Automatic Cardiac Event Recorders Reveal Paroxysmal Atrial Fibrillation after Unexplained Strokes or Transient Ischemic Attacks

Background: The etiology of stroke or transitory ischemic attack (TIA) remains frequently unknown. While paroxysmal atrial fibrillation (PAF) is often suspected, its presence remains difficult to establish. Therefore, we investigated the occurrence of PAF episodes in such a population using a long‐term automatic cardiac event recorder. Methods: We prospectively investigated 60 consecutive subjects admitted in our university hospital for stroke (n = 44) or TIA (n = 16) , adding long‐term automatic cardiac event recorders, with a target duration of 4 days, to standard investigations, which included 12‐lead ECGs and 24‐hour Holter recordings. Results: In 28 patients no etiology was found for their stroke or TIA. However, one or more than one PAF episode was found in 4 of them (14.3%) using the long‐term automatic event recorder. In the 32 remaining patients, 8 presented with PAF, and this was considered as the cause of their stroke. In both groups, AF was paroxysmal. The PAF episodes' duration went from 1 to 96 hours (mean ± standard deviation, 18 hours and 30 minutes ± 30 hours). Conclusions: Patients suffering PAF episodes after ischemic stroke or TIA were statistically less often recognized using the 24‐hour Holter ECG recording alone than the R‐Test Evolution alone.     

Assessment of Rhythm and Rate Control in Patients with Atrial Fibrillation

A recent series of randomized prospective clinical trials that compared rate control with rhythm control in patients with atrial fibrillation (AF) found no significant difference in primary outcome between the two strategies. However, these trials lacked clear criteria for defining "successful" rate or rhythm control. Various measures have been used to gauge the success of antiarrhythmic drug therapy, including time to first recurrence of AF, any AF recurrence, AF burden, and a reduction in symptoms. Determining the success of antiarrhythmic therapy can be relatively straightforward by using how patients feel during therapy as a key endpoint. Most patients are satisfied with a major reduction in symptomatic AF episodes and can live comfortably with occasional episodes of AF. For those who are bothered by even infrequent, brief AF episodes, a treatment regimen that eliminates nearly all AF recurrences is required, although often hard to achieve. Catheter ablation may be necessary to achieve a successful outcome in these patients. Suppression of AF in a patient at high risk of stroke does not, however, remove the need for concomitant warfarin therapy. The endpoints of ventricular rate control are not clear, and the recently published rhythm versus rate control trials lacked standard criteria for judging acceptable rate control. One relatively simple method is to try and achieve a 24-hour heart rate that mimics expected normal sinus rhythm. It is important to achieve good rate control to minimize symptoms and the risk of tachycardia-mediated cardiomyopathy.     

阵发性心房颤动发生的相关研究进展

尽管对阵发性心房颤动的认识已增加了不少,但是对自然状态下发作的阵发性心房颤动的触发方式的细节研究还是少之又少。通过对其相关心电图特征的研究以更好的了解阵发性心房颤动的发生。     

Silent Cerebral Events/Lesions Related to Atrial Fibrillation Ablation: A Clinical Review

Brain magnetic resonance imaging (MRI) has identified a high incidence of cerebral ischemia in asymptomatic patients after atrial fibrillation (AF) ablation (silent). Detection of cerebral ischemic events on MRI is based on acute hyperintense lesions on diffusion‐weighted imaging. In the literature, the incidence is related to specifications of MRI and depends on the definition applied. In comparative studies, silent cerebral events (SCE, diffusion‐weighted MRI [DWI] positive only) appear to be approximately 3 times more common compared to using a definition of silent cerebral lesions (SCL; without fluid attenuated inverse recovery sequence [FLAIR] positivity). Whereas the FLAIR sequence may turn positive within days after the ischemic event, SCE definition is highly sensitive for early phases of ischemic brain damage. SCE/SCL appear to represent cerebral ischemic infarcts and determine the “embolic fingerprint” of a specific ablation technology and strategy used. The optimum time point for detecting SCE is early after AF ablation (24–72 hours), whereas detection of SCL can only be performed within the first 2–7 days (due to delay of FLAIR positivity). Different technology‐, procedure‐, and patient‐related parameters have been identified to play a role in the multifactorial genesis of SCE/SCL. In recent years, evidence has been gathered that there may be differences of SCE/SCL rates depending upon the ablation technology used, but small patient numbers and a large number of potential confounders hamper all studies. As major findings of recent studies, mode of periprocedural and intraprocedural anticoagulation has been identified as a major predictor for incidences of SCE/SCL. Whereas procedural characteristics related to higher SCE/SCL‐rates may be modified, unchangeable patient‐related factors should be taken into account for future individualized risk assessment. Novel ablation devices introduced into the market should be tested for their potential embolic fingerprint and refinements of ablation procedures to reduce their embolic potential should be prompted. The knowledge of “best practice” in terms of low SCE/SCL rates has prompted changes in work‐flow, which have been implemented into ablation procedures using novel ablation devices. So far, no study has linked SCE/SCL to neuropsychological decline and the low number of AF‐ablation‐associated events needs to be weighted against the multitude of preexisting asymptomatic MRI‐detected brain lesions related to the course of AF itself. Future studies are needed to evaluate if more white matter hyperintensities due to AF may be prevented by AF ablation (producing only a small number of SCE/SCL).     

Silent cortical strokes associated with atrial fibrillation

To clarify whether silent cortical strokes (SCS) could be a predictor of symptomatic stroke in patients with atrial fibrillation (AF), 72 patients with AF (50 with chronic AF, 22 with paroxysmal AF) were studied. Patients with mitral stenosis, history of myocardial infarction, or dilated cardiomyopathy were excluded from this study. Using cranial magnetic resonance imaging (MRI), the patients were divided into those with SCS (23 patients, Group 1) and those without SCS (49 patients, Group 2). The incidence of symptomatic stroke was then compared between the two groups. Three patients (13%) in Group 1 developed symptomatic brain infarction; this is statistically significant (p < 0.05), compared with the patients in Group 2, none of whom experienced symptomatic stroke. We suggest that SCS is a predictor of symptomatic cerebral infarct in patients with AF. Therefore, it is thought to be important to diagnose SCS using cranial MRI or computed tomography and to keep patients with SCS under close surveillance.     

Pilot Study: Noninvasive Monitoring of Oral Flecainide's Effects on Atrial Electrophysiology during Persistent Human Atrial Fibrillation Using the Surface Electrocardiogram

Background: The relation between flecainide's plasma level and its influence on human atrial electrophysiology during acute and maintenance therapy of atrial fibrillation (AF) is unknown. Therefore, this study determined flecainide plasma levels and atrial fibrillatory rate obtained from the surface ECG during initiation and early maintenance of oral flecainide in patients with persistent lone AF and assessed their relationship. Methods and Results: In 10 patients (5 males, mean age 63 ± 14 years, left atrial diameter 46 ± 3 mm) with persistent lone AF, flecainide was administered as a single oral bolus (day 1) followed by 200–400 mg/day (days 2–5). The initial 300 mg flecainide bolus resulted in therapeutic plasma levels in all patients (range 288–629 ng/ml) with no side effects. Flecainide plasma levels increased on day 3 and remained stable thereafter. Day 5 plasma levels were lower (508 ± 135 vs 974 ± 276 ng/ml, P = 0.009) in patients with daily mean flecainide doses of 200 mg compared to patients with higher maintenance doses. Fibrillatory rate obtained from the surface electrocardiogram measuring 378 ± 17 fpm at baseline was reduced to 270 ± 18 fpm (P < 0.001) after the flecainide bolus but remained stable thereafter. Fibrillatory rate reduction was independent of flecainide plasma levels or clinical variables. Conclusion: A 300 mg oral flecainide bolus is associated with electrophysiologic effects that are not increased during early maintenance therapy in persistent human lone AF. In contrast to drug plasma levels, serial analysis of fibrillatory rate allows monitoring of individual drug effects on atrial electrophysiology.     

Analysis of the Surface Electrocardiogram for Monitoring and Predicting Antiarrhythmic Drug Effects in Atrial Fibrillation

Specific antiarrhythmic therapy with class I and III drugs for atrial fibrillation (AF) conversion and prevention of its recurrence is frequently utilized in clinical practice. Besides being only moderate effective, the utilization of antiarrhythmic drugs may be associated with serious side effects. In the clinical setting it is difficult to directly evaluate the effects of antiarrhythmic drugs on the individual patient’s atrial electrophysiology, thereby predicting their efficacy in restoring and maintaining sinus rhythm. Analysis of the surface electrocardiogram in terms of P-wave signal averaged ECG during sinus rhythm and spectral characterization of fibrillatory waves during AF for evaluation of atrial antiarrhythmic drug effects is a new field of investigation. Both techniques provide reproducible parameters for characterizing atrial electrical abnormalities and seem to contain prognostic information regarding antiarrhythmic drug efficacy. Further research is needed which elucidates the most challenging clinical questions in AF management whom to place on antiarrhythmic drug treatment and what antiarrhythmic drug to prescribe. Analysis of the surface ECG might have the potential to answer these questions.     

Atrial Ectopics Prior to Atrial Fibrillation Onset

Background: This study examined the possible role of atrial ectopics and short runs of atrial tachycardia in the initiation of episodes of paroxysmal atrial fibrillation (PAF). Methods: Holter recordings from patients participating in pharmacotherapy trials for the prevention of PAF were examined. Treatment comprised placebo, digoxin, disopyramide, or atenolol. The frequency of atrial ectopic beats during each 30 seconds over the 5 minutes prior to PAF and whether this was also associated with atrial tachycardia (3 or more ectopics in succession) was calculated. Results: The mean number of ectopics was 4.1 in the final minute, but patients receiving disopyramide or atenolol had significantly more ectopics than those on placebo (P > 0.05 for both). Those on digoxin had a similar number of ectopics to placebo patients. There was no relationship between heart rate at PAF onset and ectopic frequency, nor any association between the presence of one or more episodes of atrial tachycardia and ectopic frequency. Conclusion: Atrial ectopics increase in frequency prior to PAF onset, and this study suggests that antiarrhythmic therapy may increase the number of ectopics required to initiate PAF.     

Clinical Relevance of Silent Atrial Fibrillation: Prevalence, Prognosis, Quality of Life, and Management

Although first described about 100yr ago, atrial fibrillation (AF) is now recognized as the most common of all arrhythmias. It has a substantial morbidity and presents a considerable health care burden. Improved diagnosis and an ageing population with an increased likelihood of underlying cardiac disease results in AF in more than 1% of population. AF is associated with an approximately two-fold increase in mortality, largely due to stroke which occurs at an annual rate of 5–7%. Another risk to survival is heart failure, which is aggravated by poor control of the ventricular rate during AF. Usually AF is associated with a variety of symptoms: palpitations, dyspnea, chest discomfort, fatigue, dizziness, and syncope. Paroxysmal AF is likely to be symptomatic and frequently presents with specific symptoms, while permanent AF is usually associated with less specific symptoms. However, in at least one third of patients, no obvious symptoms or noticeable degradation of quality of life are observed. This asymptomatic, or silent, AF is diagnosed incidentally during routine physical examinations, pre-operative assessments or population surveys. Recently, a very large incidence of generally short paroxysms of AF has been seen in patients with implantable pacemakers or defibrillators and these arrhythmias are often silent. Pharmacological suppression of arrhythmia may be associated with a conversion from a symptomatic to an asymptomatic form of AF. Holter monitoring and transtelephonic monitoring studies have demonstrated that asymptomatic episodes of AF exceed symptomatic paroxysms by twelve-fold or more.Although symptoms may not stem directly from AF, the risk of complications is probably the same for symptomatic and asymptomatic patients. AF is found incidentally in about 25% of admissions for a stroke. Studies in patients with little or no awareness of their arrhythmia condition indicate that unrecognized and untreated AF may cause congestive heart failure. In patients with coronary bypass, AF may not only represent risk for immediate postoperative morbidity and increase hospital resource utilization, but being unrecognized, may produce a significant impact on long-term survival and quality of life. Although silent AF merits consideration for anticoagulation and rate control therapy according to standard criteria, whether antiarrhythmic therapy is relevant in this condition remains unclear.