Clinical Summaries

Abstract

HomeCirculationVol. 118, No. 9Clinical Summaries Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBClinical Summaries Originally published26 Aug 2008https://doi.org/10.1161/CIRCULATIONAHA.108.190523Circulation. 2008;118:897–898Cardiac Memory in Patients With Wolff-Parkinson-White Syndrome: Noninvasive Imaging of Activation and Repolarization Before and After Catheter AblationECG 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.Neural Mechanisms of Paroxysmal Atrial Fibrillation and Paroxysmal Atrial Tachycardia in Ambulatory CaninesParoxysmal 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.Use of Cardiac Resynchronization Therapy in Patients Hospitalized With Heart FailureDespite 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.Quantitative Control of Adaptive Cardiac Hypertrophy by Acetyltransferase p300Cardiac 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.Primary Prevention of Stroke by Healthy LifestyleAn 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.Increased Risk of Stroke in Patients With Coronary Artery Disease and Sleep Apnea: A 10-Year Follow-UpWe 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.Different Calculations of Ankle-Brachial Index and Their Impact on Cardiovascular Risk PredictionPeripheral 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. Previous Back to top Next FiguresReferencesRelatedDetails August 26, 2008Vol 118, Issue 9 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.108.190523 Originally publishedAugust 26, 2008 PDF download Advertisement