornerstone
for catheter ablation of paroxysmal AF. The results of this study
also indicate that CFAE ablation alone should not be considered
as an alternative strategy for paroxysmal patients but should be
reserved only for selected patients, unless a better identification
of critical CFAE zones becomes widely available and is proven
effective.
Conclusions: No difference in terms of success rate was seen
between pulmonary vein antrum isolation alone and pulmonary vein
antrum isolation associated with defragmentation. CFAE ablation
alone had the smallest impact on AF recurrences at 1-year follow-up.
These results suggest that antral isolation is sufficient to treat most
patients with paroxysmal AF.11
Mechanisms Underlying the Lack of Effect of
Implantable Cardioverter-Defibrillator
Therapy on Mortality in High-Risk Patients
With Recent Myocardial Infarction: Insights
From the Defibrillation in Acute Myocardial
Infarction Trial (DINAMIT)
Paul Dorian, MD, MSc; Stefan H. Hohnloser, MD; Kevin E. Thorpe, MMath;
Robin S. Roberts, MTech; Karl-Heinz Kuck, MD; Michael Gent, DSc;
Stuart J. Connolly, MD
Summary: In the Defibrillation in Acute Myocardial Infarction
Trial (DINAMIT) study, implanted defibrillators did not reduce
mortality in high-risk patients if implanted early after myocardial
infarction. In patients randomly assigned to an implantable
cardioverter-defibrillator (ICD), sudden deaths were reduced but
nonarrhythmic mortality was increased. In an analysis of the
potential causes of this finding, patients who are destined to
receive therapy from their ICD (compared with those destined not
to receive therapy) have clinical features that also increase their
risk of nonsudden death, including risks related to heart failure
and recurrent ischemic events. During follow-up, patients who
receive therapy from their ICD are more likely to have intercurrent cardiac clinical adverse events both before and after ICD
therapy compared with patients who receive no therapy or do not
have an ICD. In an early post–myocardial infarction setting, the
same clinical circumstances that increase the risk of ventricular
arrhythmias also increase the risk of nonsudden death; in addi-
Most Read in Ventricular Arrhythmias
e79
tion, ICD therapies themselves may increase the risk of subsequent death. These findings underscore the limitations of a
strategy of ICD implantation in certain high-risk groups, especially early after acute myocardial infarction.
Conclusions: In patients receiving ICDs early after myocardial infarction, those factors that are associated with arrhythmia requiring
ICD therapy are also associated with a high risk of nonsudden death,
negating the benefit of ICDs in this setting.12
Long-Term Recording of Cardiac Arrhythmias
With an Implantable Cardiac Monitor in
Patients With Reduced Ejection Fraction After
Acute Myocardial Infarction: The Cardiac
Arrhythmias and Risk Stratification After Acute
Myocardial Infarction (CARISMA) Study
Poul Erik Bloch Thomsen, MD; Christian Jons, MD; M.J. Pekka Raatikainen, MD;
Rikke Moerch Joergensen, MD; Juha Hartikainen, MD; Vesa Virtanen, MD;
J. Boland, MD; Olli Anttonen, MD; Uffe Jakob Gang, MD; Nis Hoest, MD;
Lucas V.A. Boersma, MD; Eivin S. Platou, MD; Daniel Becker, MSc;
Marc D. Messier, PhD; Heikki V. Huikuri, MD; for the Cardiac Arrhythmias and Risk
Stratification After Acute Myocardial Infarction (CARISMA) Study Group
Summary: Cardiac Arrhythmias and Risk Stratification After Acute
Myocardial Infarction (CARISMA) reports on long-term cardiac
arrhythmias recorded by an implantable cardiac monitor in patients
with left ventricular ejection fraction ⱕ40% after myocardial infarction. Clinically significant bradyarrhythmias and tachyarrhythmias
were documented in a substantial proportion of patients, most of
them asymptomatic. A large number of the documented arrhythmias
would result in device therapy according to the current guidelines.
The most significant arrhythmia was intermittent high-degree atrioventricular block, which was associated with a very high risk of
cardiac death. However, the study was observational, and whether
the use of implantable cardiac monitors in this population could
improve clinical outcome should be tested in larger randomized
trials.
Conclusions: This is the first study to report on long-term cardiac
arrhythmias recorded by an implantable loop recorder in patients
with left ventricular ejection fraction ⱕ40% after myocardial infarction. Clinically significant bradyarrhythmias and tachyarrhythmias
were documented in a substantial proportion of patients with
depressed left ventricular ejection fraction after acute myocardial
infarction. Intermittent high-degree atrioventricular block was associated with a very high risk of cardiac death.13
High Efficacy of ␤-Blockers in Long-QT Syndrome
Type 1: Contribution of Noncompliance and
QT-Prolonging Drugs to the Occurrence of
␤-Blocker Treatment “Failures”
G. Michael Vincent, MD; Peter J. Schwartz, MD; Isabelle Denjoy, MD;
Heikki Swan, MD; Candice Bithell, BA; Carla Spazzolini, DVM, MS;
Lia Crotti, MD, PhD; Kirsi Piippo, MD; Jean-Marc Lupoglazoff, MD, PhD;
Elizabeth Villain, MD; Silvia G. Priori, MD, PhD; Carlo Napolitano, MD, PhD;
Li Zhang, MD
Summary: ␤-Blocker noncompliance, the use of QT-prolonging
drugs, or both in combination are responsible for almost all cardiac
events while patients are “on” ␤-blockers, rather than “␤-blocker
failures.” Being ␤-blocker compliant and receiving no QTprolonging drugs dramatically reduce cardiac events to a mean
yearly rate of 0.06 (range, 0.05– 0.07) for cardiac arrest or sudden
death. This has equally important ramifications for the selection of
therapy for long-QT syndrome type 1 patients. Being so efficacious,
␤-blockers should be the initial treatment for all asymptomatic
patients at diagnosis, those with remote symptoms, and those with
syncope (and possible even a cardiac arrest) who were not on a
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December 2011
␤-blocker at the time of the event. Furthermore, early diagnosis and
treatment, before the high-risk time of preteens through the 20s, is
very important for preventing cardiac events, particularly cardiac
arrest and sudden death. Physicians should carefully discuss the
importance of full compliance with ␤-blockers and the avoidance of
any QT-prolonging drugs at the time of first contact and indicate the
danger of not adhering to these recommendations. This discussion
should be repeated regularly during follow-up. Patients who will not
or cannot take ␤-blockers may be candidates for implantable
converter-defibrillators or left stellectomy therapy.
Conclusions: ␤-Blockers are extremely effective in long-QT syndrome type 1 and should be administered at diagnosis and ideally
before the preteen years. ␤-Blocker noncompliance and use of
QT-prolonging drug are responsible for almost all life-threatening
“␤-blocker failures.” ␤-Blockers are appropriate therapy for asymptomatic patients and those who have never had a cardiac arrest or
␤-blocker therapy. Routine implantation of cardiac defibrillators in
such patients does not appear justified.14
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Arrhythmogenic Right Ventricular Dysplasia/
Cardiomyopathy Diagnostic Task Force
Criteria: Impact of New Task Force Criteria
Moniek G.P.J. Cox, MD; Jasper J. van der Smagt, MD; Maartje Noorman, MSc;
Ans C. Wiesfeld, MD, PhD; Paul G.A. Volders, MD, PhD;
Irene M. van Langen, MD, PhD; Douwe E. Atsma, MD, PhD; Dennis Dooijes, PhD;
Arjan C. Houweling, MD, PhD; Peter Loh, MD, PhD; Luc Jordaens, MD, PhD;
Yvonne Arens, MD, PhD; Maarten J. Cramer, MD, PhD;
Pieter A. Doevendans, MD, PhD; J. Peter van Tintelen, MD, PhD;
Arthur A.M. Wilde, MD, PhD; Richard N.W. Hauer, MD, PhD
Summary: Arrhythmogenic right ventricular dysplasia/cardiomyopathy
(ARVD/C) is characterized by progressive loss of predominantly RV
myocardium, which is replaced by fibrofatty tissue. Typically, affected
individuals present with ventricular tachycardia between the 2nd and 4th
decades of life, but ARVD/C can also cause sudden death in adolescence. Clinical diagnosis is made according to generally accepted task
force criteria (TFC). This initial set of criteria, dating from 1994, was
highly specific but lacked sensitivity. Therefore, a modified set of TFC
was recently proposed. In new TFC, scoring by major and minor criteria
is maintained. Structural abnormalities are quantified and TFC highly
specific for ARVD/C are upgraded to major. Furthermore, new criteria
are added: terminal activation duration of QRS ⱖ55 ms, ventricular
tachycardia with left bundle-branch block morphology and superior
axis, and genetic criteria. In the present study, we applied new TFC to
3 groups: (1) 105 patients with proven ARVD/C according to 1994
TFC, (2) 89 of their family members, and (3) 39 patients with probable
ARVD/C (ie, 3 points by 1994 TFC). In total, 35 individuals were newly
diagnosed with ARVD/C: 10 of 89 (11%) relatives and 25 of 39 (64%)
previously classified as probable index patients. On the contrary, 3 of
105 ARVD/C patients previously classified as “proven” did not fulfill
new TFC. ECG criteria and pathogenic mutations especially contributed
to new diagnosis. Therefore, newly proposed TFC have a major impact
in increasing diagnostic yield of ARVD/C.
Conclusions: In this first study applying new TFC to patients suspected
of ARVD/C, 64% of probable ARVD/C patients and 11% of family
members were additionally diagnosed. ECG criteria and pathogenic
mutations especially contributed to new diagnosis. Newly proposed
TFC have a major impact in increasing diagnostic yield of ARVD/C.15
Left Atrial Appendage: An Underrecognized
Trigger Site of Atrial Fibrillation
Luigi Di Biase, MD; J. David Burkhardt, MD; Prasant Mohanty, MBBS, MPH;
Javier Sanchez, MD; Sanghamitra Mohanty, MD;
Rodney Horton, MD; G. Joseph Gallinghouse, MD; Shane M. Bailey, MD;
Jason D. Zagrodzky, MD; Pasquale Santangeli, MD; Steven Hao, MD;
Richard Hongo, MD; Salwa Beheiry, MD; Sakis Themistoclakis, MD;
Aldo Bonso, MD; Antonio Rossillo, MD; Andrea Corrado, MD; Antonio Raviele, MD;
Amin Al-Ahmad, MD; Paul Wang, MD; Jennifer E. Cummings, MD;
Robert A. Schweikert, MD; Gemma Pelargonio, MD; Antonio Dello Russo, MD;
Michela Casella, MD; Pietro Santarelli, MD; William R. Lewis, MD;
Andrea Natale, MD, FHRS
Summary: Several studies have shown that together with the pulmonary veins, many extrapulmonary vein areas may be the source
of initiation and maintenance of atrial fibrillation. The most
common sites are the superior vena cava, ligament of Marshall,
coronary sinus, crista terminalis, and left atrial posterior wall.
This study is the first to report firing from the left atrial
appendage as a possible site of origin of atrial fibrillation in a
consecutive series of patients. The prevalence of this finding in
our population was 27%, and in 8.7% of patients, the left atrial
appendage was the only target of ablation during redo procedures.
We performed electric isolation of the left atrial appendage.
Similar to what was observed for the isolation of the pulmonary
veins, isolation of the left atrial appendage with segmental or
circumferential lesions led to a higher probability of achieving
long-term freedom from atrial fibrillation/atrial tachyarrhythmia
than focal ablation. The clinical relevance of left atrial appendage
isolation and its consequences with respect to potential complications require further investigation.
Conclusions: The left atrial appendage appears to be responsible for
arrhythmias in 27% of patients presenting for repeat procedures.
Isolation of the left atrial appendage could achieve freedom from
atrial fibrillation in patients presenting for a repeat procedure when
arrhythmias initiating from this structure are demonstrated.16
Incidence and Risk Factors of Arrhythmic
Events in Catecholaminergic Polymorphic
Ventricular Tachycardia
Meiso Hayashi, MD; Isabelle Denjoy, MD; Fabrice Extramiana, MD, PhD;
Alice Maltret, MD; Nathalie Roux Buisson, MD; Jean-Marc Lupoglazoff, MD, PhD;
Didier Klug, MD; Miyuki Hayashi, MD; Seiji Takatsuki, MD; Elisabeth Villain, MD;
Joël Kamblock, MD; Anne Messali, MD; Pascale Guicheney, PhD;
Joël Lunardi, MD, PhD; Antoine Leenhardt, MD
Summary: Catecholaminergic polymorphic ventricular tachycardia is a rarely recognized but important cause of sudden cardiac
death in the young. This multicenter observational study of 101
subjects (50 probands, 51 family members) was conducted to
characterize the clinical course of the disease. Catecholaminergic
polymorphic ventricular tachycardia was diagnosed from clinical
features in 84 subjects and from genotyping in 17 subjects. During
the follow-up of 7.9⫾4.9 years, 27 patients (27%), including 2 silent
gene mutation carriers, had syncope, aborted cardiac arrest, or
sudden cardiac death events that were fatal or near-fatal in 13
subjects. The estimated 8-year event rate was 32%, with a 13% rate
of fatal or near-fatal events. The event rates between the probands
and family members were comparable. A younger age at diagnosis,
a history of aborted cardiac arrest, and the absence of ␤-blockers
were predictors of events, but ␤-blocker therapy was not completely
protective. These results suggest that ␤-blockers should be prescribed even if the diagnosis is made from genotyping when there is
not a history of symptomatic arrhythmias. Additional therapies,
including implantable defibrillators, verapamil, or left cardiac sympathetic denervation, should be considered in patients with markers
of increased risk.
Conclusions: Cardiac and fatal or near-fatal events were not rare in
both catecholaminergic polymorphic ventricular tachycardia probands and affected family members during the long-term follow-up,
even while taking ␤-blockers, which was associated with a lower
event rate. Further studies evaluating concomitant therapies are
necessary to improve outcome in these patients.17
The Editors
Genetic Testing for Long-QT Syndrome:
Distinguishing Pathogenic Mutations From
Benign Variants
Suraj Kapa, MD; David J. Tester, BS; Benjamin A. Salisbury, PhD;
Carole Harris-Kerr, PhD; Manish S. Pungliya, MS; Marielle Alders, PhD;
Arthur A.M. Wilde, MD, PhD; Michael J. Ackerman, MD, PhD
Downloaded from http://circep.ahajournals.org/ by guest on May 2, 2017
Summary: Genetic testing for congenital long-QT syndrome
(LQTS) has become an established part of the clinical armamentarium for physicians encountering patients with a personal or
family history of ventricular tachyarrhythmias and sudden cardiac
death. However, the presence of a positive genetic test result must
be reviewed carefully. Most mutations identified in cases of
LQTS are novel missense mutations and thus must be distinguished as either background noise or function-altering/diseasecausing mutations. Specifically, even in the general healthy
population, genetic variation, including known polymorphisms
and novel, rare variants, may be demonstrated. Thus, the presence
of a genetic mutation should be interpreted as a probabilistic
measure of likelihood of disease rather than as a binary indicator
of its presence or absence. This work indicates that mutation type,
mutation location, and ethnic-specific background rates are critical factors in predicting the pathogenicity of novel mutations.
However, in certain cases, distinguishing pathogenic mutations
from rare variants may not be possible without additional functional characterization or linkage analyses. Although mutations
localizing to certain specialized regions may be expected with
high probability to be disease causing, mutations in other regions
should be seen as variants of uncertain significance and should be
interpreted in the clinical context and lead to further investigation
rather than prompting assumption of disease presence and resulting therapeutic interventions. This classification of genetic test
results as a probabilistic rather than absolute measure of disease
causation has potential implications when counseling patients,
especially as genetic testing becomes less expensive, more easily
available, and more commonly used. These findings may also
have implications for other genetic disorders involving mutational
analysis in which benign genetic variation is sure to exist and
must be distinguished from disease-causing mutations.
Conclusions: Distinguishing pathogenic mutations from rare variants is of critical importance in the interpretation of genetic
testing in LQTS. Mutation type, mutation location, and ethnicspecific background rates are critical factors in predicting the
pathogenicity of novel mutations. Novel mutations in lowestimated predictive value regions such as the interdomain linker
of SCN5A should be viewed as variants of uncertain significance
and prompt further investigation to clarify the likelihood of
disease causation. However, mutations in regions such as the
transmembrane, linker, and pore of KCNQ1 and KCNH2 may be
defined confidently as high-probability LQTS-causing mutations.
These findings will have implications for other genetic disorders
involving mutational analysis.18
Predicting Ventricular Arrhythmias in Patients
With Ischemic Heart Disease: Clinical
Application of the ECG-Derived QRS-T Angle
C. Jan Willem Borleffs, MD; Roderick W.C. Scherptong, MD; Sum-Che Man, MD;
Guido H. van Welsenes, MS; Jeroen J. Bax, MD, PhD; Lieselot van Erven, MD, PhD;
Cees A. Swenne, PhD; Martin J. Schalij, MD, PhD
Summary: A depressed left ventricular ejection fraction identifies
a large number of high-risk patients who receive implantable
cardioverter-defibrillators (ICDs) for primary sudden death prevention. The minority, however, will have an appropriate therapy
for ventricular tachycardia/fibrillation, and a similar number may
have complications or unnecessary therapy (often shocks). Thus,
there remains a need for better risk stratification to identify
patients likely to benefit. This investigation evaluated the ECG-
Most Read in Ventricular Arrhythmias
e81
derived QRS-T angle for predicting spontaneous arrhythmias and
mortality in an observational study of 412 primary prevention
defibrillator recipients with ischemic heart disease and a left
ventricular ejection fraction ⱕ40%. A widened spatial QRS-T
angle predicted spontaneous ventricular tachycardia/fibrillation,
with an adjusted hazard ratio of 7.3. Interestingly, in patients with
a spatial QRS-T angle ⱕ100°, the incidence of life-threatening
arrhythmias was as low as 2% during study follow-up. Similar
characteristics were observed for the planar QRS-T angle, which
is the frontal projection of the QRS-T angle but with lower
discriminative power (adjusted hazard ratio, 2.9). Further study of
the spatial QRS-T angle for risk stratification is warranted.
Conclusions: A wide QRS-T angle is a strong predictor of appropriate device therapy in primary prevention ICD recipients with
ischemic heart disease. Furthermore, a spatial QRS-T angle ⱕ100°
might be of value in the identification of patients in whom, although
currently indicated, ICD treatment should be reconsidered.19
J Wave, QRS Slurring, and ST Elevation in
Athletes With Cardiac Arrest in the Absence of
Heart Disease: Marker of Risk or
Innocent Bystander?
Riccardo Cappato, MD; Francesco Furlanello, MD; Valerio Giovinazzo, MD;
Tommaso Infusino, MD; Pierpaolo Lupo, MD; Mario Pittalis, MD; Sara Foresti, MD;
Guido De Ambroggi, MD; Hussam Ali, MD; Elisabetta Bianco, MD;
Roberto Riccamboni, MD; Gianfranco Butera, MD; Cristian Ricci, PhD;
Marco Ranucci, MD, Antonio Pelliccia, MD; Luigi De Ambroggi, MD
Summary: The ECG pattern of early repolarization (ie, J wave,
QRS slurring, and/or ST-segment elevation) in the inferior and
lateral ECG leads is a common finding in the general population
and is even more frequently observed in athletes. Recent studies
have suggested a potential proarrhythmic significance of these
findings in the general population, but data are lacking in athletes.
We investigated whether QRS-ST changes are markers of risk for
cardiac arrest or sudden death in athletes without underlying heart
disease. In a selected group of 21 young competitive athletes who
had cardiac arrest in the absence of heart disease, the prevalence
of J wave and/or QRS slurring in the inferior (II, III, and aVF) and
lateral leads (V4 to V6) was significantly higher in cases than in
control athletes. After sport discontinuation during 36-month
follow-up, arrhythmia recurrences did not differ between subgroups with and without J wave or QRS slurring. Because of
discrepancy between the frequency of early repolarization pattern
on 12-lead ECG and the rarity of cardiac arrest/sudden death, the
incidental finding of a J wave/QRS slurring in a healthy athlete
should be considered as a marker that minimally increases the
arrhythmic risk. The present findings provide novel insights on
clinical profiles of athletes at possible risk of cardiac arrest.
Conclusions: J wave and/or QRS slurring was found more frequently among athletes with cardiac arrest/sudden death than in
control athletes. Nevertheless, the presence of this ECG pattern
appears not to confer a higher risk for recurrent malignant
ventricular arrhythmias.20
New ECG Criteria in Arrhythmogenic Right
Ventricular Dysplasia/Cardiomyopathy
Moniek G.P.J. Cox, MD; Jasper J. van der Smagt, MD; Arthur A.M. Wilde, MD, PhD;
Ans C.P. Wiesfeld, MD, PhD; Douwe E. Atsma, MD, PhD; Marcel R. Nelen, PhD;
Luz-Maria Rodriguez, MD, PhD; Peter Loh, MD, PhD; Maarten J. Cramer, MD, PhD;
Pieter A. Doevendans, MD, PhD; J. Peter van Tintelen, MD, PhD;
Jacques M.T. de Bakker, PhD; Richard N.W. Hauer, MD, PhD
Summary: Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is characterized by progressive loss of predominantly right ventricular myocardium, which is replaced by
fibrofatty tissue. Typically, affected individuals present with
ventricular tachycardia between the 2nd and 4th decade of life,
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December 2011
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but ARVD/C is also a major cause of sudden death in adolescence. Clinical diagnosis was made according to generally accepted task force criteria (TFC). These criteria are highly specific
but lack sensitivity. After demonstration of high sensitivity and
specificity in a previous study, we showed that our newly
proposed additional ECG criteria improved ARVD/C diagnosis.
Patients highly suspected of ARVD/C, that is, with 3 points
according to current TFC (TFC3), were studied, being 21 index
patients and 12 family members of patients with proven ARVD/C.
Prolonged terminal activation duration is a new parameter on
right ventricular activation delay. Although only 1 of these
patients had an ␧ wave, 15 (45%) showed right ventricular
activation delay by prolonged terminal activation duration,
mainly family members. The new parameters on ventricular
tachycardia morphology, ventricular tachycardia with left bundlebranch block morphology and superior-axis and multiple ventricular tachycardia morphologies, were recorded in 12 of 21 (57%)
TFC3 index patients but not in family members. Altogether, 70%
of highly suspicious patients fulfilled ARVD/C diagnosis when
newly proposed criteria were applied additionally to current TFC.
Thus, adding our newly proposed ECG criteria would improve
sensitivity of current TFC and thereby ARVD/C diagnosis. By
this means, affected individuals can be recognized in an earlier
stage of disease, and appropriate therapeutic measures can be
taken to prevent arrhythmias and sudden death.
Conclusions: Adding the newly proposed criteria to current TFC for
ARVD/C will improve identification of affected individuals importantly, independent of outcome of DNA analyses.21
Clinical Characteristics and Genetic
Background of Congenital Long-QT Syndrome
Diagnosed in Fetal, Neonatal, and Infantile
Life: A Nationwide Questionnaire Survey
in Japan
Hitoshi Horigome, MD; Masami Nagashima, MD; Naokata Sumitomo, MD;
Masao Yoshinaga, MD; Hiroya Ushinohama, MD; Mari Iwamoto, MD;
Junko Shiono, MD; Koh Ichihashi, MD; Satoshi Hasegawa, MD;
Tadahiro Yoshikawa, MD; Tamotsu Matsunaga, MD; Hiroko Goto, MD;
Kenji Waki, MD; Masaki Arima, MD; Hisashi Takasugi, MD;
Yasuhiko Tanaka, MD; Nobuo Tauchi, MD; Masanobu Ikoma, MD;
Noboru Inamura, MD; Hideto Takahashi, PhD; Wataru Shimizu, MD;
Minoru Horie, MD
Summary: The congenital long-QT syndrome (LQTS) diagnosed
at perinatal life and through infancy is associated with high
morbidity and mortality rates. However, data on the clinical
presentation and genotype-phenotype correlation of this youngest
age group of LQTS are limited. A nationwide survey was
conducted in Japan, and 58 cases (18 fetuses, 31 neonates, and 9
infants) were registered. Among them, the peak age at diagnosis
was 0 –2 days, and the 3 most frequent clinical presentations
included sinus bradycardia, ventricular tachycardia/torsade des
pointes, and atrioventricular block. The genotype was confirmed
in 29 (71%) of 41 patients who underwent genotyping; the
incidence resembled that of child LQTS. Patients who presented
with early-onset ventricular tachycardia/torsade des pointes and
atrioventricular block were almost exclusively those with LQT2
and LQT3 among the 3 major genes, but a considerable number of
genetically unidentified ones were included. Sudden cardiac
death/aborted cardiac arrest were prevalent in the latter. LQT1
patients tended to show only sinus bradycardia or positive family
history of LQTS. These results mean that many life-threatening
episodes observed in early-onset LQTS should be treated immediately and aggressively even without knowledge of the genotype.
On the other hand, the present study was encouraging in that the
outcome of patients was favorable with multiple pharmaceutical
agents, typically with ␤-blockers, mexiletine, and magnesium and
with pacemaker implantation/implantable cardioverterdefibrillator, independent of the genotype. Further application of
gene testing is needed to establish the most appropriate genotypespecific strategy for these patients.
Conclusions: Patients with LQTS who showed life-threatening arrhythmias at perinatal periods were mostly those with LQT2, LQT3,
or no known mutations. Independent of the genotype, aggressive
intervention resulted in effective suppression of arrhythmias, with
only 7 deaths recorded.22
Outcomes of Early Risk Stratification and
Targeted Implantable Cardioverter-Defibrillator
Implantation After ST-Elevation–Myocardial
Infarction Treated With Primary Percutaneous
Coronary Intervention
Sarah Zaman, MBBS; Gopal Sivagangabalan, MBBS, FRACP; Arun Narayan, RN;
Aravinda Thiagalingam, MBChB, FRACP, PhD; David L. Ross, MBBS, FRACP;
Pramesh Kovoor, MBBS, PhD, FRACP
Summary: Selection of myocardial infarction (MI) survivors to
receive prophylactic implantable cardioverter-defibrillator (ICD)
therapy for primary prevention of sudden death requires further
elucidation. Although there is a mortality benefit for patients with
significantly depressed left ventricular function when ICDs are
implanted late after MI, a recent study found no benefit for patients
implanted early after MI, despite studies demonstrating a higher risk
of sudden death during the early months after MI that decreases with
time. The optimal clinical approach to protecting these patients is not
known, and data in the present era of primary percutaneous coronary
intervention are limited. Our study recruited consecutive patients
treated with primary percutaneous coronary intervention for acute
ST-elevation–myocardial infarction (STEMI). Patients with left
ventricular ejection fraction ⱕ40% underwent electrophysiological
study followed by ICD implantation in those with inducible ventricular tachycardia ⱖ200-ms cycle length. The overall mortality of 3%
at 1 year was low compared with previous primary prevention
studies, and there was no evidence of excess mortality with ICD
implantation early after MI. In addition, patients with inducible
ventricular tachycardia selected to receive an ICD had a relatively
high rate of spontaneous ICD therapy for ventricular arrhythmias of
22%. Although not randomized, this study suggests favorable outcomes with a uniform, systematic primary prevention protocol
integrated within an STEMI primary percutaneous coronary intervention service. This approach appears to be a rational approach to
safely allocate ICD implantation early after STEMI.
Conclusions: Early ICD implantation limited to patients with inducible ventricular tachycardia enables a low overall mortality in
patients with impaired left ventricular ejection fraction after primary
percutaneous coronary intervention for STEMI.23
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Circulation: Arrhythmia and Electrophysiology Editors' Picks: Most Read Articles on the
Topic of Ventricular Arrhythmias
The Editors
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Circ Arrhythm Electrophysiol. 2011;4:e76-e83
doi: 10.1161/CIRCEP.111.968941
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