Circulation. 2008;118:897-898
doi: 10.1161/CIRCULATIONAHA.108.190523
(Circulation. 2008;118:897-898.)
© 2008 American Heart Association, Inc.
Clinical Summaries
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Cardiac Memory in Patients With Wolff-Parkinson-White Syndrome: Noninvasive Imaging of Activation and Repolarization Before and After Catheter Ablation
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ECG imaging, a noninvasive imaging modality for cardiac electrophysiology,
determines the locations of Wolff-Parkinson-White accessory
pathways with greater accuracy than the conventional ECG-based
Arruda algorithm. This capability makes ECG imaging an effective
tool for guiding accessory pathway ablation procedures, possibly
shortening their time and reducing the associated iatrogenic
risks. ECG imaging also can be used to evaluate the outcome
of ablation. The study shows that persistent preexcitation,
which constitutes a natural model for prolonged ventricular
pacing from the accessory pathway insertion site, leads to high
dispersion of repolarization and a prolonged activation-recovery
interval (action potential duration) at the preexcited (paced)
region. The abnormal repolarization gradients resolve over a
period of 1 month after a return to normal sinus rhythm by successful
ablation. This time course is consistent with long-term cardiac
memory, possibly involving transcriptional changes that trigger
remodeling processes that alter the molecular determinants of
action potential duration. The results of this study may apply
to other clinical situations like cardiac pacing in which a
high dispersion of repolarization in a structurally abnormal
heart might provide a possible mechanistic basis of pacing-induced
proarrhythmia reported in the literature. See p
907.
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Neural Mechanisms of Paroxysmal Atrial Fibrillation and Paroxysmal Atrial Tachycardia in Ambulatory Canines
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Paroxysmal atrial fibrillation (PAF) is a common cardiac arrhythmia.
In the present study, we developed a canine model of PAF induced
by intermittent rapid atrial pacing. Continuous autonomic nerve
recordings showed that simultaneous sympathovagal discharge
is a common trigger for PAF in this model. Cryoablation of the
stellate ganglion and cardiac branch of the vagal nerve prevented
PAF. A clinical implication of this study is that similar procedures
designed to reduce sympathetic and vagal outflow to the heart
might prevent PAF in human patients. Stellate ganglion ablation
has been used for more than 30 years to prevent recurrent ventricular
arrhythmias in patients with long-QT syndrome, catecholaminergic
polymorphic ventricular tachycardia, and coronary artery diseases.
The results of the present study suggest that similar procedures
might be useful in reducing the frequencies of PAF. Because
nerve sprouting and sympathetic hyperinnervation are prominent
features of the PAF model used in the present study, we propose
that patients with evidence of autonomic mechanisms of PAF might
be most likely to benefit from this procedure. In addition to
surgical interventions, these studies also have implications
for pharmacological therapy of PAF. Because simultaneous sympathovagal
discharges are often the triggers of PAF, drugs that inhibit
both β-blockers and acetylcholine-sensitive potassium current
(
IKACh) may be more effective in preventing PAF than drugs without
these actions. Amiodarone, for example, is a drug that blocks
both β-receptors and
IKACh. Drugs with similar actions
but with lower toxicity might improve the management of PAF.
See p
916.
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Use of Cardiac Resynchronization Therapy in Patients Hospitalized With Heart Failure
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Despite the significant improvements in clinical outcomes observed
with cardiac resynchronization therapy (CRT) in randomized trials
and the current guideline recommendations for CRT, few data
are available regarding CRT use outside clinical trials. To
explore CRT use in a clinical practice setting, we analyzed
CRT implantation in the Get With the Guidelines registry. Among
33 898 patients admitted for heart failure, 12.4% were discharged
with CRT. Nearly 10% of new CRT implants occurred in patients
with a left ventricular ejection fraction >35%. Major factors
associated with an increased likelihood of CRT use included
white race, hospitalization in the western United States, decreasing
left ventricular ejection fraction, and increasing age up to
70 years of age. CRT use varies by age, race, hospital site,
and geographic region. Further research is needed to understand
the reasons for the variations in CRT use at the patient, physician,
and hospital levels and to implement programs to improve the
awareness and promotion of evidence-based use of medical devices
in heart failure. See p
926.
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Quantitative Control of Adaptive Cardiac Hypertrophy by Acetyltransferase p300
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Cardiac hypertrophy is a process that adapts the heart to sustained
increases in workload. Although frequently subdivided into pathological
and physiological hypertrophy, it is a matter of active debate
whether these are truly distinct entities or whether hypertrophy
is in fact a single process with a unitary outcome. Because
hypertrophy is a frequent precursor of heart failure, the answer
to this question has ramifications for the treatment of hypertrophy
as a disease entity. Here, we show that cardiac hypertrophy
develops as the direct result of the stress-activated accumulation
of a chromatin-remodeling enzyme, p300. This enzyme is responsible
for the activation of gene expression programs that remodel
the myocyte to permit growth and addition of sarcomeres. Our
data indicate that hypertrophy promoted by p300 is initially
physiological with preserved systolic function but, after 6
to 8 months, becomes pathological, with the onset of heart failure,
ventricular dilatation, and adverse molecular changes. Our most
important finding is that hypertrophy is quantitatively controlled
by the availability of p300, so a 50% loss of p300 results in
a 50% reduction in the amount of cardiac growth and, importantly,
in the attendant risk of heart failure. This finding suggests
that drugs that specifically attenuate p300 acetyltransferase
activity may represent a novel and valid approach to the prevention
of heart failure. A close analogy can be made to the inhibition
of angiotensin-converting enzyme or β-adrenergic signaling,
both of which are vital for basic functions in the cardiovascular
system but cause harm by sustained overactivity. See p
934.
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Primary Prevention of Stroke by Healthy Lifestyle
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An overall healthy lifestyle, which includes not smoking, eating
a prudent diet, exercising, and maintaining optimal body weight,
may be more effective in lowering risk of cardiovascular disease,
diabetes, and cancer than any 1 single factor. The cause of
stroke may differ from these other chronic diseases and may
not share the same risk factors. We prospectively studied >114
000 male and female health professionals for up to 20 years
to assess the burden of stroke that may be attributed to unhealthy
lifestyle choices. Individuals with a low-risk lifestyle (not
smoking, exercising daily, consuming a prudent diet [including
moderate alcohol], and having a healthy weight during midlife)
had a significantly lower risk of total and ischemic stroke
than individuals without a low-risk lifestyle. Within these
study populations, more than one third of total strokes and
half of ischemic strokes could be attributed to unhealthy lifestyle
factors. Our results suggest that a low-risk lifestyle that
is associated with a reduced risk of multiple chronic diseases,
including coronary disease and diabetes, also may be beneficial
in the prevention of stroke, especially ischemic stroke. This
study further supports the benefits of a low-risk lifestyle
for the primary prevention of chronic disease and long-term
well-being. See p
947.
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Increased Risk of Stroke in Patients With Coronary Artery Disease and Sleep Apnea: A 10-Year Follow-Up
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We studied the effect of sleep apnea on incident stroke, acute
myocardial infarction, and death among 392 men and women referred
for coronary arteriography at the Department of Cardiology,
Umeå, Sweden. Sleep apnea, defined as a mean of 5 or more
apnea and hypopnea events per hour of sleep, occurred in 54%
of the patients at baseline. Stroke occurred in 47 (12%) of
the patients during 10 years of follow-up. Sleep apnea was associated
with an almost tripled risk of stroke, independent of age, body
mass index, left ventricular function, diabetes mellitus, gender,
coronary artery intervention, hypertension, atrial fibrillation,
a previous stroke or transient ischemic attack, and smoking.
There was a dose-dependent relationship, and patients with 5
to 15 apnea and hypopnea events per hour of sleep had a 2.4
times increased risk of stroke, whereas patients with
15 apnea
and hypopnea events per hour of sleep had a 3.6 times increased
risk. Intervention in the form of coronary artery bypass grafting
or percutaneous coronary intervention was related to a longer
survival but did not affect the incidence of stroke. We conclude
that sleep apnea, which is a treatable disorder, is significantly
associated with the risk of stroke among patients with coronary
artery disease who are being evaluated for coronary intervention.
See p
955.
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Different Calculations of Ankle-Brachial Index and Their Impact on Cardiovascular Risk Prediction
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Peripheral arterial disease (PAD) is highly prevalent in the
United States and Europe, and these patients are at increased
risk for cardiovascular events. The ankle-brachial index (ABI;
ratio of ankle and brachial systolic blood pressure) is regarded
as an easy, reliable, and noninvasive measure to identify symptomatic
and asymptomatic patients with PAD. Usually, systolic blood
pressure of both anterior and posterior tibial arteries and
both brachial arteries is measured. According to the current
guidelines of the American Heart Association, the higher of
both ankle pressures and the higher of both arm pressures should
be used for ABI calculation, and PAD is considered present if
an ABI <0.9 is detected in at least 1 leg. This concept has
been challenged by recent studies that suggest the use of the
lower ankle pressure for ABI calculation. In the present study,
we compared the prognostic value of different models for ABI
calculation with regard to cardiovascular events. In total,
812 patients were included, and cardiovascular events (cardiovascular
death, stroke, and myocardial infarction; n=157; 19.3%) were
evaluated after a median of 6.6 years. We found that using the
higher of both ankle pressures for ABI calculation, a group
of patients at high risk for cardiovascular events is overlooked.
With a simple modification of ABI (use of the lower instead
of the higher ankle pressure), more patients at risk could be
identified. On the basis of the present data, use of the lower
of both ankle pressures for ABI calculation should be considered
for cardiovascular risk prediction. See p
961.
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