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Junctional ectopy or tachycardia have been mapped and ablated in the atrioventricular node or its posterior extensions. There is no report of Hisian ectopy convincingly demonstrated and then successfully treated by ablation. A 39-year-old man presented with a 9-year history of recurrent supraventricular ectopy refractory to medical treatment. Intracardiac mapping revealed that the ectopy originated from the His bundle, which was indicated by a reversed His bundle activation sequence during ectopy compared to that during sinus rhythm, while the right bundle branch potential was anterogradely activated. Low power RF energy delivered to the site of earliest activation completely abolished the ectopic activity without modification of Hisian or atrioventricular conduction. After a 12-month followup, the patient remains free of recurrence.

We report the case of a patient with paroxysmal atrial fibrillation in whom the background cardiac rhythm falsely mimicked sinus rhythm but actually originated from the left superior pulmonary vein. P waves during the ectopic rhythm were flat in lead I, negative in lead aVL, and without a typical "dome-and-dart" feature in precordial leads. Radiofrequency applications inside the left superior pulmonary vein eliminated both atrial fibrillation and the ectopic pacemaker.

Objective: To assess the effect of adding propafenone to atrial overdrive for the prevention of atrial arrhythmia episodes in patients with DDD pacemakers., Design: 22 patients (8 female, 14 male, mean (SD) age 67 (9) years, range 48 to 77) with DDD pacemakers and frequent paroxysmal atrial arrhythmia episodes were evaluated in a randomised crossover study., Setting: University hospital., Methods: Atrial overdrive was defined as a paced rate of 10 paced beats/min above the mean ventricular rate stored for the last 24 hours in the pacemaker memory function. The protocol consisted of two phases of one month each. The first phase consisted of atrial overdrive alone, while in the second phase, propafenone (600 mg/day) was added to atrial overdrive (atrial overdrive + propafenone). All 22 patients underwent the two phases in random order., Results: Mean ventricular rate was 72 (8) beats/min with atrial overdrive v 73 (6) with atrial overdrive + propafenone (NS). With atrial overdrive, 14 patients (64. 6%) had no recorded atrial arrhythmia v 15 (68.2%) with atrial overdrive + propafenone (NS). There was no statistical difference between the atrial overdrive and atrial overdrive + propafenone phases with regard to the number of atrial arrhythmia episodes (14 (27) v 13 (28)), their total duration (30 (78) v 29 (63) h), and their maximum duration (41 (72) v 31 (58) min). However, in the brady-tachy subgroup with persistent atrial arrhythmias, atrial overdrive + propafenone produced a shorter mean cumulative duration of atrial arrhythmia than atrial overdrive (104 (115) v 178 (149) h, p = 0.04), with a significant decrease in the number of atrial arrhythmia episodes (134 (98) v 102 (83), p = 0.05). The proportion of asymptomatic atrial arrhythmia episodes increased only in the AV block group during atrial overdrive + propafenone (p = 0.03). Three patients had atrial arrhythmias during atrial overdrive + propafenone but not with atrial overdrive alone., Conclusions: In DDD paced patients, the overall effect of propafenone during atrial overdrive is variable. Propafenone may increase the proportion of asymptomatic atrial arrhythmia episodes. A proarrhythmic effect of propafenone was documented (aggravation of atrial arrhythmias). These results need to be confirmed by further larger randomised studies.

The relation between left ventricular electromechanical delay and the acute hemodynamic effect of right ventricular pacing was studied in heart failure patients with and without complete left bundle branch block. Whereas right ventricular pacing provided a shorter electromechanical delay that correlated with an improvement in left ventricular function in patients with left bundle branch block, the converse was observed in patients without left bundle branch block.

A young woman symptomatic for tachycardia showed right ventricular preexcitation on the surface ECG with a pattern during induced atrial fibrillation suggestive of multiple APs. Noninvasive imaging techniques performed prior to catheter ablation demonstrated the presence of a giant right atrial diverticulum confirmed by hemodynamic procedure. This structure functioned as an enormous accessory AP. We performed catheter ablation of this pathway using a special 4-mm multipolar catheter inside the diverticulum. This is the first case of such as anomaly being successfully treated with catheter ablation.

Ablation of the atrioventricular junction consists in creating a therapeutic AV block to facilitate the treatment of symptoms caused by atrial arrhythmias refractory to drug therapy. The technical performance of ablation has been improved by restricting the indication to atrial fibrillation, by using radiofrequency currents, by choosing a nodal rather than His bundle ablation site, and by improving the function of cardiac pacemakers (rate adapting, back-up). The functional results are excellent but the outcome is punctuated by rare cases of sudden death, the cause of which is not fully understood (dependance, ventricular arrhythmias, ...). To avoid permanent pacing, it has been suggested that atrioventricular conduction should be modulated rather than completely interrupted. Modulation of the fast pathway has been shown to be ineffective; that of the more complex, slow pathway, seems to be more promising. Although this obviates the need for a pacemaker, it does not suppress irregularity of the ventricular rhythm, the main cause of symptoms in paroxysmal atrial fibrillation and of the haemodynamic changes associated with permanent atrial fibrillation.

In several tissues including gastric mucosa, somatostatin displays various biological effects. Five seven-transmembrane-domain somatostatin receptor subtypes (SSTR1-5) have been recently cloned and only SSTR1 has been shown to be present in the human stomach. We used the polymerase chain reaction on reverse transcripts (RT-PCR) to characterize further the SSTR's mRNAs in human and rat gastric mucosae and in the human gastric tumoral cell-line HGTL. The SSTR1-5's mRNAs were found in both human fundic and antral mucosae as well as in the HGT1 cell and rat antrum. The four SSTR2-5's mRNA's but not SSTR1's were detected in the rat fundic mucosa. Furthermore, the use of rat isolated and purified fundic mucosal cells allowed us to localize SSTR2-5 in the parietal cell-enriched fraction, whereas SSTR2 and SSTR5 were the only subtypes found in the endocrine cell-enriched fraction. These results are the first to demonstrate the presence of five SSTR's mRNA subtypes in the stomach.

Serum apolipoprotein A-I measurement was compared in alcoholic patients according to presence or absence of chronic pancreatitis and liver fibrosis. Among alcoholic patients without liver disease, apolipoprotein A-I was significantly lower in patients with chronic pancreatitis (157 +/- 70 mg/dl) than in patients without pancreatitis (209 +/- 74 mg/dl, p less than 0.001). In cirrhotic patients, apolipoprotein A-I was lower in patients with chronic pancreatitis (82 +/- 35 mg/dl) than in patients without pancreatitis (102 +/- 45 mg/dl), but this difference was not significant. The decrease of serum apolipoprotein A-I was independent of nutritional parameters whether or not there was cirrhosis. Immunohistochemical study of pancreatic samples with chronic pancreatitis showed that apolipoprotein A-I was located in the pancreatic fibrosis whereas lobules were unstained. This study suggests that apolipoprotein A-I is trapped by the pancreatic extracellular matrix and that this sequestration might explain, in part, the decrease of the serum apolipoprotein A-I.

Factors influencing the prognosis were studied in 165 patients with polyarteritis nodosa (PAN) and Churg-Strauss angiitis. One hundred and forty-seven of the patients fulfilled histological and/or arteriographic diagnostic criteria, and in 18 patients the diagnosis was based on clinical criteria. The patients' mean age on diagnosis was 48.4 +/- 16.4 years. The main symptoms were fever (69%), weight loss (66%), arthritis (44%), mononeuritis multiplex (67%), cutaneous signs (46%), renal involvement (26%), gastrointestinal symptoms (31%), asthma (29%), hypertension (31%) and cardiac failure (18%). Ninety-two per cent of the patients survived for at least 1 year after diagnosis of the disease, 79% for 2 years, and 63% for 5 years. The immediate causes of death were gastrointestinal bleeding or peritonitis in 11 cases, pancreatitis in two, renal insufficiency in six, cardiac failure in five, infectious complications in four, stroke in three and other causes in 11. We studied the prognosis of necrotizing angiitis in relation to clinical symptoms and laboratory findings. The association of four conditions were associated with a poor prognosis: age over 50, gastrointestinal problems, cardiomyopathy and renal signs. The survival rates in patients with these conditions were: for gastrointestinal problems, 55% 5-year survival (versus 67%); and for age over 50, 68% 3-year survival (versus 78%; p less than 0.09). One hundred and fifty-nine patients were treated with steroids for at least 18 months. Forty-eight also received cytotoxic agents (27%) and 46 plasma exchange. Patients who were treated with plasma exchange and prednisone were randomly assigned to additional treatment with cyclophosphamide. Survival rates were comparable in both groups.