Systematic characterization of the reentrant circuit during atrioventricular nodal reentrant tachycardia.

This study was conducted to systematically characterize the excitable gap and conduction properties of the reentrant circuit during atrioventricular nodal reentrant tachycardia (AVNRT). Previous studies have attempted to analyze these properties by introducing single ventricular extrastimuli during tachycardia. These studies have been limited, however, by the inability of single extrastimuli to engage the circuit in the majority of patients studied. Thus, in most cases, the nature of the excitable gap and the conduction properties of the anterograde and retrograde limbs of the circuit during tachycardia remain undefined. In this series, 11 patients with typical AVNRT were studied. During tachycardia, both single and double ventricular extrastimuli (the first extrastimulus acting as a conditioning stimulus) were used to scan diastole. The resetting response of the reentrant circuit, as well as the conduction properties of the retrograde fast and anterograde slow pathways, was recorded and analyzed. Whereas atrial preexcitation and resetting of the reentrant circuit could be demonstrated in only 1 patient with single ventricular extrastimuli, resetting was achieved in all 11 patients with closely coupled double ventricular extrastimuli. Over the full range of coupling intervals used, no retrograde delay in fast pathway conduction could be demonstrated before tachycardia termination or ventricular refractoriness. Penetration of the reentrant circuit resulted in a progressive increasing delay in the anterograde portion of the subsequent return cycle and an increasing resetting response pattern in all cases. Thus, the reentrant circuit during AVNRT demonstrates heterogeneous excitability. While the fast pathway remains fully excitable during tachycardia, the slow pathway uniformly demonstrates decremental conduction, resulting in an increasing resetting response pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Relation of induced to spontaneous ventricular tachycardia from analysis of stored far-field implantable defibrillator electrograms.

Predischarge testing of implantable cardioverter-defibrillators is often used to tailor antitachycardia pacing algorithms based on the response of induced ventricular tachycardia (VT) to pacing. Despite this practice, little is known about the relation between VT induced at predischarge study and VT that occurs spontaneously. To clarify this relation, we identified 19 patients with VT induced at predischarge study and compared the characteristics of the induced VT with the first episode of spontaneous VT. VT morphology, tachycardia cycle length, and response to antitachycardia pacing were measured from far-field electrograms stored by the implantable cardioverter-defibrillator. All subjects had coronary artery disease and previous myocardial infarction. The mean time from baseline study until a spontaneous VT episode was 162+/-121 days. Analysis of far-field electrograms revealed that spontaneous VT was morphologically different from predischarge-induced VT in 13 of 19 cases (68%). The cycle length of induced VT was significantly shorter than spontaneous VT when VT morphologies were different but not when spontaneous and induced VT had an identical morphology. Antitachycardia pacing was effective in terminating 18 of 19 (95%) induced VTs and 14 of 18 (78%) spontaneous VTs. Antitachycardia pacing was effective in terminating 9 of 12 episodes of morphologically different spontaneous VTs and 5 of 6 episodes of morphologically identical spontaneous VTs (p = NS). Thus, the characteristics of VT induced at predischarge study correlate poorly with those of subsequent spontaneous VT episodes due to the induction of faster "nonclinical" VTs at predischarge testing. This may limit the applicability of predischarge testing in tailoring antitachycardia pacing algorithms.

Evaluation of sampling methods in research reported in selected clinical nursing journals: implications for nursing practice.

This article summarizes standards relating to sampling methodology, identifies deviations from these standards in research studies reported in selected clinical nursing journals, and provides suggestions for improving sampling methods to enhance the applicability of research for nursing practice. A random sample of 30 research reports published in 1986 in five clinical nursing journals was examined. Nearly 97 per cent of the published studies contained at least one major deficiency in sampling methodology. More than two thirds failed to describe the sampling frame, sample size, or number of refusals, withdrawals, and/or cases lost. Thirteen per cent did not report sampling methods. More than half made generalizations that were inappropriate for the sampling method used; 43 per cent did not acknowledge any limitations of their sample. Sample sizes were small, and statistical power to detect significant differences was low. These deficiencies in sampling procedures could detract from the value of the research that nurses are encouraged to use as a basis for practice. This article provides specific recommendations for remedying these deficiencies to help ensure the scientific merit of the research published for nursing practice.

Pathophysiologic substrate for sustained ventricular tachycardia in coronary artery disease.

Sustained ventricular tachycardia (VT) in the presence of coronary artery disease (CAD) is almost always associated with prior infarction. Its mechanism is reentrant excitation and it can be initiated > 95% of the time. Disrupted and delayed endocardial activation and prolonged, fragmented electrograms recorded during sinus rhythm distinguish patients with VT from those with normal ventricles and those of prior infarction without VT. The extent of abnormalities of activation and number of abnormal, fragmented and late electrograms are greatest in patients with sustained VT. These abnormalities are associated with scar tissue separating the viable myocytes. Fragmented electrograms are due to discontinuous activation due to nonuniform anisotropy caused by the scar tissue. Patients with CAD demonstrate depressed excitability and prolonged relative refractory periods (ie, an upward shift in the strength-interval curve) at sites of infarction but effective refractory periods measured at 10 mA comparable to normals and dispersion of refractory periods. However the associated abnormalities of conduction and activation produce an abnormal dispersion of recovery. Intraoperative mapping of patients with CAD has shown that most of the abnormalities of endocardial activation and conduction are in the subendocardial layers and subendocardial resection of these areas cures VT and abolishes delayed, fragmented electrograms and split potentials and normalizes the electrograms recorded from the subjacent tissue. This supports the hypothesis that abnormalities of conduction are the critical pathophysiologic substrate of VT in CAD.

Nonuniform anisotropy is responsible for age-related slowing of atrioventricular nodal reentrant tachycardia.

INTRODUCTION: AV nodal reentrant tachycardia cycle length has been shown to be longer in the elderly population. Microfibrosis associated with aging producing nonuniform anisotropic conduction or changes in membrane ionic properties could explain this finding. METHODS AND RESULTS: Forty-five patients (33 women and 12 men) with typical AV nodal reentrant tachycardia were studied to analyze the effects of age on electrophysiologic characteristics of the tachycardia using high-density catheter mapping of the triangle of Koch. We classified patients into group A (age < or = 45 years, mean [+/-SD] 32.7 +/- 8.8, n = 27) and group B (age > 45 years, mean [+/-SD] 61.1 +/- 10.2, n = 18). Retrograde atrial activation was recorded during tachycardia by means of a 2-mm decapolar catheter at the His bundle, a quadripolar catheter at the high right atrium, a multipolar catheter (6 to 10 poles) in the coronary sinus, and a deflectable quadripolar catheter at the posterior triangle of Koch. The AH interval at the AV junction as well as HA intervals at several atrial sites were measured during tachycardia. HA intervals at all atrial recording sites except in the posterior triangle of Koch were significantly longer in group B, as well as the tachycardia cycle length (362 vs 329 msec, P = 0.01). The mean AH interval was prolonged by 24 msec in group B, but this difference did not reach statistical significance. A sequential pattern of retrograde atrial activation during tachycardia was more frequently recorded in group B. CONCLUSIONS: Since the delayed activation to the atrium was heterogeneous, transverse nonuniform anisotropic conduction is a likely explanation of these age-related modifications of AV nodal reentrant tachycardia characteristics.

Twiddler's syndrome variants in ICD patients.

Three cases of twiddler's syndrome in patients with an abdominally implanted cardioverter defibrillator (ICD) and an endocardial lead system are reported. The condition was detected when an increase in pacing threshold or lead impedance was noted at routine follow-up. Successful revision was possible in all patients; however, a recurrence in one patient necessitated removal of the device. Elderly female patients with some degree of obesity appear most susceptible. Minimizing pocket size and suturing of the device to the fascia should decrease the chance of developing this problem.

Hybrid pharmacologic and ablative therapy: a novel and effective approach for the management of atrial fibrillation.

INTRODUCTION: Maintenance of sinus rhythm in patients with recurrent atrial fibrillation is often difficult to achieve with pharmacologic therapy. Complex catheter ablative procedures are being developed, but efficacy and safety issues remain to be clarified. We hypothesized that combined pharmacologic and simple ablative therapies in a targeted subset of patients will improve success in the treatment of atrial fibrillation. METHODS AND RESULTS: We identified 13 patients (mean age 61.5 +/- 16.2 years) with atrial fibrillation who converted to electrocardiographic atrial flutter during antiarrhythmic drug treatment. Surface ECG suggested "typical" atrial flutter in 11 patients and "atypical" atrial flutter in 2. Intracardiac mapping and entrainment studies revealed 9 patients had counterclockwise isthmus-dependent atrial flutter, and the remaining 4 had complex activation patterns, suggesting the presence of multiple wavefronts. All 9 patients with typical atrial flutter underwent successful ablation. None of the 4 patients with complex activation patterns had successful ablation. Patients were followed for recurrences of atrial arrhythmias via clinic visits, record review, and interviews. In patients who underwent successful ablation and continued on antiarrhythmic drugs, 88.9% remain in sinus rhythm after a mean follow-up of 14.3 +/- 6.9 months (range 1 to 28). CONCLUSION: In patients who experience conversion of atrial fibrillation to atrial flutter during antiarrhythmic drug treatment, ablation and continuation of pharmacologic therapy is a safe and effective means of achieving and maintaining sinus rhythm.

La brecha excitable en la taquicardia auriculoventricular por reentrada nodal / The excitable gap in atrioventricular nodal reentrant tachycardia

La taquicardia auriculoventricular por reentrada nodal es una causa común de taquicardia con complejos angostos y es la arritmia supraventricular paroxística encontrada más frecuentemente en la práctica clínica. Los avances en las técnicas de ablación por catéter han descartado la importancia del conocimiento más completo del sustrato anatómico y electrofisiológico de esta taquiarritmia. El circuito más común resulta de la disociación longitudinal de la conducción en el nódulo AV, en un componente anterógrado "lento" y otro retrógrado "rápido". Cuando la taquicardia se debe a reentrada funcional o anatómica, una brecha excitable está presente comúnmente entre la cola de refractariedad del último impulso de la taquicardia y el nuevo frente de onda. Un extraestímulo debería ser capaz de penetrar el circuito de reentrada en un momento apropiado y activar el tejido excitable de un modo similar al del frente de onda reentrante. Este fenómeno se denomina reciclado (resetting). Cuando el circuito de la taquicardia es penetrado por un tren de extraestímulos, resultando en un reciclado repetitivo, el fenómeno se denomina entrecruzamiento (entrainment)

La brecha excitable en la taquicardia auriculoventricular por reentrada nodal / The excitable gap in atrioventricular nodal reentrant tachycardia

La taquicardia auriculoventricular por reentrada nodal es una causa común de taquicardia con complejos angostos y es la arritmia supraventricular paroxística encontrada más frecuentemente en la práctica clínica. Los avances en las técnicas de ablación por catéter han descartado la importancia del conocimiento más completo del sustrato anatómico y electrofisiológico de esta taquiarritmia. El circuito más común resulta de la disociación longitudinal de la conducción en el nódulo AV, en un componente anterógrado "lento" y otro retrógrado "rápido". Cuando la taquicardia se debe a reentrada funcional o anatómica, una brecha excitable está presente comúnmente entre la cola de refractariedad del último impulso de la taquicardia y el nuevo frente de onda. Un extraestímulo debería ser capaz de penetrar el circuito de reentrada en un momento apropiado y activar el tejido excitable de un modo similar al del frente de onda reentrante. Este fenómeno se denomina reciclado (resetting). Cuando el circuito de la taquicardia es penetrado por un tren de extraestímulos, resultando en un reciclado repetitivo, el fenómeno se denomina entrecruzamiento (entrainment) (AU)