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The German Cardiac Society is the oldest national cardiac society in Europe, founded on June 3, 1927, in Bad Nauheim by Dr. Bruno Kisch and Professor Arthur Weber. They were actively supported by Dr. Franz Groedel, who together with Kisch became co-founders of the American College of Cardiology in 1949. Both Groedel and Kisch would be proud to see the fulfillment of their visions and dreams, which was commemorated at the joint session of the two societies held during the 78th annual meeting of the German Cardiac Society in Mannheim, Germany. “It is ironic that their dreadful years in Germany and their loss to German Cardiology helped to contribute to advances in American and international Cardiology,” said Dr. Simon Dack, American College of Cardiology president in 1956 and 1957. The legacy of Groedel might be reflected by his own words: “We will meet the future not merely by dreams but by concerned action and inextinguishable enthusiasm.”

There is hardly a symptom that has impressed patients and physicians since ancient times more than an irregular heartbeat. In most cases, atrial fibrillation is the cause of the rhythm disturbance. However, it took many centuries before we were able to clearly understand fibrillation and to counteract it efficiently. The history of arrhythmia therapy with drugs is long and fascinating. Digitalis was probably the first “antiarrhythmic”. It was discovered by Leonhart Fuchs in the 16th century and introduced in the clinical practice by William Withering from Birmingham. Today's rhythm agents are of a much later date. Quinidine, an optical isomer of quinine, became clinically available in 1918. Other antiarrhythmic drugs were only developed in the 60s and 70s of the previous century, e.g. disopyramide, beta-receptor blockers, propafenone, flecainide, amiodarone, adenosine, ibutilide, and dofetilide. Among the latest commercially available antiarrhythmic substances are dronedarone and vernakalant, which were clinically introduced in 2009 and 2010, respectively. Thanks to the further development of innovative pharmaceuticals and modern electrotherapeutic methods, it can be expected that the previously therapy-resistant cases of atrial fibrillation will be lastingly reduced.

Das Herz ist mit Abstand das bekannteste und seit langer Zeit identifizierte Organ. Die myogene Herzmuskelpumpschwache mit linksventrikularer Dysfunktion ist nach wie vor die Herzerkrankung mit der schlechtesten Prognose bei zunehmender Pravalenz und Inzidenz. Neben verschiedenen mystischen Behandlungsversuchen und dubioser Krautermedizin etablierte sich schon fruh der Aderlass als ein uberragendes Heilmittel, das bei nahezu allen kardialen Erkrankungen Verwendung fand. Die erste und vielleicht wichtigste Herzdroge war Digitalis, das Glykosid des roten und mehr noch des weisen Fingerhuts, im Jahr 1552 beschrieben durch Leonhart Fuchs. In den 1980er Jahren erganzten Vasodilatatoren und Inotropika die klassischen Arzneimittel Digitalis und Diuretika. In den 1990er Jahren kamen ACE-Hemmer und Betarezeptorenblocker hinzu. Um die Jahrtausendwende wurden die kardiale Resynchronisationstherapie (CRT) und Linksherzunterstutzungssysteme entwickelt; letzthin ergaben sich zellulare bzw. genetische Ansatze sowie die Xenotransplantationen. Erste Resultate mit der Stammzelltechnologie sind ermutigend, jedoch werden bis zur klinischen Anwendung – wenn uberhaupt – noch Jahre vergehen.

Organophosphate poisoning is associated with a high mortality rate due to respiratory failure, dysrhythmias, and multi-organ failure. We report two cases of survival after "in-the field" antidote treatment of very severe organophosphate poisonings. Two patients orally ingested large amounts of the organophosphorous agent oxydemeton-methyl in suicide attempts, resulting in the hypercholinergic syndrome in both. Resuscitation included early administration of antidote by emergency medical personnel as well as high-dose atropine. Plasma levels of pseudo cholinesterase were initially very low in both patients. Long-term mechanical ventilation was necessary, and both patients developed aspiration pneumonia. At discharge, no major neurological deficits were present. Prompt antidote treatment and aggressive supportive emergency and intensive care unit therapy contribute to improved survival after acute organophosphate poisoning. We believe that in cases of mass poisonings--for example, terrorist activity--therapy must be available on the scene as soon as possible. This also may require decentralized antidote storage.

If compared to two-dimensional echocardiography (2DE), myocardial contrast echocardiography (MCE) improves detection of coronary artery disease (CAD) during pharmacological stress, but data on MCE vs. 2DE during supine bicycle stress is limited. Although previous myocardial infarction (MI) influences sensitivity of 2DE, its effect on MCE has not been evaluated.The study sought to determine the incremental benefit of MCE over 2DE for evaluation of CAD during supine bicycle stress and to assess the impact of previous MI on diagnostic values of both methods.We studied 103 consecutive patients scheduled for coronary angiography. Prior to coronary angiography, all patients underwent supine bicycle stress. 2DE and MCE were performed during this stress test. The diagnosis of obstructive CAD (or =50% stenosis) was based on the presence of inducible wall motion and perfusion abnormalities.Quantitative coronary angiography revealedor =50% stenosis in 53 of 77 patients without previous MI and in 21 of 26 patients with previous MI. If compared to 2DE, MCE was more sensitive (68% vs. 86%; p0.001) and more accurate (73% vs. 86%; p0.001) to detector =50% stenosis. In patients without previous MI, 2DE and MCE yielded sensitivity of 65% and 85% (p0.01) and accuracy of 71% and 85% (p0.01), whereas in patients with previous MI sensitivity was 79% and 90% (p=NS) and accuracy 79% and 88% (p = NS), respectively.MCE enhances sensitivity and accuracy of 2DE in detection of obstructive CAD during supine bicycle stress. The incremental benefit of MCE is especially present in patients without previous MI.

There is a risk of atrial fibrillation for 1 in 4 adults over the age of 40 years. In most cases the cause of atrial fibrillation is an underlying organic disease. Approximately 2.5 million mostly elderly male patients in Europe are affected by this dysrhythmia and it is expected that the number of patients will more than double by the year 2050. With a few exceptions every form of fibrillation should be treated regarding the underlying disease, the risk of thrombo-embolization and the arrhythmogenic symptoms. However, it must be questioned whether every case of atrial fibrillation must be anti-arrhythmically treated or in which cases rate control of ventricle function is adequate or whether rhythm control, i.e. conversion into sinus rhythm, is necessary. Arguments for conversion into a sinus rhythm are improved cardiac output, decreased risk of thrombo-embolization and hypercoagulability as well as a reduction of tachycardiomyopathies. A decline in clinical symptoms leads to improvement in the quality of life and also in many cases brain function.

Vorhofflimmern ist die haufigste anhaltende Herzrhythmusstorung des Erwachsenen. Bei Vorhofflimmern ohne organisches Herzleiden gelten die 1 c-Antiarrhythmika Flecainid und Propafenon als Mittel der Wahl. Bei vorbestehender koronarer Herzkrankheit waren Betablocker als erstes anzuwenden, bei ausgepragter linksventrikularer Dysfunktion ist Amiodaron angezeigt. Bei einer Tachyarrhythmia absoluta ist zunachst eine Normalisierung der Kammerfrequenz durch den Einsatz von Kalziumantagonisten, Betarezeptorenblockern, Digitalsglykosiden oder Amiodaron sowie anderen Antiarrhythmika zur Senkung der AV-nodalen Leitungskapazitat anzustreben. Sprechen die Patienten auf die medikamentose Therapie nicht an, so steht als wirksame Masnahme die Ablation des AV-Knotens mit konsekutiver Schrittmacherimplantation zur Verfugung. – Bei der haufigen Form des anfallsweisen – also paroxysmalen – Vorhofflimmerns hat das neue Konzept der Pill-in-the-pocket-Strategie besonderes Interesse gefunden. Diese besagt, dass die in der Tasche mitgefuhrte antiarrhythmische Medikation anfallsbezogen einzunehmen ist. Das Prinzip besteht darin, bei paroxysmalem Vorhofflimmern keine dauerhafte Medikation zu verabreichen, sondern Rhythmusmittel ereignisbezogen durch den Patienten selbst einnehmen zu lassen mit dem Ziel der unmittelbaren Regularisierung der Herzschlagfolge. Hier werden vor allem Flecainid und Propafenon empfohlen. Von speziellem Interesse ist auch die Kombination von pharmakologischen und elektrotherapeutischen Behandlungsstrategien, wie sie bei der sog. Hybridtherapie Verwendung finden. Die modernen elektrischen sowie medikamentosen, in standiger Weiterentwicklung befindlichen Therapieoptionen dienen dem Ziel, den Patienten durch individuell angepasste therapeutische Masnahmen die Ruckkehr in das gewohnte soziale Umfeld zu ermoglichen, verbunden mit der gebotenen Alterskompetenz bei hoher Lebensqualitat.

Die Moglichkeiten der antiarrhythmischen Therapie von Vorhofflimmern sind heute vielfaltiger und effektiver, aber auch komplizierter als noch vor wenigen Jahren. Dies gilt gleichermasen fur die Indikation zur Therapie allgemein wie fur den Entschluss zu einer bestimmten therapeutischen Masnahme und die Kontrolle der antiarrhythmischen Behandlung selbst. Bei einer Tachyarrhythmia absoluta ist eine Normalisierung der Kammerfrequenz uber den Einsatz von Calciumantagonisten, β-Blockern, Digitalis, Glykosiden oder Amiodaron zur Senkung der AV-nodalen Leitungskapazitat anzustreben. Sprechen die Patienten auf die medikamentose Therapie nicht an, steht als wirksame Masnahme die Ablation des AV-Knotens mit konsekutiver Schrittmacherimplantation (meist VVIR-Stimulation) zur Verfugung. Bei medikamentoser Therapieresistenz und ausgepragter Symptomatik stehen auch die praventive Schrittmachertherapie sowie kathetergestutzte Ablationstechniken zu Gebote. Bei ausreichender Kenntnis der medikamentosen und interventionellen antiarrhythmischen Moglichkeiten durften therapieresistente Formen von Vorhofflimmern und Risiken der Arrhythmiebehandlung auf ein Minimum zu reduzieren sein.

An antiarrhythmic treatment was done in 56 patients with recurrent ventricular tachycardias using amiodarone. The dosage was 400 to 600 mg/d following a loading dosage of 1000 mg for 8 to 12 days. Amiodarone and desethylamiodarone concentration in serum (control group n = 33) and in erythrocyte haemolysate (control group n = 13) were determined in relapses of ventricular tachycardias (n = 7) and in pulmonary fibrosis as serious side effect (n = 3). It was shown that amiodarone levels rise continuously during loading treatment until the 8th to 12th day and that desethylamiodarone can be demonstrated after the 3rd day of treatment. The mean concentrations (+/- standard deviation) of amiodarone and desethylamiodarone were 2.21 +/- 0.89 microgram/ml and 1.3 +/- 0.74 microgram/ml in serum and 0.97 +/- 0.65 microgram/ml and 1.95 +/- 1.9 micrograms/ml in erythrocyte haemolysate. Amiodarone levels did not correlate with efficacy and with incidence of side effects. However, in pulmonary fibrosis high desethylamiodarone concentrations in serum (greater than 2.5 micrograms/ml) and in erythrocyte haemolysate (greater than 4 micrograms/ml) were found. Four out of 7 patients with recurrent ventricular tachycardia showed relatively low desethylamiodarone concentrations in serum (desethylamiodarone/amiodarone ratio less than 0.4). Thus control of amiodarone treatment can be enlarged by determination of desethylamiodarone levels as its concentrations correlate with relapses of ventricular tachycardias and serious side effects.

BACKGROUND AND OBJECTIVE Epidemiological studies have demonstrated a circadian distribution of sudden cardiac death (SD) and acute myocardial infarction (AMI), with a maximum frequency of events during the morning hours. Recently an analysis of computer recordings of implanted cardioverter/defibrillators has confirmed these findings with respect to SD. The majority of these studies concerned patients with coronary heart disease. In a prospective study we evaluated the circadian and weekly distribution of malignant ventricular tachyarrhythmias (VTA) in patients with a nonischaemic cardiac disease, namely dilated cardiomyopathy (CMP), and those with coronary heart disease (CHD). PATIENTS AND METHODS Over a mean period of 25 +/- 9 months computer-stored data and cardiac electrograms recorded from the implanted cardioverter/defibrillators (ICD) were analysed in 28 patients with CHD and 11 with DCMP. The circadian and weekly distribution of VTA was obtained, using customary arrhythmia classification and the stored and timed events. RESULTS Patients with CHD had a maximal frequency of VTA or ventricular fibrillation (VF) during the morning, with a peak between 9 and 10 o/c, while those with DCMP were at a higher risk of VTA or VF in the later afternoon and early evening. Regarding the frequency of events during the week, a significantly higher incidence of VTA was recorded on Saturdays in those with CHD, but on Mondays and Wednesdays in those with DCMP. INTERPRETATION The circadian and weekly distribution of VTA differs significantly between patients with CHD and those with DCMP. A possible reason for this difference may be different trigger mechanisms in the two types of cardiac disease, since transient ischaemia is unlikely to be the cause in patients with nonischaemic DCMP.

Incidence, type and clinical significance of cardiac involvement in advanced HIV infection was determined in 32 patients (30 men, two women; mean age 34.2 [21-52] years; mean CD4-cell number 52.2 [0-192]/microliters) over a period of 31 months. Any cardiac involvement was assessed diagnostically by one- and two-dimensional and Doppler echocardiography, complemented by other examinations and results of treatment. 14 patients (43.8%) had abnormal cardiac findings, presumably AIDS-associated. This included left ventricular pump dysfunction of various degrees of severity (n = 11), left ventricular dilatation (n = 2), pericardial effusion (n = 11), as well as cor pulmonale in primary pulmonary arterial hypertension (n = 2). In one patient the first manifestation of AIDS was tubercular pericarditis; in two patients there was a likely connection to disseminated pneumocystis infection and toxoplasmosis, respectively. In 11 patients no specific cause was found for the cardiac involvement. Nine of the 14 patients (64%) had symptoms due to the cardiac involvement. These findings indicate that the incidence and clinical significance of cardiac involvement must be taken into account in any treatment concept for AIDS.

The efficacy of ajmaline (50-75 mg i.v.) or lidocaine (100-200 mg i.v.) in terminating persistent, haemodynamically stable ventricular tachycardia (VT) was compared in a prospective, randomized trial of 31 patients. There were no significant differences as to age, underlying heart disease, ejection fraction and rate of ventricular tachycardia between the two treatment groups. Ajmaline terminated VT in 10 of the 15 patients receiving it, lidocaine in only 2 of 16 (P less than 0.01). The frequency of VT was not significantly changed by lidocaine, while mean cycle length during VT changed under ajmaline from 369 +/- 82 ms to 452 +/- 11 ms (P less than 0.01). In contrast to lidocaine, QRS duration under ajmaline lengthened from 166 +/- 18 ms to 200 ms +/- 28 ms (P less than 0.01), but return cycles after tachycardia termination were similar (ajmaline, 863 +/- 296 ms; lidocaine, 917 +/- 367 ms). Both drugs were equally well tolerated, but in this series ajmaline was more effective in the acute treatment of persistent VT.

In einer randomisierten Doppelblindstudie bei 116 Patienten mit leichter bis mittelschwerer chronischer Herzinsuffizienz (NYHA II-III) wurde die Wirksamkeit einer Kombination von Captopril und Diuretika (Gruppe I) mit der einer Kombination von Digitalis und Diuretika (Gruppe II) verglichen. Die Therapie wurde uber zwolf Monate mit einer Kombination von 50 mg Captopril (zweimal 25 mg/d per os) oder 0,2 mg Digoxin (zweimal 0,1 mg/d per os) und Hydrochlorothiazid (HCT) durchgefuhrt. In einer Vorbehandlungsphase uber 3-4 Wochen erhielten die Patienten der Gruppe I eine mittlere HCT-Dosis von 37,7 mg, in der Gruppe II von 34,9 mg taglich. Nach 12 Monaten waren in Gruppe I der echokardiographisch bestimmte Ventrikeldurchmesser und die Belastungstoleranz gegenuber den Ausgangswerten sowie im Vergleich mit Gruppe II signifikant gebessert. Die klinische Bewertung der Herzinsuffizienz nach der NYHA-Klassifizierung zeigte in Gruppe I eine Verbesserung um im Mittel einen Schweregrad bei 51,8 % (n = 61) und in Gruppe II bei 40,7 % (n = 47) (P

Lymphocyte subpopulations in peripheral blood and bronchoalveolar lavage fluid (BAL) were examined in 29 patients with AIDS (26 men, three women; median age 32 [16-55] years). Patients in group 1 (n = 12) had no lung disease, in group 2 (n = 11) had Pneumocystis carinii pneumonia, in group 3 (n = 6) had other lung disease. There were 13 men and two women (median age 48 [21-80]) in the control group (bronchoscoped for mild pulmonary symptoms: no abnormal findings in the BAL). Compared with the control group, patients with AIDS had a significant deficiency in helper cells, both in blood (7-23% vs 50%; P < 0.01) as well as in the BAL (7-24% vs 52%; P < 0.001). There was a correlation of the percentage helper cell proportion in peripheral blood and BAL (for both group 1 and 2, rs = 0.75; P < 0.05). The proportion of helper cells in peripheral blood and BAL in AIDS patients was significantly lower in those with than without lung disease (group 1: 23% blood, 24% BAL vs group 2: 9% blood, 7% BAL; group 3: 7% blood, 7% BAL; P < 0.02 blood, P < 0.004 BAL). The percentage proportion of suppressor cells was greater in both blood and BAL in AIDS patients (group 1: blood 47%, BAL 63%; group 2: blood 44%, BAL 76%; group 3: blood 52%, BAL 75%) than in the controls (blood 28%, BAL 33% [P < 0.01], but there was no correlation between peripheral blood and BAL. In addition, the absolute number of suppressor cells in the lavage (30 cells/microliters in group 1 and 3, 65 cells/microliters in group 2) was significantly higher than in the controls (8 cells/microliters).--In AIDS patients there occurs a lymphocytosis in the BAL, while in blood there is a lymphopenia. The concordant decrease in helper cells in blood and BAL is decisive for the severity of any pulmonary infections.

In eleven patients serum levels of amiodarone and its desethyl metabolite were determined after a single dose of 400 mg amiodarone given with and without subsequent administration of colestyramine. In addition, the elimination half-life was measured in three patients after discontinuation of long-term amiodarone therapy. Mean serum levels of amiodarone at 7 1/2 hours after dosing (n = 11) were 0.42 +/- 0.11 micrograms/ml without colestyramine and 0.21 +/- 0.14 micrograms/ml with colestyramine (P less than 0.01). Elimination half-life after discontinuing long-term amiodarone therapy (n = 3) was 23 1/2, 29 and 32 days, respectively (half-life in eight controls: 35-58 days). The results indicate that colestyramine significantly reduces the enterohepatic circulation of amiodarone. Therefore, colestyramine should be capable of accelerating the regression of dose-dependent side-effects of amiodarone by enhancing its elimination.

A 53-year-old man known to have Wolff-Parkinson-White syndrome suffered an acute posterior-wall myocardial infarction. Despite successful thrombolysis treatment with streptokinase he continued to have attacks of supraventricular tachycardia with angina. The ECG showed a short P-R interval and pre-excitation with positive delta waves in leads V1-6, as well as signs of re-infarction. The tachycardias could not be satisfactorily suppressed by drug treatment. Coronary angiography revealed triple vessel disease. During this investigation ventricular extrasystoles occurred which initiated orthodromic supraventricular tachycardia and angina, as well as monophasic S-T elevations in leads II, III and aVF. This provided the indication for immediate high-frequency catheter ablation left laterally at the mitral anulus after a left-lateral accessory conduction pathway had been identified. Three days later the stenoses of the circumflex and anterior interventricular branches were dilated. The patient has been free of symptoms for 3 months and can exercise up to 150 W. The tachycardias have not recurred.

Systemic peripheral resistance, right and left heart pressures, cardiac output and left ventricular ejection fraction were measured in 12 patients with severe heart failure (stages III-IV of the NYHA), before and after intravenous injection of indoramin (0.2-0.4 mg/kg bodyweight). Peripheral resistance decreased from a mean of 2738.5 to 1294.4 dyn X s X cm-5 (P less than 0.001), mean pulmonary artery pressure from 39.4 to 21.4 mm Hg (P less than 0.001), mean aortic pressure from 105.3 to 86.0 mm Hg (P less than 0.001), left ventricular end-diastolic pressure from 35.3 to 18.3 mm Hg (P less than 0.001), arterio-venous oxygen difference from 36.1 to 25.4% (P less than 0.001), while cardiac output rose from 2.1 to 3.3 l X min-1 X m-2 (P less than 0.001), and the ejection fraction increased from 29.0 to 42.5% (P less than 0.001). Heart rate remained nearly unchanged. There were no significant side effects, such as hypotension or arrhythmias. The results indicate that the parenteral injection of indoramin favourable influences haemodynamic parameters of patients in severe heart failure.

History and clinical findings A 78-year-old patient experienced dizziness, impairment of mnemic and cognitive function, chronic fatigue and recurrent syncope. Investigations Hypertensive heart disease, reduced left ventricular function, and ventricular ectopia classification Lown IVb was documented. Computed tomography showed minimal brain atrophia. Stenoses of the brain supplying arteries and of other intracranial diseases were excluded. A distinct correlation between cardiac output and cerebral blood flow in correspondence to changes of heart rate were found (cardiac output 4.2 l/min during sinus rhythm, 7.4 l/min during temporary atrial pacing--AAI-Mode with a pacing rate of 90/min; 4.8 l/min--AAI-Mode with a pacing rate of 120/min; cerebral blood flow: 70, 74 and 62 ml/100 g per minute, respectively). Thus, impairment of cerebral blood flow autoregulation can be assumed. Treatment and course After implantation of a permanent pacemaker the patient was without any complaints. The mnemic and cognitive function improved, dizziness and fatigue disappeared. Synopsis did not occur. 14 months later a sudden onset of complaints occurred caused by atrial fibrillation (heart rate 120/min). Cardiac output and cerebral blood flow were now 4.0 l/min and 35 ml/100 g per minute. After antiarrhythmic drug therapy and restoration of sinus rhythm cardiac output and cerebral blood flow increased and the complaints disappeared again. Conclusion In patients with impaired capacity of cerebral autoregulation a reduced cardiac function and output can induce a reduction of cerebral blood flow. Thus, impairment of mnemic and cognitive function as well as other unspecific neurological deficits can be caused. In these cases pacemaker therapy has to be discussed as an effective therapeutical concept.

BACKGROUND AND OBJECTIVE There is an increasing number of pointers towards a causative connection between Chlamydia pneumoniae and atherosclerosis. But the pathogenetic mechanism and intimal structures that are involved remain unclear. Starting with the hypothesis of a chronic infection, as demonstrated by the presence of the chlamydial stress (heat-shock) protein 60 (HSP 60), the presence and localization of these bacterial products in coronary atheromas was investigated. PATIENTS AND METHODS Coronary atheroma tissue from primary stenoses in 42 patients (36 men, 6 women, mean age 60.2 +/- 7.3 years) was studied immunohistochemically in the course of a retrospective analysis for chlamydial HSP 60. The findings in clinically acute coronary syndrome (Braunwald's classification) present in 27 patients were compared with those in 15 patients with acute angina and evaluated in relation to expression and site of predilection. RESULTS An immune reaction to chlamydial HSP 60 was demonstrated in 27 of 42 atheromas (64%). Intact, non-atherosclerotic vessels, such as the mammary artery and sphenous vein, showed no such signals. Chlamydial HSP 60 was localized in maximally 23% of all plaque cells, mostly in macrophages/foam cells, more rarely in smooth muscle cells. Chlamydia in foam cells most often revealed ultrastructural patterns that pointed to the persistence of the pathogen. Sites of predilection of chlamydial HSP were predominantly foam cell areas and cell-poor regions, more rarely inflammatory infiltrates and areas of rupture. When comparing both types of lesion, signals for chlamydial HSP 60 were present in 21 of the 27 atheromas (78%) with unstable angina or acute myocardial infarction, but in only 6 of the 15 atheromas (40%) with stable angina. Within the group with the acute coronary syndrome, the prevalence of chronic chlamydial infection was independent of a previous myocardial infarction. CONCLUSIONS Chlamydial HSP 60 can often be demonstrated in primary coronary stenosis of symptomatic patients. It is most frequently found in macrophages/foam cells and is highly prevalent in the acute coronary syndrome. In-situ findings suggest a pathogenetically relevant role of chronic persistent infection of Chlamydia pneumoniae in unstable coronary plaques.

BASIC PROBLEM AND OBJECTIVE Untreated patients with obstructive sleep apnoea (OSA) have an increased risk of death from cardiovascular (cv) disease. This study was undertaken to determine the disease spectrum in patients with sonographically proven OSA (apnoea-hypopnoea index > or = 5), with special reference to cv risk factors and accompanying diseases in relation to the severity of their respiratory abnormalities. The study's aim was to clarify what risk factors and accompanying diseases were associated with different degrees of OSA. PATIENTS AND METHODS A systematic recording of cv risk factors and accompanying diseases as well as their association to the severity of nocturnal respiratory disorders was made for 175 patients (165 men, 10 women, mean age 54 +/- 10.2 years) with sonographically proven OSA (mean apnoea-hypopnoea index 37 +/- 24.4). RESULTS The body mass index (BMI) was significantly related to the severity of the respiratory disorder (apnoea-hypopnoea index, AHI, P or = 20). The incidence of left ventricular hypertrophy rose with an increasing severity of nocturnal OSA. CONCLUSION These data indicate that in patients with high-grade OSA (AHI > or = 20) there is a further grouping together of cardiovascular risk factors, namely increasing body weight, diabetes mellitus, arterial hypertension and left ventricular hypertrophy; they explain the increased mortality rate among these patients from vascular complications.

History and clinical findings A 67-year-old man with chronic obstructive pulmonary disease (COPD) for many years and a heavy smoker was hospitalized because of increasing dyspnoea and moderately productive cough. His general condition was clearly impaired. He was markedly cyanotic, he had a barrel-shaped chest, and there were wheezing rhonchi throughout the lung. Body temperature was 37.8 degrees C. He had mild ankle oedema. The preliminary diagnosis was exacerbation of the COPD with global respiratory failure. Tests There was severe hypoxaemia (pO2 48 mm Hg) with hypercapnia (pCO2 46 mm Hg). Vital capacity was reduced to 1.81, one-second forced expiratory volume 0.91. Chest radiograph revealed multiple nodular opacities, such as seen in bronchial carcinoma with metastases. But computed tomography showed fluid-filled bronchi. Bronchoscopy demonstrated large amounts of dirty-white, sticky secretions as high up as the trachea, confirming the preliminary diagnosis. Klebsiella oxytoca and haemophilus influenzae were cultured from the secretions. Treatment and course Immediate administration of amoxycillin and clavulanic acid (2.2 g daily) quickly led to clinical improvement. Chest x-ray was normalized after 10 days. But long-term oxygen treatment was instituted because of persisting resting hypoxaemia (pO2 46 mm Hg), after which he was discharged free of dyspnoea. Conclusion To clarify nodular pulmonary opacities in a chest radiograph computed tomography should be performed before bronchoscopy.

Transvenous electrical ablation of AV conduction was performed in 15 patients with drug-resistant supraventricular tachycardia. Eight patients had paroxysmal AV nodal reentry tachycardia, one had permanent junctional reentry tachycardia, five had recurrent atrial flutter and one paroxysmal atrial tachycardia. The intracardiac ablation was done with 150-350 J, on average twice per patient. Permanent 3 degrees AV block was achieved in ten patients, in none of whom there was a recurrence of the tachycardia. In four patients with re-established AV conduction the clinical symptoms had nonetheless improved; despite repeated use of His-bundle ablation, permanent junctional reentry tachycardia could not be controlled satisfactorily and required surgical section of the accessory pathway. Apart from septic fever in one patient there were no serious complications. Implantation of a pacemaker, however, was required in all those patients in whom a permanent 3 degrees AV block had been produced. For this reason alone, His-bundle ablation should only be used in drug-refractory supraventricular tachycardias. But in these this method presents an important advance in treatment.

Quality of life after implantation of an automatic implantable cardioverter/defibrillator (ICD) was assessed by questionnaire in 43 patients (38 males, 5 females; mean age 57 +/- 16 years) with treatment-resistant symptomatic ventricular arrhythmias. 37 of the 43 patients felt better after ICD implantation. 23 were always conscious of having an ICD, but 18 had got used to it in less than 2 months. 15 patients reported being afraid of an ICD shock, while eight noted physical discomfort caused by the ICD. Limitations concerning their professional, recreational and social activities were reported by six patients. 41 of the 43 patients confirmed that the ICD had been helpful, enabling 23 to return to an active life. 42 would recommend implantation to others if indicated. These data demonstrate that there is a remarkably high degree of acceptance of the ICD. Survival rate after implantation is thus not the only criterion of success. All aspects of the quality of life should be taken into consideration before implantation is decided upon.

Forty-two patients (6 women, 36 men; mean age 55 [39-69] years), with one-, two- or three-vessel disease on coronary angiography, were studied using single-photon emission computer tomography with 15-p-123I-iodophenyl-pentadecanoic acid (IPPA), in order to evaluate this new method of demonstrating abnormalities of myocardial perfusion. The reference range for fatty acid turnover was determined in eleven controls (4 women, 7 men; mean age 41 [20-51] years) with no coronary stenosis. 185 MBq (5 mCi) of IPPA was administered intravenously during submaximal stress on a bicycle ergometer. Comparison between different regions of the tomograms revealed changes in fatty acid utilization typical of ischaemia. The sensitivity, specificity and predictive value of a positive result compared with coronary angiography were 95%, 89% and 93%, respectively, for the area supplied by the anterior interventricular artery, 92%, 91% and 93% for the circumflex branch and 89%, 91% and 90% for the right coronary artery. In 25 out of 31 patients (81%) with myocardial infarction, IPPA scintigraphy infarct localization agreed with the clinical findings. In two cases with unremarkable scintigrams left ventriculography showed hypokinesia, while in four cases neither method demonstrated any abnormality. There was one false-positive scintigram. IPPA scintigraphy has greater sensitivity and specificity than conventional nuclear medicine techniques in the demonstration of coronary heart disease.

Various parameters relating to the radio-frequency ablation of accessory pathways were studied in 53 patients (27 males, 26 females: mean age 38.5 [14-64] years) with a history of paroxysmal tachycardia (over 1 month to 50 years), shown to be caused by an accessory pathway (Wolff-Parkinson-White syndrome). In all patients the following values were obtained: (1) number of procedures necessary to achieve permanent blockage of the accessory pathway (1-4); (2) duration of each procedure (45-420 min); (3) duration of fluoroscopy (5-102 min); (4) number of necessary radio-frequency applications (1-48); and (5) cumulative energy per procedure. To ablate left-lateral pathways (n = 10) required fewer procedures, shorter duration per procedure, shorter fluoroscopy time, fewer current applications and less total energy than coagulation of right-sided pathways (n = 10). Those various parameters were greatest for ablation of septal and para-septal pathways (n = 9). Pathways which conducted only retrogradely (n = 15) were more difficult to ablate than those with anterograde conduction (n = 38). There were two complications. In one case a tension pneumothorax occurred after faulty puncture of the subclavian vein; in the other, the left ventricle was perforated causing an acute tamponade which required pericardiocentesis with subsequent suture closure of the perforation. It is concluded that, in principle, all accessory pathways, regardless of their conduction potential and site, can be ablated by a radio-frequency current.

Muscle potentials as a cause of pacemaker malfunction are often unrecognized, because control examinations are usually performed without physical exercise. Two observations are cited to illustrate how malfunctioning of different modes of stimulation can be caused by interference from muscle potentials. In addition to the known suppression of impulse production, fixed-rate stimulation may occur. These observations indicate that pacemaker function should be tested also during physical activity. Any malfunction can almost always be stopped by re-programming amplifier sensitivity.

BACKGROUND AND OBJECTIVE There is seroepidemiologic and experimental evidence for a link between Chlamydia (C.) pneumoniae and arteriosclerosis. However, the clinical importance and the pathogenic pathways implicated remain unclear. In the present study, we sought to evaluate the presence and the location of C. pneumoniae in coronary atheroma, as well as a potential prevalence with unstable versus stable angina. PATIENTS AND METHODS Retrospectively, coronary plaque material of primary lesions from 51 consecutive patients (44 men, 7 women, mean age 59.6 +/- 9.4 years) was examined for the presence of C. pneumoniae by use of immuno-histochemistry and transmission electron microscopy. The findings associated with clinically acute coronary syndrome according to Braunwald's classification (n = 31) were compared to those with stable angina (n = 20) and regarded for potential relations to characteristic intimal features. RESULTS Immunoreaction for C. pneumoniae was found in 32 of 51 (63%) coronary plaques. Signals (% prevalence of specific intimal features) were present with necrotic areas (40%), sparse cellularity (40%), neo-vascularization (29%), thrombi (20%), ruptured plaque areas (19%), and fields rich in foam cells and calcifications (13%). Intimal hyperplasia and inflammatory infiltrates showed no signals. As the central finding in this report, C. pneumoniae immunoreaction was more frequently (P < 0.001) found in 26 of 31 (84%) lesions associated with unstable angina or acute myocardial infarction, compared to 6 of 20 (30%) lesions with stable angina (P < 0.001). Intact vessels devoid of arteriosclerotic disease, such as mammarial arteries and saphenous veins, were without C. pneumoniae signals (negative controls). Ultrastructurally, chlamydial elementary bodies were found in foam cells and phagocytosing macrophages, also in fragmented extracellular matrix adjacent to apoptotic and necrotic intimal cells. CONCLUSIONS Chlamydiae pneumoniae were detected in 32 of 51 (63%) coronary primary lesions of symptomatic patients. Most importantly, there was a highly significant prevalence of lesions associated with acute coronary syndrome. Predilection sites of C. pneumoniae were areas that revealed small healing activity and (or) propensity to plaque rupture. The present in situ findings indicate a pathogenic role of Chlamydiae pneumoniae in human (coronary) plaque rupture.

AIM OF STUDY: To investigate how medical permission to drive in patients with a cardioverter defibrillator is handled in various European countries. METHODS: A specially developed questionnaire was sent to all 46 delegates of the pacemaker groups of the European Society of Cardiology. They were asked to provide information on the procedures and criteria used in the various countries regarding a driving ban after cardioverter defibrillator implantation (ICD). RESULTS: 39 answers (83%) were received from representatives of 24 countries. 22 (56%) of those replying advised their patients not to drive. A permanent driving ban was recommended by 13 (33%), a temporary one of 3-18 (mean 9 +/- 4) months by 26 (67%). Presyncope was named as a criterion for a ban by 15 (38%), syncope by 13 (33%) and multiple defibrillator shocks by two (5%). Contrary to medical advice not to drive about one third of patients resumed driving, half of them after 6 months. 12 months after implantation most of the patients were again driving. Defibrillator discharges occurred in 2 patients, without consequence. One patient had a fatal car accident, unrelated to loss of consciousness or defibrillator shock. CONCLUSIONS: 1. ICD discharges are an extremely rare cause of driving accidents. 2. About half of the cardiologists recommended a driving ban for a mean of 9 months after ICD. 3. Despite medical ban about half of the patients resumed driving after 6 months. 4. There are as yet no uniform criteria in Europe for judging fitness to drive. Language: de

HISTORY AND CLINICAL FINDINGS A 68-year-old woman was hospitalized because of fever and tiredness for 3 months. Her general condition was clearly impaired. She had a mild fever of 38.5 degrees C and on auscultation a 3/6 systolic murmur, maximal parasternally in the 3rd intercostal space, transmitted to the apex. There were distant râles over both lungs, the neck veins were distended and there was ankle oedema. INVESTIGATIONS C-reactive protein was raised to 17.3 mg/dl (normal up to 0.9 mg/dl), WBC count 19,300/microliter. beta-haemolysing streptococcus (S. agalactiae) was grown in the blood culture. The ECG showed sinus tachycardia (rate of 98/min) and transthoracic echocardiography demonstrated a small pericardial, enlarged ventricles, marked mitral regurgitation and a large vegetation on the posterior mitral leaflet, as well as a 3 x 4 cm mass in the posterior wall of the ventricle, originating from the posterior mitral valve ring and communicating with the vegetation on the mitral valve. The posterior mitral leaflet was perforated. TREATMENT AND COURSE As endocarditis of the mitral valve with a complicated course was suspected-abscess of the posterior mitral valve ring and septic myocardial aneurysm with associated pericarditis and haemodynamically insignificant effusion-she was transferred to the intensive care unit where she died suddenly of circulatory arrest only 30 min after transfer. Autopsy confirmed the echocardiographic findings. CONCLUSION Paravalvular abscess in the course of mitral valve endocarditis is rare, but should be looked for at transthoracic echocardiography so that any necessary surgical intervention can be undertaken early.

PURPOSE To evaluate the independent prognostic impact of the chest radiograph for mortality from community-acquired pneumonia requiring hospitalization. METHODS Chest radiographs of 67 patients with hospital-treated community-acquired pneumonia were analyzed with regard to the prognostic implications of radiographic patterns, extent and density of infiltrates, and its evolution during treatment. RESULTS Non-survivors had a significantly higher extent of infiltrates (p = 0.008), density of infiltrates (p = 0.05), and radiographic spread during follow-up within 48-75 hours (p = 0.0001). In multivariate analysis, persistent or progressive infiltrates were associated with a 47-fold increase, and persistent or progressive density of infiltrates with an 18-fold increase in risk of mortality. The presence of both parameters could correctly predict 96% of survivors and 90% of non-survivors. CONCLUSIONS The chest radiograph is an independent predictor of the severity of pneumonia. Both persistent or progressive infiltrates and persistent or progressive density of infiltrates are independently associated with mortality from community-acquired pneumonia.

BACKGROUND Patients with atrial fibrillation (AF) often exhibit abnormalities of P wave morphology during sinus rhythm. We examined a novel method for automatic P wave analysis in the 24-hour-Holter-ECG of 60 patients with paroxysmal or persistent AF and 12 healthy subjects. METHODS Recorded ECG signals were transferred to the analysis program where 5-10 P and R waves were manually marked. A wavelet transform performed a time-frequency decomposition to train neural networks. Afterwards, the detected P waves were described using a Gauss function optimized to fit the individual morphology and providing amplitude and duration at half P wave height. RESULTS >96% of P waves were detected, 47.4 +/- 20.7% successfully analyzed afterwards. In the patient population, the mean amplitude was 0.073 +/- 0.028 mV (mean variance 0.020 +/- 0.008 mV(2)), the mean duration at half height 23.5 +/- 2.7 ms (mean variance 4.2 +/- 1.6 ms(2)). In the control group, the mean amplitude (0.105 +/- 0.020 ms) was significantly higher (P < 0.0005), the mean variance of duration at half height (2.9 +/- 0.6 ms(2)) significantly lower (P < 0.0085). CONCLUSIONS This method shows promise for identification of triggering factors of AF.

Die Moglichkeiten der antiarrhythmischen Therapie von Vorhofflimmern sind heute vielfaltiger und effektiver, aber auch komplizierter als noch vor wenigen Jahren. Dies gilt gleichermasen fur die Indikation zur Therapie allgemein wie fur den Entschluss zu einer bestimmten therapeutischen Masnahme und die Kontrolle der antiarrhythmischen Behandlung selbst. Bei einer Tachyarrhythmia absoluta ist eine Normalisierung der Kammerfrequenz uber den Einsatz von Calciumantagonisten, Betablockern, Digitalis, Glykosiden oder Amiodaron zur Senkung der AV-nodalen Leitungskapazitat anzustreben. Sprechen die Patienten auf die medikamentose Therapie nicht an, steht als wirksame Masnahme die Ablation des AV-Knotens mit konsekutiver Schrittmacherimplantation (meist VVIR-Stimulation) zur Verfugung. Bei medikamentoser Therapieresistenz und ausgepragter Symptomatik stehen auch die praventive Schrittmachertherapie sowie kathetergestutzte Ablationstechniken mit linearen atrialen Lasionen oder Isolation von Pulmonalvenenarealen bei fokal induziertem Vorhofflimmern zu Gebote. Bei ausreichender Kenntnis der medikamentosen und interventionellen antiarrhythmischen Moglichkeiten durften therapieresistente Formen von Vorhofflimmern und Risiken der Arrhythmiebehandlung auf ein Minimum zu reduzieren sein.

Der implantierbare Cardioverter/Defibrillator (ICD) ist das einzige Therapiemodul, welches eine lebensbedrohliche ventrikulare Tachyarrhythmie erkennen und den hierdurch hervorgerufenen plotzlichen Herztod durch eine Elektrostimulation oder -schockabgabe verhindern kann. Aufgrund zahlreicher aktueller Studienergebnisse haben sich die Indikationen fur die Primar- und Sekundarpravention erheblich gewandelt. Nach adaquater Identifikation eines Risikopatienten kann durch die Implantation eines ICD die kardiale und daruber hinaus die Gesamtmortalitat positiv beeinflusst werden. Eine genaue Kenntnis der Parameter, die zur Erkennung solcher Risikopatienten fuhren, ist essenzieller Bestandteil des diagnostischen Vorgehens. In der vorliegender Arbeit werden klare Ablaufe der notwendigen Voraussetzungen und der Wahl des ICD-Aggregates vorgestellt, um dem im Alltag tatigen Internisten strukturierte Vorgehensweisen fur eine adaquate Therapie seiner Patienten an die Hand zu geben.

Echocardiography is an established method to estimate left-ventricular mass (LVM) in mice. Accuracy is determined by cardiac size and morphology and influenced by mathematical models. We investigated accuracy of three common algorithms in three early developmental stages. High-resolution echocardiography was performed in 35 C57/BL6-mice. Therefore, two-dimensional-guided M-mode echocardiography and parasternal short- and long-axis views in B-mode were obtained. LVM was assessed in vivo applying Penn (P), Area Length (AL), and Truncated Ellipsoid (TE) algorithms and validated with histomorphometry. Regression analysis of all mice showed fair estimation of LVM assessed with M-mode-based Penn algorithm (y = 0.6*x - 0.12, r: 0.71). In contrast two-dimensional assessment of LVM revealed close linear relationship with histomorphometry (y(AL)= 1.21*x - 12.1, r: 0.88, y(TE)= 1.38*x - 2.88, r: 0.86). Bias was lowest for LVM-AL at diastole underestimating 3.2%. In concordance with the summarized data, LVM-P revealed lower regression coefficients and significant underestimation in all three subgroups. Small hearts (

Background The population of patients likely to respond to selected pacing algorithms for maintenance of sinus rhythm is unknown. Objectives The purpose of this study was to identify patients with specific onset patterns of paroxysmal atrial fibrillation (AF). Methods Dual-chamber pacemakers with advanced diagnostic functions were implanted in 112 patients with conventional indications for antibradycardia pacing and a history of paroxysmal AF. Pacemaker diagnostic data were analyzed after 97.5 ± 40.9 days. According to the frequency of premature atrial contractions (PACs) during the 5 minutes before AF onset, patients were assigned to one of three groups: group A (high PAC activity), group B (moderate PAC activity), or group C (low PAC activity). Results AF burden was lower in group A (4.6% ± 2.4%) than group B (15.8% ± 3.0%, P = .003) and group C (15.5% ± 3.1%, P = .003). Fewer AF episodes occurred in group A (2.1 ± 1.3 per day) than group B (3.8 ± 1.2 per day, P = .006). Mean AF episode duration was shorter in group A (11.4 ± 10.2 hours) than group C (41.4 ± 27.5 hours, P = .03). Conclusion The coincidence of low PAC activity before AF onset, high AF burden, and extended arrhythmia episode duration appears to be the consequence of a high atrial substrate factor. In these "substrate fibrillators," the efficacy of pacing algorithms for maintenance of sinus rhythm may be limited. In contrast, "trigger fibrillators" exhibiting low AF burden despite high PAC incidence may represent the target population for specific PAC-suppressing pacing algorithms.

Aims Amiodarone is one of the most efficient and safe antiarrhythmic drugs in the treatment of atrial fibrillation (AF). Although pro-arrhythmic effects of amiodarone therapy are rare, the aim of the present study was to identify clinical constellations which may lead to amiodarone-associated pro-arrhythmia. Methods and results Sixty-three consecutive patients (pts) (49 males; 64+ 10.3 years; 35 with coronary heart disease, 17 with lone AF) were retrospectively included in this study. All received an oral (92.1%) or iv (7.9%) loading dose of amiodarone for the treatment of AF. Cardiac diseases, concomitant medical treatment, and incidence of pro-arrhythmic effects were analysed. Three pts (4.8% of the total population) developed a clinical relevant, polymorphic ventricular tachyarrhythmia, 3–48 h after initiation of amiodarone loading. Coronary heart disease was present in all of these pts, and in two of them left ventricular ejection fraction was severely reduced. The mean QTc in these pts was only slightly prolonged; mean heart rate was significantly decreased compared with the total study population (61.0+ 7.5 vs. 74.5+ 24.1 bpm; P � 0.05). In all pts with pro-arrhythmia, amiodarone (two pts iv, one patient oral) was initiated during concomitant beta-blocker/digitalis therapy. Twenty-five per cent of the patients receiving this ‘triple’ therapy developed ventricular arrhythmia. Conclusion The present study implies that initiation of amiodarone therapy in pts with structural heart disease and AF that are concomitantly treated with beta-blockers and digitalis may have an increased risk of amiodarone-associated pro-arrhythmia.

Background: Patients with atrial fibrillation (AF) and atrial thrombi have an increased risk for cerebral embolism. However, there is little knowledge about the long-term fate of atrial thrombi and the incidence of cerebral embolism in patients under oral anticoagulation. Methods: Consecutive patients with persistent or permanent AF and left atrial (LA) thrombi were included in the study. We performed serial and prospective transesophageal echocardiography, cranial magnetic resonance imaging, and clinical examinations during a period of 3 years. Oral anticoagulation was continued or initiated in all patients. A target INR of 2.5 was intended in all patients. Results: Forty-three patients with LA thrombi and persistent or permanent AF were included. During the follow-up period 31(72%) of the thrombi disappeared. Patients with disappearance of thrombi had significantly smaller thrombi (P < 0.01), a lower echogenicity of thrombi (P < 0.01), and a lower LA volume (P = 0.02). Twenty-two (51%) patients suffered from cerebral embolism and/or death during the observation period. Five patients died due to embolic events. The only independent predictors of cerebral embolism were an elevated peak emptying velocity of the LA appendage (P < 0.001) and a history of previous thromboembolism (P < 0.01). Conclusions: Patients with persistent or permanent AF and atrial thrombi have a high long-term risk of cerebral embolism and/or death (51%) even despite the oral anticoagulation therapy. Thrombus size may predict thrombus resolution under continued anticoagulation.

Amiodarone is one of the most efficient and safe antiarrhythmic drugs in the treatment of atrial fibrillation (AF). Yet, though rare, proarrhythmic effects remain a clinical problem. We present three cases of amiodarone-associated "Torsade de pointes" tachycardia (Tdp) in patients treated concomitantly with heart rate controlling medication for AF. Amiodarone loading therapy was started for the treatment of tachyarrhythmic AF in all the three patients. All presented with a history of coronary heart disease, resulting in a severely reduced left ventricular ejection fraction in two patients. One received oral amiodarone loading, in the others, amiodarone was administered intravenously because of hemodynamically relevant AF episodes. Amiodarone therapy was combined with a heart rate controlling medication including a beta-blocking agent and digitalis in all the cases. All the subjects suffered from clinically relevant Tdp in the early run after initiation of amiodarone loading (max. 48 hours). The mean QTc in all patients before induction of Tdp was prolonged. The present case reports imply that amiodarone in combination with beta-blocker/digitalis therapy may be associated with an elevated proarrhythmic risk in selected patients with structural heart disease and AF.

Question of the study We have recently demonstrated that application of CPAP in patients with obstructive sleep apnoea syndrome (OSAS) results in an immediate decrease of N-terminal fragment of BNP pro-hormone (NT-pro BNP) in previously untreated normotensive and, in particular, hypertensive OSAS patients. However, there is uncertainty about whether nasal continuous positive airway pressure (CPAP) has a sustained effect on NT-pro BNP and whether chronic use of CPAP produces a even more pronounced decrease of NT-pro BNP. Therefore, we evaluated the long-term impact of CPAP treatment on B-type natriuretic peptide (BNP) in normotensive and hypertensive OSAS patients.

Objectives: The VIP registry investigated the efficacy of preventive pacing algorithm selection in reducing atrial fibrillation (AF) burden. Background: There are few data identifying which patients might benefit most from which preventive pacing algorithms. Methods: Patients, with at least one documented AF episode and a conventional antibradycardia indication for pacemaker therapy, were enrolled. They received pacemakers with AF diagnostics and four preventive algorithms (Selection and PreventAF series, Vitatron). A 3-month Diagnostic Phase with conventional pacing identified a Substrate Group (>70% of AF episodes with

OBJECTIVE Patients with atrial fibrillation (AF) have a risk of cerebral embolism. Echocardiographic parameters elevate this risk significantly. However, there is little knowledge about the long-term fate and the rate of clinically silent cerebral embolism under continued oral anticoagulation. The aims of our study were to assess prognosis of patients with AF and determine a high risk group with an increased risk of cerebral embolism under oral anticoagulation. METHODS Consecutive patients with persistent or permanent AF and left atrial (LA) thrombi, dense spontaneous echo contrast (SEC) and/or reduced LA appendage peak emptying velocities (LAAv) were included in the study (N = 128). Patients with AF and without echocardiographic risk factors (N = 114) served as controls. All patients were examined with transesophageal echocardiography, cranial magnetic resonance imaging and clinically during a period of three years. RESULTS During the three-year follow-up period 6 (5%) of the high risk patients had cerebral embolism with neurological deficits. 4 (3%) patients died due to embolic events and 17 (13%) patients had silent embolism as documented on MRI. In the control group 8 (7%) patients had embolic events (n = 1 clinically apparent and n = 7 silent embolism) documented on MRI, one was clinically apparent. Study patients with an event had more commonly previous thromboembolism (p < 0.0001). CONCLUSIONS Patients with peristent or permanent AF and LA thrombi, dense SEC or reduced LAAv have an explicitly increased risk of cerebral embolism (21%) despite oral anticoagulation. Previous thromboembolic event is another important predictor for an event.

Study objectives To evaluate the impact of obstructive sleep apnea syndrome (OSAS) on serum creatine phosphokinase (CK) levels. Design Single-center prospective cross-sectional study. Setting Academic sleep disorder center. Patients Two hundred one consecutive patients (mean [± SD] age, 54.9 ± 11.0 years; 155 men and 46 women; mean body mass index, 31.3 ± 6.9 kg/m2) with suspected sleep-disordered breathing. Measurements and results OSAS was confirmed in182 patients (apnea-hypopnea index [AHI], > 5 events per hour) and was ruled out in 19 patients (control subjects) by standard polysomnography. Sixty-six OSAS patients and 1 control patient showed an unexplained CK elevation. The mean baseline CK level was significantly higher in patients with severe OSAS (AHI, > 30 event per hour; n = 89) compared to those with mild-to-moderate OSAS (AHI, 5 to 30 events per hour; n = 93) and control subjects (191.4 ± 12.9 vs 134.3 ± 7.5 vs 107.1 ± 7.9 U/L, respectively; p 148 U/L (r = 0.660) for CK, which yielded a positive predictive value of 99%, a sensitivity of 43%, and a specificity of 95% for the diagnosis of OSAS. The mean nocturnal oxyhemoglobin saturation was the main predictor of CK level (r = 0.47; p Conclusions One third of our study population showed a mild-to-moderate elevation in CK level, which was highly predictive of OSAS. The application of CPAP therapy in OSAS patients resulted in a significant decrease in CK level. We speculate that OSAS may account for a substantial number of cases of unexplained CK elevation (ie, hyperCKemia). Further studies should address the prevalence of OSAS in patients with mild-to-moderate hyperCKemia.

Several experimental and clinical studies have demonstrated that platelet size and function correlate since large platelets are hemostatically more reactive than platelets of normal size. Since platelets play a crucial role in vascular remodeling after percutaneous transluminal coronary angioplasty (PTCA), we investigated the influence of the mean platelet volume (MPV), a parameter of platelet size, on restenosis after PTCA.The retrospective study comprised 174 patients who underwent elective PTCA and follow-up angiography within 6 months thereafter. According to the follow-up angiograms, the patients were assigned to group A ("restenosis", n=74) or group B ("no restenosis", n=100). Both groups were compared in regard to pre-procedural hematological routine parameters including MPV, platelet count, hematocrit, white blood cell count and fibrinogen.MPV was significantly increased in group A, compared with that in group B (8.75+/-0.99 fl vs. 8.04+/-0.74 fl, p0.001). This difference in MPV was evident in patients with stable and unstable angina pectoris. In addition, MPV had an impact on the time-related incidence of angiographic restenosis, as early restenosis was associated with higher pre-procedural MPV values. Platelet count correlated inversely with MPV (r=-0.36, p0.01) and was significantly lower in group A than in group B. The remaining hematological parameters were not different in both groups.The MPV seems to be a marker of coronary restenosis in patients undergoing PTCA. Patients with high pre-procedural MPV values might benefit from an intensified antiplatelet therapy after coronary interventions.

Pseudomembranous and obstructive Aspergillus tracheobronchitis (PMATB/OATB) are still considered to be refractory to therapy and to have a fatal outcome. To evaluate the optimal diagnostic strategy and to describe factors affecting the outcome of PMATB and OATB. Retrospective analysis of four new cases of PMATB and OATB combined with 16 previously reported cases over a 10-year period (1995-2004). Among the four new cases reported and the 16 published cases, four patients survived their infection. The mortality rate was significantly higher in the group of ventilated patients [94% (15 of 16 patients)] than in the group of non-ventilated patients [25% (1 of 4 patients), P < 0.05, Fisher's exact test]. In all 20 patients, diagnosis was established by bronchoscopy. Culture examination of mucous plugs was positive in 8 of 10, culture of the tracheobronchial aspirate was positive in 8 of 12, and bronchoalveolar lavage was diagnostic in 7 of 13 patients. All bronchoscopic techniques were complementary in improving the yield of bronchoscopy. However, microscopy of mucous plugs and/or necrotic material was the best diagnostic modality [positive in 94% (17 of 18 patients)]. Prognosis of PMATB and OATB remains poor. Microscopy of respiratory specimens is the most sensitive tool to confirm the diagnosis. The characteristic appearance of the disease makes it possible to start antifungal therapy immediately.

Die Erstmanifestation einer Miliartuberkulose bei einer jungen, nicht immunsupprimierten Patientin in Form eines schwerwiegenden neurologischen Krankheitsbildes stellt die Besonderheit der vorgestellten Kasuistik dar. Exemplarisch zeigt diese Kasuistik die Schwierigkeiten der Diagnosesicherung, die Charakteristika des Krankheitsbildes sowie die im Einzelfall auch ohne mikrobiologische Sicherung erforderliche Entscheidung uber die Einleitung einer antituberkulosen Therapie bei dieser seltenen, aber lebensbedrohlichen Form der Tuberkulose. Eine 32-jahrige marokkanische Patientin zeigte nach neurochirurgischer Versorgung einer intrazerebralen Massenblutung das Bild einer Sepsis. Bei Vorliegen einer normochromen Anamie fanden sich eine deutliche Erhohung des C-reaktiven Proteins, der Kreatininkinase, der Lactatdehydrogenase und der γ-Glutamyltransferase sowie eine Hypokalzamie, Hyponatriamie und Normokaliamie. Anamnestisch und in der weiterfuhrenden Diagnostik (Echokardiographie, Abdomensonographie, Blut-/Urinkulturen) ergaben sich keine Hinweise auf einen Infektfocus. Die radiologische Bildgebung (Rontgen-Thorax in zwei Ebenen, Computertomographie des Thorax) zeigte eine feinnodulare Zeichnungsvermehrung beider Lungen. In der bronchoalveolaren Lavage fanden sich eine negative mikroskopische und PCR-Diagnostik (Polymerase-Kettenreaktion) auf Tuberkuloseerreger. Aufgrund des fehlenden Ansprechens auf eine antimikrobielle Therapie sowie des charakteristischen radiologischen Befunds erfolgte die Einleitung einer antituberkulosen Vierfachtherapie (Rifampicin, Isoniazid, Pyrazinamid, Ethambutol) sowie einer additiven Cortisontherapie. Darunter kam es zu einer raschen Entfieberung, Normalisierung des Blutdrucks und Verbesserung des Allgemeinzustands. Im weiteren Verlauf gelang der kulturelle Nachweis von Mycobacterium tuberculosis. Die ausgepragte hypotone Hyponatriamie wurde als Ausdruck eines assoziierten Schwartz-Bartter-Syndroms (SIADH) gewertet. Im Weiteren normalisierten sich die Natriumwerte. Nach 5-monatiger Therapie zeigte sich eine deutliche Regredienz der miliaren Lungenrundherde. Nach Abschluss der 12-monatigen antituberkulosen Therapie war die Patientin bis auf ein neurologisches Defizit beschwerdefrei. Eine Miliartuberkulose stellt eine seltene Differentialdiagnose beidseitiger infiltrativer Lungenveranderungen dar. Die Diagnosesicherung kann durch eine initial unauffallige mikrobiologische Diagnostik (Mikroskopie, PCR) erschwert sein. Aufgrund der hohen Mortalitat des Krankheitsbildes muss im Einzelfall die Entscheidung zur Einleitung einer spezifischen Therapie aufgrund klinischer und bildgebender Befunde erfolgen.