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ZusammenfassungVorhofflimmern ist ein häufiger Grund für einen Schlaganfall. Insbesondere Patienten ohne adäquate Antikoagulation haben ein erhöhtes Risiko für thromboembolische Ereignisse (ca. 5–7%). Es liegt eine Assoziation zwischen Kardioversionen und embolischen Ereignissen vor. Durch eine orale Antikoagulation (OAK) mit Nicht-Vitamin-K-Antagonisten (NOAK) kann dieses Risiko auf unter 1% reduziert werden. Es gibt 2 unterschiedliche Kardioversionsstrategien. Zum einen kann eine Kardioversion nach 3-wöchiger effektiver Antikoagulation ohne weitere Bildgebung durchgeführt werden. Zum anderen kann nach Ausschluss einer intrakardialen Thrombenbildung durch eine TEE umgehend sicher kardiovertiert werden. Bei Vorhofflimmern sollte nach der Kardioversion eine effektive Antikoagulation für mindestens 4 Wochen erfolgen, unabhängig vom CHA2DS2-VASc-Score. Eine Bildgebung mittels TEE ist notwendig, wenn die Dauer einer effektiven Antikoagulation

A 58-year-old woman fainted on the ward a few days after an emergency appendectomy. Due to recurrent loss of consciousness, immediate resuscitation was started and a ventricular torsades de pointes tachycardia was documented. Further diagnostic procedures did not reveal any underlying cardiac disease or channelopathy and different potential causes were ruled out. For optimal diagnostic accuracy in a situation where a reversible/preventable cause might have been present, a loop recorder was implanted for continuous ECG monitoring of the patient.

A 58-year-old woman fainted on the ward a few days after an emergency appendectomy. Due to recurrent loss of consciousness, immediate resuscitation was started and a ventricular torsades de pointes tachycardia was documented. Further diagnostic procedures did not reveal any underlying cardiac disease or channelopathy and different potential causes were ruled out. For optimal diagnostic accuracy in a situation where a reversible/preventable cause might have been present, a loop recorder was implanted for continuous ECG monitoring of the patient.Eine 58-jährige Patientin synkopierte wenige Tage nach einer notfallmäßigen Appendektomie auf der Station. Wegen rezidivierendem Bewusstseinsverlust wurde eine sofortige Reanimation eingeleitet, und es wurde eine Torsade-de-Pointes-Tachykardie dokumentiert. In der weiteren diagnostischen Aufarbeitung fand sich kein Hinweis auf eine zugrundeliegende kardiale Erkrankung oder Kanalerkrankung; verschiedene Ursachen der Tachyarrhythmie konnten ausgeschlossen werden. Um eine optimale diagnostische Sicherheit in einer Situation zu gewährleisten, in der reversible oder vermeidbare Ursachen für eine Torsade-de-Pointes-Tachykardie nicht sicher auszuschließen waren, wurde ein Loop-Rekorder implantiert, der eine kontinuierliche EKG-Überwachung der Patientin gewährleistete.

Patients with coronary heart disease are subject to an increased risk for sudden cardiac death (SCD). Within the first 30-90 days after the myocardial infarct the risk is particularly high. In times of implantable cardioverter-defibrillator (ICD) on the one hand and the ability to bridge high-risk periods with e. g. wearable defibrillator vests on the other, adequate risk stratification is essential. Currently, the main parameter for this is the left ventricular ejection fraction (LVEF). However, risk stratification by measurement of the LVEF has severe limitations, especially since the majority of patients suffering from SCD have a normal LVEF. Various other methods like ventricular ectopy, signal-averaged ECG, QRS width, microvolt T-wave alternans and programmed ventricular stimulation have been previously evaluated. None of these methods alone or in combination with a left ventricular function assessment was capable of improving the predictability of arrhythmic events significantly. Considering the multiple mechanisms that can lead to SCD, a single risk stratifier seems unrealistic. However, patients with chronic total occlusion of a coronary artery and residual or provocable ischemia have an increased risk for SCD. Therefore a combination of clinical and angiographic parameters seems reasonable. Advanced echocardiographic parameters e.g. mechanical dispersion could be used on a complementary role.

The aim of this study was to assess the incidence, clinical predictors, and outcome of patients developing contrast medium induced nephropathy (CIN) after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS). CIN is associated with significant higher morbidity and mortality after coronary intervention. Recently it was shown, that patients undergoing percutaneous coronary intervention for acute myocardial infarction have a significant higher risk of developing CIN. Non-ST-elevating myocardial infarction (NSTEMI) patients (pts) might be at an even higher risk developing CIN than patients with ST-elevating myocardial infarction (STEMI), because of presenting older and more often with diabetes. In 392 consecutive ACS patients developing myocardial infarction and therefore undergoing emergent coronary angiography between October 2004 and March 2007, we measured serum creatinine concentration (Cr) at baseline and each day of the following 3 days. Contrast medium induced nephropathy was defined as an increase in Cr > 0.5 mg/dl. ACS was defined according to the guidelines of the German Society of Cardiology. Overall, 392 pts were included: 203 (51.8%) with STEMI and 189 (48.2%) with NSTEMI. Patients with STEMI developed more often a cardiogenic shock (18 vs. 6%; P

Background: Acute myocardial infarction (AMI) due to acute simultaneous proximal occlusion of two major coronary arteries (ASOMC) is a rare but life-threatening situation. Most patients die suddenly or go into cardiogenic shock (CS). In patients with AMI due to ASOMC identified by coronary angiography (CA), percutaneous coronary intervention (PCI) performed in both infarct-related arteries (IRAs) at the same time as diagnostic CA is the fastest option to complete revascularization. However, no prospective studies regarding the outcome of such procedures have been published so far. Methods: In this prospective single-center study, between October 2004 and March 2007, consecutive patients with acute coronary syndrome (ACS) reporting to our university hospital and regional referral center were evaluated for ASOMC by means of emergent CA. When diagnosed with ASOMC, PCI of the IRAs was performed. Clinical data were obtained at baseline, discharge, after 6 months, and after 1 year. Results: Out of 417 patients with ACS, 379 patients (90.9%) suffered an AMI. In 5 patients CA revealed an ASOMC. PCI was performed in 4 patients. One patient with severe triple-vessel disease was referred for emergent coronary artery bypass graft (CABG) surgery after conventional PCI of one IRA. One patient died in-hospital due to early in-stent thrombosis after PCI. At 6-month follow-up and at 1-year follow-up, 4 patients were alive. Conclusion: In spite of the complex interventions, PCI patients had low in-hospital mortality and good clinical results at 1-year follow-up. Our observations are important in the clinical decision-making process of AMI due to ASOMC.

The purpose of this first in vivo study was to assess the incidence of thermal influence to the right coronary artery (RCA) during ablation of common type atrial flutter (Aflu) by measuring the fractional flow reserve (FFR) in the vessel before, under and after ablation.In thirty three patients ablated we performed coronary angiography (CA) before and at the end of the procedure. The FFR wire was positioned in the distal, the isthmus underlying, part of the RCA. Before and after the procedure FFR measurement was done at baseline and during adenosine administration. During the whole ablation procedure FFR measurement was continuously carried on, to monitor a transient thermal impact to the RCA.Of the 33 patients observed, 25 males, 8 females, mean age 58 +/- 9.5 years, none with CAD, all patients, except one with unidirectional block, were successfully ablated. The FFR at rest and under medication with adenosine before and after ablation was 0.985/0.949 and 0.981/0.942, respectively (p = ns). The CA of the RCA did not reveal any morphological change. The mean FFR while ablation declined from 0.94 to 0.904 (p = ns). Twenty-six patients (78.8%) had no or moderate decrease in FFR, seven patients (21.2%) demonstrated a substantial decrease [five patients (15.2%), FFR0.9 and0.75] or significant change [two patients (6.1%)], FFR0.75 consistent with a remarkable or significant reduction of coronary flow.Ablation of AFlu did not alter RCA morphology; simultaneous FFR measurement showed severe depression of the FFR in a few patients, consistent with impairment in myocardial perfusion.

The ablation of common type atrial flutter is mainly performed by two approved techniques, whose efficacy and outcome in terms of quality of life have not been evaluated so far in a long-term follow-up study over years. A high proportion of patients suffer from coexistent atrial fibrillation, which may worsen the ablation result. The question arises whether one technique is more effective than the other when immediate ablation results, the occurrence of atrial fibrillation and the quality of life are compared. Considering these facts, it is reasonable to think about new ablation strategies for common type atrial flutter in the era of new concepts in catheter ablation of atrial fibrillation. In a retrospective study we evaluated a detailed questionnaire in 132 patients who underwent ablation of common type between 1999 and 2004. Radiofrequency ablation was performed irrespective of coexistent atrial fibrillation either with an irrigated tip or the 8 mm tip electrode. Acute and long-term ablation outcome, and the associated quality of life, pre-, under- and post-ablation was compared in the two different ablation groups. Recurrent tachycardia were re-evaluated by 12 lead ECG analysis and assessed for both ablation groups. 88 (67%) of the 132 patients contacted answered the questionnaire polling the perceived benefits of the procedure. Of the other 44 patients (33%); 4 (3%) had died, 7 (5.3%) had moved, 33 patients (25%) could not be included due to missing or incoherent answers. Independent of the ablation technique there was a high acute and long-term ablation success rate at about 95%. After a mean of 3 years of follow-up this benefit persists in spite of a high proportion of recurrent tachycardia, mainly atrial fibrillation (55/88 patients, 59.1%). Despite the occurrence of secondary tachycardia, there was a high significant long-term symptomatic benefit in the state of healthy and daily practice work, evaluated with a p-value of < 0.0005. The frequency of episodes and the symptom "tachycardia" were significantly reduced after effective ablation of common type atrial flutter, p-values of 0.003 and 0.002, respectively. Therefore the need for hospitalization was significant reduced (p = 0.001). Comparison of both approaches revealed that there was no significant difference related to the incidence and occurrence of atrial fibrillation. The two mainly accepted and applied techniques for the ablation of common type atrial flutter show an excellent outcome under the aspect of ablation efficacy and quality of life in longterm follow-up. Three years after the ablation procedure the majority of patients consider the intervention beneficial. Despite the relatively high appearance of atrial fibrillation in the long-term follow-up this effect is still traceable.

In contrast to Kawasaki syndrome the formation of coronary aneurysms caused by atherosclerosis has hardly been demonstrated. We report on a 56-year old patient, admitted to our hospital for cardiovascular evaluation before carotid surgery. He had no anginal pain, but a history of coronary artery disease with previous anterior myocardial infarction. Angiography revealed a collateralized LAD occlusion. Myocardial scintigraphy only demonstrated fixed perfusion defects. Surprisingly, MR imaging revealed large coronary aneurysms of the RCX and RCA. Angiographic follow up showed a rapid progression of ectatic towards aneurysmatic coronary lesions within 3 years. General pathophysiological mechanisms promoting ectatic coronary artery disease as a structural failure of the atherosclerotic remodelling process itself and chronic dilatatory stimuli due to endogenous and exogenous factors are discussed.

Bei Erwachsenen ist das vagale Vorhofflimmern von besonderer klinischer Relevanz. Pathophysiologisch ist der muskarinerge Kaliumionenstrom IK(ACh) ursachlich an der Entstehung des vagal induzierten Vorhofflimmerns beteiligt. Die selektive Inhibition des IK(ACh) erscheint therapeutisch vielversprechend. Die Anwendung von Amiodaron, dem derzeit wichtigsten Wirkstoff in der Therapie des Vorhofflimmerns, wird durch ein komplexes Nebenwirkungsprofil limitiert. KB130015, ein neues Amiodaronderivat, und Ibutilide sind neue Klasse-III-Antiarrhythmika. Mittels der “whole-cell voltage-clamp”-Technik wurde die Wirkung von KB130015 und Ibutilide auf den muskarinergen Kaliumionenstrom an isolierten atrialen Myozyten von Meerschweinen untersucht. 50 µM KB130015 und 50 µM Ibutilide inhibierten den IK(ACh) vollstandig und reversibel. Die benotigte Konzentration fur eine halbmaximale Inhibition des IK(ACh) betrug fur KB130015 0,8 µM und fur Ibutilide 2,8 µM. Die Hemmung des IK(ACh) war unabhangig vom Modus seiner Aktivierung. Sowohl der adenosin- als auch der acetylcholininduzierte Ionenstrom waren durch beide Wirkstoffe supprimierbar. Ebenso inhibierten beide Substanzen auch den durch GTP-γ-S irreversibel induzierten Ionenstrom. Intrazellulare Applikation zeigte dagegen keinen Effekt auf den IK(ACh). KB130015 und Ibutilide sind potente Inhibitoren des IK(ACh). Eine direkte Hemmung des IK(ACh) durch Interaktion mit dem extrazellular gelegenen Anteil des Ionenkanals ist wahrscheinlich. Akute Effekte von KB130015 auf das Ventrikelmyokard konnten bislang nicht nachgewiesen werden, Ibutilide dagegen inhibiert zusatzlich den IKr. KB130015 scheint daher das vielversprechendere der beiden Pharmaka zur Therapie des vagal induzierten Vorhofflimmerns zu sein. Eine signifikante Proarrhythmie ist im Vergleich zu Ibutilide nicht zu erwarten.

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 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).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.

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 (KBor =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.

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

Patients with coronary heart disease are subject to an increased risk for sudden cardiac death (SCD). Within the first 30-90 days after the myocardial infarct the risk is particularly high. In times of implantable cardioverter-defibrillator (ICD) on the one hand and the ability to bridge high-risk periods with e. g. wearable defibrillator vests on the other, adequate risk stratification is essential. Currently, the main parameter for this is the left ventricular ejection fraction (LVEF). However, risk stratification by measurement of the LVEF has severe limitations, especially since the majority of patients suffering from SCD have a normal LVEF. Various other methods like ventricular ectopy, signal-averaged ECG, QRS width, microvolt T-wave alternans and programmed ventricular stimulation have been previously evaluated. None of these methods alone or in combination with a left ventricular function assessment was capable of improving the predictability of arrhythmic events significantly. Considering the multiple mechanisms that can lead to SCD, a single risk stratifier seems unrealistic. However, patients with chronic total occlusion of a coronary artery and residual or provocable ischemia have an increased risk for SCD. Therefore a combination of clinical and angiographic parameters seems reasonable. Advanced echocardiographic parameters e.g. mechanical dispersion could be used on a complementary role.

Der Notarzt bringt einen 72-jahrigen Patienten in die Notaufnahme, der seit ca. 2 h uber starkes retrosternales Brennen und leichte Luftnot klagt. Vom Notarzt war dies als akutes Koronarsyndrom eingestuft und entsprechend medikamentos behandelt worden. Bei Eintreffen klagt der Patient uber zunehmende Luftnot. Bei der orientierenden Untersuchung lassen sich beidseits basal feuchte Rasselgerausche auskultieren; der Patient erhalt 6 l/min Sauerstoff uber eine Maske und 5 mg Morphin i.v. zur Schmerztherapie. Auserdem wird der Patient mit dem Oberkorper 30° hochgelagert und erhalt wegen eines beginnenden Lungenodems insgesamt 40 mg Furosemid.

In daily practice, moderate types of congenital coronary artery anomalies (CAA) remain unrecognized unless the patient is evaluated for coronary artery disease (CAD) due to clinical symptoms, often...

Atrial fibrillation (AF) occurs commonly in patients with acute myocardial infarction (AMI) and has been established as a marker of adverse prognosis. There are only few clinical trials that investigate differences between new-onset and chronic AF in AMI. We hypothesize that chronic AF is associated with an increased rate of adverse short- and long-term outcomes. In a single center study, over a period of 28 months, 375 consecutive patients with AMI were included [337 patients without AF (89.9%) and 38 with AF (10.1%)]. As much as 16 patients had new-onset AF (42.1%) and 22 had chronic AF (57.9%). Patients with severe coronary artery disease develop AF more often in AMI, and the existence of AF was associated with a poor prognosis. Compared to patients with new-onset AF, chronic AF was more frequently associated with advanced age (75 vs. 70 years, p not significant), reduced left ventricular ejection fraction (44.8 vs. 54.0%, p

Pharmacological treatment of atrial fibrillation (AF) is limited by induction of malignant ventricular arrhythmias. Developing new drugs, a promising strategy is a more specific treatment of the atria. Muscarinic potassium current (IK[ACh]) is predominantly expressed in supraventricular tissue and mediates the induction of vagus-induced AF. The authors investigated the profile of representative class III drugs in respect to their effect on IK(ACh).In rat atrial myocytes, IK(ACh) was activated by acetylcholine (ACh) measured with the whole-cell voltage clamp method. Drugs used: selective IKs blocker chromanole 293B (Cro); IKr blockers sotalol (Sot), dofetilide (Dof), ibutilide (Ibu), and terikalant (Ter). Data are expressed as mean values +/- standard deviation (SD).ACh-induced IK(ACh) density was 73 +/- 9 pA/pF (n= 9). IK(ACh) was almost completely desensitized in the presence of 50 micro M Ter, Ibu, or Dof. IC(50) of IK(ACh) inhibition by the three drugs was 0.9, 2.8, and 4.2 micro M (Dof, Ibu, and Ter, respectively). Receptor-independent GTP-gamma-S-induced IK(ACh) was sensitive to Ter, Ibu, and Dof as well. Sot is known to be a weak inhibitor of IKr. Inhibition of IK(ACh) by Sot was much less potent (IC(50) = 35.5 micro M) than inhibition by the high-affinity IKr blockers Ter, Ibu, and Dof. Superfusion of the cells with the IKs blocker Cro showed no desensitization of IK(ACh). Applied via the patch pipette (40 min) none of the class III drugs were effective.The results indicate inhibition of IK(ACh) and IKr but not IKs to be of similar mechanism (direct ion channel inhibition from the external side of the membrane). Potent desensitization of muscarinic potassium current could be of clinical relevance especially in patients with vagus-induced AF.