Should Radiofrequency Therapy Be Performed in Every Symptomatic Patient with Supraventricular Tachycardia? (Pro Drug Position)

The indication for treatment of paroxysmal supraventricular tachycardia depends on the frequency and severity of the tachycardia attacks. If the tachycardia attacks are mildly symptomatic and occur only once or twice a year, there is no indication for either continuous drug therapy or radiofrequency oblation. The only therapeutic measure required is termination of each acute event. If symptoms occur frequently, long-term antiarrhythmic drug therapy is then indicated and will be effective for chronic prophylaxis in most individuals with a low risk of proarrhythmic events. Only in patients with severe or life-threatening symptoms or cases refractory to drug therapy would radiofrequency ablation possibly be justified.     

Generation of Cell-Derived Factors Suppressing IgE Synthesis of Nippostrongylus brasiliensis-Infected Mice in Vitro

Modulation of de novo IgE synthesis in vitro was studied using the parasitic infection of mice with the nematode Nippostrongylus brasiliensis. Cell-derived factors were generated by stimulation of splenic and mesenteric lymph node cells of BALB/c mice with monoclonal IgE in vitro. High molecular weight (greater than 50,000) and low molecular weight (less than 50,000) culture supernatants were prepared. De novo IgE synthesis of BALB/c lymphocytes--obtained from N. brasiliensis-reinfected mice that secreted pronounced quantities of IgE in vitro--was markedly reduced by the addition of high molecular weight supernatants. A dose-dependent suppression of IgE synthesis was obtained, whereas IgG synthesis, viability, and cell proliferation were not inhibited. After fractionation of low molecular weight supernatants with IgE-Sepharose the glycine/HCl eluate fractions markedly inhibited the in vitro IgE synthesis. Low molecular weight factors which suppressed IgE synthesis without modulating IgG production were obtained from IgE high responder B6D2F1 normal mouse cells. Thus, our results demonstrate the generation of IgE-specific suppressor factors in vitro upon stimulation with IgE. The suppression of IgE synthesis by eluate fractions of low molecular weight supernatants absorbed with IgE-Sepharose suggest a potential role for IgE binding factors on de novo IgE synthesis in vitro.     

Slowing of the Ventricular Rate During Atrial Fibrillation by Ablation of the Slow Pathway of AV Nodal Reentrant Tachycardia

Influence of Slow Pathway Ablation on Atrial Fibrillation. Introduction : The mechanisms whereby radiofrequency catheter modification of AV nodal conduction slows the ventricular response are not well defined. Whether a successful modification procedure can be achieved by ablating posterior inputs to the AV node or by partial ablation of the compact AV node is unclear. We hypothesized that ablation of the well-defined slow pathway in patients with AV nodal reentrant tachycardia would slow the ventricular response during atrial fibrillation.
Methods and Results : In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1-week follow-up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 ± 76,500 ± 121, and 405 ± 91 msec to 429 ± 84 (P < 0.01), 673 ± 161 (P < 0.01), and 535 ± 98 msec (P < 0.01), respectively. These effects remained stable during follow-up at 1 week. The AV block cycle length increased from 343 ± 68 msec to 375 ± 60 msec (P < 0.05) immediately and to 400 ± 56 msec (P < 0.01) at 1-week follow-up. The effective refractory period of the AV node prolonged from 282 ± 83 msec to 312 ± 89 msec and to 318 ± 81 msec after 1 week (P < 0.05), respectively.
Conclusion : This study shows a decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of posterior inputs to the AV node.     

Changes in Plasma Epinephrine Concentration and in Heart Rate During Head-Up Tilt Testing in Patients with Neurocardiogenic Syncope:

Sympathetic Activation in Neurocardiogenic Syncope. Introduction : Tilt table testing is widely used in the management of patients with neurocardiogenic syncope. However, the exact pathophysiologic mechanism of this disorder is still under debate. Likewise, therapy of these patients continues to represent a challenge in many cases. Therefore, the present study aimed to gain further insight into the pathophysiology of this syndrome and to examine easily accessible clinical parameters that can improve therapy selection.
Methods and Results : In 16 patients with neurocardiogenic syncope, changes in endogenous catecholamine concentrations were determined during repeated tilt table testing before and during treatment with metoprolol. Tachycardia preceded syncope in 8 of 10 responders compared to only 1 of 6 nonresponders (P < 0.05). In responders, the relative increase in epinephrine levels averaged 197%± 51% during drug-free tilting and 75%± 33% during repeated testing while on β-blocker therapy (P < 0.05). In nonresponders, there was a smaller relative increase in epinephrine averaging 137%± 35% at baseline tilt. During repeated tilt testing, a similar increase was observed in these patients with recurrent syncope (156%± 104%; P = NS compared to baseline).
Conclusion : In patients with neurocardiogenic syncope who show both an increase in epinephrine concentration during tilt test and sinus tachycardia prior to the onset of symptoms, β-blocker treatment is very effective. These findings confirm the major role of sympathetic activation as a trigger of syncope. Particularly, heart rate changes at the onset of syncope may allow early identification of patients responding to antiadrenergic therapy.     

Pressure‐Guided Cryoballoon Isolation of the Pulmonary Veins for the Treatment of Paroxysmal Atrial Fibrillation

Pressure‐Guided Cryoballoon Pulmonary Vein Isolation. Background: Pulmonary vein (PV) isolation using a balloon‐mounted cryoablation system is a new technology for the percutaneous treatment of atrial fibrillation (AF). Complete PV occlusion during balloon ablation has been shown to predict successful electrical isolation. The aim of this study was to correlate mechanical PV occlusion with changes in a pressure curve recorded at the distal tip of the cryoballoon catheter. Methods and Results: We analyzed 51 PVs in 12 patients (61 ± 6 years old) with paroxysmal AF. At first, PV occlusion via the cryoballoon was documented by changes in the pressure curve. Once the PV is occluded, the pressure curve registered in the vein converts from a left atrial pressure curve to a pulmonary artery pressure curve: the PV wedge curve. Occlusion was then confirmed by transesophageal echocardiography (TEE). Following 2 cryoablation applications, electrical PV isolation was assessed with a circumferential mapping catheter. Under the exclusive guidance of changes in the pressure curve at the tip of the cryoballoon, mechanical occlusion confirmed by TEE was achieved in 47 of 51 PVs (92%). Three PVs required further TEE guidance to achieve occlusion. All 50 occluded veins were electrically isolated after cryoablation. One right inferior vein, which could not be occluded with the balloon, displayed conduction post cryoablation and was isolated by focal ablation. Conclusions: Occlusion and electrical isolation of PVs during cryoballoon ablation can be predicted by the appearance of a PV wedge curve at the tip of the catheter. This new straightforward parameter may facilitate the procedure. (J Cardiovasc Electrophysiol, Vol. 21, pp. 120‐125, February 2010)