Brugada-like electrocardiographic pattern induced by an episode of anemia.

The mechanisms responsible for the undulating pattern of ST-segment elevations in the Brugada syndrome are still a matter of discussion. This report describes a young man with a Brugada-like electrocardiographic pattern. The specific ST-segment elevations were unmasked during an episode of anemia due to a duodenal ulcer.

Multiple AV nodal pathways in patients with AV nodal reentrant tachycardia--more common than expected?

AIMS: It was the purpose of this study to determine the incidence of more than two AV nodal pathways in patients with AVNRT. METHODS AND RESULTS: In 78 consecutive patients with AV-nodal reentrant tachycardias (AVNRT) (50 females, 28 males, mean age 52.8 +/- 14.6 years), the number of sudden AH increases by 50 ms or more (AH-jump) was analysed during atrial extrastimulation. The incidence of two AV nodal pathways was accepted to be present in patients with AVNRT without an AH-jump ('smooth curve'). The following forms of tachycardia were induced: a typical AVNRT (slow-fast) in 67 patients, an atypical AVNRT (fast-slow) in 12 patients and a slow-slow-AVNRT in 4 patients. Five patients had two forms of AVNRT. 47 patients (60.3%) showed two AV nodal pathways, 27 patients (34.6%) had three AV-nodal pathways and 4 patients (5.1%) exhibited four AV-nodal pathways. For successful catheter ablation of AVNRT in patients with more than two pathways, more radiofrequency energy applications were required (9.2 +/- 6.3) compared with patients with only two pathways (6.7 +/- 4.8). Furthermore, in patients with more than two AV-nodal pathways, the catheter intervention resulted more frequently in a modulation of slow pathway conduction than in an ablation of the slow pathway(s). CONCLUSION: The incidence of more than two AV-nodal pathways in patients with AVNRT was unexpectedly high at about 40%. Thus, these tachycardias require a meticulous electrophysiological evaluation for successful ablation.

AV nodal pathways in the R-R interval histogram of the 24-hour monitoring ECG in patients with atrial fibrillation.

BACKGROUND: Patients with more than one AV nodal pathway show two and more peaks in the histogram of the R-R intervals of the Holter monitoring ECG during atrial fibrillation. It was the purpose of the present study to determine the number of patients showing more than one AV nodal pathway in a larger patient group with permanent atrial fibrillation by analyzing the Holter monitoring ECG. METHODS: 250 patients with permanent atrial fibrillation during Holter monitoring ECG were studied; 203 patients had structural heart disease. The number of peaks in the R-R interval histogram of each patient was determined. The distribution of the number of peaks in the R-R interval histogram in different patient groups was analyzed. RESULTS: 153 patients (61%) had one peak, 80 patients (32%) two peaks, 13 patients (5%) three peaks, and four patients (2%) four peaks, reflecting the number of different AV nodal pathways. In the different patient groups, in the patients with or without structural heart disease, with coronary heart disease, with a history of syncope, and in patients with a mean heart rate of more than 100/min, there was no significant difference in the distribution of the number of peaks in the R-R interval histogram. CONCLUSIONS: In more than one third of all patients with permanent atrial fibrillation there are two, three, or four AV nodal pathways. It is suggested that this number of different AV nodal pathways found in the studied group can be applied to all humans. 38.8% of all patients with permanent atrial fibrillation have more than one AV nodal pathway; 6.4% of all patients with atrial fibrillation would benefit from an ablation of AV nodal pathways with shorter refractory periods for reduction of the heart rate.

[Terminating supraventricular tachycardia with adenosine--comparing the effectiveness of 12 mg and 18 mg]. / Terminierung supraventrikulärer Tachykardien durch Adenosin--Vergleich der Wirkung von 12 mg und 18 mg.

OBJECTIVES: This study was done to answer the question if intravenous application of 18 mg adenosine is superior to 12 mg adenosine for the termination of supraventricular tachycardias. PATIENTS AND METHODS: 31 patients (17 men, 14 women, mean age 53 +/- 15 years [range 15-76 years]) had electrophysiological tests. In 25 patients AV nodal reentrant tachycardias were induced during programmed stimulation, 6 patients had inducible AV reentrant tachycardias with an accessory pathway. After induction of the supraventricular tachycardia (mean rate 183 +/- 29/minute, range 115-240/minute), in each patient 12 or 18 mg adenosine was applied in a bolus for terminating of the tachycardia. After the second induction of the tachycardia, a dose of 18 or 12 mg adenosine was given. The different doses of adenosine were chosen in a randomized and prospective manner in a crossover design. RESULTS: In 25 of the 31 patients (81%) the tachycardia was terminated by 12 mg adenosine. In 29 of the 31 patients (94%) the induced tachycardia was terminated by the application of 18 mg adenosine (no significant difference). In one patient, the tachycardia cessation was observed after 12 mg adenosine, but not after 18 mg adenosine. In another patient the tachycardia was not terminated by either 12 mg or by 18 mg adenosine. The termination of the tachycardia was seen after 25 +/- 8 seconds (13-51 seconds) when 12 mg adenosine was given. After the application of 18 mg adenosine the tachycardia ended after 25 +/- 8 seconds (14-44 seconds) (not significant). The asystole directly after tachycardia termination was 976 +/- 63 milliseconds (540-1700 milliseconds) with 12 mg adenosine, and 1070 +/- 628 milliseconds (530-4000 milliseconds) after the application of 18 mg adenosine (not significant). The longest asystole after termination of a tachycardia by 18 mg adenosine was 9.03 seconds. In one patient the tachycardia was reinitiated by spontaneous atrial extrasystoles after 12 mg adenosine, and reinduction of tachycardia was seen twice after 18 mg adenosine. After the administration of 18 mg adenosine, atrial fibrillation was observed in one patient. No serious complication occurred. CONCLUSIONS: In AV nodal reentrant tachycardias and AV reentrant tachycardias with an accessory pathway, which can not be terminated by the administration of adenosine in a dose of 12 mg, the tachycardia can be terminated more effectively by the application of 18 mg adenosine.

Capture and fusion beats during atrial fibrillation and ventricular tachycardia.

Two patients were presented, and two previously unreported observations were made. Patient 1, a 50 year old man with episodic palpitations and dizziness for 10 years, exhibited initiation of idiopathic ventricular tachycardia (VT) by atrial fibrillation (AF). Patient 2, a 43 year old woman with a structurally normal heart but recurrent palpitations for one year, demonstrated fusion and capture beats during simultaneous VT and AF. An explanation is given as to why the latter phenomenon is rarely observed.

[Typical AV nodal reentry tachycardia in 4 anterograde AV nodal pathways. Successful high frequency ablation of slow AV nodal pathways]. / Typische AV-Knoten-Reentry-Tachykardie bei vier antegrad leitenden AV-Knoten-Bahnen. Erfolgreiche Hochfrequenzablation der langsamen AV-Knoten-Bahnen.

CASE REPORT: A 26-year-old patient was referred to our department for electrophysiologic evaluation of recurrent paroxysmal tachycardias with narrow QRS-complexes (< 120 ms). Three jumps in the AV-nodal conduction curve were detected during programmed atrial extrastimulation in sinus rhythm and at a cycle length of 600 ms indicating of 4 antegrade conducting AV-nodal pathways. After intravenous application of orciprenaline an AV-nodal re-entrant-tachycardia (AVNRT) of the common type was induced with a cycle length of 290 ms. During tachycardia, antegrade conduction occurred via one of the slow conducting pathways, retrograde conduction via the fast pathway ("slow-fast"-AVNRT). Application of radiofrequency energy was able to ablate all slowly conducting AV-nodal pathways at one site in the infero-posterior region of Koch's triangle. During control stimulation with and without orciprenaline no AH-jump or inducible tachycardia was found. CONCLUSION: This case shows the rare finding of 4 antegrade AV-nodal pathways in a patient with the common type of AVNRT. Application of radiofrequency current was able to ablate all slow conducting AV-nodal pathways successfully.

[Does heparin modify the course of chronic abscess-forming peritonitis in the animal model?]. / Beeinflusst Heparin den Verlauf einer chronischen abszedierenden Peritonitis im Tiermodell?

After laparotomy and inoculation of a Bacteroides fragilis suspension (2 ml with 10(8) CFU/ml), we induced chronic abscess-forming peritonitis in rats (n = 19, untreated). Fifteen animals were treated with heparin 30 IU, administered s.c. from day 1 after inoculation of the bacteria onwards. The main groups were divided into three subgroups (n = 8/5/6 and n = 5/5/5), which were observed for 3/7/14 days, respectively. On days 3 and 7, abdominal swabs were not only B. fragilis positive, but also showed severe polyvalent mixed infection after translocation of intestinal bacteria into the abdominal cavity. In the heparin group, B. fragilis positive swabs were reduced and translocation was inhibited (P < 0.05 for days 3 and 7). In the untreated group, blood cultures were B. fragilis positive on days 3/7/14 in 3/2/1 animals versus 0/1/1 in the heparin group. Adhesions were found in the untreated group in 1/4/5 animals, whereas in the heparin group there were no adhesions (P < 0.05 for days 7 and 14). However, intra-abdominal abscesses were also diminished in the heparin group (0/2/1) compared with the untreated animals (2/4/6, P < 0.05 for day 14). Therefore, heparin was shown to have a favourable influence on chronic abscess-forming peritonitis in an animal model.

[Persistent dilatation of non-stenosed epicardial arteries in 24- and 48-hour nitroglycerin infusion]. / Persistierende Dilatation nichtstenosierter Epikardarterien unter 24- und 48stündiger Nitroglycerin-Infusion.

UNLABELLED: It is still a matter of dispute to what extent a direct loss of nitrate mediated vasodilatation (true tolerance) contributes to the development of nitrate tolerance. Aim of this study was to assess to what extent the dilatation of non-obstructed segments of epicardial arteries is attenuated during a continuous 24- and 48-h-infusion of nitroglycerin. In a prospective, randomized and blinded study we investigated 32 patients who underwent diagnostic coronary angiography. All cardiac medication was withdrawn at least for 24 h; patients were randomized to either a 24 h NTG-infusion (group A; 0-24 h saline infusion followed by a 24 h NTG-infusion; n = 16) or a 48 h NTG-infusion (group B; 0-48 h of NTG-infusion; n = 16) in a dosage of 1.5 micrograms/ kg/min. The patients were included if 5 proximal segments of the left coronary artery showed no visible atherosclerosis. A coronary angiography was performed after 24 and 48 h respectively. The lumen diameters were measured by quantitative coronary analysis at baseline and 1 and 3 min after application of 0.2 mg of NTG intracoronarially (i.c.). Blood samples were drawn before and after 24 and 48 h of infusions to measure hematocrit and neurohormones. In group A after 24 h of saline infusion there was a significant increase in lumen diameter from 3.14 +/- 0.17 mm at baseline to 3.51 +/- 0.11 mm (p < 0.001) and 3.60 +/- 0.21 mm (p < 0.001) after 1 and 3 min of NTG i.e. respectively. After 24 h of NTG-infusion there were no significant changes in baseline and values after further NTG i.e. In group B after 24 h of NTG-infusion no significant change in lumen diameter was detectable after NTG i.e. (3.57 +/- 0.23 mm to 3.63 +/- 0.13 mm) and the mean diameter remained unchanged after prolongation of NTG to 48 h (3.58 +/- 0.33 mm). There were no significant differences between the baseline values and the responses to i.e. NTG after 24 and 48 h of NTG infusion. Hematocrit and aldosterone levels decreased significantly after NTG-infusion but not following saline. Renin and norepinephrine remained unchanged throughout the NTG-infusion-periods. IN CONCLUSION: The vasodilatation of non-obstructed segments of epicardial arteries persists during a prolonged infusion period and there is no induction of vascular tolerance between the 24 and 48 h infusion period. These findings further support that there is a different susceptibility of arteries and veins to nitrate tolerance.