THE POSSIBLE ROLE OF SHIGELLA IN SPORADIC ENTERIC REACTIVE ARTHRITIS

Reactive arthritis (ReA) occurs after a urogenital infectionusually with Chlamydia trachomatis or an enteritis due to Yer-sinia,Salmonella, Campylobacter or Shigella, Shigella, except duringepidemics, is not considered to be a frequent cause of entericreactive arthritis. However this might be due to the lack ofa reliable antibody test, which makes diagnosis difficult. Wecompared synovial and peripheral blood lymphocyte proliferationto various bacterial antigens in 19 consecutive patients withReA or undifferentiated oligoarthritis. In five patients Shigellawas identified as the causative microbe by a specific synoviallymphocyte proliferation. All five patients had a history ofsymptomatic diarrhoea and had negative stool cultures by thetime arthritis developed. Four of the five were HLA B 27 positive.We conclude that Shigella may be underestimated as a cause ofnon-epidemic ReA. KEY WORDS: Reactive arthritis, Shigella, Antigen specific lymphocytes, Synovial fluid     

Hereditary deficiency of triosephosphate isomerase in four unrelated families

Triosephosphate isomerase deficiencies in erythrocytes and leucocytes were discovered in three unrelated families by a heterozygote screening of 3000 blood samples. In addition, a family found by Schroter et al. [not published] was studied. In these four families, only heterozygote carriers were found. In the family described by Freycon et al. with hetero- and homozygote carriers of triosephosphate isomerase deficiency, the heterozygotes were reinvestigated. There was 51% of normal enzyme activity in three of the families. In the other two families the enzyme activity was 64% and 71% of normal. Two of the eleven heterozygotes, both children, were diseased, but it seems unlikely that the disorders resulted from the deficiencies. The activities of thirteen enzymes, the Km of triosephosphate isomerase for glyceraldehyde phosphate and the concentrations of metabolites were normal. Antibody titration showed normal specific activities in four families and 50% of normal in one family. No electrophoretic variant was detected. From the proved heredity, a heterozygous frequency of at least 1/1000 is indicated. A maximal frequency of 5/1000 is estimated by using further instances of triosephosphate isomerase deficiency where heredity has not yet been investigated. An explanation for the small number of known cases is that this enzyme is not routinely assayed.     

Heart Rate Variability in Isolated Rabbit Hearts

The presence of heart rate variability (HRV) in patients with cardiac denervation after heart transplantation raised our interest in HRV of isolated, denervated hearts. Hearts from seven adult white ELCO rabbits were transferred to a perfusion apparatus. All hearts were perfused in the working mode and in the Langendorff mode for 20 minutes each. HRV was analyzed in the frequency domain. A computer simulated test ECG at a constant rate of 2 Hz was used for error estimation of the system. In the isolated, denervated heart, HRV was of random, broadband fluctuations, different from the well-characterized oscillations at specific frequencies in intact animals. Mean NN was 423 ± 51 ms in the Langendorff mode, 406 ± 33 ms in the working heart mode, and 500 ms in the test ECG. Total power was 663 ± 207 ms², 817 ± 318 ms², and 3.7 ms², respectively. There was no significant difference in any measure of HRV between Langendorff and working heart modes. The data provide evidence for the presence of HRV in isolated, denervated rabbit hearts. Left atrial and ventricular filling, i.e., the working heart mode, did not alter HRV, indicating that left atrial or ventricular stretch did not influence the sinus nodal discharge rate.     

Effects of Overdrive Stimulation on Functional Reentrant Circuits Causing Ventricular Tachycardia in the Canine Heart:

Overdrive Stimulation and Functional Reentry, introduction: The purpose of the experiments described in this article was to investigate the effects of overdrive stimulation on functional anisotropic reentrant circuits causing ventricular tachycardia in infarcted canine ventricles. We determined how overdrive stimuli affect reentrant circuits to alter characteristics of the tachycardia.
Methods and Results: Activation patterns were determined In mapping excitation with a 192 bipolar electrode array. We found that overdrive stimuli could activate the circuits with the same pattern as the reentrant wavefront and that after overdrive stopped either the last or the next to last stimulated wavefront continued propagating through the circuit as a new reentrant impulse and tachycardia continued. When the circuit was not altered after overdrive, the exit route that the stimulated wavefront took from the circuit to activate the rest of the ventricles was also not altered and the tachycardia after overdrive had the same cycle length and QRS morphology as prior to overdrive. In some experiments, however, the overdrive stimuli did not follow the original reentrant pathway but led to the formation of a different circuit with a different exit route to the ventricles. As a result, after overdrive stimulation tachycardia had a different QRS morphology and cycle length than prior to stimulation. When the new circuit after overdrive was small and the revolution time of the reentrant impulse around the circuit was short, fibrillation occurred.
Conclusion: Functional reentrant circuits can either be maintained or altered after a period of overdrive stimulation. The results explain many of the effects that have been seen during overdrive stimulation of clinical ventricular tachycardia.     

Sarcoid Myocarditis With Ventricular Tachycardia Mimicking ARVD/C

Sarcoid Myocarditis with VT Mimicking ARVD/C.   Cardiac sarcoidosis (CS) is a multisystem granulomatous disorder of unknown etiology with frequent cardiac involvement. We describe a patient presenting with a ventricular tachycardia, presumably originating in the right ventricle (RV). This patient had a malignant clinical course with initial diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C); however, at postmortem histopathology revealed epithelioid granulomas with fibrosis localized in the interventricular septum, typical for sarcoidosis, without signs of extracardiac sarcoidosis. In conclusion, sarcoid myocarditis may present with signs and symptoms of ARVD/C and only histopathology can differentiate the 2 diseases. In the cases of atypical clinical presentation or when histopathological proof of ARVD is absent, a close follow-up is advisable to identify other potentially treatable disorders. (J Cardiovasc Electrophysiol, Vol. 21, pp. 94–98, January 2010)     

Metabolism of a bisphosphonate ester (PNU-91638) in rat

1. Metabolites of the cyclic bisphosphonate ester, 4-[2,2′-bis-(5,5-dimethyl-1,3,2-dioxaphosphorinan-2-yl)] butanoyl-3-fluoro-benzene (PNU-91638) in bile or urine of the male Sprague-Dawley rat were characterized by mass spectrometry. The chronically bile duct/duodenal-cannulated male rats received a single oral dose of 100?mg/kg [¹³C] [¹³C]PNU-91638. Bile and urine samples were analysed for radioactivity and profiled by hplc with radiometric and UV detection. 2. The 0-28-h bile and urine accounted for 46.0 and 19.7% of dose respectively. The structures of radioactive peaks were investigated by ionspray and liquid secondary ion mass spectrometry (LSIMS) and LSIMS/MS analysis. 3. Major metabolites in urine included two regioisomeric phenol glucuronides, a gem-methyl hydroxylated metabolite of the bisphosphonate heterocycle, a phenol metabolite, parent drug and a benzylic alcohol metabolite. Additional metabolites in bile included an unstable phenol glutathione adduct (from a putative epoxide intermediate) with several minor isobaric regioisomers, and a carboxylic acid derived from the gem methyl hydroxylated bisphosphonate ring. 4. The structures proposed have not been confirmed by nmr due to discontinuation of the development of PNU-91638.     

Directional Coronary Atherectomy of In-stent Restenosis: A Two-Center Experience

Background: Tissue proliferation is the major cause of in-stent restenosis (ISR). Thus, debulking of material should be the most favorable method to treat ISR. The present study was performed to test the clinical and angiographic outcome of directional coronary atherectomy (DCA) in the treatment of restenosis within different stents. Methods and Results: Fifty patients with ISR in single stents (12 Palrnaz-Schatz stents, 8 Pura stents, 10 Multilink stents, 10 NIR stents, 8 Wallstents, and 2 Microstents) underwent DCA with adjunctive balloon angioplasty in 38 patients. Primary success was achieved in 48 patients (96%). Two patients developed CK-MB elevations, one with a Q-wave infarction. Some minor technical problems occurred with respect to the different stent types. The percent diameter stenosis decreased from 76 ± 7% at baseline to 29 ± 6% after atherectomy (P < 0.0001) and 20 ± 4% after adjunctive PTCA, and it increased to 45 ± 19% at 4-month angiography (P < 0.0001). Angiographic restenosis occurred in 14 (29.2%) of 48 patients who were reevaluated after 4 months. Conclusion: While DCA is able to remove u significant amount of intimal tissue in selected patients with in-stent restenosis, new atherectomy catheter designs are required to make this a feasible and safe procedure.     

Clinical Evaluation of a Prototype Passive Fixation Dual Chamber Single Pass Lead For Dual Chamber ICD Systems

Dual chamber ICD systems use two separate leads for sensing. We developed and tested a new prototype of a single pass dual chamber passive fixation lead for dual chamber ICDs. Methods and Results: The prototype was a modification of the Guidant CPI Endotak DSP lead. The additional sensing electrode for the right atrium consisted of a side-mounted porous atrial ring electrode (AR). Atrial signals were recorded from the lead in patients during normal sinus rhythm (NSR), atrial fibrillation (AFib), and/or atrial flutter (AFl) with the AR in stable contact with the atrial wall or floating. During NSR, with the AR in contact with the atrial wall, an average P wave amplitude of 7.2 ± 1.5 mV (mean ± SD, n = 12) was measured. After induction of AFib/AFl, the single amplitude decreased to 3.6 ± 1.5 mV (n = 8) during AFib and 3.4 ± 1.7 mV (n = 9) during AFl. Amplitudes dropped between 53% and 75% when the AR lost atrial wall contact. The atrial pacing threshold was 1.0 ± 0.4 V (n = 16) when the AR was in contact with the atrial wall. Conclusions: In future dual chamber ICDs the signals from a passive fixation single pass lead could be used for atrial sensing and pacing as long as the sensing electrode for the right atrium remains in contact with the atrial wall. This system might lead to a simpler, less invasive implantation of dual chamber ICD systems.