Incidence of Atrial Fibrillation in Patients with Different Mode of Pacing. Long-term Follow-up

We evaluated the incidence of atrial fibrillation in 189 patients (92males, 97females, mean age 75 ± 12yrs, range 41–100yrs) with pacemaker, during a mean follow-up of 5.5yrs (range 1–24yrs). The indications for implant were: complete AV block (115pts), second degree Möbilz 2 AV block (51pts). bifascicular block (5pts). sick sinus syndrome (14pts), symptomatic bradycardia (4pts). The mode of stimulation considered were VVI (105pt), VVI rate responsive (21pts), single lead VDD (43pts), DDD (20pts). The occurrence of retrograde VA conduction in patients with VVI or VVI rate responsive pacing was also evaluated. Atrial fibrillation occurred in 40 pts (21%). The highest incidence was evidenced in patients with sick sinus syndrome (9pts, 64%), and in patients with VVI stimulation (28pts, 27%). On the contrary, the lowest incidence was found in single lead VDD stimulation (4pts, 9%). The patients with dual chamber pacing showed a relatively high incidence of the arrhythmia (5pts, 25%). Atrial fibrillation occurred in 9 out of 32 patients with retrograde VA conduction, and in 22 out of 94 patients without retrograde conduction (28% versus 23%, p=NS). In conclusion, it is confirmed that patients with sick sinus syndrome are at high risk for atrial fibrillation. Single lead VDD stimulation seems to be the better mode of pacing in preventing atrial fibrillation, while dual chamber pacing showed minor efficacy. The presence of retrograde VA conduction could not predict the occurrence of the arrhythmia.     

Prospective Evaluation of New and Old Criteria to Discriminate Between Supraventricular and Ventricular Tachycardia in Implantable Defibrillators

This study was designed to evaluate the ability to distinguish between supraventricular tachycardias (SVTs) and ventricular tachycardias (VTs) based on onset, stability, and width criteria in an implantable defibrillator. Inappropriate detection of atrial fibrillation and sinus tachycardia is a common problem in patients with implantable defibrillators. The onset, stability, and width criteria were studied in 17 patients who underwent implantation of a Medtronic 7218C implantable defibrillator by inducing sinus tachycardia and atrial fibrillation. Additional data on the width criteria was obtained by pacing at separate sites in both the left and right ventricle. Patients were studied at different times for up to 6 months to determine any changes in the criteria. The onset and stability criteria caused inappropriate detections in 36% and 12% of the episodes, respectively. The addition of the width criteria decreased the inappropriate detection using the onset and stability criteria to 5% and 2%, respectively. Pacing from the RV apex, RV outflow tract, and LV apex was appropriately detected as wide in 76%, 41%, and 94%, respectively. The width criteria changed over time in individual patients, but was stable by 6 months in all but one patient. No single criterion is satisfactory for distinguishing between SVT and VT in this patient population, but the combination of criteria seems to provide better discrimination. The width criteria can change dramatically over time and needs to be monitored carefully. Newer algorithms will need to be developed to allow better detection of supraventricular tachycardias.     

Tridimensional Mapping: Guided Modification of the Sinus Node

Tridimensional Mapping: Guided Modification of the Sinus Node. Radiofrequency (RF) catheter modification of the sinus node appears to he a promising therapeutic modality for the treatment of inappropriate sinus tachyeardia Modification, as opposed to total obliteration, of the atrial pacemaker requires precise localization of the sinus node. This has been successfully achieved with a multicatheter approach guided by intracardiac echocardiography. This article describes the first clinical use of a tridimensional nonfluoroscopic mapping system to guide successful RF modification of the sinus node in two cases of inappropriate sinus tachycardia. This system simplifies the current approach and greatly reduces the fluoroscopy time.     

Time- and Dose-Dependent Effects of Chronic Wound Fluid on Human Adult Dermal Fibroblasts

BACKGROUND Wound healing is a biologic process that is altered in patients affected by chronic venous ulcers. The wound microenvironment is reflected in the chronic wound fluid (CWF), an exudate containing serum components and tissue-derived proteins.
OBJECTIVES We investigated the effects of increasing doses of CWF collected from patients suffering from chronic venous ulcers on human adult dermal fibroblasts cultured in vitro and the relationship among CWF effects and treatment length.
METHODS Fibroblasts were treated with 60, 240, and 720 μg/mL CWF for 3 and 7 days. We evaluated cell proliferation and viability by MTT and Trypan blue assay, cell morphology by light microscopy, F-actin microfilaments organization by tetramethylrhodamine B isothiocyanate-conjugated phalloidin, α-smooth muscle actin expression by immunofluorescence, and senescence-associated β-galactosidase activity.
RESULTS CWF induced an increase in cell proliferation in the first 3 days of treatment. In contrast, at 7 days, a strong decrease in cell viability was observed. These changes were related to a cytoskeletal F-actin reorganization and not to fibroblast–myofibroblast differentiation nor to changes in cellular senescence.
CONCLUSIONS This study shows a dose-dependent and biphasic effect of CWF on dermal fibroblasts, suggesting that a continuous exposure to chronic wounds microenvironment may induce late cellular dysfunctions possibly involved in the delayed wound healing.     

Evidence for a Therapeutic Effect of Plasmapheresis in Patients with Systemic Lupus Erythematosus

Fourteen patients with active systemic lupus erythematosus (SLE)have been treated with plasmapheresis at a rate of two litresdaily on three to four days per week, over a period of two tothree weeks. Plasma was replaced isovolemically with eitherfresh frozen plasma or with human plasma protein fractions.Ten patients were receiving treatment with prednisone at thetime of plasmapheresis, and four had received no prior treatment.Eight patients showed evidence of either clinical improvementor clinical and immunochemical improvement, at the time of plasmapheresis.In the three patients who showed high levels of circulatingcomplexes before treatment, there was a sudden fail in the levelof circulating immune complexes, which was quantitatively greaterthan could be explained by the amount removed. This suggeststhat in some patients with SLE, clearance of complexes by themononuclear phagocytic system is initially blocked by high levelsof circulating complexes and that one effect of plasmapheresismay be to relieve this blockade. Five patients showed a clinicalresponse to plasmapheresis despite the fact that tests for immunecomplexes were negative. Three patients showed no response toplasmapheresis, and three were regarded as unevaluable. In a limited number of patients, who show a high level of circulatingimmune complexes, and whose condition is deteriorating despitetreatment with corticosteroids, there may he an important therapeuticrole for plasmapheresis.     

Neural Control Mechanisms and Vasovagal Syncope

Vasovagal Syncope, Patients with recurrent unexplained syncope may have cardioinhibitory and vasodepressor responses provokable with head-up tilt with or without exogenousbeta-adrenergic stimulation. Although these responses are believed to be neurally mediated, the neural mechanisms involved are pourly understood. Numerous studies have documentedperipheral vasodilation, hypotension, and bradycardia at the time of syncope and several casereports have shown sudden withdrawal of vasoconstrictor sympathetic neural outflow to skeletal muscle in human subjects. In cats and rats, a similar response can be provoked with hemorrhage and is prevented by interruption of cardiac vagal C-fiber afferents. In dogs, however, section of these fibers does not prevent the development of a vasodepressor response. Theprovocation of vasodepressor syncope during nitroprusside infusion in a heart transplantrecipient with presumed ventricular denervation also suggests that cardiac afferent nerves maynot be required for the development of vasodepressor responses in humans. Other potentialmechanisms include release of endogenous opioids or nitric oxide that may inhibit sympatheticnerve firing, and primary central nervous system activation (as in partial seizures) that triggerscardioinhibitory and vasodepressor responses. This article reviews our current understandingof the mechanisms involved in the development of neurally mediated syncope.