Circulation. 2008;117:2567-2569
doi: 10.1161/CIRCULATIONAHA.107.189726
(Circulation. 2008;117:2567-2569.)
© 2008 American Heart Association, Inc.
Clinical Summaries
 |
Catheter Ablation for Atrial Fibrillation in Patients With Obesity
|
|---|
The present study reports the clinical outcomes of catheter-based
ablation (Lasso-guided pulmonary vein isolation or 3-dimensional
mapping-guided wide-area pulmonary vein isolation) for symptomatic
atrial fibrillation, focusing on an obese patient population.
The patients were grouped by body mass index (lean, <25 kg/m
2;
overweight, 25 to 29.9 kg/m
2; obese,
30 kg/m
2). The vast majority
of patients who underwent catheter ablation therapy for symptomatic
atrial fibrillation were obese (38%) or overweight (44%). The
obese population with atrial fibrillation appears to be more
symptomatic with lower Medical Outcomes Study 36-item Short-Form
General Health Survey scores for quality of life than lean patients.
At the 12-month follow-up, there was no significant difference
in atrial fibrillation elimination rate (75%, 72%, and 70% in
the lean, overweight, and obese patients, respectively) without
the use of antiarrhythmic drugs. The present study conveys that
most patients who underwent catheter ablation therapy for symptomatic
AF were obese or overweight and provides an encouraging outcome
of using catheter ablation in treating patients with obesity
and atrial fibrillation. Although weight reduction, an appropriate
exercise program, and treatment of hypertension, dyslipidemia,
diabetes mellitus, and obstructive sleep apnea are of importance,
curative pulmonary vein isolation is a reasonable option in
the armamentarium of therapies for obese patients with symptomatic
atrial fibrillation. See p
2583.
|
Independent Prognostic Importance of a Restrictive Left Ventricular Filling Pattern After Myocardial Infarction: An Individual Patient Meta-Analysis: Meta-Analysis Research Group in Echocardiography Acute Myocardial Infarction
|
|---|
We try to predict the future of our patients with myocardial
infarction to improve our understanding of the disease, intervene,
and improve the prognosis for individual patients. Echocardiography
provides an easily available, attractive tool to identify high-risk
patients. The Meta-Analysis Research Group in Echocardiography
(MeRGE) study is an individual patient meta-analysis, representing
the largest cohort with comprehensive Doppler echocardiography
in the setting of acute myocardial infarction. The study demonstrates
that a restrictive mitral filling pattern is an important prognostic
indicator in a wide range of patients after acute myocardial
infarction. Restrictive filling, characterized by a high mitral
E-to-A ratio and short deceleration time, is easily identified
from standard echocardiography, and even though it usually is
seen when systolic function is impaired, it may also be seen
if systolic function appears to be only mildly impaired. This
filling pattern occurs in
20% of patients after myocardial infarction
and when present is associated with a nearly 3-fold increase
in mortality. This study clearly demonstrates that this relationship
is independent of age, left ventricular size, ejection fraction,
and Killip class, highlighting the importance of the assessment
of left ventricular filling with echocardiography in all patients
after myocardial infarction, regardless of infarct size, presence
and degree of systolic impairment, or extent of left ventricular
remodeling. Assessment of left ventricular filling pattern is
simple, quick, and easily applied and should be part of the
routine risk assessment after myocardial infarction. See p
2591.
|
Left Ventricular Morphology and Systolic Function in Sleep-Disordered Breathing: The Sleep Heart Health Study
|
|---|
The present study evaluates the association of obstructive sleep-disordered
breathing with left ventricular morphology and function in a
community-based sample of adults drawn from the Cardiovascular
Health Study, Framingham Heart Study, and Strong Heart Study.
The primary outcome measure was left ventricular mass index,
an important predictor of cardiovascular mortality and morbidity.
There was a significant association between sleep-disordered
breathing at a severity commonly encountered in the general
population and increased left ventricular mass index, after
adjustment for known and potential causes of left ventricular
hypertrophy, including age, sex, body mass index, hypertension,
history of diabetes mellitus and myocardial infarction, smoking,
and alcohol consumption. Left ventricular hypertrophy in subjects
with sleep-disordered breathing had a pattern of eccentric rather
than concentric hypertrophy. Modestly reduced global left ventricular
systolic function was also observed. The results of the present
study add to the growing literature supporting an association
of sleep-disordered breathing and cardiovascular disease and
suggest that obstructive sleep-disordered breathing should be
considered as a possible causative factor in the development
of left ventricular hypertrophy and dilated cardiomyopathy.
See p
2599.
|
Results of the Predictors of Response to CRT (PROSPECT) Trial
|
|---|
Cardiac resynchronization has revolutionized the care of a substantial
portion of patients with advanced heart failure; for those with
appropriate indications, cardiac resynchronization therapy appears
to improve clinical status in
70% of those treated. Although
this degree of response is very encouraging, numerous echocardiographic
techniques, based largely on tissue Doppler measurements, have
been developed to better distinguish responders from nonresponders.
Ideally, the ability to accurately predict likelihood of response
will enhance the quality and substance of the physician-patient
conversation before treatment. These methods attempt to detect
mechanical dyssynchrony more accurately than with the QRS under
the assumption that correction of dyssynchrony is the main mechanism
of action with cardiac resynchronization therapy. However, there
had not been a large multicenter study to evaluate these methods
prospectively. In 426 patients, Predictors of Response to CRT
(PROSPECT) studied 12 echocardiographic methods for their ability
to predict response and showed that in the multicenter setting,
they lacked sensitivity and specificity to affect clinical decisions.
We therefore recommend that these methods not be used routinely
in evaluating a patient for cardiac resynchronization therapy.
Other methods are under investigation (eg, strain measurements,
3-dimensional imaging, scar location) that may be able to distinguish
responders from nonresponders with more accuracy. However, before
they can be recommended for general use, their applicability
should be tested in a multicenter setting. See p
2608.
|
Comparison of Echocardiographic Dyssynchrony Assessment by Tissue Velocity and Strain Imaging in Subjects With or Without Systolic Dysfunction and With or Without Left Bundle-Branch Block
|
|---|
Because a substantial number of patients who meet current clinical
and ECG criteria for cardiac resynchronization therapy (CRT)
do not improve after biventricular pacing, the importance of
using a mechanical dyssynchrony parameter as an additional selection
criterion has been emphasized. Intraventricular dyssynchrony
measured by timing differences in peak systolic tissue velocity
was found to be a major predictor of the effect of CRT. Currently,
echocardiographic dyssynchrony indexes are regarded as a standard
method for measuring dyssynchrony and are used as a tool to
select patients for CRT, to monitor the effect of CRT, and to
optimize biventricular pacing. These indexes also have been
shown to be frequently positive in heart failure patients with
normal QRS duration and/or normal ejection fraction, indicating
that CRT may improve their symptoms. Most of these studies,
however, are from a single center and are not randomized in
a relatively small number of patients. Moreover, how often this
echocardiographically derived dyssynchrony is present in normal
subjects and in patients with heart failure but without conduction
delay is not well known. Our study demonstrated that tissue
velocity–derived dyssynchrony is common in normal healthy
control subjects and that there is a large overlap of these
values among groups who may or may not be a candidate for CRT.
The strain-derived dyssynchrony index was found to be better
than tissue velocity–derived dyssynchrony in distinguishing
groups of different ejection fractions and QRS durations. Further
clinical investigations are necessary to identify the best echocardiographic
dyssynchrony parameters and to determine the role of echocardiography
in CRT. See p
2617.
|
Reversal of Cardiac Hypertrophy and Fibrosis From Pressure Overload by Tetrahydrobiopterin: Efficacy of Recoupling Nitric Oxide Synthase as a Therapeutic Strategy
|
|---|
Sustained pressure overload induces profound ventricular remodeling
and is a leading cause of cardiac failure. An important mechanism
for this maladaptive response is stimulation of reactive oxygen
species, and recent studies indicate that functional uncoupling
of nitric oxide synthase (NOS) plays an important role in this
pathophysiology. A key determinant of NOS coupling, and thus
its generation of NO versus O
2–, is the level and redox
state of its cofactor tetrahydrobiopterin (BH4), which becomes
compromised from pressure-overload stress. Here, we tested whether
exogenous administration of BH4 could restore NOS coupling and
function, reduce oxidant stress, and block or reverse maladaptive
remodeling in hearts with already advanced disease induced by
pressure overload. In mice subjected to proximal aortic constriction,
BH4 stopped progressive chamber dilation and dysfunction, reversed
fibrosis and hypertrophy, and improved myocyte function and
calcium handling. NOS became recoupled, and oxidant stress potently
declined. The effects of BH4 were linked to NO–reactive
oxygen species interactions and became manifest when NOS activity
started to decline after induction of pressure overload. Parallel
studies performed with a broad antioxidant (Tempol) did not
replicate BH4 effects on reverse remodeling even though oxidant
stress was reduced. Furthermore, selective enhancement of BH4
in endothelial cells did not mimic the response to exogenous
BH4, highlighting the importance of myocyte NOS uncoupling.
These findings support the potential therapeutic utility of
BH4 as a treatment for advanced hypertrophic heart disease.
They also highlight the notion that not all antioxidant strategies
are equivalent and that targeting NOS uncoupling could prove
to be a particularly potent approach. See p
2626.
|
Effect of Short Call Admission on Length of Stay and Quality of Care for Acute Decompensated Heart Failure
|
|---|
We studied the quality of care delivered for patients admitted
to an academic-affiliated Veterans Affairs Medical Center for
acute decompensated heart failure. We were concerned that patients
who were admitted to a resident short call team might have delays
in the processes of their care such as the time to second diuretic
dose and subsequently a longer length of stay. Short call teams
(primary team) admit during the daytime and transfer patient
care to physicians for overnight coverage (long call). Care
is then transferred back to the primary team in the morning.
These transfers potentially result in delays in care. We studied
218 patients with acute decompensated heart failure admitted
to either short call or long call between July 1, 2003, and
June 30, 2005. Patients admitted to short call had a longer
median length of stay than patients admitted to long call (5.2
versus 3.9 days;
P=0.0004). After adjustment for patient characteristics
and comorbidities, short call patients had a 44% increase in
length of stay compared with long call patients. Short call
patients received fewer diuretic doses in the first 24 hours
of hospitalization (1.80 versus 2.12;
P=0.01) and had a longer
median time to the second dose of loop diuretics compared with
long call patients (17.9 versus 16.2 hours;
P=0.04). Additional
studies are needed to clarify the impact of short call admission
at academic medical centers on inpatient quality of care. See
p
2637.
|
Novel Role for Inhibitor of Differentiation 2 in the Genesis of Angiotensin II–Induced Hypertension
|
|---|
The mechanisms by which hypertension damages the heart and kidneys
are not known, but immune responses are involved. Angiotensin
(Ang) II is a blood pressure–raising and potentially organ-damaging
substance that is inhibited or blocked by drugs directed at
the renin-angiotensin system. We studied mice lacking the basic
helix-loop-helix transcription factor Id2 that is responsible
for antigen-presenting Langerhans dendritic cell production
and T-cell function. These mice were remarkably resistant to
the blood pressure–raising or organ-damaging effects of
Ang II. Oddly, the vessels constricted appropriately after acute
intravenous injections of Ang II and norepinephrine, with an
increase in blood pressure. To our surprise, bone marrow transplant
of Id2-containing marrow cells did not restore the Ang II responses,
nor did Id2
–/– kidneys transplanted to wild-type
mice produce the Id2
–/– phenotype. Crossing Id2-deficient
mice with transgenic mice that produce Ang II yielded the same
responses as the Ang II infusions. In primary vascular smooth
muscle cells, we also observed that Id2 deficiency was associated
with increased peroxisome proliferator-activated receptor-
and
decreased peroxisome proliferator-activated receptor-
expression.
Furthermore, Id2 deficiency protected vascular smooth muscle
cells from senescence. Id2 is a downstream molecule of transforming
growth factor-β signaling. Ang II is known to activate
transforming growth factor-β. Although we do not yet understand
the mechanisms and cell type involved, our findings underscore
the role of the transforming growth factor-β–Id2
axis in chronic hypertension-induced vascular disease and could
be of therapeutic relevance in the future. See p
2645.
|
Endothelial Dysfunction and Cytomegalovirus Replication in Pediatric Heart Transplantation
|
|---|
Cardiac allograft vasculopathy, the major limiting factor to
the long-term success of pediatric heart transplantation, is
associated with the development of endothelial dysfunction in
the donor coronary arteries. Cytomegalovirus (CMV) has been
shown to be a significant risk factor for the development of
cardiac allograft vasculopathy. Recent work has demonstrated
CMV DNA in leukocytes in the absence of direct allograft infection,
suggesting that vascular changes may not be limited to the allograft.
The present project used flow-mediated dilation in the brachial
artery to illustrate decreased native endothelial function in
children who had shown CMV replication after heart transplantation.
Importantly, none of the patients enrolled in the present study
were CMV DNA polymerase chain reaction positive at the time
of their scan, and only 1 developed clinical CMV disease. In
addition, it was interesting to note that neither the pretransplantation
CMV status of donor or recipient nor CMV mismatch was associated
with changes in brachial endothelial function. The present work
demonstrates that the effects of posttransplantation CMV are
not limited to the allograft and that traditional risk factors
for CMV disease may not be adequate to identify those patients
who are most likely to suffer CMV-mediated complications. It
also promotes the idea that subclinical CMV replication may
be an important influence on later vascular health, even after
virus is no longer detectable in the blood. Further studies
are required to prove a link between systemic endothelial dysfunction
and the later development of cardiac allograft vasculopathy
in these patients. See p
2657.
|
Inhibition of Interleukin-1 by Anakinra Improves Vascular and Left Ventricular Function in Patients With Rheumatoid Arthritis
|
|---|
Atherogenesis shares similar pathophysiological mechanisms with
the inflammatory process in patients with rheumatoid arthritis,
including increased nitrooxidative stress and release of proinflammatory
cytokines and endothelins. Interleukin-1 mediates atherogenesis
and coronary vasoreactivity. Anakinra, a human recombinant interleukin-1a
receptor antagonist, is currently used for the treatment of
rheumatoid arthritis. In the present study, we have shown that
treatment with anakinra improves coronary flow and endothelial,
arterial, and left ventricular function compared with placebo
and is related to a concomitant reduction of nitrooxidative
stress, inflammation, and endothelin in patients with rheumatoid
arthritis. Additionally, anakinra was more effective than corticosteroids
in improving vascular and left ventricular function after 30
days of treatment. In a large study of patients with rheumatoid
arthritis and comorbidities, including coronary artery disease,
there were no differences in cardiovascular events or serious
infections after anakinra compared with placebo. Anakinra has
a more favorable safety profile than other humoral regimens
that improve vascular function. Thus, inhibition of interleukin-1
activity may improve outcome by improving vascular and left
ventricular function in patients with rheumatoid arthritis and
may be a potential therapeutic target in patients with coronary
artery disease. See p
2662.
|
Anakinra, a Recombinant Human Interleukin-1 Receptor Antagonist, Inhibits Apoptosis in Experimental Acute Myocardial Infarction
|
|---|
Acute myocardial infarction remains a major cause of morbidity
and mortality despite current strategies for early reperfusion.
Many patients die early during the course, and those who survive
are at risk of dying late as a result of adverse cardiac remodeling
and heart failure. The initial ischemic damage to the myocardium
activates reparative events that are initially beneficial but
entrain late events that eventually lead to adverse cardiac
remodeling and heart failure. Ventricular remodeling is a complex
process mediated by alterations in stereotypic pathways that
can trigger hypertrophy and apoptosis (programmed cell death),
resulting in a delicate balance between cardiomyocyte death
and survival. Interventions that limit the extent of infarction
and/or inhibit apoptosis have the potential to prevent adverse
cardiac remodeling and heart failure–related deaths. Interleukin-1
(IL-1) receptor antagonist (IL-1Ra) is part of the IL-1 family
and competes with IL-1β for its receptor acting as an antiinflammatory
protein. IL-1Ra levels are consistently elevated in patients
with acute myocardial infarction and behave as a marker of disease.
Using an established model of acute myocardial infarction with
surgical ligation of the left coronary artery, we have found
that IL-1Ra promotes cell survival through an intrinsic antiapoptotic
activity. Administration of anakinra, an exogenous recombinant
human IL-1Ra, within 24 hours of acute myocardial infarction
in this model resulted in amelioration of postinfarction cardiac
remodeling and heart failure. These findings may open a new
therapeutic window for the treatment of ischemic injury and
remodeling for the prevention and treatment of ischemic heart
failure, which may ultimately benefit several thousands of patients.
See p
2670.
Related Articles:
-
Catheter Ablation for Atrial Fibrillation in Patients With Obesity
- Yong-Mei Cha, Paul A. Friedman, Samuel J. Asirvatham, Win-Kuang Shen, Thomas M. Munger, Robert F. Rea, Peter A. Brady, Arshad Jahangir, Kristi H. Monahan, David O. Hodge, Ryan A. Meverden, Bernard J. Gersh, Stephen C. Hammill, and Douglas L. Packer
Circulation 2008 117: 2583-2590.
[Abstract]
[Full Text]
-
Left Ventricular Morphology and Systolic Function in Sleep-Disordered Breathing: The Sleep Heart Health Study
- Hassan A. Chami, Richard B. Devereux, John S. Gottdiener, Reena Mehra, Mary J. Roman, Emelia J. Benjamin, and Daniel J. Gottlieb
Circulation 2008 117: 2599-2607.
[Abstract]
[Full Text]
-
Endothelial Dysfunction and Cytomegalovirus Replication in Pediatric Heart Transplantation
- Jacob Simmonds, Matthew Fenton, Catherine Dewar, Elizabeth Ellins, Clare Storry, David Cubitt, John Deanfield, Nigel Klein, Julian Halcox, and Michael Burch
Circulation 2008 117: 2657-2661.
[Abstract]
[Full Text]
-
Inhibition of Interleukin-1 by Anakinra Improves Vascular and Left Ventricular Function in Patients With Rheumatoid Arthritis
- Ignatios Ikonomidis, John P. Lekakis, Maria Nikolaou, Ioannis Paraskevaidis, Ioanna Andreadou, Theophania Kaplanoglou, Pelagia Katsimbri, Grigorios Skarantavos, Panayiotis N. Soucacos, and Dimitrios T. Kremastinos
Circulation 2008 117: 2662-2669.
[Abstract]
[Full Text]
-
Comparison of Echocardiographic Dyssynchrony Assessment by Tissue Velocity and Strain Imaging in Subjects With or Without Systolic Dysfunction and With or Without Left Bundle-Branch Block
- Chinami Miyazaki, Brian D. Powell, Charles J. Bruce, Raul E. Espinosa, Margaret M. Redfield, Fletcher A. Miller, David L. Hayes, Yong-Mei Cha, and Jae K. Oh
Circulation 2008 117: 2617-2625.
[Abstract]
[Full Text]
-
Reversal of Cardiac Hypertrophy and Fibrosis From Pressure Overload by Tetrahydrobiopterin: Efficacy of Recoupling Nitric Oxide Synthase as a Therapeutic Strategy
- An L. Moens, Eiki Takimoto, Carlo G. Tocchetti, Khalid Chakir, Djahida Bedja, Gianfranco Cormaci, Elizabeth A. Ketner, Maulik Majmudar, Kathleen Gabrielson, Marc K. Halushka, James B. Mitchell, Shyam Biswal, Keith M. Channon, Michael S. Wolin, Nicholas J. Alp, Nazareno Paolocci, Hunter C. Champion, and David A. Kass
Circulation 2008 117: 2626-2636.
[Abstract]
[Full Text]
-
Independent Prognostic Importance of a Restrictive Left Ventricular Filling Pattern After Myocardial Infarction: An Individual Patient Meta-Analysis: Meta-Analysis Research Group in Echocardiography Acute Myocardial Infarction
- Meta-Analysis Research Group in Echocardiography (MeRGE) AMI Collaborators
Circulation 2008 117: 2591-2598.
[Abstract]
[Full Text]
-
Anakinra, a Recombinant Human Interleukin-1 Receptor Antagonist, Inhibits Apoptosis in Experimental Acute Myocardial Infarction
- Antonio Abbate, Fadi N. Salloum, Elena Vecile, Anindita Das, Nicholas N. Hoke, Stefania Straino, Giuseppe G.L. Biondi-Zoccai, Jon-Erik Houser, Ian Z. Qureshi, Evan D. Ownby, Edoardo Gustini, Luigi M. Biasucci, Anna Severino, Maurizio C. Capogrossi, George W. Vetrovec, Filippo Crea, Alfonso Baldi, Rakesh C. Kukreja, and Aldo Dobrina
Circulation 2008 117: 2670-2683.
[Abstract]
[Full Text]
-
Effect of Short Call Admission on Length of Stay and Quality of Care for Acute Decompensated Heart Failure
- Jennifer L. Schuberth, Tom A. Elasy, Javed Butler, Robert Greevy, Theodore Speroff, Robert S. Dittus, and Christianne L. Roumie
Circulation 2008 117: 2637-2644.
[Abstract]
[Full Text]
-
Results of the Predictors of Response to CRT (PROSPECT) Trial
- Eugene S. Chung, Angel R. Leon, Luigi Tavazzi, Jing-Ping Sun, Petros Nihoyannopoulos, John Merlino, William T. Abraham, Stefano Ghio, Christophe Leclercq, Jeroen J. Bax, Cheuk-Man Yu, John Gorcsan, III, Martin St John Sutton, Johan De Sutter, and Jaime Murillo
Circulation 2008 117: 2608-2616.
[Abstract]
[Full Text]
-
Novel Role for Inhibitor of Differentiation 2 in the Genesis of Angiotensin II–Induced Hypertension
- Petra Gratze, Ralf Dechend, Carolin Stocker, Joon-Keun Park, Sandra Feldt, Erdenechimeg Shagdarsuren, Maren Wellner, Faikah Gueler, Song Rong, Volkmar Gross, Michael Obst, Ralph Plehm, Natalia Alenina, Ana Zenclussen, Jens Titze, Kersten Small, Yoshifumi Yokota, Martin Zenke, Friedrich C. Luft, and Dominik N. Muller
Circulation 2008 117: 2645-2656.
[Abstract]
[Full Text]
Top
Catheter Ablation for Atrial...
Independent Prognostic...