Intra-atrial reentrant tachycardia with ambiguous data from activation mapping: what to do next?
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OBJECTIVES: This study was designed to determine the association between race and atrial fibrillation (AF) among patients with heart failure (HF). BACKGROUND: Atrial fibrillation is known to complicate HF, but whether its prevalence varies by race, and the reasons why, are not well understood. METHODS: We identified adults hospitalized with confirmed HF within a large integrated healthcare delivery system. We obtained information on demographics, comorbidity, vital signs, medications, and left ventricular systolic function status. "Atrial fibrillation" was defined as AF or atrial flutter documented by electrocardiogram or prior physician-assigned diagnoses. We evaluated the independent relationship between race and AF using multivariable logistic regression. RESULTS: Among 1,373 HF patients (223 African Americans, 1,150 Caucasians), the prevalence of AF was 36.9% (95% confidence interval [CI] 34.3% to 39.5%). Compared with Caucasians, African Americans were younger (mean age 67 vs. 74 years, p < 0.001) and more likely to have hypertension (86.6% vs. 77.7%, p < 0.01) and prior diagnosed HF (79.4% vs. 70.7%, p < 0.01). African Americans had less prior diagnosed coronary disease, revascularization, hypothyroidism, or valve replacement. Atrial fibrillation was much less prevalent in African Americans (19.7%) than Caucasians (38.3%, p < 0.001). After adjustment for risk factors for AF and other potential confounders, African Americans had 49% lower odds of AF (adjusted odds ratio 0.51, 95% CI 0.35 to 0.76). CONCLUSIONS: In a contemporary HF cohort, AF was significantly less common among African Americans than among Caucasians. This variation was not explained by differences in traditional risk factors for AF, HF etiology and severity, and treatment.
PURPOSE OF REVIEW: Device therapy for atrial fibrillation remains contentious despite the recognized benefit of atrial pacing in sinus node dysfunction. There are various new specialized pacing algorithms that aim to provide rhythm or rate control in atrial fibrillation. We review the various options for device therapy and the evidence available concerning their effectiveness. RECENT FINDINGS: Randomized trials on preventative algorithms for atrial fibrillation have not shown consistent benefit. Anti-tachycardia pacing for atrial fibrillation has inherent problems illustrated in this review and has failed to demonstrate objective improvement except in the case of atrial flutter. Several large randomized trials have demonstrated an adverse outcome with right ventricular apical pacing. These studies have shown an increase in atrial fibrillation with ventricular pacing. Recent studies have emphasised the importance of right ventricular apical pacing in burden of atrial fibrillation and therefore we discuss the likely confounding effect on previous trials and speculate on future directions. SUMMARY: The use of a device with atrial fibrillation prevention algorithms in a patient with a bradycardia indication for pacing is not unreasonable but there is no hard evidence of benefit. Patients with sinus node dysfunction should be paced in the atrium alone. There is no indication for use of a device for atrial fibrillation without a conventional indication for pacing.
Atrioventricular (AV) node ablation to control ventricular response was attempted in two patients with recurrent drug refractory atrial flutter. Standard radiofrequency (RF) procedure, which delivers energy through the 4-mm tip electrode of an ablation catheter positioned at the right AV junction and a large back plate (unipolar mode), failed in both patients. As an accepted second step, high energy direct current (DC) ablation under general anesthesia was then performed in patient one. After two shocks of 200 J, complete AV block occurred, but complete recovery was noted 3 hours later. In a third session for patient 1 and in the first session for patient 2 (after 15 unsuccessful unipolar right-sided RF applications), a second ablation catheter was introduced via the femoral artery on the left side of the His bundle area under the aortic valves. Energy was then delivered in a bipolar fashion between the tip electrodes of the right-sided and the left-sided catheter. Complete and permanent AV block (follow-up: 3 and 1 months) was created within 4 and 1.5 seconds, respectively, in each patient. No complication was encountered and echocardiograms and blood levels of cardiac enzymes were all normal after the procedures. This new approach, after further evaluation, may represent a useful additional step in the strategy of AV node ablation and could be applied before high energy DC shock when the standard RF procedure is unsuccessful.
INTRODUCTION: Dogs with rapid ventricular pacing (RVP)-induced congestive heart failure (CHF) have inducible atrial tachycardia, flutter, and fibrillation (AF). We tested the hypothesis that rapid atrial activation in multiple regions and at different rates is responsible for sustained AF in this CHF model. METHODS AND RESULTS: We studied 12 episodes of sustained (>10 minutes) AF induced in 12 dogs with CHF produced by 3-6 weeks of RVP at 230 beats/minute. High-density mapping of AF was performed using 382 unipolar atrial electrograms recorded simultaneously from epicardial electrodes on the right (RA) and left atria (LA) and Bachmann's bundle. AF mechanisms were based on Fast Fourier Transform (FFT) analysis and activation sequence mapping. A driver was defined as a rapid stable activation region with a single dominant frequency peak in FFT analysis. During AF, three FFT and activation patterns were seen: (1) a single LA driver (7.8 +/- 1.1 Hz) near the pulmonary veins (PVs) with irregular activation in the rest of the atria (n = 4); (2) simultaneous, multisite, biatrial drivers at differing frequencies (LA vs RA dominant frequency gradient: 1.3 +/- 0.8 Hz) near the PVs (8.4 +/- 0.3 Hz) and high RA (8.5 +/- 1.5 Hz) (n = 7); and (3) biatrial irregular activation with multiple and/or broadband frequency peaks without a dominant frequency. (LA: 7.1-11.4 Hz; RA: 5.9-7.7 Hz) (n = 1). Atrial drivers had either a focal activation pattern or were due to a macroreentrant circuit around the PVs. CONCLUSIONS: In this CHF model, FFT analysis and activation sequence mapping demonstrate that sustained AF is characterized by single and multiple, stable LA and RA drivers with predominant sources in the PVs and high RA causing fibrillatory conduction.
BACKGROUND: The mechanisms underlying the transition of typical atrial flutter (Afl) to fibrillation (AF) remain unclear. We set out to test the hypothesis that Afl disorganizes to AF via alternans of atrial action potentials. METHODS AND RESULTS: In 38 patients with Afl, monophasic action potentials (MAPs) were recorded at the isthmus and either high or low right atrium (HRA, LRA) during overdrive pacing to 160 ms or to the initiation of AF, whichever came first. MAP duration measured at 90% repolarization was longer at the isthmus in all patients, and failed to shorten with rate, compared with the HRA (n=38) or LRA (n=5). In 20 patients who developed AF, progressive pacing first caused alternans of isthmus MAP duration and amplitude at mean cycle length of 219+/-45 ms, followed by AF at a mean onset cycle length of 184+/-38 ms. Subsets of this group showed spontaneous action potential duration alternans at the isthmus (11 of 20 patients) and 2:1 isthmus conduction block immediately preceding AF (4 of 20 patients). In the 18 patients who did not develop AF, MAP alternans was less common (9 of 18 patients; P<0.0003), and occurred only at faster pacing (cycle length=169+/-25 ms; P<0.05). CONCLUSIONS: In patients with typical Afl, action potential duration rate maladaptation at the isthmus may lead to action potential duration alternans and conduction block preceding the transition to AF. These isthmus characteristics may enable the spontaneous initiation of AF through wavefront fractionation and may explain the benefits of isthmus ablation in preventing AF recurrence.
251 untreated patients with mild to moderate hypertension were included in a multicenter study aimed 1) to detect arrhythmias (24-H Holter recording) and 2) to assess the efficacy of sotalol on blood pressure and possible arrhythmias. Patients with coronary heart disease or previously documented arrhythmias were excluded. Atrial arrhythmias such as premature beats, fibrillation, flutter and paroxysmal atrial tachycardia were detected in 16% of patients. Monomorphic ventricular premature contractions (VPCs) (Lown I and II) were detected in 41% of patients and polymorphic VPCs or duplets/triplets (Lown III and IV) in 14%. A correlation seems to exist between the level of hypertensive cardiopathy, judged on electrocardiographic data (Tarazi classification), age of patients and severity of arrhythmias. Sotalol was administered during 2 months at a mean dose of 160 mg per day. The treatment was effective on blood pressure and arrhythmias (82% improvement of severe VPCs) and the drug was well tolerated. It was difficult to conclude if these good results are due to the betablocking properties or specific class II antiarrhythmic effects of sotalol or to the combined activity.
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The prevalence of arrhythmia increases with age. Considered as an "ordinary" event in elderly patients, these arrhythmias may nevertheless have serious consequences. This study was undertaken to determine the clinical, aetiological and prognostic features of serious arrhythmias in a population of elderly subjects (> or = 70 years) hospitalised over a 20 months period and comprising 202 patients (103 women, 99 men, mean age 79.6 +/- 5.9 years). Supraventricular arrhythmias are the most common by far (84.2%): 51.4% of patients had atrial fibrillation, 15.3% had atrial flutter; 12.9% had focal atrial tachycardia, 4.5% had junctional tachycardia. Of the ventricular arrhythmias (15.8%), there were 12 sustained ventricular tachycardias, 4 torsades de pointes and 1 ventricular fibrillation. The increased duration of hospital stay (10 +/- 6 days on average) is related not to age but to the type of arrhythmia (longer for ventricular arrhythmias) and to left ventricular dysfunction. The main complications of arrhythmias were cardiac failure (52.4%), neurological deficits (37.4%) and angina (18.6%). Electrocardiographic signs of atrioventricular block were present in 62% of cases and QRS changes in 47.3% of cases. Ventricular arrhythmias were more commonly associated with intraventricular conduction defects, signs of myocardial necrosis and prolongation of the QT interval; they were also common in patients with left ventricular dysfunction and when the left ventricle was dilated. The aetiology of ventricular arrhythmias was mainly iatrogenic (50%) and ischaemic (21.8%), whereas the aetiologies of the supraventricular arrhythmias were varied, 14.7% of cases being idiopathic. Conversion to stable sinus rhythm was obtained in half the patients. A pacemaker was implanted in 10.8% of cases. The hospital mortality was 4.9%.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: The true risk of thromboembolic events after cardioversion of atrial flutter was not addressed carefully. Nevertheless, thromboembolic events were thought to be rare and less likely to occur after cardioversion of atrial fibrillation. The aim of this study was to prospectively evaluate if the interruption of persistent typical atrial flutter could be safely performed without anticoagulation in a group of patients at low risk for thromboembolic events. METHODS: We studied 64 subjects selected among 138 consecutive patients with persistent typical atrial flutter (minimal duration 72 hours) in whom a transesophageal atrial pacing was performed in our electrophysiology laboratory from October 1994 to May 1999. Exclusion criteria included: anticoagulation therapy during the previous 4 weeks; previous history of atrial fibrillation; recent (< 1 month) myocardial infarction; history of thromboembolic events; left ventricular ejection fraction < 40%; presence of moderate or severe mitral regurgitation or stenosis; induction of sustained (> 6 hours) atrial fibrillation during transesophageal atrial pacing. Patients in whom atrial flutter persisted in spite of transesophageal atrial pacing underwent external direct current cardioversion or right atrial overdrive pacing within 24 hours. Thromboembolic events were checked for 4 weeks after the restoration of sinus rhythm. RESULTS: Sinus rhythm was restored in 54 patients by transesophageal atrial pacing, in 8 patients by electrical cardioversion, and in 2 by right atrial pacing. The mean duration of atrial flutter was 18 +/- 19 days, the mean left atrial size 41.3 +/- 6.2 mm, and the mean left ventricular ejection fraction 54.8 +/- 7.3%. During the study period no episodes of thromboembolism were recorded. CONCLUSIONS: Cardioversion of persistent typical atrial flutter in non-anticoagulated patients at low risk for thromboembolic events appears safe.