H.-J. Trappe

Positionspapier zur ?Automatisierten Externen Defibrillation?

Herausgegeben vom Vorstand der Deutschen Gesellschaft für Kardiologie – Herzund Kreislaufforschung – in Zusammenarbeit mit der Deutschen Gesellschaft für Internistische Intensivmedizin und Notfallmedizin Bearbeitet im Auftrag der Kommission für klinische Kardiologie (R. H. Strasser, D. Andresen, G. Ertl, F. de Haan, H. Mudra, A. Osterspey, H.-J. Trappe, K. Werdan, außerdem G. Arnold, E. Fleck, H. M. Hoffmeister)

Positionspapier zur „Automatisierten Externen Defibrillation“

Herausgegeben vom Vorstand der Deutschen Gesellschaft für Kardiologie – Herzund Kreislaufforschung – in Zusammenarbeit mit der Deutschen Gesellschaft für Internistische Intensivmedizin und Notfallmedizin Bearbeitet im Auftrag der Kommission für klinische Kardiologie (R. H. Strasser, D. Andresen, G. Ertl, F. de Haan, H. Mudra, A. Osterspey, H.-J. Trappe, K. Werdan, außerdem G. Arnold, E. Fleck, H. M. Hoffmeister)

Disproportionate shortening of left ventricular diastolic duration in patients with dilated cardiomyopathy

ZusammenfassungHintergrund und Ziel:Das Verhältnis von Systolen- und Diastolendauer wird als eine wichtige Determinante der Herzfunktion angesehen. Bei Kindern mit dilatativer Kardiomyopathie (DCM) konnte eine abnorme Verkürzung der Diastolendauer beobachtet werden. In der vorliegenden Studie wurde untersucht, ob sich dieser Befund bei Erwachsenen reproduzieren lässt und welches Verhalten der diastolische Anteil des Herzzyklus unter stufenweiser ergometrischer Belastung zeigt.Patienten und Methodik:Die Untersuchung schloss konsekutiv 61 Patienten mit DCM im NYHA-Stadium (New York Heart Association) II–III ein. Bei diesen wurde unter ergometrischer Belastung eine Radionuklidventrikulographie mit hoher zeitlicher Auflösung durchgeführt. Aus der Zeit-Aktivitäts-Kurve wurde neben der linksventrikulären Ejektionsfraktion die Dauer von linksventrikulärer Systole und Diastole abgeleitet. Als Vergleichskollektiv dienten 26 Patienten, bei denen eine normale linksventrikuläre Pumpfunktion mittels Radionuklidangiographie vor geplanter Chemotherapie sichergestellt wurde.Ergebnisse:Der Vergleich der relativen Systolendauer ergab bei Patienten mit DCM bereits in Ruhe eine signifikante Verlängerung gegenüber Herzgesunden (23,9 vs. 21,5 s/min; p = 0,006). Dieser Befund blieb unter maximaler Belastung signifikant (29,2 vs. 26,7 s/min; p = 0,01), obwohl der Herzfrequenzanstieg in der Patientengruppe vermindert war (118 vs. 127/min; p = 0,04). Um den Einfluss der Herzfrequenz auf die Diastolendauer der DCM-Patienten zu eliminieren, wurden die beobachteten Werte mit den rechnerisch aus der Regressionsgleichung Herzgesunder ermittelten Werten verglichen. Dieses Vorgehen bestätigte eine signifikante Verkürzung der Diastolendauer auf maximaler Belastungsstufe und eine Zunahme des Verlusts an diastolischer Zeit pro Herzschlag gegenüber dem Ruhewert.Schlussfolgerung:Patienten mit fortgeschrittener DCM weisen eine abnorme Verkürzung der linksventrikulären Diastolendauer auf. Diese ist unter körperlicher Belastung besonders ausgeprägt und kann die kardiale Effizienz durch Restriktion von ventrikulärer Füllung und Perfusion beeinträchtigen.AbstractBackground and Purpose:Cardiac performance can be characterized in terms of the relative duration of systole and diastole. In pediatric patients with dilated cardiomyopathy (DCM), a disproportionate shortening of left ventricular diastole was observed. The present study was intended to reproduce these findings in an adult patient group and to evaluate exercise-related changes of both time intervals.Patients and Methods:Exercise radionuclide angiography was used in 61 patients with DCM NYHA (New York Heart Association) stage II–III. The phases of the cardiac cycle were derived from a radionuclide time-activity curve with high temporal resolution. The control group consisted of 26 patients referred for ventricular function assessment with radionuclide angiography before cardiotoxic cancer treatment.Results:When the duration of systole was expressed as the product of systolic time and heart rate, DCM patients exhibited a significant increase in left ventricular systolic time at rest (23.9 vs. 21.5 s/min; p = 0.006) and during peak exercise (29.2 vs. 26.7 s/min; p = 0.01). The prolongation of left ventricular systole at peak exercise was evident, although the peak heart rate was significantly lower in the patient group than in the control group (118 vs. 127/min; p = 0.04). In DCM patients the diastolic time loss per beat was further quantified using a regression equation obtained from the healthy control group. A significant shortening of left ventricular diastolic time was confirmed during peak exercise. Furthermore, a progressive loss in diastolic time per beat from rest to peak exercise was noted.Conclusion:Cardiac cycle abnormalities of patients with DCM are characterized by a prolongation of left ventricular systole and an abnormal shortening of left ventricular diastole. The systolic-diastolic mismatch is accentuated during exercise and has the potential to impair the cardiac reserve in these patients by restricting ventricular filling and perfusion.

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

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 A1 receptors, we investigated the effect of diadenosine pentaphosphate (Ap5A) in rabbit myocardium. Parameters of supraventricular electrophysiology and atrial vulnerability were measured in Langendorff‐perfused rabbit hearts. Muscarinic potassium current (IK(ACh/Ado)) and ATP‐sensitive potassium current (IK(ATP)) were measured by using the whole‐cell voltage clamp method. Ap5A prolonged the cycle length of spontaneously beating Langendorff perfused hearts from 225±14 (control) to 1823±400 ms (Ap5A 50 μM; 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). Ap5A1 μM reduced AERP (100 μM, 58±11 ms; n=6). Extrastimuli delivered to hearts perfused with Ap5A‐ or adenosine ( μM)‐induced atrial fibrillation, the incidence of which correlated to the concentration added to the perfusate. The selective A1‐receptor antagonist CPX (20 μM) inhibited the Ap5A‐ and adenosine‐induced decrease of AERP. Atrial fibrillation was no longer observed in the presence of CPX. The described Ap5A‐induced effects in the multicellular preparation were enhanced by dipyridamole (10 μM), which is a cellular adenosine uptake inhibitor. Dipyridamole‐induced enhancement was inhibited by CPX. Ap5A (1 mM) did neither induce IK(Ado) nor IK(ATP). No effect on activated IK(Ado/ATP) was observed in myocytes superfused with Ap5A. However, effluents from Langendorff hearts perfused with Ap5A 100 μM activated IK(Ado) by using A1 receptors. Ap5A did not activate A1 receptors in rabbit atrial myocytes. The Ap5A induced A1‐receptor‐mediated effects on supraventricular electrophysiology and vulnerability suggest that in the multicellular preparation Ap5A is hydrolyzed to yield adenosine, which acts via A1 receptors. An influence on atrial electrophysiology or a facilitation of atrial fibrillation under conditions resulting in increased interstitial Ap5A concentrations might be of physiological/pathophysiological relevance.

Mitral valve disease as well as uncommon extensive epipericardial and intramyocardial calcification secondary to massive mitral annular calcification

A 71-year-old woman with a history of childhood pulmonary tuberculosis was admitted to our hospital for exertional dyspnoea (NYHA functional class II). Transthoracic and transoesophageal echocardiography demonstrated moderate to severe mixed mitral valve disease due to massive mitral annular calcification (MAC) and extensive infiltrative calcification of the atrioventricular groove. In addition, a very uncommon intramyocardial calcification of the ventricular septum and the lateral free wall was diagnosed. This case demonstrates a rare combination of mitral valve disease secondary to MAC, and a small hypertrophied left ventricle, as well as epipericardial and myocardial calcification likely due either to the massive MAC with myocardial extension or to former tuberculous perimyocarditis. The multidimensional imaging approach, which has been used in this particularly case, provided an excellent visualization and clinical evaluation of this rare finding.

Propranolol inhibits IK(Ado) by competetive A1-receptor interaction

Propranolol ist einer der am meisten verwendete β-Blocker in der Klinik und wird experimentell als Antiadrenergikum genutzt. In der Literatur wurde berichtet, dass in bestimmten Patientenkollektiven die Inzidenz von Vorhofflimmern unter Propranolol abnimmt. Seine antiischämischen Eigenschaften sollen antiarrhythmisch wirken. Da die Aktivierung des muskarinergen Kaliumstroms (IK(ACh)) und des ATP abhängigen Kaliumstroms (IK(ATP)) Vorhofflimmern begünstigt, untersuchten wir die Wirkung von Propranolol auf den IK(ACh) und den IK(ATP). Der IK(ACh) wurde mittels Adenosin (Ado) oder Azetylcholin (ACh) aktiviert. Wir nutzten das „whole-cell voltage clamp“ Verfahren zur Erfassung der Ionenströme an isolierten Vorhofmyozyten von Ratten. Angaben erfolgen als Mittelwerte ±SD. Propranolol 50 μM sowie (+)-Propranolol (ein Isomer ohne β-blockierende Eigenschaften) hemmte den IK(Ado) vollständig (n = 6), hingegen war Esmolol signifikant schwächer wirksam. Der IC50 betrug 7 μM (n = 7). Die Strom-Spannungsbeziehung des gehemmten Stromes zeigte eine streng einwärts gleichrichtende Eigenschaft, die typisch für den muskarinergen Kaliumstrom ist. Die Inhibition war innerhalb von wenigen Sekunden reversibel. Der Effekt auf den Azetylcholin und GTP-γ-S induzierten muskarinergen Kaliumstrom war geringer (EC50 29 bzw. 31 μM), die intrazelluläre Applikation von Propranolol zeigte keinerlei Wirkung. Der IK(ATP) war kaum Propranolol sensitiv. Propranolol hemmt den IK(Ado) unabhängig von der Aktivität der G-Protein gekoppelten Rezeptoren. Die Inhibition ist nicht an die β-blockierende Eigenschaft der Substanz gebunden und daher unabhängig von der Anwesenheit von β-Mimetika. Der Adenosin induzierte IK(Ado) ist besonders empfindlich; es erscheint eine direkte Hemmung auf A1-Rezeptorebene wahrscheinlich. Als eine Ursache einer Propranolol bedingten Reduktion der Inzidenz von Vorhofflimmern ist die Hemmung des IK(ACh) denkbar. Bei der Anwendung von Propranolol in experimentellen kardiologischen Studien sollte eine mögliche Hemmung des IK(ACh) bei der Interpretation der Resultate berücksichtigt werden. 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). 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 μM) completely inhibited IK(Ado). IC50 was 7 μM. Inhibition of acetylcholine induced current (IK(ACh)) and GTP-γ-S induced muscarinic potassium current was less potent (IC50 29 μM and 31 μM 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 μM). 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.

Plötzlicher Herztod und automatisierte externe Defibrillatoren

Sudden cardiac death (SCD) is one of the major problems in the western world with approximately 70.000-100.000 SCD patients (pts) in Germany and 450.000 SCD victims in the US. SCD is not caused by a single factor but is a multifactorial problem. SCD is caused by ventricular tachyarrhythmias in approximately 90% of pts, whereas SCD is caused by bradyarrhythmias in 5-10%. In 50% of SCD victims, sudden cardiac death is the first manifestation of a heart disease. There is general agreement that early defibrillation with automated external defibrillators (AED) is an effective tool to treat pts with ventricular fibrillation. Nevertheless, further stragies on cardiopulmonary resuscitation and AED therapy are necessary to improve survival of patients with cardiac arrest.

Verfügbarkeit von Patientenverfügungen in einer interdisziplinären Notaufnahme

INTRODUCTION Despite an increasing attention to living wills, the effects of such living wills on patient care in the emergency departments remains unknown. MATERIAL AND METHODS All patients who were admitted to our emergency department between September 24th, 2014 and November 23th, 2014 were asked, whether they have signed living wills previously and if so, whether they have it on hand at admission. RESULTS 496 patients (229 men (46.2 %), 267 women (53.8 %)) with a mean age of 64.9 ± 18.8 years were included in this survey. 138 patients (27.8 %) had a living will but only 16 patients (3.2 %) had it on hand.Altogether, the existence of living wills increased with an increasing patient`s age; only 5 of 117 patients aged 50 years old or younger (4,3 %) had a living will, but 133 of 379 patients older than 50 years (35,1 %). DISCUSSION AND CONCLUSION Despite an obviously broad acceptance of living wills especially in the elderly population, there are hardly any consequences on the daily patient care in an emergency department by now, as hardly any patient has hers or his living will on hand at admission. We therefore see the need for further educational work to guarantee that living wills get adequate priority in patient care at emergency departments.

Dünndarm-Perforation durch einen verschluckten Tabletten-Blister nach postinterventioneller Koronarperforation

HISTORY AND ADMISSION FINDINGS A 70-year-old woman was admitted to hospital with progressive chest pain. Coronary angiography demonstrated a significant stenosis of the left descending artery (LAD), which was treated by percutaneous coronary intervention (PCI) and stent implantation. During this intervention, a coronary perforation occurred which was remedied immediately. Five days after the intervention, the patient complained about severe atypical chest and abdominal pain with nausea and vomitting, but no fever. Physical examination revealed an acute abdomen of uncertain origin. INVESTIGATIONS Laboratory tests revealed leukocytosis and elevated levels of C-reactive protein while cardiac enzymes were in normal range. The electrocardiogram showed no signs of acute myocardial ischemia. Abdominal x-ray was performed without any pathological findings. Further diagnostic tests, especially computed tomography of the abdomen, revealed an ingestion of a blister-wrapped tablet which had caused small bowel perforation and peritonitis. DIAGNOSIS, TREATMENT AND COURSE An acute abdomen due to ingestion of a foreign body was diagnosed and an emergency laparotomy was performed immediately. The blister pack was removed by ileostomy. The further course was uneventful. CONCLUSION The clinical presentation of abdominal pain is a frequent medical condition in hospital. Determining the cause requires precise assessment and examination and implicates a variety of differential diagnosis including non-cardiac and cardiac pain. Iatrogenic causes must be considered in differential diagnosis.

Herzrhythmusstörungen bei der Schwangeren und beim Fetus

For the acute treatment of supraventricular (SVT) and ventricular tachycardias (VT) in pregnant women, electrical cardioversion with 50-100 J is indicated in all unstable patients. In stable SVT the initial therapy includes vagal maneuvers or intravenous adenosine. For long-term therapy, beta-blocking agents with beta(1)-selectivity are first-line drugs or specific anti-arrhythmic drugs. An implantable cardioverter-defibrillator is another approach. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of pregnancy. Evaluation of fetal arrhythmias in clinical practice is based on assessment of the chronological relationship between atrial and ventricular contraction (M-mode and Doppler ultrasound or magnetocardiography). Most forms of SVT can be treated with transplacental administration of anti-arrhythmic drugs. Atrioventricular (AV) block in fetuses with structural heart disease is frequently associated with hydrops fetalis and intrauterine death. Administration of corticoids and beta-mimetic drugs is used to treat antibody-mediated AV block and cardiomyopathy.