BACKGROUND:

Although the pulmonary veins are accepted as preferential trigger sites for paroxysmal atrial fibrillation/flutter (AF/AFL), the intrinsic basis for reentrant excitation is undetermined in persistent AF/AFL.

OBJECTIVE:

To identify histoanatomic substrates for reentrant AF/AFL in rats.

METHODS:

Spatiotemporal patterns of impulse propagation were visualized optically on the posterior surface of the atria in di-4ANEPPS-stained Langendorff-perfused rat heart/lung preparations. The relevant histology was also analyzed.

RESULTS:

Burst (S1-S2) pacing at the right atrium provoked AF/AFL in 15 of 19 hearts, and most cases developed by organized reentrant excitation through the coronary sinus (CS) and left atrium (LA) roof, with non-organized irregular propagation in 3 cases. The reentrant circuit developed along 2 pathways of propagation: a slower pathway at the LA roof (conduction velocity, 42.4 ± 16.6 cm/s) and a faster pathway along the CS (conduction velocity, 53.3 ± 9.2 cm/s). Upon extra stimulus (S2) after consecutive S1 pacing, the impulse at the roof propagated retrogradely from the CS, resulting in reentrant propagation anchored by the atrial septum and posterior LA. Histologic quantification revealed significantly lower myocardial density in the posterior LA and the septum than elsewhere in the atria. Moreover, myocytes in the LA roof, vs. the CS, were of lower density, more randomly arranged in the direction of conduction, and characterized by more disorganized distribution of connexin 43 over the entire cell membrane, consistent with the slower impulse propagation there.

CONCLUSION:

The intrinsic histoanatomic heterogeneity in the LA would constitute a pro-reentrant substrate responsible for perpetuating AF/AFL.

The American College of Chest Physicians provides recommendations for the use of anticoagulant medications for several indications that are important in the primary care setting. Warfarin, a vitamin K antagonist, is recommended for the treatment of venous thromboembolism and for the prevention of stroke in persons with atrial fibrillation, atrial flutter, or valvular heart disease. When warfarin therapy is initiated for venous thromboembolism, it should be given the first day, along with a heparin product or fondaparinux. The heparin product or fondaparinux should be continued for at least five days and until the patient's international normalized ratio is at least 2.0 for two consecutive days. The international normalized ratio goal and duration of treatment with warfarin vary depending on indication and risk. Warfarin therapy should be stopped five days before major surgery and restarted 12 to 24 hours postoperatively. Bridging with low-molecular-weight heparin or other agents is based on balancing the risk of thromboembolism with the risk of bleeding. Increasingly, self-testing is an option for selected patients on warfarin therapy. The ninth edition of the American College of Chest Physicians guidelines, published in 2012, includes a discussion of anticoagulants that have gained approval from the U.S. Food and Drug Administration since publication of the eighth edition in 2008. Dabigatran and apixaban are indicated for the prevention of systemic embolism and stroke in persons with nonvalvular atrial fibrillation. Rivaroxaban is indicated for the prevention of deep venous thrombosis in patients undergoing knee or hip replacement surgery, for treatment of deep venous thrombosis and pulmonary embolism, for reducing the risk of recurrent deep venous thrombosis and pulmonary embolism after initial treatment, and for prevention of systemic embolism in patients with nonvalvular atrial fibrillation.

OBJECTIVE:

The purpose of this study is to report a single institution's experience with abdominal coarctation in children and report associated comorbidities.

BACKGROUND:

Abdominal coarctation is a rare condition, accounting for less than 2% of aortic coarctations. Single patients with abdominal coarctation have been reported with additional vascular disease in pediatric patients.

METHODS:

Our echocardiography database between January 2001 and January 2012 was searched to identify all patients with abdominal coarctation. Relevant clinical data were reviewed.

RESULTS:

Nine patients were identified with abdominal coarctation. Median age at diagnosis was 4.7 years (IQR 1.1-14.3 years). Additional cardiac diagnoses were found in three patients: one had moderate aortic regurgitation and aortic root dilatation; one had mild aortic regurgitation, severe mitral regurgitation, and atrial flutter; and one had a thoracic coarctation previously repaired. Eight patients (89%) had an associated noncardiac comorbidity. Comorbidities included: Takayasu arteritis (n = 3), systemic lupus erythematosus (n = 1), epidermal nevus syndrome (n = 1), abdominal hemagioma (n = 1), Williams syndrome (n = 1), and renal artery stenosis (n = 2). Intervention was performed in four patients (57%): two underwent surgical grafting and two had angioplasty with stent placement. Patients with surgical grafting required no further intervention, whereas both patients who underwent angioplasty and stenting required further stent placement.

CONCLUSION:

Abdominal coarctation is a rare anomaly. It is frequently associated with other vascular abnormalities. Vasculitis should be suspected in children with abdominal coarctation. All patients, even if treated, require continued close observation.

OBJECTIVES:

The aim of our study was to demonstrate that the use of contrast microbubbles during transesophageal echocardiography (TEE) guided cardioversion will improve interpretation of the TEE images.

BACKGROUND:

TEE-guided cardioversion of atrial flutter or fibrillation (AF) is a safe and proven method to restore sinus rhythm. However, artifacts and dense spontaneous echo contrast in the left atrial appendage (LAA) can sometimes decrease the level of confidence in excluding the presence of thrombus.

METHODS:

One hundred patients referred for TEE-guided cardioversion were prospectively enrolled and microbubble contrast agent (DEFINITY) was administered after the clinical decision had been made regarding suitability for cardioversion. Noncontrast and contrast images were compared during subsequent offline analysis.

RESULTS:

LAA dimensions and contractility indices were higher, artifacts were significantly differentiated, previously unsuspected LAA filling defects were identified, and the level of confidence in excluding thrombus was enhanced in the contrast images when compared to the noncontrast images. After 4 months follow-up, 1 stroke-associated death occurred in a patient who had LAA thrombus recognized only by contrast. Left atrial appendage visualization is enhanced with microbubble contrast agent use during transesophageal echocardiography guided cardioversion and is useful in identification of intracardiac thrombus.

Major atrial coronary arteries, including the sinus node artery (SNA), were commonly found in the areas involved in atrial fibrillation (AF) ablation and could cause difficulties in achieving linear block at the left atrial (LA) roof. The SNA is a major atrial coronary artery of the atrial coronary circulation. This study aimed to determine impact of the origin of SNA on recurrence of AF after pulmonary vein isolation (PVI) in patients with paroxysmal AF.Seventy-eight patients underwent coronary angiography for suspected coronary heart disease, followed by catheter ablation for paroxysmal AF. According to the origin of SNA from angiographic findings, they were divided into right SNA group (SNA originating from the right coronary artery) and left SNA group (SNA originating from the left circumflex artery). Guided by an electroanatomic mapping system, circumferential pulmonary vein ablation (CPVA) was performed in both groups and PVI was the procedural endpoint. All patients were followed up at 1, 3, 6, 9 and 12 months post-ablation. Recurrence was defined as any episode of atrial tachyarrhythmias (ATAs), including AF, atrial flutter or atrial tachycardia, that lasted longer than 30 seconds after a blanking period of 3 months.The SNA originated from the right coronary artery in 34 patients (43.6%) and the left circumflex artery in 44 patients (56.4%). Freedom from AF and antiarrhythmic drugs (AADs) at 1 year was 67.9% (53/78) for all patients. After 1 year follow-up, 79.4% (27/34) in right SNA group and 59.1% (26/44) in left SNA group (P = 0.042) were in sinus rhythm. On multivariate analysis, left atrium size (HR = 1.451, 95%CI: 1.240 - 1.697, P < 0.001) and a left SNA (HR = 6.22, 95%CI: 2.01 - 19.25, P = 0.002) were the independent predictors of AF recurrence.The left SNA is more frequent in the patients with paroxysmal AF. After one year follow-up, the presence of a left SNA was identified as an independent predictor of AF recurrence after CPVA in paroxysmal AF.

The interrelationship between atrial fibrillation (AF) and atrial flutter (AFL) has long been recognized both in patients and animal models(1). There are two important aspects of this interrelationship relevant to the paper by Mohanty et al.(2) in this issue of this journal. First is the fact that AF virtually always precedes the onset of classical cavotricuspid isthmus (CTI) dependent AFL, and second, the development of classical CTI AFL requires the development or presence of a line of block in the right atrium between the venae cavae(1). The first aspect probably was initially recognized by Sir Thomas Lewis(3), who, in studies in the normal canine heart, burst paced the right atrium, and obtained mostly transient AF, but sometimes sustained AFL. Lewis "mapped" the AFL, and concluded that AFL was due to reentry around the great veins, i.e., the superior and inferior vena cavae. This conclusion became well accepted. The second aspect was addressed by Rosenbleuth and Garcia-Ramos(4), who postulated that the reason it was so difficult for Lewis et al. to induce AFL was because there was short circuiting of the AFL reentrant circuit by conduction across the atria in the region between the vena cavae (from the left atrium or to the right atrium or vice versa) making the reentrant circuit impossible to sustain. Therefore, in studies in the canine heart (1947), they created conduction block between the vena cavae, either with a crush lesion (permanent block) or by painting cocaine on the atrial epicardium in the intercaval region (transient block), and, with burst atrial pacing, easily induced AFL. The latter occurred consistently in the presence of the crush lesion, but only transiently with the use of cocaine, as the effects of the cocaine wore off.

Abstract

Objectives:

Data regarding efficacy and safety of three-dimensional localisation systems (3D) are limited. We performed a meta-analysis of randomized trials comparing combined fluoroscopy and 3D guided to fluoroscopically-only guided procedures.

Design:

A systematic search was performed using multiple databases between 1990- 2010. Outcomes were acute and long-term success, ablation, procedure and fluoroscopic times, radiation dose (RD), and complications.

Results:

Thirteen studies involving 1292 patients were identified. 3D were tested against fluoroscopic guidance in 666 patients for supraventricular tachycardia (SVT), atrial flutter (AFL), atrial fibrillation (AF) and ventricular tachycardia (VT). Acute and long-term freedom from arrhythmia were not significantly different between 3D and control for AFL (acute success 97% vs. 93%, p=0.57; chronic success 93% vs. 96%, p=0.90) or SVT (acute success 94% vs. 100%, p=0.36; chronic success 88% vs. 88%, p=0.80). A shorter fluoroscopic time was achieved with 3D in AFL (p<0.001) and SVT (p=0.002). RD was significantly less for both AFL (p=0.002) and SVT (p=0.01). Ablation & procedure time and complications were not statistically different.

Conclusions:

Success, procedure time, and complications were similar between fluoroscopic and 3D-guided ablations. Fluoroscopic time and RD were significantly reduced for ablation of AFL and SVT with 3D.

Purpose:

To determine the diagnostic yield of the 24-hour Holter monitoring in the patients who were evaluated for palpitations.

Methods:

A prospective, single-centre study was performed to evaluate the diagnostic yield of the Holter monitoring. The inclusion criteria was age greater then 18 years with the symptom of unexplained recurrent palpitations. The exclusion criteria was patients with known medical causes of palpitation, a history of documented arrhythmias, or a history of or the current use of anti-arrhythmic drugs. The outcomes included a diagnostic Holter monitor recording.

Results:

The data analysis of the 335 patients who were studied, showed that there were 160 (47.8%) females and 175 (52.2%) males with a mean age of 55± 18.85 years (18 to 90 years). Ventricular ectopics as bigeminy in 36.7% patients and as couplets in 20% patients, were detected. Non-sustained VT was detected in 5.7% patients, VT was detected in 0.9% cases and SVT was detected in 12.5% cases. 3.58% cases had paraxosymal atrial flutter/fibrillation. The ST segment shift which is suggestive of silent ischaemia, was present in 17.6% of the study population. Second or higher degrees of AV blocks were noted in 2 cases, while one patient had the WPW syndrome. Ventricular bigeminy, couplets, VT,SVT and AF were statistically significant in the patients who were over the age of 50 years as compared to those who were less than 50 years.

Conclusion:

In patients with non-specific symptoms, Holter monitoring has a significant role in the primary diagnosis of myocardial ischaemia or arrhythmia as a cause of such symptoms in the older age groups.

BACKGROUND AND PURPOSE:

It is unknown whether supraventricular arrhythmias other than atrial fibrillation or flutter are associated with stroke.

METHODS:

To examine the association between paroxysmal supraventricular tachycardia (PSVT) and stroke, we performed a retrospective cohort study using administrative claims data from all emergency department encounters and hospitalizations at California's nonfederal acute care hospitals in 2009. Our cohort comprised all adult patients with ≥1 emergency department visit or hospitalization from which they were discharged alive and without a diagnosis of stroke. Our primary exposure was a diagnosis of PSVT recorded at an encounter before stroke or documented as present-on-admission at the time of stroke. To reduce confounding, we excluded patients with diagnoses of atrial fibrillation. We defined PSVT, stroke, and atrial fibrillation using International Classification of Diseases, Ninth Revision, Clinical Modification codes previously validated by detailed chart review.

RESULTS:

Of 4806830 eligible patients, 14121 (0.29%) were diagnosed with PSVT and 14402 (0.30%) experienced a stroke. The cumulative rate of stroke after PSVT diagnosis (0.94%; 95% confidence interval, 0.76%-1.16%) significantly exceeded the rate among patients without a diagnosis of PSVT (0.21%; 95% confidence interval, 0.21%-0.22%). In Cox proportional hazards analysis controlling for demographic characteristics and potential confounders, PSVT was independently associated with a higher risk of subsequent stroke (hazard ratio, 2.10; 95% confidence interval, 1.69-2.62).

CONCLUSIONS:

In a large and demographically diverse sample of patients, we found an independent association between PSVT and ischemic stroke. PSVT seems to be a novel risk factor that may account for some proportion of strokes that are currently classified as cryptogenic.

 A 70-year-old man with atrial flutter (AFL) following pulmonary vein (PV) isolation (PVI) underwent electrophysiologic testing. The AFL exhibited positive P waves in the inferior leads and lead V1. Left atrial activation mapping revealed 2 remote sites with early activation that were located at the antrum of the left superior PV roof and the left inferior PV bottom. A single irrigated radiofrequency ablation targeting the earliest PV activation at the left PV carina eliminated the AFL. This case demonstrated that PV carina tachycardia with multiple conduction gaps and inter-PV conduction after PVI might mimic double focal atrial tachycardias.