Circulation. 2008;118:793-794
doi: 10.1161/CIRCULATIONAHA.108.190522
(Circulation. 2008;118:793-794.)
© 2008 American Heart Association, Inc.
Circulation: Clinical Summaries
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Physical Activity and Incidence of Atrial Fibrillation in Older Adults: The Cardiovascular Health Study
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Physical activity is often considered to increase the risk of
atrial fibrillation (AF), on the basis of anecdotal reports,
case series, and retrospective studies evaluating vigorous exertion
and endurance training in younger and middle-aged athletes;
however, most AF cases do not occur in athletes but in the general
population of older adults (
65 years old), in whom 10-year risk
of AF approaches 20%. At these ages, AF risk factors include
long-standing hypertension, reduced ventricular compliance,
and structural heart disease, all of which are risk factors
that might be improved or prevented by habitual light to moderate
activity. However, relationships of physical activity with incidence
of AF in older adults had not been evaluated. We prospectively
investigated associations of habitual light to moderate activity,
including leisure-time activities and walking, with AF incidence
among 5446 adults
65 years of age over a 12-year period. After
adjustment for other risk factors, both leisure-time activity
and walking were associated with significantly lower AF incidence,
including a 36% lower risk for the highest versus lowest quintile
of leisure-time activity and a 50% lower risk for the highest
versus lowest category of walking distance/pace. Strenuous exertion
was not required: Lower risk was seen with regularly walking
5 to 10 blocks per week and at 2- to 3-mph paces (greater distances
and paces were associated with even lower risk). Although these
observational findings do not prove causality, the strength
and consistency of associations, including among individuals
with and without preexisting cardiovascular disease, and the
known biological effects of exercise suggest that regular light
to moderate activity may reduce AF incidence in older adults.
This provides additional strong impetus for clinicians and policy
makers to focus on regular physical activity, including leisure-time
activities and walking, to maintain cardiovascular health in
older adults. See p
800.
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Contemporary Analysis of Descending Thoracic and Thoracoabdominal Aneurysm Repair: A Comparison of Endovascular and Open Techniques
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Numerous comparisons have been conducted between open and endovascular
repair of aortic lesions; however, in nearly all reports, with
the exception of the prospective randomized trials involving
infrarenal abdominal aortic aneurysm, significant anatomic differences
exist between groups. The present contemporary comparison of
724 consecutive patients treated with open surgery (372) or
pure endovascular (352) procedures with thoracic and branched
technology contrasted outcomes in the context of the anatomic
extent of the repair. The results demonstrate similar incidences
of paraplegia and 30-day and 12-month mortality irrespective
of the repair technique used; however, an inherent treatment
bias existed toward the repair of younger healthier patients
with conventional treatments, whereas endovascular repair was
reserved for less fit patients. Endovascular patients were on
average 9 years older and were sicker by nearly every metric
considered (cardiac, pulmonary, and renal disease; diabetes
mellitus; smoking; and cancer). The highest risk for death and
paraplegia occurred with the most extensive aneurysms (type
II), whereas the lowest risks were associated with the least
extensive aneurysms (isolated thoracic aneurysms), with paraplegia
occurring in <1% of these individuals. Prior distal aortoiliac
operations were associated with a higher incidence of paraplegia
in endovascular patients, and chronic dissections also increased
the incidence of paraplegia in patients who underwent open surgical
repair. On the basis of the observations of this study, it is
clear that endovascular repair of extensive aneurysms is feasible
and capable of producing results similar to open surgical techniques,
even in more physiologically challenged patients. See p
808.
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Improvement in Left Ventricular Remodeling by the Endothelial Nitric Oxide Synthase Enhancer AVE9488 After Experimental Myocardial Infarction
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Nitric oxide (NO) generated by the endothelial NO synthase (eNOS)
plays a key role in vascular tone and cardiomyocyte contractility
and protects against hypertrophy and atherosclerosis. Cardiac
and vascular NO bioavailability is reduced in heart failure,
contributing to contractile dysfunction, ventricular hypertrophy,
and remodeling, as well as endothelial dysfunction. Overexpression
of the eNOS gene in endothelial cells or cardiomyocytes improved
cardiac performance in mice after myocardial infarction. Various
established pharmacological interventions in heart failure enhance
NO bioavailability. Nitrates are powerful NO donors widely used
in coronary artery diseases and heart failure. However, nitrate
tolerance and the induction of reactive oxygen species formation
limit their benefits. In the present study, we tested the concept
of directly augmenting eNOS by pharmacological intervention.
The novel compound AVE9488, shown to elevate eNOS expression
and NO production, improved left ventricular remodeling and
contractile dysfunction in rats after coronary artery ligation.
Myocardial molecular alterations were prevented by AVE9488;
endothelial vasomotor dysfunction and superoxide formation were
attenuated; and levels of circulating endothelial progenitor
cell were elevated. Importantly, the phenomenon of eNOS uncoupling,
which may lead to production of superoxide anions instead of
NO, was not observed after treatment with AVE9488. Thus, a pharmacological
intervention to increase eNOS expression and subsequent NO formation
constitutes a promising therapeutic approach for the amelioration
of postinfarction ventricular remodeling and heart failure.
See p
818.
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Smoothelin-B Deficiency Results in Reduced Arterial Contractility, Hypertension, and Cardiac Hypertrophy in Mice
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The causes of essential hypertension remain largely unknown,
although it is commonly accepted that vascular smooth muscle
dysfunction is a potential culprit. Improved insight into the
mechanics and regulation of smooth muscle contraction may provide
additional therapeutic targets to treat pathologies such as
hypertension. However, our current understanding of these 2
aspects of smooth muscle function is limited. Here, we introduce
smoothelin, a protein specifically expressed in fully differentiated,
contractile smooth muscle cells, as a crucial component of the
vascular smooth muscle cell contractile apparatus. We demonstrate
for the first time that smoothelin is necessary for physiological
vascular smooth muscle contraction. Smoothelin deficiency in
mice resulted in severely reduced contractile potential, particularly
in smaller arteries. Paradoxically, this was accompanied by
hypertension and concomitant cardiac hypertrophy. Analyses of
differently sized blood vessels indicated that the cause of
the hypertension is likely to be downstream of vessels like
the saphenous artery and/or mediated by overcompensation of
blood pressure regulatory systems like the renin-angiotensin
system. Recently, imatinib, a drug used in clinical practice,
was shown to specifically promote smoothelin expression in vascular
smooth muscle cells. Considering the currently reported data,
such an increase in smoothelin concentration not only may indicate
a more contractile phenotype of the vascular smooth muscle cell
but also may improve vascular smooth muscle contractile potential.
The combination of an increased knowledge of smoothelin function
and the availability of pharmacological tools that affect smoothelin
expression provides interesting opportunities to treat pathologies
originating from vascular smooth muscle cell dysfunction. See
p
828.
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Cardiac Magnetic Resonance With T2-Weighted Imaging Improves Detection of Patients With Acute Coronary Syndrome in the Emergency Department
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Cardiac magnetic resonance (CMR) is emerging as an alternative
noninvasive diagnostic test for rapid and accurate assessment
of patients with acute chest pain who present to the emergency
room, particularly for patients with intermediate risk of developing
an acute coronary syndrome. We demonstrated that CMR with T2-weighted
imaging and left ventricular wall thickness analysis provided
not only high diagnostic accuracy for detection of patients
with acute coronary syndrome but also allowed the differentiation
of patients with acute versus old myocardial infarction. Furthermore,
the CMR changes presented before the rise of cardiac enzymes
in patients with non–ST-segment myocardial infarction
(6±2 hours), and the combination of T2-weighted imaging,
a signature of myocardial edema, and delayed hyperenhancement,
which represents myocardial necrosis, allowed further characterization
as unstable angina or non–ST-segment myocardial infarction.
Finally, the CMR data provided significant incremental value
over initial clinical assessment and traditional cardiac risk
factors (odds ratio 129.4, 95% confidence interval 11.8 to >999.9).
These data suggest that a 30-minute CMR protocol is feasible
and accurate in the emergency department setting. Future studies
will need to determine the impact of CMR in clinical decision
making and assess the cost-effectiveness of CMR in the emergency
department setting. See p
837.
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Mitral Leaflet Adaptation to Ventricular Remodeling: Occurrence and Adequacy in Patients With Functional Mitral Regurgitation
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Left ventricular remodeling after myocardial infarction or in
dilated cardiomyopathy creates mismatch between mitral leaflet
and ventricular size, which leads to ischemic mitral regurgitation,
a source of increased heart failure and mortality. We explored
whether the valve itself adapts to the stresses imposed by the
dilating ventricle. Three-dimensional echocardiography, validated
against excised valves, measured diastolic leaflet area in 80
patients and control subjects. Leaflet area was an average of
35% greater in patients with left ventricular dysfunction than
in control subjects. Leaflet area showed comparable adaptation
to annular area in all groups (nearly 2-fold ratio). However,
leaflet area was a strong independent predictor of mitral regurgitation,
and patients with mitral regurgitation had reduced ratios of
total leaflet area to the tented leaflet area required to close
the annular orifice in systole. The valve therefore adapts to
the increased size of remodeled ventricles, but the degree of
adaptation may be insufficient to prevent mitral regurgitation
by meeting the geometric demands imposed on the stretched leaflets.
Understanding the mechanisms of mitral valve adaptation can
potentially provide new therapeutic targets. See p
845.
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Electroanatomic Mapping of the Left Ventricle in a Porcine Model of Chronic Myocardial Infarction With Magnetic Resonance–Based Catheter Tracking
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During catheter ablation of cardiac arrhythmias, the importance
of delineating the cardiac anatomy is undisputed. Currently,
image integration with either computed tomographic or magnetic
resonance (MR) imaging is used both to enhance the acquisition
of 3-dimensional electroanatomic mapping and to guide radiofrequency
ablation. Typically, the imaging is performed before the procedure
and registered to the patient’s anatomy at the time of
the procedure using fiducial landmarks. However, a more ideal
paradigm would be to perform these procedures completely in
an MR imaging environment. Both errors in registration and exposure
to ionizing radiation could theoretically be eliminated. Superior
anatomic visualization could be possible with the generation
of vascular roadmaps by MR angiography and visualization of
abnormal infracted or ablated myocardium with myocardial delayed
enhancement imaging. In this porcine study, MR tracking of microcoils
embedded in electrophysiology catheters was used to navigate
the catheters to the left ventricle at rates approaching that
of x-ray fluoroscopy (13 to 15 frames per second) using MR angiography
vascular roadmap guidance. With myocardial delayed enhancement
images, it was possible to accurately maneuver the catheter
within the chamber, to measure intracardiac electrograms, and
to project this spatial and electrogram information onto the
MR angiography–generated 3-dimensional left ventricle
models. In infracted animals, MR imaging–based voltage
maps were compared with standard x-ray–based electroanatomic
voltage maps to establish the equivalency of this MR-tracking
approach to ventricular mapping. This article demonstrates that
it may be possible to use these imaging techniques with active
MR tracking to perform electrophysiology procedures in a clinically
relevant manner completely in an MR imaging environment. See
p
853.
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