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Background Oral anticoagulation (OAC) reduces thromboembolic events and mortality in patients with atrial fibrillation (AF). Anticoagulation rates have substantially increased over recent years. Still, a number of patients are not receiving guideline recommended OAC. Purpose To investigate clinical factors and reasoning associated with non-prescription of OAC in a current German registry. Methods The German AFNET 2 registry is a prospective multi-center registry on atrial fibrillation comprising a total of 3491 patients from all levels of medical care (general practitioners, cardiologists, hospitals; enrolment 5/2014 to 3/2016). The registry was conducted in collaboration with the EORP program of the ESC. Here, only patients with non-valvular AF and at least two clinical risk factors for stroke (using CHA2DS2-VASc score) were considered. Results The study population consisted of 2856 patients, 58.4% male, mean age 75.5±7.8 years, mean CHA2DS2-VASc score 4.1±1.5, mean HAS-BLED score 1.8±1.0. Overall, the rate of OAC was 94.3%. 54% of these received Vitamin K antagonists (VKA) and 46% NOAC. 2.3% received antiplatelets only. Patients newly initiated on OAC mostly received a NOAC (82.5% of patients). Anticoagulation rate was lower in elderly patients (age Conclusions Within registries, the guideline recommended use of OAC is very high in Germany indicating high guideline adherence by prescribing physicians. However, use of antiplatelet therapy was associated with non-prescription of OAC. In addition, a high HAS-BLED score appears to be a relevant argument for withholding proven OAC for stroke prevention in patients with AF. Acknowledgement/Funding BMS Germany; DZHK

Die damalige Deutsche Gesellschaft fur Kreislaufforschung, heute Deutsche Gesellschaft fur Kardiologie – Herz- und Kreislaufforschung, wurde 1927 von Bruno Kisch und Arthur Weber gegrundet. Lange Zeit dominierten die „Theoretiker“ (Physiologen, Pathologen, Pharmakologen) die Gesellschaft. Zu Beginn der 1970er-Jahre forderten die klinisch tatigen Mitglieder der Gesellschaft fur sich einen groseren Einfluss in der Gesellschaft. Es bestand die Gefahr der Grundung einer eigenen Gesellschaft. In dieser Situation entstand 1971 wahrend der 37. Mitgliederversammlung der Deutschen Gesellschaft aus dem „Ausschuss fur Klinische Kommission“ die Kommission fur Klinische Kardiologie (KKK). Es war die Zeit der Entstehung neuer Herzkathetertechniken und neuer Herzkatheterlabore. Die KKK initiierte und organisierte ab 1974 die klinisch orientierten Herbsttagungen der Gesellschaft, griff Fragen der klinischen Kardiologie auf und verfasste und publizierte Leitlinien, damals zuerst Richtlinien genannt. Die erste erschien 1983 und damit vor den ersten ACC/AHA Clinical Practice Guidelines. Heute werden die Leitlinien durch internationale Leitlinien der European Society of Cardiology, angepasst an deutsche Verhaltnisse, erganzt und seit 1996 auf der Internetseite der Gesellschaft publiziert. Auserdem wurde 1982 der erste von nachfolgend 25 (2010) Berichten uber Struktur und Leistungszahlen der Herzkatheterlabore in der Bundesrepublik Deutschland (heute Herzbericht) publiziert.

Approximately 10% of ischemic strokes are associated with atrial fibrillation (AF) first diagnosed at the time of stroke. Detecting asymptomatic AF would provide an opportunity to prevent these strokes by instituting appropriate anticoagulation. The AF-SCREEN international collaboration was formed in September 2015 to promote discussion and research about AF screening as a strategy to reduce stroke and death and to provide advocacy for implementation of country-specific AF screening programs. During 2016, 60 expert members of AF-SCREEN, including physicians, nurses, allied health professionals, health economists, and patient advocates, were invited to prepare sections of a draft document. In August 2016, 51 members met in Rome to discuss the draft document and consider the key points arising from it using a Delphi process. These key points emphasize that screen-detected AF found at a single timepoint or by intermittent ECG recordings over 2 weeks is not a benign condition and, with additional stroke factors, carries sufficient risk of stroke to justify consideration of anticoagulation. With regard to the methods of mass screening, handheld ECG devices have the advantage of providing a verifiable ECG trace that guidelines require for AF diagnosis and would therefore be preferred as screening tools. Certain patient groups, such as those with recent embolic stroke of uncertain source (ESUS), require more intensive monitoring for AF. Settings for screening include various venues in both the community and the clinic, but they must be linked to a pathway for appropriate diagnosis and management for screening to be effective. It is recognized that health resources vary widely between countries and health systems, so the setting for AF screening should be both country- and health system-specific. Based on current knowledge, this white paper provides a strong case for AF screening now while recognizing that large randomized outcomes studies would be helpful to strengthen the evidence base.

Die Deutsche Gesellschaft fur Kardiologie (DGK) legt hiermit ein Curriculum zur Erlangung einer Zusatzqualifikation „Spezielle Rhythmologie“ vor, um besondere Kenntnisse, Erfahrungen und Fertigkeiten anzuerkennen, das sich an die Anforderungen der European Heart Rhythm Association (EHRA) anlehnt. Neben dem Erwerb der Zusatzqualifikation „Spezielle Rhythmologie“ (24 Monate) konnen auch die Blocke „Invasive Elektrophysiologie“ bzw. „Aktive Herzrhythmusimplantate“ separat erworben werden (jeweils 15 Monate). Die Erteilung des Zertifikats setzt die Anerkennung als „Arzt fur Innere Medizin und Kardiologie“ voraus. Beschrieben werden Ziele und die zugehorigen theoretischen und praktischen Inhalte des Programms. Zusatzlich wurden Kriterien fur die Eignung einer Statte zur Erlangung der Zusatzqualifikation und fur die Qualifikation des Leiters formuliert. Der Ablauf der Zusatzqualifikation wird in einem Logbuch dokumentiert. Die Akkreditierung der Zentren und der Leiter erfolgt durch eine Kommission „Zusatzqualifikationen in der Kardiologie“ der DGK. Fur die Zeitdauer von 2 Jahren gelten Ubergangsregelungen. Dieses strukturierte Programm zur optionalen Erlangung der Zusatzqualifikation soll einer optimalen Patientenversorgung dienen sowie die Attraktivitat der Speziellen Rhythmologie innerhalb der Kardiologie erhohen.

The German Competence Network on Atrial Fibrillation (AFNET) is a national interdisciplinary research network funded by the Federal Ministry of Education and Research (BMBF). AFNET was initiated in 2003 and aims at improving treatment of atrial fibrillation (AF), the most frequent sustained cardiac arrhythmia. AFNET has established a nationwide patient registry on diagnostics, therapy, course and complications of AF in Germany. The data analyzed to date demonstrate that patients with AF are likely to have multiple co-morbidities, such as hypertension, valvular heart disease, coronary artery disease, diabetes mellitus and advanced age. Oral anticoagulation is provided to the majority of patients in accordance with the recommendations given by guidelines. Further areas of research deal with the optimal duration of antiarrhythmic therapy following electrical cardioversion of atrial fibrillation and the value of strategies to prevent arrhythmogenic changes, such as fibrosis in the atria, for prevention of further episodes of atrial fibrillation. Additional registry projects were established for patients with catheter-based interventional therapy of atrial fibrillation and surgical ablation to define success, complications and long term results of these recently developed procedures more clearly. Data and insights gathered from these projects were used to further develop standards of care in two international conferences.

Drug-induced proarrhythmia is a serious medical problem that causes relevant morbidity and mortality. It is also a relevant problem for the development of novel pharmacological compounds. Therefore, there is a need for sensitive, specific and high-throughput preclinical tests to detect a risk for drug-induced proarrhythmia early in the development of new drugs. The review focuses on the potential role of transgenic models with altered repolarisation but without overt structural heart disease for drug-induced proarrhythmia screening. Today, selected murine models with alterations in K+, Na+ channels and ankyrin are available. In the future, transgenic rabbit and Zebra fish models may also be used.

The correct diagnosis of a wide complex tachycardia (WCT)—QRS duration > 120 ms—remains a challenge despite numerous established criteria for the differentiation of ventricular from supraventricular tachycardia (SVT) with aberrant conduction. Making the correct diagnosis is important for the acute as well as long term management of patients with WCT. The objective of the present review is to discuss the major causes as well as clinical and electrophysiologic criteria of WCT (table 1) in patients without structural heart disease. View this table: Table 1 Causes of wide complex tachycardias (WCTs) in patients without structural heart disease Broad categories of WCTs include ventricular tachycardia (VT), SVT with abnormal intraventricular conduction, and ventricular paced rhythms. A lack of underlying structural heart disease does neither exclude a VT nor imply a benign prognosis. However, if a patient has had similar episodes during previous years, SVT is more likely than VT. Termination of a tachycardia by the Valsalva manoeuvre or adenosine injection also suggests a supraventricular origin, although some VT can also be terminated by these manoeuvres (for example, fascicular VT). A WCT in a patient who is alert and haemodynamically stable is not necessarily of supraventricular origin. The clinical presentation depends on the haemodynamic consequences it produces. These depend partly on tachycardia rate, the degree of myocardial dysfunction, the circumstances and suddenness of initiation, and autonomic factors. Physical examination in a patient presenting with WCT may indicate haemodynamic distress (low blood pressure, heart failure or cardiogenic shock). When cardiac output and blood pressure are maintained and/or when the tachycardia is short lived, the arrhythmia may present as palpitations, breathlessness or just discomfort. Intraventricular conduction delay can result from heart rate changes, as well as from fixed pathological lesions in the conduction system. In patients with pre-existing or “fixed” (present during the normal baseline rhythm) bundle branch block (BBB), …

Der plotzliche Herztod ist eine haufige Todesursache. Er wird vor allem durch tachykarde Herzrhythmusstorungen verursacht. Angeborene genetische Veranderungen von kardialen Ionenkanalen, Proteinen des kontraktilen Apparats, der intrazellularen Calciumspeicher oder von Zell-Struktur-Proteinen konnen angeborene arrhythmogene Erkrankungen verursachen. Bei der Herzhypertrophie und der Herzinsuffizienz treten adaptative Veranderungen der Genexpression und Proteinfunktion auf, die arrhythmogene Folgen haben. Teilweise finden sich ahnliche molekulare Mechanismen der Arrhythmogenese bei erworbenen adaptativen und angeborenen arrhythmogenen Erkrankungen.

Eine 18-jahrige Patientin mit antiepileptischer Medikation wurde morgens leblos im Bett aufgefunden, vom Notarzt bei dokumentiertem Kammerflimmern reanimiert und auf die Intensivstation verbracht. Dort wurde nach EKG-Kriterien die Diagnose eines Long-QT-Syndroms (LQTS) gestellt. Im weiteren Verlauf verstarb die Patientin am hypoxischen Hirntod. Die erweiterte Anamnese ergab, dass die Patientin zuvor rezidivierende Synkopen erlitten hatte, die als epileptische Anfalle gedeutet wurden. Die 17-jahrige Schwester der Patientin war acht Wochen zuvor aus ungeklarter Ursache am plotzlichen Herztod verstorben, ebenso eine Tante (Zwillingsschwester der Mutter) mit 37 Jahren. Ein EKG-Screening bei der Familie brachte sechs weitere Familienmitglieder mit LQTS zu Tage. Eine molekulargenetische Analyse bei diesen fuhrte zur Identifizierung einer nicht-bekannten Mutation (888 delG insAA) im LQT2-Gen (HERG), die zu einem Aminosaurenabbruch (360X) auf Proteinebene in der Untereinheit des IKr-Kanals fuhrt. Die Kasuistik verdeutlicht einige klassische Aspekte des LQTS (typischer adrenerger Triggermechanismus, klassische Fehldiagnose "Epilepsie") und zeigt neue Erkenntnisse wie die Moglichkeit einer genotypischen Zuordnung aus phanotypischen EKG-Charakteristika. Der Fall reprasentiert ein ungewohnliches Beispiel eines LQTS mit hochmaligner Penetranz, welches aggressive Therapiemasnahmen bei den uberlebenden Familienmitgliedern erforderte.

About three years ago, the German Government initiated a complete change in the reimbursement system for costs of the in-hospital treatment of patients. A commission of representatives from every component of the German health system decided to adapt the Australian refined Diagnosis Related Groups (AR-DRG system). The AR-DRG system was selected as it would fit best to the German system and because of its high flexibility and preciseness reflecting severity of diseases and treatments. In October 2002, the first German Diagnosis Related Groups (G-DRGs) were calculated from the data of about 116 hospitals. These data now allow first analyses in how far a correct and precise grouping of patients in specific hospital settings is indeed performed and corresponds to the actual costs. Thus, we thoroughly calculated all costs for material and personnel during the in-hospital stay for each patient discharged during the first 4 months of 2002 from our cardiological department. After performing the grouping procedure for each patient, we analyzed in how far inhomogeneous patient distribution in the DRGs occurred and which impact this had on costs and potential reimbursements. Several different problems were identified which should be outlined in this work regarding three G-DRGs: costs of patients who received an implantable cardioverter defibrillator (F01Z) were markedly influenced by multimorbidity and additional expensive interventions which were not reflected by this G-DRG. Use of numerous catheters and expensive drugs represented a major factor for costs in patients with coronary angioplasty in acute myocardial infarction (F10Z) but seemed to be not sufficiently included in the cost weight. A specific area of patient management in our department is high frequency ablation of tachyarrhythmias which is included in other percutaneous interventions (F19Z). Complex procedures such as ablation of ventricular tachycardia or new innovative procedures as ablation of atrial fibrillation were associated with high costs leading to inadequate reimbursement. Furthermore, problems in the associated codes for diseases and procedures became apparent. Opportunities for future optimization such as specific new DRGs, splitting of DRGs, or the impact of changes in reimbursement for high-outliers were discussed.

Wir berichten uber den Langzeitverlauf eines kombinierten fusiformen Aneurysmas der Arteria subclavia dexter sowie des Abgangs des Truncus thyreocervicalis (3,2×2,8×2,2cm (Breite×Hohe×Tiefe)) bei einem 33-jahrigen Patienten. Bereits perinatal wurde der klinische Verdacht auf das Vorliegen einer Aortenisthmusstenose geausert, allerdings zum damaligen Zeitpunkt kein Interventionsbedarf gesehen. Die weitere Entwicklung des Kindes verlief zunachst normal, bis im Alter von 11 Jahren der Patient erneut aufgrund nach sportlicher Aktivitat verspurten Schwindelgefuhls kardiologisch vorgestellt wurde. Bei klinisch evidenter Progression wurde eine Herzkatheterdiagnostik durchgefuhrt, die eine juxtaductale Aortenisthmusstenose zeigte. Diese wurde konsekutiv mittels End-zu-End-Anastomose 1981 operativ korrigiert. Daneben zeigte sich bereits eine aneurysmatisch veranderte Arteria subclavia dexter, wobei diesbezuglich ein konservatives Procedere vorgeschlagen wurde. Der Patient stellte sich in regelmasigen Abstanden zu einer Verlaufskontrolle in unserer Ambulanz vor und ist seitdem vollstandig asymptomatisch. Der vorliegende Bericht zeigt den nunmehr uber 20-jahrigen asymptomatischen Verlauf eines fusiformen Aneurysmas der Arteria subclavia dexter unter Einbeziehung des ebenfalls fusiform aneurysmatisch veranderten Abgang des Truncus thyreocervicalis und bietet einen Uberblick der Literatur zu diesem Thema.

Das Jervell- und Lange-Nielsen-(J-LN)Syndrom ist eine besondere Form des kongenitalen QT-Syndroms. Im Gegensatz zum autosomal-dominant vererbten Romano-Ward (R-W)Syndrom liegt neben der charakteristischerweise mit Synkopen einhergehenden Verlangerung des QT-Intervalls zusatzlich eine Innenohrschwerhorigkeit (sog. surdokardiales Syndrom) und ein autosomal rezessiver Erbmodus vor. In jungster Zeit konnten die zugrundeliegenden genetischen Defekte bei einem Teil der an der Erkrankung leidenden Familien aufgeklart werden. Bei den kurzlich identifizierten Genen KCNQ1 und KCNE1 handelt es sich um die gleichen Gene, die auch bei Patienten mit R-W-Syndrom Mutationen aufweisen. Es ergeben sich allerdings Unterschiede im Vererbungsmodus; eine rezessiv homozygote Vererbung und eine kombinierte Heterozygotie konnen differenziert werden. Die vorliegende Arbeit fasst klinische und genetische Gemeinsamkeiten und Unterschiede des J-LN-Syndroms verglichen mit dem R-W-Syndrom sowie das diagnostische und therapeutische Management der J-LN-Patienten zusammen.

In selected patients, biventricular pacing leads to improvement in left ventricular (LV) performance, especially in the presence of pre-existing marked asynchrony of LV contraction. Improvements are sustained in the great majority of cases, and are accompanied by reduced symptoms, increased walking distance and reduced need for hospitalization. The degree of asynchrony of LV contraction and the amount of myocardial scarring are important parameters that determine the response to cardiac resynchronization therapy (CRT). Improvements in haemodynamics are due not to a positive inotropic effect of pacing but rather to elimination of an unsynchronized energy-wasting contraction pattern. Mortality trials are in progress to assess the effect of CRT on total mortality, arrhythmic mortality and mortality from heart failure.

The European Society of Cardiology has convened a Task Force on Sudden Cardiac Death in order to provide a comprehensive, educational document on this important topic. The main document has been published in the European Heart Journal in August 2001[1]. The Task Force has now summarized the most important clinical issues on sudden cardiac death and provided tables with recommendations for risk stratification and for prophylaxis of sudden cardiac death. The present recommendations are specifically intended to encourage the development and revision of national guidelines on prevention of sudden cardiac death. The common challenge for cardiologists, physicians of other medical specialties and health professionals throughout Europe is to realize the potential for sudden cardiac death prevention and to contribute to public health efforts to reduce its burden.

There is an ongoing debate whether female gender is associated with increased cardiovascular morbidity and mortality, especially after coronary interventions. The impact of gender on the outcome of patients undergoing emergency coronary artery bypass grafting (CABG) for failed PTCA was analyzed. Clinical and procedural data of all patients who underwent PTCA and subsequent emergency CABG at our institution from 1989 to 1998 were assessed. During these 10 years, 6681 PTCA procedures were performed, 1312 in women (19.6%). Subsequently, 110 patients underwent emergency CABG of whom 32 were females (29.1%). Postoperatively, 9 women and 5 men died (mortality 12.7%). Women presented with higher age (61.2 +/- 2.1 vs. 58.3 +/- 1.0 years, n.s.), smaller height (1.61 +/- 0.01 vs. 1.76 +/- 0.01 m, p0.0001), lower weight (67.7 +/- 2.4 vs. 82.1 +/- 1.2 kg, p0.0001), smaller body surface area (1.70 +/- 0.04 vs. 1.98 +/- 0.02 m2, p0.0001), and higher comorbidity as expressed by their Cleveland score (7.9 +/- 0.3 vs. 7.1 +/- 0.2, p = 0.013). The risk for failure of PTCA with subsequent emergency CABG was higher in women than in men (2.4% vs. 1.5%, p = 0.012, odds ratio 1.66) as well as for postoperative death (28.1% vs. 6.4%, p = 0.004, odds ratio 4.39). Women had longer in-hospital stays (19.7 +/- 4.2 vs. 12.9 +/- 1.3 days, p = 0.044). Logistic regression analyses found lower weight (p = 0.003), higher number of diseased coronary vessels (p = 0.024) and higher Cleveland score (p = 0.023) to be independent predictors of operative mortality. A Kaplan-Meier model (follow-up 5.3 +/- 2.5 years) showed an increased in-hospital mortality in women (p = 0.0034, log rang test), but a comparable long-term survival. Women had an increased risk for failure of PTCA and a markedly higher operative mortality after emergency CABG. In multivariate analyses, however, gender was not an independent predictor of postoperative death.

Torsade de pointes (TdP) is a serious complication which is induced by a large variety of cardiovascular and non-cardiovascular drugs. Many clinical conditions and risk factors for the occurrence of TdP during administration of drugs with a proarrhythmic potential have been identified. All such drugs have in common that they reversibly alter myocardial repolarization due to the prolongation of the action potential (acquired QT interval prolongation) which is per se not arrhythmogenic. TdP is initiated (acquired long QT (LQT) syndrome) only when a threshold level is reached leading to early after-depolarizations (EADs) and triggered beats together with a marked dispersion in recovery of excitability. The underlying mechanisms of TdP are not yet satisfactorily elucidated but, in general, alterations in cardiac ion currents which tune the normal action potential play a major role in arrhythmogenesis. Following recent advances in molecular biology and genetics, it has become clear that in some clinical instances (e.g. congestive heart failure or cardiac hypertrophy) ion channel genes become less expressed (down-regulated) and the consequent reduced ion currents (e.g. IKr) are likely to cause prolonged myocardial repolarization. In this setting, the use of drugs with action potential-prolonging properties could possibly be harmful and could not be compensated by the normal cardiac ‘repolarization reserve’. In congenital LQT syndrome some of the same ion channel components were found to be genetically altered, suggesting that either quantitative or qualitative changes of ion currents may be involved in ventricular arrhythmogenesis through similar mechanisms (‘final common pathway’). A variable clinical expressivity and, especially, an incomplete penetrance has been found in patients carrying the same LQT genotype, even when near-relatives, which raises the question on the frequency and importance of ‘silent’ (i.e. minor functional) ion channel gene mutations that may become functionally significant in presence of action potential prolonging drugs and other coexisting factors. The observation of adverse drug reactions in apparently healthy (‘normal heart’) individuals is suggestive of a genetic susceptibility for ‘acquired’ arrhythmias. This report reviews and summarizes the recent knowledge on unapparent ion channel gene mutations and preliminary concepts about ‘acquired’ arrhythmias.

The members of the Task Force on Sudden Death dedicate this paper to the memory of our former friend and colleague, Professor Ronald W. F. Campbell. Ronnie spent his life working in the field of sudden cardiac death; he contributed much and helped many. But his own life fell victim to this very problem, sadly illustrating its unexpected nature. With Ronnie’s memory in mind the Task Force has worked diligently to describe the extent of our expanding knowledge in this field, hoping that our small contribution might help to appease his sad and sudden death.

WEBER, M., et al.: Antitachycardia Pacing for Rapid VT During ICD Charging: A Method to Prevent ICD Shocks. In patients with ICDs, rapid VTs are usually treated with shocks. It is unknown, if antitachycardia pacing (ATP) delivered once for rapid VT during capacitor charging can avoid painful shocks without increasing the risk of syncope. In patients in whom rapid monomorphic VT (cycle length 300–220 ms) could be reproducibly induced during predischarge ICD testing, the success of cardioversion (defibrillation threshold plus 10 J) and a single ATP attempt (burst with 8 or 16 stimuli) was compared using a randomized crossover study design. Consciousness of the patients was checked by the signal from a button constantly pushed by the patient. In 20 patients (ejection fraction 0.50 ± 0.19) rapid VTs (253 ± 26 ms) were reproducibly induced. A single burst successfully terminated 11 (55%) of 20 rapid VTs, 6 episodes could not be terminated with a single burst pacing and 3 VTs accelerated. Rapid VTs not terminated by ATP were significantly faster than those that could be terminated (246 vs 258 ms, P = 0.026). Cardioversion (19 ± 3 J) terminated the VTs in all cases. No patient suffered syncope during rapid VTs. A single ATP may terminate rapid VT with cycle lengths < 300 ms in 55% of patients without increasing the risk of syncope. Therefore, in rapid VTs one attempt of ATP may be suitable as an additional therapy option during ICD capacitor charging to avoid painful shocks without compromise of safety. Thus, future ICDs should implement the option of ATP during charging of capacitors.

Objectives This study is designed to examine the immediate and short-term outcomes of patients who have undergone slow pathway ablation/modification for atrioventricular nodal reentrant tachycardia. Background Targeting the slow pathway has emerged as the superior form of treatment for atrioventricular nodal reentrant tachycardia. This technique has been found effective and is associated with a low complication rate. However, little is known of the long-term outcome of patients undergoing this procedure. Methods Over a 40-month period the slow pathway was targeted in 379 consecutive patients with proven atrioventricular nodal reentrant tachycardia. The case records of all patients were examined. Accurate follow-up data is available in 96% of patients a mean of 20·6 months after the procedure. Results The initial success rate was 97%. The incidence of complete heart block was 0·8% and the mean fluoroscopy duration was 27·3min. The recurrence rate was 6·9%. Age, number of pulses and fluoroscopy time were positively associated with either initial failure or recurrence. A total of 11·3% of patients were still taking antiarryhthmic medication at follow-up. Conclusions Targeting the slow pathway is an effective form of treatment for atrioventricular nodal reentrant tachycardia. The technique has a high initial success rate, a low complication rate and a low recurrence rate at long-term follow-up. Slow pathway modification is associated with similar success rates and recurrence rates as slow pathway ablation and may confer theoretical long-term benefits.

In recent in vivo studies using positron emission tomography (PET) our group demonstrated that the myocardial beta adrenoceptor (betaAR) density is reduced in arrhythmogenic right ventricular cardiomyopathy (ARVC) and idiopathic right ventricular outflow tract tachycardia (RVO-VT) associated with an increased presynaptic catecholamine washout. It was hypothesised that the reduction of myocardial betaAR density is secondary to an increase of local catecholamines in the myocardium resulting from the presynaptic dysfunction since circulating plasma catecholamines were demonstrated to be unchanged in these conditions. To further prove this hypothesis of an organ-limited adrenergic nervous dysfunction of the heart, this study aimed to investigate betaAR density in another thoracic organ, the lung.Pulmonary and myocardial betaAR density was measured in 7 ARVC patients, 8 RVO-VT patients and in a group of healthy controls (n = 13) using the non-selective beta-blocker [11C]-CGP 12177 and PET.Pulmonary betaAR density was similar in controls (12.4 +/- 1.7 pmol/g tissue), ARVC (11.6 +/- 1.7 pmol/g tissue, p = ns) and RVO-VT (12.8 +/- 2.0 pmol/g tissue, p = ns), whereas myocardial betaAR density was significantly reduced in ARVC (6.3 +/- 1.1 pmol/g tissue, p = 0.006) and RVO-VT (6.8 +/- 1.2 pmol/g tissue, p=0.02) as compared to controls (8.8+/-1.5 pmol/g tissue).The unchanged pulmonary betaAR density in the presence of a previously described significant reduction in myocardial betaAR density in the same patient principally supports our pathophysiological hypothesis that the myocardial betaAR density may be reduced in ARVC and RVO-VT because of an increase in local synaptic catecholamine levels due to an organ-limited presynaptic adrenergic dysfunction of the heart. Since in the present study only pulmonary betaAR density was measured, future functional studies excluding pulmonary betaAR desensitisation are required to finally prove the unchanged pulmonary sympathetic innervation in ARVC and RVO-VT.

Patienten, z.B. fur eine Therapie mit Antikoagulanzien, lassen sich hieraus nicht ableiten. Ein neuer moglicher Ansatz fur eine individuell abgestimmte Behandlung besteht in der Detektion zirkulierender Mikroemboli mittels transkranieller Dopplersonographie. Mit dieser Technik lassen sich kleinste gasformige oder solide Partikel im Blutstrom detektieren, die aufgrund der geringen Grose selbst nicht zu einem klinisch fassbaren thromboembolischen Ereignis fuhren. Ihr Auftreten korreliert aber nach den Ergebnissen zahlreicher Studien eng mit einem klinisch relevanten Embolierisiko. Zur Untersuchung wird ein Schallkopf am Kopf des Patienten befestigt, der dopplersonographisch Flusssignale der Arteria cerebri media erfasst. Diese werden akustisch und optisch auf zirkulierende Mikroemboli ausgewertet. In der Neurologie wird diese Methode bereits fur eine individuelle Risikostratifizierung von Patienten eines Hochrisikokollektivs eingesetzt, z.B. bei der Indikationsstellung zu einer Antikoagulanzientherapie oder Karotisendatherektomie. In der Kardiologie wird die Mikroembolus-Detektion bisher nicht routinemasig eingesetzt und wurde nur in geringem Mas durch klinische Studien evaluiert. In diesem Uberblick sollen die grundlegenden Prinzipien, die methodisch-technischen Voraussetzungen sowie Moglichkeiten und Grenzen der Mikroembolus-Detektion dargestellt werden. Weiterhin werden die wesentlichen Studienergebnisse zum Einsatz dieser Technik bei kardiologischen Erkrankungen und kardiovaskularen Interventionen zusammengefasst.

Antiarrhythmic Drug Efficacy in Patients with an ICD. There are a number of novel ways in which implantable cardioverter defibrillator (ICD) endpoints can he used in clinical trials to evaluate antiarrhythmic drugs. The advances in ICD technology (storage, retrieval, and accurate interpretation of ICD electrograms) expand the potential to include the use of an ICD endpoint as a clinical surrogate for sudden death. The ICD also provides the necessary safety net to test new drugs. The frequent need for‘antiarrhythmic drugs in patients already fitted with an ICD (e.g., for atrial fibrillation) necessitates knowledge of the drugs' effect on defibrillator threshold. There are interpretative problems and challenges associated with all types of ICD trials. A particular difficult issue is the degree to which the results of data on antiarrhythmic drug efficacy and safety acquired in the context of an ICD endpoint trial might he extrapolated to patient populations in which the device is not used. These and other challenging issues are discussed, with the goal of enhancing the design and interpretation of clinical trials featuring ICD endpoints.

Objectives The Cholesterol Lowering Atherosclerosis PTCA Trial (CLAPT) is a prospective, randomized trial with blinded angiographic end-points to assess the effect of 2-year's treatment with lovastatin initiated 4 weeks prior to PTCA, compared to usual care on non-dilated coronary segments and on dilated coronary lesions in male patients with total cholesterol between 200 and 300mg.dl−1who underwent elective PTCA. Methods and Results Two hundred and twenty six patients were randomized 4 weeks prior to PTCA to special care (diet plus lovastatin n=112) or usual care (diet; n=114). One hundred and ninety-nine patients underwent PTCA at baseline and were finally included in the study. Quantitative coronary angiographic assessment was performed on blinded cinefilms at baseline (PTCA) and repeated after 4 and 24 months in 91% and 81% of the patients. The primary end-point was a change in the mean segment diameter of non-dilated segments. The mean lovastatin dose was 33mg.day−1. Total- and LDL-cholesterol decreased by 21% and 29% in the special care group and by 7% and 11% in the usual care patients. After 2 years, the mean segment diameter of non-dilated segments decreased by 0·03mm in the usual care group and 0·004mm in the special care group ( P =0·27). The decrease in the mean segment diameter of dilated lesions was 0·17mm (usual care) and 0·06mm (special care) ( P =0·04) after 4 months; 0·16mm (usual care) and 0·002mm (special care) after 24 months, respectively ( P =0·05). In both groups, the mean segment diameter of dilated lesions increased between 4 and 24 months after PTCA compared to a decrease in mean segment diameter of non-dilated segments ( P 50% diameter stenosis at follow-up) occurred in 28·4% of usual care and 22·2% of special care patients ( P =0·17). Conclusions Lovastatin reduced the progression of dilated lesions in men with elective PTCA. Independent of treatment allocation, the dilated lesions regressed and the non-dilated segments progressed during the study follow-up. Four weeks of pre-treatment with lovastatin did not influence the rate of restenosis. Lovastatin had no statistically significant effect on non-dilated segments.

Hardware-related complications in implantable cardioverter/defibrillators (ICD) are still a common problem. Identifying underlying reasons becomes more and more difficult as the complexity of ICD systems increases. We report a patient with a dual chamber ICD (DDD-ICD) who suffered multiple complications. These included: ventricular oversensing causing inappropriate shocks and episodes of asystole; an insulation defect resulting in ineffective shocks as a consequence of a short circuit between the active can device and a defective high voltage cable; and device dysfunction requiring several hospitalizations and operative system revisions.

Lady1999199919991999 The European Society of CardiologyThe European Society of CardiologyThe European Society of CardiologyThe European Society of CardiologyThatcher: Copyright They are exactly what they say, guidelines, they are not the law. They are guidelines .Ms Baxendale: Do they have to be followed? Lady Thatcher: Of course, they have to be followed, but they are not strict law. That is why they are guidelines and not law and, of course they have to be applied according to circumstances.

Abstract —This study presents an analysis of the expression of type VIII collagen mRNA in response to cholesterol diet and balloon injury in the rabbit iliac artery. The design of the animal experiments was as follows: 28 male New Zealand White rabbits were divided into the 3 different treatment groups. Group 1 received regular chow; group 2 was fed with a 1% cholesterol diet for 6 weeks and normal chow for 5 weeks; and group 3 underwent balloon injury, then 6 weeks of a 1% cholesterol diet, which was followed by 5 weeks of normal chow. The expression pattern of type VIII collagen mRNA was compared with that of the fibrillar collagen types I and III, transforming growth factor-β1, a factor known to exert the most potent stimulatory effect on collagen synthesis in vitro, and matrix metalloproteinase 1, a collagen-degrading enzyme. The cholesterol diet resulted in an upregulation of type VIII collagen, fibrillar collagens, transforming growth factor-β1, and matrix metalloproteinase I in the adventitia. Although the number of type VIII collagen mRNA–expressing cells in the media increased, no significant difference in overall expression levels was detectable by northern blot analysis. The ratio of medial smooth muscle cells expressing type VIII collagen mRNA to those expressing type I and type III collagen mRNA (CVIII:CI:CIII) changed from 1:1.88:0.03 in the normal media to 1:0.78:0.29. When cholesterol feeding was preceded by balloon injury, type VIII collagen mRNA expression concomitant with the fibrillar collagens was further upregulated over and above that level reported after cholesterol diet alone. In general, low levels of transforming growth factor-β1 mRNA correlated with high expression of matrix metalloproteinase I. Our study indicates that a cholesterol diet resulted in a balanced reorganization of the collagen composition but did not result in marked collagen accumulation. This may provide an extracellular environment that favors migration and proliferation processes during early atherogenesis. It also demonstrates that type VIII collagen is highly expressed and deposited at later stages, and this may be linked to processes such as tissue reorganization during vascular repair and plaque stabilization.

Our knowledge on the molecular genetics of inherited cardiac arrhythmias is very recent in comparison to the advances of genetics achieved in other inherited cardiac disorders. This is related to the high mortality and early disease onset of these arrhythmias resulting in mostly small nucleus families. Thus, traditional genetic linkage studies that are based on the genetic information obtained from large multi-generation families were made difficult. In 1991, the first chromosomal locus for congenital long-QT (LQT) syndrome was identified on chromosome 11p15.5 (LQT1 locus) by linkage analysis. Meanwhile, the disease-causing gene at the LQT1 locus (KCNQ1), a gene encoding a K+ channel subunit of the IKs channel, and three other, major genes, all encoding cardiac ion channel components, have been identified. Taken together, LQT syndrome turned out to be a heterogeneous channelopathy. Moreover, the power of linkage studies to reveal the genetic causes of the LQT syndrome was also important to identify unknown but fundamental channel components that contribute to the ion currents tuning ventricular repolarization. In-vitro expression of the altered ion channel genes demonstrated in each case that the altered ion channel function produces prolongation of the action potential and thus the increasing propensity to ventricular tachyarrhythmias. Since these ion channels are pharmacological targets of many antiarrhythmic (and other) drugs, individual and potentially deleterious drug responses may be related to genetic variation in ion channel genes. Very recently, also in acquired LQT syndrome, which is a frequent clinical disorder in cardiology a genetic basis has been proposed in part since mutations in LQT genes have been specifically found. The discovery of ion channel defects in LQT syndrome represents the major achievement in our understanding and implies potential therapeutic options. The knowledge of the genomic structure of the LQT genes now offers the possibility to detect the underlying genetic defect in 80-90% of all patients. With this specific information, containing the type of ion channel (Na+ versus K+ channel) and electrophysiological alteration by the mutation (loss-of-function versus change-of-function mutation), gene-directed, elective drug therapies have been initiated in genotyped LQT patients. Based on preliminary data, that were supported by in vitro studies, this approach may be useful in recompensating the characteristic phenotypes in some LQT patients. Mutation detection is a new diagnostic tool which may become of more increasing importance in patients with a normal QTc or just a borderline prolongation of the QTc interval at presentation. These patients represent approximately 40% of all familial cases. Moreover, LQT3 syndrome and idiopathic ventricular fibrillation are allelic disorders and genetically overlap. In both mutations in the LQT3 gene SCN5A encoding the Na+ channel alpha-subunit for INa have been reported. Thus, the clinical nosology of inherited arrhythmias may be reconsidered after elucidation of the underlying molecular bases. Meanwhile, genotype-phenotype correlations in large families are on the way to evaluate intergene, interfamilial, and intrafamilial differences in the clinical phenotype reflecting gene specific, gene-site specific, and individual consequences of a given mutation. LQT syndrome is phenotypically heterogeneous due to the reduced penetrance and variable expressivity associated with the mutations. This paper discusses the current data on molecular genetics and genotype-phenotype correlations and the implications for diagnosis and treatment.

Die arrhythmogene rechtsventrikulare Kardiomyopathie (ARVCM) ist insbesondere bei jungen Patienten eine nicht zu unterschatzende Ursache ventrikularer Tachykardien (VT). Im Vordergrund der Therapie steht die Behandlung der Kammertachykardien und die Prophylaxe des plotzlichen Herztodes. Bei einzelnen Patienten mit ausgepragter und progressiver ARVCM besteht eine manifeste Herzinsuffizienz, die nach ublichen Therapierichtlinien medikamentos behandelt wird.

Atrial fibrillation, a commonly encountered arrhythmia, has in recent years, been the subject of increased interest and intensive clinical research. There is also increasing awareness that atrial fibrillation is a major cause of embolic events which in 75% of cases are complicated by cerebrovascular accidents[1,2]. Atrial fibrillation is often associated with heart disease but a significant proportion of patients (about 30%) have no detectable heart disease[3]. Symptoms, occasionally disabling, haemo-dynamic impairment and a decrease in life expectancy are among the untoward effects of atrial fibrillation, resulting in an important morbidity, mortality and an increased cost for the health care provider[4]. The Working Group of Arrhythmias of the European Society of Cardiology created a Study Group on Atrial Fibrillation in order to establish recommen-dations for the better management of this arrhythmia and to promote multicentre studies. The purpose of this paper is to briefly outline the state of our knowledge on the clinical presentation, the causes, the mechanisms and therapeutic approaches currently available and to propose recommendations for management. Although atrial flutter can coexist with atrial fibrillation, it is considered a different arrhythmia and will not be covered in the present paper.

Radiofrequency catheter ablation of a right septal accessory pathway was performed in a 66-year-old patient with incessant orthodromic atrioventricular reentrant tachycardia. Intravenous administration of flecainide, ajmaline, verapamil, and d,l-sotalol had been ineffective in controlling the tachycardia. After the ablation procedure, precordial T-wave inversion was observed during sinus rhythm. These repolarization abnormalities persisted and were suggested to represent "cardiac memory." Three days later, atrial fibrillation with a fast ventricular response developed and oral d,l-sotalol, which had been well tolerated previously on a long-term basis, was started again. However, at this time, and in the presence of the persisting repolarization abnormalities, the T waves became deeper and broader within a few hours after the introduction of d,l-sotalol. Marked QT prolongation that was paralleled by the occurrence of repeated episodes of torsade de pointes developed. Serum electrolytes were normal. Direct current cardioversion was necessary due to the degeneration of torsade de pointes into ventricular fibrillation. Further sustained arrhythmia episodes were suppressed by temporary endocardial ventricular pacing. The patient recovered without any sequela. This case demonstrates that repolarization abnormalities after catheter ablation, which may be due, at least in part, to the "cardiac memory," are not always benign but may contribute significantly to proarrhythmia.

Hintergrund: Patienten nach atrialen Umkehroperationen (Mustard- oder Senning-Operation) zur Korrektur einer Transposition der grosen Arterien (TGA) unterscheiden sich in einem wesentlichen Punkt von anderen Patienten mit kongenitalen Vitien: Der anatomisch rechte (vorne gelegene) Ventrikel fungiert bei ihnen als Systemventrikel. Da eine wachsende Zahl derart operierter Patienten das Erwachsenenalter erreicht, gewinnt die Frage, ob eine Schwangerschaft fur die so operierten Patientinnen wegen der dabei auftretenden, ausgepragten hamodynamischen Veranderungen eine Gefahrdung darstellt, zunehmende Bedeutung. Patienten: Initiiert durch die Vorstellung einer schwangeren Patientin in unserer Klinik konnten durch Literatursuche in MEDLINE weitere 26 Kasuistiken uber Schwangerschaften nach Mustard-Operation identifiziert werden. Bei den somit insgesamt 27 Patientinnen wurde uber 39 Schwangerschaften berichtet. Fetale Komplikationen: Es kam zu drei Fruhaborten im 1. Trimenon und einer Fehlgeburt in der 23. Schwangerschaftswoche. Weiterhin wurde ein elektiver Abort im 1. Trimenon durchgefuhrt. 35 Kinder (ein Zwillingspaar) wurden lebend geboren ohne kardiovaskulare Fehlbildungen. Mutterliche Komplikationen: Von den Muttern verstarb keine. Acht Patientinnen entwickelten eine therapiebedurftige Herzinsuffizienz, wobei alle drei Patientinnen mit vormals komplexer TGA (zusatzliche andere kardiale Fehlbildungen) betroffen waren. Von diesen erholten sich vier Patientinnen innerhalb der Nachbeobachtungszeit, die anderen vier Patientinnen zeigten eine anhaltende Verschlechterung ihrer korperlichen Leistungsfahigkeit oder klinische Zeichen einer Herzinsuffizienz. Als weitere Komplikationen kam es bei funf Patienten zu supraventrikularen Tachykardien und bei 22% der Patientinnen zu einer Hypertonie/Pra-Eklampsie. Schlusfolgerung: Zusammenfassend zeigt sich eine gute Prognose fur Mutter nach Mustard-Operation und ihre Kinder, ein intensives und spezielles Monitoring vorausgesetzt.

Der Nutzen einer postoperativ routinemasig durchgefuhrten Uberprufung der Defibrillationsfunktion implantierbarer Kardioverter/Defibrillatoren (ICDs) ist unklar. Um die Indikationen zu diesen den Patienten belastenden Untersuchungen zu uberprufen, analysierten wir retrospektiv 844 ICD-Teste bei 439 Systemen und 409 Patienten. 755 ICD-Teste (89,4%) waren routinemasig (57 % vor Entlassung; 43% wahrend der Nachverfolgung) durchgefuhrt worden. Auserplanmasig erfolgten 58 ICD-Teste (6,9%) nach Aufsattigung mit einem Antiarrhythmikum und 24 ICD-Teste (2,9%) nach Austausch oder Revision einer Komponente des ICD-Systems. Sieben ICD-Teste (0,8 %) wurden durchgefuhrt, weil eine Fehlfunktion des Systems vermutet wurde. Routinemasig durchgefuhrte ICD-Teste ergaben bei sechs Patienten (0,8%) eine mangelhafte Defibrillationsfunktion. Bis auf einen Patienten fanden sich bei allen jedoch bereits vor der Testung Besonderheiten, die auf einen Fehlfunktion hatten schliesen lassen konnen. Wegen einer Anderung der Antiarrhythmika-Medikation auserplanmasig durchgefuhrte ICD-Testungen ergaben bei drei von 58 Patienten (5,2%) eine mangelhafte Defibrillationsfunktion (Amiodaron: n = 2; Flecainid: n = 1). In vier von sieben Fallen (57%), in denen eine Fehlfunktion des ICD-Systems vermutet wurde, ergab die auserplanmasige ICD-Testung eine mangelhafte Defibrillationsfunktion. Nach Revision oder Austausch einer Systemkomponente zeigte der ICD-Test stets eine effektive Defibrillation. Bei 16 ICD-Testen (1,9%) traten Komplikationen auf. Am haufigsten waren unnotige Schocks (n = 10; 1,2 %). Am schwerwiegendsten waren passagere neurologische Symptome bei vier Patienten (0,48%). Somit fuhren postoperative Uberprufungen der Defibrillationsfunktion implantierter Defibrillatoren selten zu therapierelevanten Erkenntnissen. Routinemasig erscheinen die fur den Patienten belastenden und nicht komplikationsfreien Tests verzichtbar, wenn nach einer Uberprufung der Sensing-Signale bei Sinusrhythmus, der Schrittmacherreizschwelle und der Rontgen-Thoraxbilder keine Hinweise auf eine Systemdysfunktion bestehen und intraoperativ eine Defibrillationsschwelle mit einem ausreichenden Sicherheitsabstand bestand. Nach Aufsattigung mit einem Klasse-1- oder Klasse-III-Antiarrhythmikum sollte die Defibrillationsfunktion durch einen erneuten Test sichergestellt werden.

Die akute thorakale Aortendissektion ist eine potentiell lebensbedrohliche Erkrankung, die eine rasche Diagnosestellung und Therapie erfordert. In dieser Kasuistik wird uber eine 65jahrige Patientin berichtet, bei der aufgrund einer ungewohnlichen Befundkonstellation die Diagnose einer akuten thorakalen Aortendissektion erschwert wurde. Heftige Brustschmerzen und akrale Durchblutungsstorungen fuhrten bei der bis dahin gesunden Patientin zur notfallmasigen Klinikaufnahme. Die korperliche Untersuchung ergab eine Bradykardie von 40 Schlagen pro Minute, Zeichen einer Durchblutungsstorung der Akren ahnlich einer „Raynaud-Symptomatik” und eine Hypotonie mit 90/50 mm Hg. Das Aufnahme-Elektrokardiogramm zeigte bei bradykardem Sinusrhythmus eine T-Negativierung in V1 und eine geringe ST-Hebung (1 mV) in V3. Funf Stunden spater bot die Patientin eine selbstterminierende polymorphe, ventrikulare Tachykardie und einen bifaszikularen Block mit einem Rechtsschenkelblock und einem linksanterioren Hemiblock. Unter der Annahme eines akuten Myokardinfarktes wurde eine Streptokinase-Lyse durchgefuhrt. Nach hamodynamischer Verschlechterung, Intubation und Beatmung erfolgte die Verlegung in unsere Klinik. Eine Koronarangiographie zeigte den Befund einer thorakalen Aortendissektion mit Verschlus der linken Koronararterie. Die Patientin verstarb noch im Katheterlabor.

BACKGROUND New recommendations for secondary prevention of coronary heart disease (CHD) were issued by the European Society of Cardiology (ESC), the European Atherosclerosis Society (EAS) and the European Society of Hypertension (ESH) in 1994. The main objective of the EUROASPIRE study (European Action on Secondary Prevention by Intervention to Reduce Events) was to evaluate to what degree the new recommendations have been implemented and whether a significant risk factor reduction in patients who presented with CHD has been achieved. The present study was conducted in the region of Munster, Westphalia, Germany, as part of the nine-country EUROASPIRE study. METHODS A total of 524 patients (58.6 +/- 8.2 years) were included in the study by abstracting data from their medical records. According to the clinical event which led to admission to the hospital, patients belonged to the following four groups: 1) coronary artery bypass graft (CABG), 2) percutaneous transluminal coronary angioplasty (PTCA), 3) acute myocardial infarction, 4) acute myocardial ischemia. Initially, a pre-specified number of patients had been recruited with the goal of having 100 patients in each of the four groups participate in the follow-up interview and examination. At least 6 months and, on average, 20 months after hospital discharge for the acute event, 74.8% of the patients came to an interview and examination for an evaluation of their risk profile. RESULTS At the interview, 15.6% of the patients smoked, 22.7% were obese, 54.6% had blood pressure levels above 140/90 mm Hg and 31.3% a total cholesterol/HDL-cholesterol-ratio greater than 5. Risk factor modification over time was insufficient as only one-fifth of patients had values of their risk factors within the target range at the time of the interview. CONCLUSION The goals of secondary prevention have not been achieved in the region of Munster-there is clearly room for improvement. Considering the treatment of patients with CHD, the recommended strategies of secondary prevention need to be applied more intensively in clinical practice.

The aim of this study was to compare findings on coronary intravascular ultrasound and thallium-201 SPECT in patients following orthotopic heart transplantation. Background: No data are available on whether pathological thallium scintigraphic findings in heart recipients are based on coronary vessel wall alterations identifiable by intravascular ultrasound. Methods: 29 patients (mean age: 50.9 ± 11.5 years; male n = 23) were investigated by means of intravascular ultrasound of selected coronary segments and thallium-201 myocardial SPECT. Patients were investigated 11.6 ± 5.4 weeks post transplantation, a subgroup of 13 patients was re-investigated 70.2 ± 18.4 weeks following transplantation. A total of 214 cross-sectional areas of the left coronary artery were examined using a 3.5 French intravascular ultrasound catheter to measure intimai index and the circumferential extension of a three-layer appearance of the vessel wall. Shortly after catheterisation, an ergometric stress-test was performed to examine all recipients by means of thallium-201 SPECT. In each patient, 20 segments of the left ventricle were evaluated using a score system to differentiate between persistent defects, redistribution, and reverse redistribution. A score was developed that measured the degree of inhomogeneity and severity of perfusion defects, respectively. Findings on scintigraphy were correlated to coronary intravascular ultrasound findings. Results: At first investigation, mean intimai index of all evaluated coronary cross-sectional areas was 0.06 ± 0.1. Sixty-four cross-sectional areas demonstrated a three-layer appearance of the vessel wall, mean circumferential extension was 72 ± 122 degrees. Thallium scintigraphy demonstrated a total of 336 (40%) pathological left ventricular segments; 168 (20%) were regarded as permanent defects, 67 (8%) demonstrated redistribution and 101 (12%) showed reverse redistribution. The score of inhomogeneity was calculated as 5.8%±2.6%. In the subgroup of patients at the follow-up study, the score was 6.4±2.8%. There was no correlation between intimai index and the score, nor could any correlation be confirmed between the score and the circumferential extension of a three-layer appearance of the vessel wall. At second investigation, no significant differences of intimai index (0.05±0.07) or circumferential extension of a three-layer appearance of the vessel wall (74±118 degrees) could be confirmed. The score was slightly, but significantly increased to 8.1 ± 4.5% at the second investigation ( P

Background Implantable cardioverter-defibrillators (ICDs) and d,l- sotalol are widely used to treat ventricular tachyarrhythmia and ventricular fibrillation (VT/VF). The purpose of this study was to compare the long-term efficacy of d,l -sotalol and ICDs in patients with coronary artery disease. Methods and Results In a case-control study, 50 patients treated with oral d,l -sotalol were matched to 50 patients treated with ICDs. Both groups were matched for sex (82 men), age (58±10 years), ejection fraction (40±12%), extent of coronary artery disease, presenting arrhythmia, and year that treatment began. In all patients in the sotalol group, VT/VF was inducible in the drug-free electrophysiological study. Induction of sustained VT/VF was suppressed by d,l -sotalol (438±95 mg/d). In the ICD group, either VT/VF was not inducible (n=5) or inducible sustained VT/VF was refractory to antiarrhythmic drug treatment (n=45). Sotalol treatment led to a marked reduction in arrhythmic events. Whereas 83% of the patients in the sotalol group were free of sudden death and nonfatal VT at 3 years, only 33% of the ICD patients did not receive appropriate ICD therapies ( P P P =.02). Conclusions In this case-control study, ICD therapy was more effective than electrophysiologically guided antiarrhythmic treatment with d,l -sotalol in prevention of sudden death and reduction of total mortality in patients with coronary artery disease. Prospective studies are needed to confirm these results.

Objectives The primary objectives of this study were to assess the feasibility of temperature-controlled radiofrequency catheter ablation of left and right sided manifest accessory pathways in patients with Wolff-Parkinson-White syndrome and to gain more insights into biophysical aspects of temperature-controlled catheter ablation in humans. Background The electrode-tissue interface temperature and other biophysical parameters are among important variables determining the efficacy and safety of radiofrequency ablation of accessory pathways. Experimental studies have shown that radiofrequency-induced tissue necrosis can be accurately predicted by monitoring of catheter tip temperature. Methods 38 consecutive patients (14 f, 24 m; aged 42 ± 12 years) with anterograde conducting accessory pathways (left sided: n=22; right sided: n=l6) underwent temperature-controlled radiofrequency ablation (HAT 200S, Dr Osypka, Germany). The electrode temperature was monitored via a thermistor embedded into a 4 mm catheter tip. Power output was adjusted automatically during energy delivery in a closed loop system (preselected temp.: 70·1 ± 5·8°C). Results Accessory pathway conduction was successfully abolished in all patients after the delivery of 2·3 ± 2·1 radiofrequency pulses (range: 1–9, median: 2). Interruption of the accessory pathway as evidenced by loss of preexcita tion occurred after 5·9 ± 5·4 s. At the time of the interruption of the accessory pathway the catheter tip temperature measured 54·2 ± 11· 2 ° C in patients with left and 44·9 ± 5·0° C in patients with right sided accessory pathways, respectively ( P

Abstract Because measurements of hemostatic factors might aid the prediction of cardiovascular clinical events, we investigated the long-term prognostic importance of selected hemostatic factors in patients with angina pectoris. At recruitment, 209 patients underwent clinical assessment and coronary angiography, and a range of hemostatic factors were measured. During the follow-up period of 9 years, 58 patients (28%) suffered a cardiac event (acute myocardial infarction or death from cardiac causes). The risk of cardiac events was positively related to baseline measurements of fibrinogen (risk ratio per SD [RR] increase 1.29, 95% confidence interval [CI] 0.99 to 1.68, P =.06) and negatively related to antithrombin III activity measurements (RR 0.75, 95% CI 0.59 to 0.95, P =.02). No other hemostatic factor measured was significantly related to the risk of having a cardiac event. Worsening of angina in the few weeks before and ejection fraction evaluation at the initial angiography were both strongly related to the risk of cardiac events. However, the relationships of fibrinogen and antithrombin III measurements to risk remained almost unchanged after adjusting for worsening of angina and ejection fraction. Fibrinogen and antithrombin III may have an important etiologic role in the prognosis of patients with angina pectoris.

Objective: The aim of this prospective study was to analyse the yield of programmed ventricular stimulation at the right ventricular apex compared with the outflow tract. Methods: A stepwise randomized cross-over protocol of programmed ventricular stimulation with alternating stimulation at both sites was used in 66 patients who were studied because of sustained ventricular tachycardia (n = 30), ventricular fibrillation (n = 7), or non-sustained ventricular tachycardia and/or syncope (n = 29). Results: There were no significant differences between the results of stimulation from either right ventricular site with regard to the presence or absence of structural heart disease, spontaneous arrhythmia, ejection fraction or effective refractory periods. Overall, monomorphic ventricular tachycardia was inducible in 33 patients (50%); in 25 patients (75.8%), this arrhythmia was induced from both sites. However, in only 17 of these 25 patients (68%) did the induced monomorphic ventricular tachycardias have the same morphologies and similar (± 50 ms) cycle lengths. Ventricular fibrillation was inducible in 11 patients (17%), mostly by three extrastimuli (n=8; 73%). Conclusions : (1) stimulation from at least two right ventricular sites is desirable because of their independent contribution to the induction of ventricular tachyarrythmias, (2) the non-inducibility or inducibility at one ventricular site does not predict the effect at another stimulation site, (3) the effective refractory period at the right ventricular apex and outflow tract do not differ, (4) the inducibility of multiple ventricular tachycardia morphologies emphasizes the importance of documenting the cause of spontaneous arrhythmias with multiple electrocardiographic leads to ensure the correct interpretation of arrhythmias induced by programmed stimulation, (5) clinical or haemodynamic features cannot predict whether one or more stimulation sites will be required for induction of ventricular tachycardia. These results are important for the diagnostic evaluation and assessment of pharmacological or non-pharmacological interventions.

In order to assess prognosis after myocardial infarction, various methods have been used: estimation of ejection fraction, Holter monitoring, detection of ventriculur late potentials using signal-averaging techniques, programmed ventricular stimulation of the heart to test the inducibility of ventricular tachyarrhythmias, and parameters that assess heart rate variability. Left ventricular dysfunction is the major determinant for prognosis after myocardial infarction, but left ventricular end-systolic volume may be better than overall ejection fraction. The presence of an ‘arrhythmogenic substrate’ may be detected by recording low-amplitude, fractionated activity or by artificially introducing premature ventricular extrasystoles using programmed ventricular stimulation. The signal-averaged ECG represents an independent tool for risk assessment. In some studies, signal-averaging and programmed ventricular stimulution proved to be more sensitive for the prediction of sustained ventricular tachycardia than for sudden death. The risk of an arrhythmic event in patients with an abnormal signal-averaged ECG or an abnormal result of programmed ventricular stimulation is increased, although the majority of these putients still do not experience a fatal or life-threatening arrhythmia. This high number of false-positive results limits the practical applicability of the signal-averaged ECG but also of other techniques such as long-term ECG recording. Recent interest has focussed on heart rate variability, which is considered an index of sympatho-vagal interaction after acute myocardial infarction. Patients with decreased heart rate variability have a poorer prognosis than those with normal parameters. Patency of the infarct-related artery is a major factor that governs the potentially beneficial effects of thrornbolyic therapy. Many, but not all, studies have shown a reduced prevalence of late potentials after successful thrombolysis or in the presence of an open infarct-related artery. Effective thrombolytic therapy may prevent the development of an abnormal electrophysiological milieu after myocardial infarction. Finally, neurological factors such as depression have been shown to be independent risk factors for mortality after acute myocardial infurction. The role of psycho-social factors and their mechanisms of action need further attention since they open the door for behavioural modification. In conclusion, there are several promising new techniques for indentification of patients at risk of ventricular tachyarrhythmias. These techniques seem to be superior to more conventional methods such as long-term ECG monitoring as well as exercise testing. Methods which determine the arrhythmogenic substrate might be combined with a parameter of left ventricular ejection fraction because of the paramount importance of left ventricular pump function. However, due to the large proportion of false-positive results obtained with any of these methods, it seems unlikely that they will clearly surpass the others and be sufficiently accurate for risk assessment in the individual patient.

Up to now there have been no descriptions in the literature of endocardial catheter mapping and successful radiofrequency catheter ablation of the right sided accessory pathway during sustained atrial fibrillation. We attempted ablation of a right posterolateral and a right lateral accessory pathway during sustained atrial fibrillation with rapid anterograde conduction over the accessory pathway in two patients with Wolff-Parkinson-White syndrome. In both patients (aged 47 and 52 years), sustained atrial fibrillation occurred during the electrophysiological study to assess accessory pathway conduction properties. The mean ventricular rate during atrial fibrillation was 180 and 170 beats.min-1, respectively. Both patients were successfully ablated with a single radiofrequency impulse. At the successful ablation sites, a potential of the accessory pathway was consistently recorded preceding the onset of preexcitation in the surface electrogram, by 25 ms in patient 1 and 30 ms in patient 2. The unipolar electrogram recorded from the ablation catheter showed a QS morphology and the accessory pathway potential preceded the intrinsic deflection by 10 ms in both patients. Onset of the ventricular electrogram (patient 1: -20 ms; patient 2: -15 ms) and its activation time (patient 1: -15 ms; patient 2: +5 ms) in relation to the onset of preexcitation in the surface electrocardiogram also indicated the close proximity of the ablation catheter to the accessory pathway. Preexcitation disappeared within 2 s after energy application in both patients. Thus, radiofrequency catheter ablation of right sided accessory pathways during sustained atrial fibrillation is feasible and may obviate the need for medical or electrical cardioversion.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular late potentials detected at the end of the QRS complex by the signal-averaged ECG have been shown to predict arrhythmic events after acute myocardial infarction. Spectral turbulence analysis is a novel technique for detecting abnormalities of cardiac electric activation inside the QRS complex. The purpose of this study was to combine these two analysis methods in order to increase the predictive power of the signal-averaged ECG in post-infarction patients. The study comprised a prospective series of 778 males under 66 years of age who survived the acute phase of myocardial infarction. Signal-averaged ECG recordings were performed before hospital discharge 2 to 3 weeks after infarction. The original Simson method was used for recording and analysing the time-domain signal-averaged ECG. Spectral turbulence analysis was performed using the same averaged vector magnitude QRS complexes (Del Mar Avionics). During the follow-up period of 6 months, 33 patients (4.2%) had an arrhythmic event (sustained monomorphic ventricular tachycardia in 13 cases, ventricular fibrillation in eight cases and sudden cardiac death in 12 cases). The predictive power of late potentials in the time domain, spectral turbulence analysis and their combinations were tested together with clinical variables using the Cox regression method. The combination of late potentials and a spectral turbulence analysis score (one or both abnormal) had the greatest influence on the prediction of arrhythmic events: late potentials+spectral turbulence analysis (regression coefficient B=0.75; P=0.0014), Selvester ECG score >10 (B=0.44; P=0.027), history of previous infarction (B=0.49; P=0.018) and non-sustained ventricular tachycardia during long-term ECG recording (B=0.50; P=0.035). The combination of late potentials and spectral turbulence analysis reached a sensitivity of 76%, a specificity of 63%, a positive predictive value of 8% a negative predictive value of 98%) and a total predictive accuracy of 61%. Patients with late potentials and/or abnormal spectral turbulence analysis were significantly less often free of arrhythmic events compared to patients with normal findings (92% vs 98%, P