Effect of sodium nitroprusside on myocardial performance and venous tone.

The action of sodium nitroprusside upon the mechanical performance of the isolated, working rat heart and on isolated bull veins has been studied. Cumulative concentrations of 1--1000 ng sodium nitroprusside per ml had no effect on left ventricular pressure, end-diastolic left ventricular pressure, dp/dtmax, cardiac output and calculated wall stiffness of isolated rat hearts with constant rate, preload and afterload. Isolated strips of bull veins contracted with noradrenaline showed a dose dependent relaxation by sodium nitroprusside in concentrations of 5--1000 ng per ml. This study shows that sodium nitroprusside has no direct effect on myocardial contractility and causes venous relaxation.

Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report.

We observed a dangerous increase of ventricular rate following the intravenous administration of amiodarone in a patient with atrial fibrillation and rapid ventricular response associated with the Wolff-Parkinson-White syndrome. The mechanism of enhanced accessory pathway conduction remains speculative. A possible explanation for the shortened antegrade effective refractory period of the accessory pathway is afforded by the hypotensive action of amiodarone or its dissolvent which might trigger beta-adrenergic reflexes. Intravenous amiodarone should be used with caution in patients with atrial fibrillation and rapid ventricular response via an accessory pathway.

Demonstration of multiple antegrade and retrograde atrioventricular pathways.

A patient with paroxysmal supraventricular tachycardia had discontinuous antegrade (1a-A2, H1-H2) and retrograde (V1-V2, A1-A2) conduction curves suggesting dual A-V nodal pathways in both directions. Atrial echoes occurred with premature atrial pacing only at short A1-A2 coupling intervals after long antegrade (A2-H2) and retrograde (H2-A3) conduction intervals. Premature ventricular stimulation revealed ventricular echoes simultaneously with a sudden increase in the V2-A2 interval. The echo zone coincided with the slow pathway curve. Following atropine the echo zone was extended over the slow and fast pathway curves. Slow pathway conduction was observed at long and sort V1-V2 coupling intervals. Following isoproterenol ventricular stimulation initiated two cycles of ventricular echoes with relatively long retrograde (V2-A2, Ve-Ae) and short antegrade (A2-He, Ae-He) conduction times, the earliest atrial activation being observed in the low right atrium before the left atrium and the high right atrium. Antegrade fast and slow pathways as well as retrograde fast pathway conduction appeared to be confined to the A-V node. Retrograde slow pathway conduction may progress through a slow or fast A-V nodal pathway slowed by antegrade concealed conduction. However, an accessory pathway with long conduction times located near the septum cannot be ruled out entirely.

Concealed accessory pathway and dual AV conduction: drug-dependent reentrant tachycardia.

Electrophysiological studies were performed in a patient with paroxysmal supraventricular tachycardia and a normal surface ECG at the time of the study. Premature atrial stimulation revealed dual AV conduction and an echo zone during AV conduction over the fast and the slow pathway. The prolongation of the AV conduction time by a calcium antagonist, Ro 11-1781, permitted the induction of tachycardias via both pathways. Premature ventricular stimulation yielded constant VA conduction times with activation of the low right atrium before the high right atrium before the left atrium. During the tachycardia, premature right ventricular beats conducted to the atrium at a time when the AV node and the His bundle would be refractory. The study suggests the simultaneous occurrence of an occult accessory bundle connecting the right ventricle to the right atrium and dual AV conduction.

[Therapy of paroxysmal supraventricular tachycardias by rapid patient-activated atrial stimulation]. / Therapie von paroxysmalen supraventrikulären Tachykardien durch patientenaktivierte rasche Vorhofstimulation.

Recurrent, drug refractory supraventricular tachycardia may present a therapeutic challenge. Following invasive electrophysiological study and the prospectively controlled therapeutic failure of all available drugs 3 patients were treated by permanent implantation of a system for atrial burst stimulation. The system consists of an implanted receiver with electrodes connected to the right atrium and a radiofrequency stimulator that requires patient activation for burst pacing. During a follow-up period of 6 to 39 months numerous attacks of recurrent tachycardia were successfully terminated without complication. The therapeutic approach which has allowed stoppage of all antiarrhythmic drugs and has obviated the need for frequent hospital admissions has met with patient approval and is highly regarded as providing an improvement in quality of life.

[Clinical and electrophysiological observations in a case of Romano-Ward syndrome ]. / Klinische und elektrophysiologische Beobachtungen bei Romano-Ward-Syndrom.

Syncope associated with atypical ventricular tachycardia of the "torsades de pointes" type was observed in a 16 year-old girl with hereditary QT prolongation. The arrhythmia occurred only during maximal prolongation of the QTc to 0.77 sec, which had possibly been aggravated by exercise and hypokalaemia. Electrophysiological studies were performed when the QTc was 0.59 sec. Incremental as well as premature ventricular pacing with single or double premature ventricular beats did not initiate ventricular arrhythmias, but revealed AV nodal and bundle branch reentry. It is postulated that these types of macroreentry are involved in the twisting of the QRS complexes in the surface ECG in torsades de pointes.

Psoriasin (S100A7) is a major Escherichia coli-cidal factor of the female genital tract.

The female urogenital tract requires an efficient defense against bacteria, potentially derived from the adjacent intestinal tract. We have thus sought to identify the factors that protect against Escherichia coli (E. coli) in the female genital tract. Vaginal fluid from healthy human donors consistently killed E. coli in vitro and vaginal epithelium strongly expressed and secreted psoriasin. Psoriasin was constitutively produced in an organotypic vaginal epithelium model, and exposure of these cells to supernatants of E. coli cultures led to an enhanced psoriasin expression. Secreted psoriasin in vaginal fluids accounted for approximately 2.5-3% of total protein. Fractionation of vaginal fluids by high performance liquid chromatography (HPLC) showed that psoriasin co-eluted with a peak of E. coli killing activity. Our data show that normal vaginal fluid contains a powerful intrinsic antimicrobial defense against E. coli and that psoriasin contributes to the innate immune response of the female genital tract.

[Inactivation of implanted demand pacemaker through external stimulation]. / Inaktivierung des implantierten Demand-Schrittmachers durch externe Stimulation.

External chest wall stimulation was performed in 87 patients in order to overdrive and thereby suppress the implanted pacemaker. The impossibility to inactivate the implanted pacer suggested a disturbed "sensing" function in 12 patients. Marked changes of the escape rhythm were found in 77 patients with suppressable pacemaker when compared with the tracings before pacemaker implantation. Increasing degree of A-V block or marked changes in heart rate were observed in 14 of 35 cases with advanced A-V block. Minor alterations were noted in cases with sick sinus syndrome and atrial fibrillation. Overdrive suppression is a helpful method for the selection of pacemaker dependent patients.

Reduction of pulmonary hypertension by nitroprusside.

The action of nitroprusside on pulmonary circulation was studied in patients with pulmonary hypertension due to mitral stenosis (group I) or to primary lung disease (group II) and in patients with normal pulmonary artery pressure (group III). Nitroprusside 20 microgram/min decreased systolic and mean pulmonary artery pressure in groups I and II while higher doses were necessary to produce a similar pressure reduction in group III. Diastolic pulmonary artery pressure was reduced by 40 microgram/min nitroprusside in all groups. Systemic arterial pressure declined during nitroprusside infusion similary in all groups in a dose-related manner; cardiac index remained unaltered. Pulmonary vascular resistance was reduced by 20 microgram/min nitroprusside in group I, not below 200 microgram/min nitroprusside in group II and remained unchanged in group III. Peripheral vascular resistance declined in all groups with nitroprusside infusion. The study suggests direct relaxation of the pulmonary vasculature by nitroprusside.

[Conservative therapy of supraventricular tachycardias]. / Die konservative Therapie supraventrikulärer Tachykardien.

The conservative management of supraventricular tachycardias is briefly surveyed and described. For exact treatment a description of different ways of origin of tachycardias such as focal activity or reentry-mechanisms is given. A diagram at the end shows the site of influence of different antiarrhythmic drugs in the atria and the AV-node as well as the accessory pathways in preexcitation. A list of antiarrhythmics according to their classification of Vaughan Williams and of Tournboul completes this survey.

Effect of tiapamil in the Wolff-Parkinson-White syndrome.

The effect of tiapamil was studied in 9 patients with the Wolff-Parkinson-White syndrome using programmed stimulation of the heart. Before the drug, sustained orthodromic tachycardias could be initiated in 7 patients and antidromic tachycardia in 2 by premature atrial and/or ventricular stimulation. An intravenous bolus of tiapamil, 2 mg/kg, terminated the tachycardia in 7 out of 8 cases by a block in the atrioventricular (AV) node. Tiapamil lengthened the effective refractory period of the AV node in the only patient in whom it could be measured and the atrial effective refractory period in 1 out of 9 cases, but the drug had no influence on antegrade or retrograde refractory periods of the accessory pathway or on that of the ventricle. The AV nodal conduction time (A-H interval) was prolonged. Following tiapamil, it was not possible to initiate the tachycardia in 4 cases, in 2 patients the tachycardia zone widened, and in 3 it was unaltered. In the latter cases, the cycle length of the tachycardia was increased. Tiapamil appears to be useful for the termination of tachycardia and also for its prevention in some cases. In others, it may facilitate the inhibition of tachycardia. The delayed AV nodal conduction during sinus rhythm augments the area of ventricular preexcitation, which may facilitate the electrocardiographic localization of the accessory pathway.

Electrophysiology of tiapamil in concealed accessory pathways.

The effect of 2 mg/kg intravenous tiapamil was studied by programmed stimulation of the heart in 6 patients. Before tiapamil, sustained tachycardias were initiated in 5, and only atrial echoes in 1. In all patients, the reentrant circuit involved an accessory pathway conducting only in the ventriculoatrial direction. When administered during tachycardia, tiapamil promptly terminated the arrhythmia in 5 cases. Tiapamil lengthened the atrio-His (A-H) interval and the effective refractory period of the A-V node. As a result of these changes, it was not possible to initiate the tachycardia in 1 patient. In 1 case, tiapamil permitted the induction of sustained tachycardia, while only echoes had been initiated before the drug. In 2 cases, the tachycardia zone narrowed, in 2 others it widened following tiapamil. The ability to sustain the arrhythmia was lost in 1 patient. Tiapamil may be useful for the termination of reentrant supraventricular tachycardia involving concealed accessory pathways. Whether tiapamil prevents or favors the initiation of tachycardia in these patients depends on the interplay between the prolongation of the effective A-V nodal refractory period and the prolongation of the transnodal conduction time in individual patients.

[Prophylaxis of supraventricular paroxysmal tachycardias on the basis of electrophysiologic examinations]. / Prophylaxe supraventrikulärer paroxysmaler tachykardien auf der basis elektrophysiologischer untersuchungen.

Paroxysmal supraventricular tachycardias (PSVT) were classified with regard to electrophysiologic criteria in 12 cases. In 6 patients the reentry circuit of the PSVT involved a concealed accessory connection, in 6 patients the reentry circuit was confined to the A-V node. Different antiarrhythmic drugs were administered orally over a 4 week period, the frequency of attacks and possible side effects were recorded. In patients with accessory pathway metoprolol (n = 3), ajmalin (n = 3), Aprindine (n = 1) and verapamil (n = 1) prevented the occurrence of PSVT. Verapamil, Ro 11-1781, metoprolol and digitalis were effective in A-V nodal reentry. PSVT could be prevented in all but one patient by at least one drug.