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H-J Trappe

Publications and source records attributed to H-J Trappe.

12 recordsLinked to original sources
PubMed2006

IEGM-online based evaluation of implantable cardioverter defibrillator therapy appropriateness.

Appropriate and inappropriate therapies of implantable cardioverter defibrillators have a major impact on morbidity and quality of life in ICD recipients. Intracardiac electrograms (IEGMs) stored in the ICD have been shown to be essential for differentiating appropriate and inappropriate ICD therapies. The recently introduced third generation of ICD Home Monitoring offers remotely transmitted IEGMs (IEGM-online). Hence, the appropriateness of ICD therapies might be remotely assessed. Validation of these electrograms is currently being performed in the RIONI study. A total of 210 episodes will be collected by about 40 European clinical centers. The study primarily investigates whether the IEGM-online based evaluation of the appropriateness of the ICD's therapeutic decision following a tachyarrhythmia episode detection is equivalent to the evaluation based on the complete ICD episode holter. The evaluation is independently performed by an expert board of three experienced ICD investigators. The equivalence of the two methods is accepted if the conclusions deviate for less than 10% of all evaluated IEGMs. Secondary endpoints investigate the IEGM-online usefulness in more detail. The conclusion of the study is expected by mid of 2007. RIONI has successfully been started for proving the reliability of IEGM-online. The expected results will significantly influence the efficacy of Home Monitoring based patient management.

Aged↗
PubMed2005

[First responder defibrillation in the USA, Europe and Germany--prerequisites, experiences, perspectives].

Sudden out-of-hospital cardiac arrest is a leading cause of death and only 5-8% of patients survive such event. Defibrillation is the mose effective treatment and should performed within 5 minutes; however, its effectiveness diminishes with each passing minute. "Early defibrillation" is the use of automated external defibrillators (AEDs) by trained public-safety personnal ("first responder"), whereas "public access" defibrillation describes AED use by persons who have no specific AED training. Several studies in the US and in Europe show that first responder defibrillation will increase the number of survivors of out-of-hospital cardiac arrest compared to paramedics. This is caused by a shorter "call-to-arrival-time" in first responders compared to paramedics. In Europe, programs for the use of automated external defibrillators exist only occasionally. Reasons for this are the lack of open-mindedness, logistic and legal problems. In Germany, there are only few AED programs with promising results. At the present time, placement of automated external defibrillators in public places frequented by a large number of susceptible people will increase overall survival. However, placement of AEDs in all public places is still debatable and further studies are necessary to estimate the potential impact of publicc access defibrillators.

Ambulatory Care↗
PubMed2005

[First responder defibrillation in the LAGO-die Therme--results and experiences].

The use of automated external defibrillator (AED) by persons other than paramedics and emergency medical technicians is advocated by several US- and European organizations. However, at the present time it is still unclear to identify public places with a high incidence of out-of-hospital cardiac arrest. There are few data on the potential impact of public access defibrillators on survival after out-of-hospital cardiac arrest in sporting arenas or water parks. Therefore, we studied prospectively incidence of out-of-hospital cardiac arrest in the LAGO-die Therme in Herne. This is one of the most important swimming parks in Europe and member of the European Waterpark Association EWA. Eight AEDs were placed in the waterpark LAGO-die Therme. The locations where the defibrillators were stored were chosen to make possible a target interval of 60 seconds from collapse to first defibrillation. Twenty waterpark officers were instructed in cardiopulmonary resuscitation and in the use of the AED. During November 16, 2001 and December 31, 2004, 2.05 Mio. visitors were counted in the LAGO. Out-of-hospital cardiac arrest occurred in none of them. AED were used in two visitors with non arrhythmogenic syncope, no shock was delivered. Questionaires were done in 588 visitors (336 males, 252 females, mean age 38+21 years) in 2002 and in 579 visitors (322 males, 257 females, mean age 37+/-25 years) in 2004. In 2002, 77% of the visitors noticed the AED and, therefore, 49% performed more sporting activities. In addition, in 2004, AED was noticed by 480 visitors (83%) and 277 visitors (48%) did more sporting activities. There were no significant differences between 2002 and 2004 (p=ns). Despite no out-of-hospital cardiac arrest in the waterpark during the 3 year follow- up, it seems reasonable to install AED in sporting places with thousands of visitors per year.

Adult↗
PubMed2005

[Automated external defibrillators: perspectives and outlook].

In Germany about 80.000 patients die of sudden cardiac death each year with enormous human, social and economic consequences. Most cases of sudden cardiac death are caused by ischemia-triggered ventricular fibrillation. A precondition for survival of the victims is an optimally and fast reacting "chain of survival". One of the central links of this chain is timely defibrillation, which is the only effective therapy for treatment of ventricular fibrillation. Automated external defibrillators proved to be a major step forward in improvement of resuscitation results. It has been convincingly demonstrated, that these devices not only are safe and efficacious in the hands of rescue personnel of different qualification degrees but also in the hands of minimally trained "first responders" and even in the hands of untrained lay people. This story of success was paralleled by the development of a new generation of biphasic defibrillators, which have a superior efficacy, are lightweight and are even cheaper than conventional devices. It must however kept in mind, that progress offered by these new opportunities will only translate in better resuscitation results, when programmes are thoroughly planned, will stay under continuous quality control with regard to performance of devices and rescuers and if new knowledge in resuscitation is adequately incorporated in action protocols.

Cardiopulmonary Resuscitation↗
PubMed2004

Propranolol inhibits IK(Ado) by competitive A1-receptor interaction.

OBJECTIVES: Betablocking agents are known to exert anti-arrhythmic effects in ischemic myocardium due to blockade of myocardial beta-1-receptors. Since adenosine (Ado) induced muscarinic potassium current (IK(Ado)) and ATP sensitive potassium current (IK(ATP)) are discussed to be activated during ischemia we studied the effect of propranolol on IK(Ado) and IK(ATP). METHODS AND RESULTS: The effect of propranolol on muscarinic potassium current and IK(ATP) was studied in isolated rat atrial myocytes by means of the whole-cell voltage clamp tech- nique. Propranolol (50 microM) completely inhibited IK(Ado). IC50 was 7 microM. Inhibition of acetylcholine induced current (IK(ACh)) and GTP-gamma-S induced muscarinic potassium current was less potent (IC50 29 microM and 31 microM respectively). Propranolol was active from the outside only. Intracellular application did not significantly affect muscarinic potassium current. (+)-propranolol, an isomer without beta-blocking properties, was as effective as (+/-)-propranolol. The inwardly rectifying potassium current IK(ATP) showed minor sensitivity to the compound (10% current reduction, propranolol 50 microM). CONCLUSIONS: Propranolol inhibits IK(Ado). Inhibition is not due to beta-receptor blockade. Predominantly an interaction with A1-receptors seems to be involved. The observations in part might explain the anti-arrhythmic properties of the drug in ischemic/fibrillating myocardium based on the prolongation of refractoriness.

Acetylcholine↗
PubMed2003

Inhibition of G protein-coupled and ATP-sensitive potassium currents by 2-methyl-3-(3,5-diiodo-4-carboxymethoxybenzyl)benzofuran (KB130015), an amiodarone derivative.

2-Methyl-3- (3,5-diiodo-4-carboxymethoxybenzyl) benzofuran (KB130015; KB), a novel compound derived from amiodarone, has been proposed to have antiarrhythmic properties. Its effect on the G protein-coupled inward rectifying K+ current [IK(ACh) or IK(Ado)], ATP-sensitive K+ current [IK(ATP)], and background inward rectifying current (I(K1)) were studied in guinea pig atrial and ventricular myocytes by the whole-cell voltage-clamp technique. Receptor-activated IK(ACh/Ado), induced in atrial myocytes by the stimulation of either muscarinic or Ado receptors was concentration dependently (IC50 value of approximately 0.6-0.8 microM) inhibited by KB. Receptor-independent guanosine 5'-O-(3-thio)triphosphate-induced and background IK(ACh), which contributes to the resting conductance of atrial myocytes, were equally sensitive to KB (IC50 value of approximately 0.9 microM). IK(ATP) induced in atrial myocytes during metabolic inhibition with 2,4-dinitrophenol (DNP) was also suppressed by KB, whereas IK1 measured in ventricular myocytes was insensitive to the drug (KB < or =50 microM). Although being effective when applied from the outside, intracellular application of KB via the patch pipette affected neither IK(ACh) nor IK(ATP). 3,3',5-triodo-L-thyronin, which shares structural groups with KB, did not have an effect on the K+ currents. Consistent with the effects on single myocytes, KB did not depolarize the resting potential but antagonized the shortening of action potential duration by carbamylcholine-chloride or by DNP in multicellular preparations and antagonized the shortening of action potential duration by acetylcholine in single myocytes. It is concluded that KB inhibits IK(ACh) and IK(ATP) by direct drug-channel interaction at a site more easily accessible from extracellular side of the membrane.

Action Potentials↗
PubMed2003

Diadenosine-5-phosphate exerts A1-receptor-mediated proarrhythmic effects in rabbit atrial myocardium.

(1) Diadenosine polyphosphates have been described to be present in the myocardium and exert purinergic- and nonreceptor-mediated effects. Since the electrophysiological properties of atrial myocardium are effectively regulated by A(1) receptors, we investigated the effect of diadenosine pentaphosphate (Ap(5)A) in rabbit myocardium. (2) Parameters of supraventricular electrophysiology and atrial vulnerability were measured in Langendorff-perfused rabbit hearts. Muscarinic potassium current (I(K(ACh/Ado))) and ATP-sensitive potassium current (I(K(ATP))) were measured by using the whole-cell voltage clamp method. (3) Ap(5)A prolonged the cycle length of spontaneously beating Langendorff perfused hearts from 225+/-14 (control) to 1823+/-400 ms (Ap(5)A 50 micro M; n=6; P<0.05). This effect was paralleled by higher degree of atrio-ventricular block. Atrial effective refractory period (AERP) in control hearts was 84+/-14 ms (n=6). Ap(5)A>/=1 micro M reduced AERP (100 micro M, 58+/-11 ms; n=6). (4) Extrastimuli delivered to hearts perfused with Ap(5)A- or adenosine (>/= micro M)-induced atrial fibrillation, the incidence of which correlated to the concentration added to the perfusate. The selective A(1)-receptor antagonist CPX (20 micro M) inhibited the Ap(5)A- and adenosine-induced decrease of AERP. Atrial fibrillation was no longer observed in the presence of CPX. (5) The described Ap(5)A-induced effects in the multicellular preparation were enhanced by dipyridamole (10 micro M), which is a cellular adenosine uptake inhibitor. Dipyridamole-induced enhancement was inhibited by CPX. (6) Ap(5)A (</=1 mM) did neither induce I(K(Ado)) nor I(K(ATP)). No effect on activated I(K(Ado/ATP)) was observed in myocytes superfused with Ap(5)A. However, effluents from Langendorff hearts perfused with Ap(5)A 100 micro M activated I(K(Ado)) by using A(1) receptors. (7) Ap(5)A did not activate A(1) receptors in rabbit atrial myocytes. The Ap(5)A induced A(1)-receptor-mediated effects on supraventricular electrophysiology and vulnerability suggest that in the multicellular preparation Ap(5)A is hydrolyzed to yield adenosine, which acts via A(1) receptors. An influence on atrial electrophysiology or a facilitation of atrial fibrillation under conditions resulting in increased interstitial Ap(5)A concentrations might be of physiological/pathophysiological relevance.

Acetylcholine↗