Detection of Atrial Fibrillation by Implanted Devices with Wireless Data Transmission Capability

Remote telemetry may facilitate the management of implantable devices. We tested the reliability of a new automatic, wireless home monitoring (HM) system that archives data every 24 hours. We retrospectively analyzed archival data from 276 consecutive pacing system implants to define temporal atrial fibrillation (AF) patterns and associated ventricular rate. An "AF day" was defined by a >20%/24 hour mode switch (MS) duration, irrespective of the MS number. Management decisions resulting from transmissions were noted. A pilot study confirmed that 89% of 22,356 transmissions were successful, of which >90% were received in <5 minutes. Data integrity was 100% preserved. Overall, AF developed in 29 patients (10.5%), representing a total of 645 AF days (mean = 22.2 ± 29.6 AF, median = 9 days), over 12 ± 2 months of monitoring. AF was infrequent (50% of 24 hours. Ventricular rates during 645 AF days in 29 patients averaged 95.1 ± 9.9 beats/min (median = 94 beats/min). Ventricular rates were >80 beats/min in 25 ± 30 AF days (median = 11 days). HM enabled rapid anticoagulation decisions. In recipients of implantable devices, automatic wireless telemetry with HM was efficient and reliable. Its application may overcome some current challenges in AF management by early notification and precise measurement of both AF burden and ventricular rate during AF.     

AZATHIOPRINE INDUCED BONE MARROW SUPPRESSION IN LIVE RELATED RENAL ALLOGRAFT RECIPIENTS

Over a follow-up period of 6 years, 4 out of 31 live related renal allograft recipients (12.9%) developed azathioprine induced bone marrow suppression. Presentation in 3 patients was with fever and 2 patients also had associated graft dysfunction. All patients had leucopenia, 2 patients in addition had anaemia and one patient had pancytopenia. Bone marrow suppression developed 9.6 months (3.5-16.0 months) following transplantation and recovery followed over a period of 30 (18-49 days) days after withdrawal of the drug. One patient succumbed during the phase of bicytopenia.KEY WORDS: Azathioprine, Bone marrow suppression, Kidney transplantation     

BETA-ADRENORECEPTORS OF THE CAT NICTITATING MEMBRANE

• 1 The relaxant effects of isoprenaline, salbutamol, adrenaline and noradrenaline on the partially contracted isolated nictitating membrane of the cat were determined in the absence and the presence of α-adrenoreceptor blockade.
• 2 It was possible to demonstrate significant relaxant effects of isoprenaline and salbutamol in the absence as well as in the presence of α-adrenoreceptor blockade. However, the relaxant effects of adrenaline and noradrenaline could not be demonstrated in the absence of α-adrenoreceptor blockade.
• 3 Molar concentrations (EC₃₀) of isoprenaline, salbutamol and adrenaline causing 30% relaxation of the tone did not significantly differ from each other; EC₃₀ of each of these agents was significantly less than that of noradrenaline.
• 4 β₁-Adrenoreceptor antagonist metoprolol was less potent than β₂-antagonist H 35/25 in antagonizing the effect of salbutamol; metoprolol was more potent than H 35/25 in antagonizing noradrenaline. Both these agents were effective antagonists of isoprenaline; however, metoprolol and H 35/25 in combination produced greater antagonism of isoprenaline than did each antagonist separately.
• 5 It is concluded that the cat nictitating membrane possesses both β₁- and β₂-adrenoreceptors which are responsible for the relaxant effects of sympathomimetic agents. A study of these receptors is, however, complicated by concomitant stimulation of α-adrenoreceptors.

     

Neurophysiological abnormalities in genuine female stress urinary incontinence

Summary. Perineal sensory and motor function was investigated in 28 women with genuine stress incontinence of urine and compared with a matched control group. Electrosensitivity of the dorsal nerve of the clitoris and of the urethral mucosa was significantly diminished in these patients (eight measurements 'insensitive'). Three different reflex latency measurements (dorsal nerve to external anal sphincter, dorsal nerve to urethral sphincter, urethral mucosa to external anal sphincter) were prolonged in incontinence (14 absent reflexes). Mean motor unit potential duration of the external anal sphincter was also prolonged, reflecting an early neuropathy. Anorectal manometry detected significantly weaker squeeze pressures in stress incontinence although other variables were unaffected.     

Inducibility of Atrial Fibrillation After GP Ablations and “Autonomic Blockade”: Evidence for the Pathophysiological Role of the Nonadrenergic and Noncholinergic Neurotransmitters

Autonomic Blockade and Atrial Fibrillation . Background: Recent clinical reports that used cholinergic and adrenergic blockade (CAB) as an alternative to ganglionated plexi (GP) ablation to terminate atrial fibrillation (AF) showed mixed results. We investigated the role of other neurotransmitters in AF inducibility. Methods: In 23 pentobarbital anesthetized dogs, a left and right thoracotomy allowed the attachment of electrode catheters to the left and right pulmonary veins and atrial appendages (AA). Programmed stimulation was used to determine the effective refractory periods (ERP) and AF inducibility, measured by the window of vulnerability (WOV). AF duration in response to acetylcholine (Ach; 100 mM) applied to the AA was measured before and after GP ablation + CAB and with vagus nerve stimulation (VNS). After GP ablation + CAB, Ach induced AF duration was determined in response to vasoactive intestinal peptide (VIP) and its specific antagonist ([Ac‐Tyr1,D‐phe2]‐VIP). Results: GP ablation + CAB significantly prolonged ERP, eliminated WOV, and suppressed the duration of Ach induced AF (P ≤ 0.01 for all). Also slowing of the heart rate by VNS was essentially blocked; however, with Ach 100 mM applied to the AA, VNS, and VIP applied to the AA markedly prolonged AF duration. This effect was blocked by the VIP antagonist. Conclusions: Neither GP ablation nor CAB can fully suppress AF inducibility arising from the atrial neural network. Our findings suggest that other neurotransmitters, such as VIP released during VNS, can promote sustained AF despite GP ablation and “autonomic blockade,” which may further define the substrate for AF outside the pulmonary vein‐atrial junctions. (J Cardiovasc Electrophysiol, Vol. 24, pp. 188‐195, February 2013)