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Circulation 2008年8月26日

心血管内科医师 · 最后编辑于 2008-08-26 · IP 浙江浙江
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这个帖子发布于 16 年零 295 天前,其中的信息可能已发生改变或有所发展。
Abstract 1 of 7
Arrhythmia/Electrophysiology

Cardiac Memory in Patients With Wolff-Parkinson-White Syndrome
Noninvasive Imaging of Activation and Repolarization Before and After Catheter Ablation

Background— Cardiac memory refers to a change in ventricular repolarization induced by and persisting for minutes to months after cessation of a period of altered ventricular activation (eg, resulting from pacing or preexcitation in patients with Wolff-Parkinson-White syndrome). ECG imaging (ECGI) is a novel imaging modality for noninvasive electroanatomic mapping of epicardial activation and repolarization.

Methods and Results— Fourteen pediatric patients with Wolff-Parkinson-White syndrome and no other congenital disease, were imaged with ECGI a day before and 45 minutes, 1 week, and 1 month after successful catheter ablation. ECGI determined that preexcitation sites were consistent with sites of successful ablation in all cases to within a 1-hour arc of each atrioventricular annulus. In the preexcited rhythm, activation-recovery interval (ARI) was the longest (349±6 ms) in the area of preexcitation leading to high average base-to-apex ARI dispersion of 95±9 ms (normal is 40 ms). The ARI dispersion remained the same 45 minutes after ablation, although the activation sequence was restored to normal. ARI dispersion was still high (79±9 ms) 1 week later and returned to normal (45±6 ms) 1 month after ablation.

Conclusions— The study demonstrates that ECGI can noninvasively localize ventricular insertion sites of accessory pathways to guide ablation and evaluate its outcome in pediatric patients with Wolff-Parkinson-White syndrome. Wolff-Parkinson-White is associated with high ARI dispersion in the preexcited rhythm that persists after ablation and gradually returns to normal over a period of 1 month, demonstrating the presence of cardiac memory. The 1-month time course is consistent with transcriptional reprogramming and remodeling of ion channels.

Abstract 2 of 7
Arrhythmia/Electrophysiology

Neural Mechanisms of Paroxysmal Atrial Fibrillation and Paroxysmal Atrial Tachycardia in Ambulatory Canines

Background— The relationship between autonomic activation and the mechanisms of paroxysmal atrial fibrillation remains unclear.

Methods and Results— We implanted a pacemaker and a radio transmitter in 7 dogs (group 1). After baseline recording, we paced the left atrium at 20 Hz for 1 week and then monitored left stellate ganglion nerve activity, left vagal nerve activity, and left atrial electrogram without pacing for 24 hours. This protocol repeated itself until sustained atrial fibrillation (>48 hours) was induced in 3±1 weeks. In another 6 dogs (group 2), we cryoablated left and right stellate ganglia and the cardiac branch of the left vagal nerve during the first surgery and then repeated the same pacing protocol until sustained atrial fibrillation was induced in 7±4 weeks (P=0.01). There were 4±2 episodes of paroxysmal atrial fibrillation per day and 10±3 episodes of paroxysmal atrial tachycardia per day in group 1. Simultaneous sympathovagal discharges were observed to immediately precede the onset of atrial arrhythmias in 73% of episodes. In comparison, group 2 dogs had no paroxysmal atrial fibrillation (P=0.046) or paroxysmal atrial tachycardia (P<0.001) episodes. Nerve sprouting, sympathetic hyperinnervation, and a massive elevation of transcardiac norepinephrine levels occurred in both groups.

Conclusions— Intermittent rapid left atrial pacing results in sympathetic hyperinnervation, paroxysmal atrial fibrillation, and paroxysmal atrial tachycardia. Simultaneous sympathovagal discharges are common triggers of these arrhythmias. Cryoablation of extrinsic sympathovagal nerves eliminated paroxysmal atrial fibrillation and paroxysmal atrial tachycardia, which suggests that simultaneous sympathovagal discharges and these arrhythmias are causally related. Because cryoablation only delayed but did not prevent sustained atrial fibrillation, autonomic nerve activity is not the only factor that determines atrial fibrillation maintenance.

Abstract 3 of 7
Heart Failure

Use of Cardiac Resynchronization Therapy in Patients Hospitalized With Heart Failure

Background— The frequency and characterization of patients receiving cardiac resynchronization therapy (CRT) are largely unknown since the publication of pivotal clinical trials and subsequent incorporation of CRT into the American College of Cardiology/American Heart Association guidelines for heart failure.

Methods and Results— We analyzed 33 898 patients admitted from January 2005 through September 2007 to 228 hospitals participating in the American Heart Association’s Get With the Guidelines–Heart Failure program. There were 4201 patients (12.4%) discharged alive with CRT, including 811 new implants. Patients discharged with CRT were older (median age, 75 versus 72 years) and had lower median left ventricular ejection fraction (30% versus 38%), more frequent ischemic cardiomyopathy (58% versus 45%), more history of atrial fibrillation (38% versus 27%), and higher rates of β-blocker and aldosterone antagonist use (P<0.0001 for all) than those without CRT. We found that 4.8% of patients with left ventricular ejection fraction 35% were discharged with a new CRT implant, which varied greatly by hospital. Ten percent of patients discharged with a new CRT implant had a left ventricular ejection fraction >35%. Major factors associated with lower rates of new CRT placement were treatment in the northeast (odds ratio, 0.40; 95% confidence interval, 0.30 to 0.53), black race (odds ratio, 0.45; 95% confidence interval, 0.36 to 0.57), increasing left ventricular ejection fraction per 10% (odds ratio, 0.56; 95% confidence interval, 0.52 to 0.60), and increasing age per 10 years in those >70 years of age (odds ratio, 0.56; 95% confidence interval, 0.48 to 0.65).

Conclusions— Although CRT is a recent evidence-based therapy for heart failure, patterns of use differ significantly from clinical trials and published guidelines. Important variations also exist for CRT therapy based on race, geographic region, comorbidities, and age and need to be addressed through further study and/or quality-of-care initiatives.

Abstract 4 of 7
Molecular Cardiology

Quantitative Control of Adaptive Cardiac Hypertrophy by Acetyltransferase p300

Background— Acetyltransferase p300 is essential for cardiac development and is thought to be involved in cardiac myocyte growth through MEF2- and GATA4-dependent transcription. However, the importance of p300 in the modulation of cardiac growth in vivo is unknown.

Methods and Results— Pressure overload induced by transverse aortic coarctation, postnatal physiological growth, and human heart failure were associated with large increases in p300. Minimal transgenic overexpression of p300 (1.5- to 3.5-fold) induced striking myocyte and cardiac hypertrophy. Both mortality and cardiac mass were directly related to p300 protein dosage. Heterozygous loss of a single p300 allele reduced pressure overload–induced hypertrophy by 50% and rescued the hypertrophic phenotype of p300 overexpressers. Increased p300 expression had no effect on total histone deacetylase activity but was associated with proportional increases in p300 acetyltransferase activity and acetylation of the p300 substrates histone 3 and GATA-4. Remarkably, a doubling of p300 levels was associated with the de novo acetylation of MEF2. Consistent with this, genes specifically upregulated in p300 transgenic hearts were highly enriched for MEF2 binding sites.

Conclusions— Small increments in p300 are necessary and sufficient to drive myocardial hypertrophy, possibly through acetylation of MEF2 and upstream of signals promoting phosphorylation or nuclear export of histone deacetylases. We propose that induction of myocardial p300 content is a primary rate-limiting event in the response to hemodynamic loading in vivo and that p300 availability drives and constrains adaptive myocardial growth. Specific reduction of p300 content or activity may diminish stress-induced hypertrophy and forestall the development of heart failure.

Abstract 5 of 7
Stroke

Primary Prevention of Stroke by Healthy Lifestyle

Background— The combination of healthy lifestyle factors is associated with lower risk of coronary heart disease, diabetes, and total cardiovascular disease. Little is known about the impact of multiple lifestyle factors on the risk of stroke.

Methods and Results— We conducted a prospective cohort study among 43 685 men from the Health Professionals Follow-up Study and 71 243 women from the Nurses’ Health Study. Diet and other lifestyle factors were updated from self-reported questionnaires. We defined a low-risk lifestyle as not smoking, a body mass index <25 kg/m2, 30 min/d of moderate activity, modest alcohol consumption (men, 5 to 30 g/d; women, 5 to 15 g/d), and scoring within the top 40% of a healthy diet score. We documented 1559 strokes (853 ischemic, 278 hemorrhagic) among women and 994 strokes (600 ischemic, 161 hemorrhagic) among men during follow-up. Women with all 5 low-risk factors had a relative risk of 0.21 (95% confidence interval [CI], 0.12, 0.36) for total and 0.19 (95% CI, 0.09, 0.40) for ischemic stroke compared with women who had none of these factors. Among men, the relative risks were 0.31 (95% CI, 0.19, 0.53) for total and 0.20 (95% CI, 0.10, 0.42) for ischemic stroke for the same comparison. Among the women, 47% (95% CI, 18 to 69) of total and 54% (95% CI, 15 to 78%) of ischemic stroke cases were attributable to lack of adherence to a low-risk lifestyle; among the men, 35% (95% CI, 7 to 58) of total and 52% (95% CI, 19 to 75) of ischemic stroke may have been prevented.

Conclusion— A low-risk lifestyle that is associated with a reduced risk of multiple chronic diseases also may be beneficial in the prevention of stroke, especially ischemic stroke.

Abstract 6 of 7
Stroke

Increased Risk of Stroke in Patients With Coronary Artery Disease and Sleep Apnea
A 10-Year Follow-Up

Background— The effect of sleep apnea on mortality and cardiovascular morbidity is mainly unknown. We aimed to study whether sleep apnea is related to stroke, death, or myocardial infarction in patients with symptomatic coronary artery disease.

Methods and Results— A total of 392 men and women with coronary artery disease referred for coronary angiography were examined by use of overnight sleep apnea recordings. Sleep apnea, defined as an apnea-hypopnea index 5, was recorded in 54% of the patients. All patients were followed up prospectively for 10 years, and no one was lost to follow-up. Stroke occurred in 47 (12%) of 392 patients during follow-up. Sleep apnea was associated with an increased risk of stroke, with an adjusted hazard ratio of 2.89 (95% confidence interval 1.37 to 6.09, P=0.005), independent of age, body mass index, left ventricular function, diabetes mellitus, gender, intervention, hypertension, atrial fibrillation, a previous stroke or transient ischemic attack, and smoking. Patients with an apnea-hypopnea index of 5 to 15 and patients with an apnea-hypopnea index 15 had a 2.44 (95% confidence interval 1.08 to 5.52) and 3.56 (95% confidence interval 1.56 to 8.16) times increased risk of stroke, respectively, than patients without sleep apnea, independent of confounders (P for trend=0.011). Death and myocardial infarction were not related to sleep apnea. 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.

Conclusions— Sleep apnea is significantly associated with the risk of stroke among patients with coronary artery disease who are being evaluated for coronary intervention.

Abstract 7 of 7
Vascular Medicine

Different Calculations of Ankle-Brachial Index and Their Impact on Cardiovascular Risk Prediction

Background— An ankle-brachial index (ABI; ratio of ankle and brachial systolic blood pressure) <0.9 indicates peripheral arterial disease (PAD) and is a strong predictor of cardiovascular events. The aim of the present study was to address the prognostic value of different methods of ABI calculation.

Methods and Results— In 831 patients admitted with chest pain for diagnostic heart catheterization, blood pressure of both anterior and posterior tibial arteries was measured. ABI was calculated for each leg with the higher of the 2 ankle pressures (current definition of the American Heart Association) or with the lower of the 2 ankle pressures (modified definition) in relation to the higher of the left or right brachial systolic blood pressure. For each patient, the lower ABI from both legs was used for further evaluation. Fifteen patients (1.8%) with ABI >1.5 were excluded. We compared patients with ABI <0.9 according to the current definition (with PAD, n=204 [25.0%]), those with ABI 0.9 according to the modified definition (without PAD, n=524 [64.2%]), and those with ABI <0.9 according to the modified definition and 0.9 according to the current definition (suspected PAD, n=88 [10.8%]). Follow-up data (median 6.6 years) were available for 812 patients (99.5%); 157 patients (19.3%) experienced cardiovascular events (cardiovascular death, myocardial infarction, or stroke). Patients without PAD had the lowest cardiovascular event rate, whereas event rates were comparable for patients with PAD and those with suspected PAD (14.8% versus 28.4% versus 25.0%, respectively). In a fully adjusted Cox regression analysis that included patients without PAD as the reference group, the hazard ratio (95% CI) was 1.56 (0.97 to 2.53) for patients with suspected PAD and 1.67 (1.16 to 2.40) for patients with PAD.

Conclusions— When the higher ankle pressure is used 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.












































































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