The adaptation of state-of-the-art computerized technology to closely monitor patients with HF with advanced-practice nurse care under the guidance of a cardiologist significantly improves HF management while reducing the cost of care.

BACKGROUND The safety and efficacy of selective fast versus slow pathway ablation using radiofrequency energy and a transcatheter technique in patients with atrioventricular nodal reentrant tachycardia (AVNRT) were evaluated. METHODS AND RESULTS Forty-nine consecutive patients with symptomatic AVNRT were included. There were 37 women and 12 men (mean age, 43 +/- 20 years). The first 16 patients underwent a fast pathway ablation with radiofrequency current applied in the anterior/superior aspect of the tricuspid annulus. The remaining 33 patients initially had their slow pathway targeted at the posterior/inferior aspect of the right interatrial septum. The fast pathway was successfully ablated in the initial 16 patients and in three additional patients after an unsuccessful slow pathway ablation. A mean of 10 +/- 8 radiofrequency pulses were delivered; the last (successful) pulse was at a power of 24 +/- 7 W for a duration of 22 +/- 15 seconds. Four of these 19 patients developed complete atrioventricular (AV) block. In the remaining 15 patients, the post-ablation atrio-His intervals prolonged from 89 +/- 30 to 138 +/- 43 msec (p less than 0.001), whereas the shortest 1:1 AV conduction and effective refractory period of the AV node remained unchanged. Ten patients lost their ventriculoatrial (VA) conduction, and the other five had a significant prolongation of the shortest cycle length of 1:1 VA conduction (280 +/- 35 versus 468 +/- 30 msec, p less than 0.0001). Slow pathway ablation was attempted initially in 33 patients and in another two who developed uncommon AVNRT after successful fast pathway ablation. Of these 35 patients, 32 had no AVNRT inducible after 6 +/- 4 radiofrequency pulses with the last (successful) pulse given at a power of 36 +/- 12 W for a duration of 35 +/- 15 seconds. After successful slow pathway ablation, the shortest cycle length of 1:1 AV conduction prolonged from 295 +/- 44 to 332 +/- 66 msec (p less than 0.0005), the AV nodal effective refractory period increased from 232 +/- 36 to 281 +/- 61 msec (p less than 0.0001), and the atrio-His interval as well as the shortest cycle length of 1:1 VA conduction remained unchanged. No patients developed AV block. Among the last 33 patients who underwent a slow pathway ablation as the initial attempt and a fast pathway ablation only when the former failed, 32 (97%) had successful AVNRT abolition with intact AV conduction. During a mean follow-up of 6.5 +/- 3.0 months, none of the 49 patients had recurrent tachycardia. Forty patients had repeat electrophysiological studies 4-8 weeks after their successful ablation, and AVNRT could not be induced in 39 patients. CONCLUSIONS These data suggest that both fast and slow pathways can be selectively ablated for control of AVNRT: Slow pathway ablation, however, by obviating the risk of AV block, appears to be safer and should be considered as the first approach.

The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p <0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p< 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amenable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia. (Circulation 1989;79:256-270) M acroreentry within the His-Purkinje system commonly referred to as bundle branch reentry (BBR) is a frequently observed phenomenon in the laboratory.1-3Although scattered cases of sustained BBR tachycardia have been reported, no large series dealing with this phenomenon exists in the literature.4-11 The incidence of BBR as a mechanism of sustained ventricular tachycardia (VT), therefore, continues to be underreported in the literature, and consequently, there is less awareness of sustained BBR tachycardia as a significant clinical arrhythmia.

During the generation of radiofrequency (RF) lesions in the ventricular myocardium, the maintenance of adequate electrode-tissue contact is critically important. In this study, lesion dimensions and temperature and impedance changes were evaluated while controlling electrode-tissue contact levels (-5, 0, +1, and +3 mm) and power levels (10, 20, and 30 W). This data was used to assess the ability of impedance and temperature monitoring to provide useful information about the quality of electrode-tissue contact. The results show that as the electrode-tissue contact increases, so does the amount of temperature rise. With the electrode floating in blood (-5 contact), the average maximum temperature increase with 20 and 30 W was only 7 +/- 1 and 11 +/- 2 degrees C, respectively. At 20 and 30 W the temperature plateaued shortly after the initiation of power application. With good electrode-tissue contact (+1 mm or +3 mm), the temperature increase within the first 10 seconds was significantly greater than the temperature increase from baseline with poor contact (0 mm or -5 mm) and reached a maximum of 60 +/- 1 degrees C after 60 seconds of power application. As the electrode-tissue contact increased, so did the rate and level of impedance decrease. However, the rate of impedance decrease was slower compared to the rate of temperature rise. With the electrode floating in blood, the maximum impedance decreases with 20 and 30 W were 6 +/- 6 omega and 9 +/- 5 omega, respectively. The impedances plateaued after a few seconds of power application. With the electrode in good contact, the maximum impedance decreases with 20 and 30 W were 25 +/- 2 omega and 20 +/- 6 omega, respectively. In these cases the rate of the impedance decrease plateaued after 40 seconds of power application. The increase in lesion diameter and depth correlate well with decreasing impedance and increasing temperature. However, lesion depth appears to correlate better with impedance than temperature. We conclude that, since the electrode-tissue contact is not known prior to the application of power to the endocardium, in the absence of a temperature control system, the power should initially be set at a low level. The power should be increased slowly over 20-30 seconds, and then maintained at its final level for at least 90 seconds to allow for maximal lesion depth maturation. The power level should be lowered if the impedance drop exceeds 15 omega.

The hemodynamic determinants of the time constant of left ventricular (LV) isovolumic pressure (P) decline were studied in 32 anesthetized dogs. The time constant, tau (an index of LV relaxation), was determined from the best exponential fit of the equation P = Poe-t/r, to LVP measured at 5-ms intervals during isovolumic relaxation; Po = LVP at maximum negative dP/dt and t = time. At a constant heart rate of 120 beats/min, tau was determined during steady-state increases in preload (volume expansion), increases in afterload (methoxamine infusion), reductions in afterload (nitroprusside infusion), and in variably afterloaded beats at a constant preload (single-beat interventions). tau was directly related to LV systolic pressure and length during the alterations in LV loading conditions, but tau was not closely related to the extent of fiber shortening. During isoproterenol infusion, relaxation was more rapid (tau), and following the administration of propranolol, relaxation was prolonged (tau). While data from the variably afterloaded contractions indicate the presence of systolic load-dependent LV relaxation velocity, the steady-state studies do not exclude the possibility that altered contractility through reflex or other mechanisms contributes to the observed changes in tau.

In patients with neurocardiogenic syncope associated with bradycardia or asystole, drug therapy is often effective in preventing syncope, whereas artificial pacing is not.

Two-dimensional echocardiography was performed during a head-up tilt test in 11 control subjects (group I) and 18 patients with recurrent unexplained syncope. In four patients (group II), the head-up tilt test was negative at baseline and after isoproterenol infusion. Syncope was induced during baseline head-up tilt in nine patients (group III) and after isoproterenol challenge in five (group IV). The echocardiographic variables assessed were left ventricular end-systolic and end-diastolic areas and percent fractional shortening. At the end of head-up tilt, end-systolic area decreased by 4.5 +/- 1.3 and 3.0 +/- 1.2 cm2 in groups III and IV, respectively, compared with 0.5 +/- 0.7 and 0.2 +/- 0.1 cm2 in groups I and II, respectively (p less than 0.04). Similarly, end-diastolic area decreased by 5.5 +/- 2.6 cm2 in group III compared with 2.7 +/- 1.9 and 1.75 +/- 0.4 cm2 in group I and II, respectively (p less than 0.04). Additionally, at the end of the baseline study, fractional shortening was significantly greater in group III and group IV (43 +/- 5%) than in groups I and II (p less than 0.01). In conclusion, syncope induced by head-up tilt is associated with vigorous myocardial contraction and a significant decrease in left ventricular end-systolic dimensions. This left ventricular hypercontractility may play an important role in the pathogenesis of syncope induced by head-up tilt.

The combination of electrophysiologic evaluation and head-up tilt testing can identify the underlying cause of syncope in as many as 74% of patients presenting with unexplained syncope. Therapeutic strategies formulated according to the results of these diagnostic tests appear to prevent syncope effectively in most patients.