Background: Infections of cardiac implantable electronic devices as a perioperative complication remain an important problem and contribute to patient morbidity and mortality. In Germany about half of the operations are done in the cath lab and half of the operations are done in the operating room. Aim of the study: Aim of the study was to evaluate the incidence of infections of CIEDs implanted in a standard cath lab compared to the infections of CIEDs implanted in a cath lab with an attire protocol similar to an operating room. Methods: We compared in this observational study the CIED infection rates in two different time frames before and after the implementation of a more strict attire protocol in our cath lab. Before 2012 our personnel changed clothes for each procedure regardless if angiography, catheter ablation or implantation of a CIED. With the beginning of the year 2012 we performed all procedures in a cath lab with a hygiene standard similar to an operationg room. It became mandatory to change clothes and to wear a surgical hat and mask before entering the lab. All staff and patients used a lock to enter the cath lab. In addition teaching about hygiene and infection prevention took place for all medical personnel involved in CIED implantations. Results: In 2011 254 implantations were performed. We implanted 170 pacemakers (30 VVI, 138 DDD, 2 CRT; 151 first implantations and 19 changes) and 84 ICDs (47 VVI, 14 DDD, 23 CRT; 61 first implantations and 23 changes). The average time of operation was 50.6 minutes for pacemakers and 85.9 minutes for ICD/CRTs. During this time period all implantations were done in a cath lab with routine hygiene standards. We had an infectious rate of 2.4% (6 infections: 3 systemic infections and 3 local infections; 4 infections occurred after a device change, 2 infections occurred after a new implantation; detection of staphylococcus epidermidis in 2 systemic infections). All infected CIEDs had to be explanted. In 2012 we implanted 266 devices. 175 pacemaker operations (30 VVI, 134 DDD, 3 CRT; 146 first implantations and 29 changes) and 91 ICD-operations (42 VVI, 15 DDD, 34 CRT, 71 first implantations and 20 changes) were performed. The median time of operation was 44.1 minutes for pacemakers and 79.5 minutes for ICD/CRTs. No single infection occurred until now. Conclusion: If the cath lab is used for implantation of CIEDs, hygiene standards similar to those in the operating room should be implemented for all procedures, with carefully teaching of the medical staff.

Reflex-mediated syncope is a common cause for syncope. The first step in evaluating the cause of syncope is to assess the risk of a life-threatening cause for syncope, e.g., ventricular arrhythmias. Reflex-mediated syncope has to be differentiated from orthostatic syncope. In orthostatic syncope, there is an insufficient autonomic response. In contrast to a reflex-mediated syncope, in which the autonomic nervous system acts inappropriately, reflex-mediated syncope is classified into the classical vasovagal form, the situational form, or due to carotid sinus hypersensitivity. In the elderly, often a mixed form is present. Treatment is difficult. Most important is educating the patient and avoiding precipitating factors. Physical maneuvers, e.g., counter pressure maneuvers, are more effective than drug treatment. Permanent pacing is rarely needed. However, before indicating a pacemaker, a correlation between bradycardia and syncope should be documented. This is often only possible by implanting a monitoring device at an early stage.

Ein 70-jähriger Patient stellt sich wegen zunehmender Dyspnoe, Anschwellen beider Arme verbunden mit Schwindel und Engegefühl im Kopf vor. Wegen eines zurückliegenden, kurativ behandelten Rektumkarzinoms vor 5 Jahren besteht noch ein implantiertes Portsystem rechts-pektoral. Bei der klinischen Untersuchung finden sich die typischen Zeichen der oberen Einflussstauung. In der venösen Angiographie über den liegenden Port konnte ein Verschluss der V. cava superior nachgewiesen werden mit ausgeprägter Kollateralisation über die V. azygos und thorakale Venen. Nach zunächst konservativer Behandlung mit Antikoagulation (Heparin, Phenprocoumon) und Armkompression kommt es im Verlauf zu einer progredienten Zunahme der Symptome im Sinne eines V.-cava-superior-Syndroms, im CT- des Thorax finden sich zunehmende Pleuraergüsse beidseits. Der Port war in der Zwischenzeit explantiert. Durch Ballondilatation und abschließendes Stenting (selbstexpandierender Wallstent 16 mm/14 mm) gelingt interventionell eine vollständige Rekanalisation der V. cava superior mit im Verlauf völliger Rückbildung der Symptome und der beidseitigen Pleuraergüsse über 8 Wochen. Bei Portpatienten sollte grundsätzlich an die Möglichkeit einer katheterassoziierten Thrombose gedacht werden. Zur Nachsorge von Portträgern gehört auch die zeitnahe Explantation bei fehlender Indikation.

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study

A 55-year-old woman developed increasing shortness of breath and breath-independent pain in the left lower chest. 20 years previously she had had an episode of pulmonary embolism and 10 years previously a central venous thrombosis in the left eye. No cause of the increased thrombogenesis had been found. On admission she had resting dyspnoea but a stable circulation. On auscultation the breath sounds were diminished over the left base and there was a diastolic murmur over the pulmonary area with an accentuated second sound. There was also marked tenderness below the left costal margin. Recurrent pulmonary embolism or left-sided pleuropneumonia was suspected.Arterial blood gases (without additional oxygen) showed severe hypoxaemia (pO2 42.3 mm Hg, pCO2 27.8 mm Hg, pH 7.455, oxygen saturation 80.5%). Transthoracic and transoesophageal echocardiography showed normal left ventricular dimensions, right atrial and ventricular dilatation, and an atrial septal aneurysm with a right to left interatrial shunt. Right heart catheterisation demonstrated severe pulmonary hypertension. Sonography, computed tomography and scintigraphy revealed multiple splenic infarcts.Heparinisation was instituted (partial thromboplastin time 70-90 s) and overlapping oral anticoagulation to a Quick value of 20%. Subsequently the calcium antagonist felodipine (15 mg daily) was given. The mean pulmonary artery pressure was 61 mm Hg before and 57 mm Hg after treatment.Splenic infarction resulting from paradoxical embolisation is rare, but should be routinely considered in the presence of thromboembolic phenomena.

Zusammenfassung Eine 51-jährige Patientin wurde mit dem Bild einer Globalherzinsuffizienz in die Innere Klinik aufgenommen. In der Folge findet sich eine manifeste Hyperthyreose bei unauffälliger morphologischer und immunologischer Schilddrüsendiagnostik, des Weiteren ein Unterbauchtumor mit einer massiven Erhöhung von HCG (1.168.000 U/ml) im Serum. Postoperativ (Nachweis einer Blasenmole) fand sich ein simultaner, rascher Abfall der Schilddrüsenhormonwerte und des HCG-Spiegels mit Erreichen einer euthyreoten Stoffwechsellage nach 2 Wochen. Im funktionellen Bioassay (CHO-TSH-R) zeigte das Patientenserum präoperativ eine signifikante Stimulation, postoperativ wieder eine Normalisierung der TSH-rezeptorstimulierenden Aktivität. Zusammenfassend konnte damit die Diagnose einer HCG-assoziierten Hyperthyreose bei Blasenmole gestellt werden. Die Diagnose einer HCG-assoziierten Hyperthyreose stützt sich auf folgende Befunde: laborchemischer Nachweis einer manifesten Hyperthyreose, morphologische, laborchemische und funktionelle Schilddrüsendiagnostik ohne richtungsweisenden Hinweis für das Vorliegen einer regionalen Autonomie oder Immunhyperthyreose sowie Nachweis exzessiv erhöhter HCG-Werte (üblicherweise >50.000 U/l). Entscheidend für das Krankheitsbild ist die enge Assoziation der Hyperthyreose mit dem Verlauf der Grunderkrankung.

Percutaneous transluminal coronary angioplasty (PTCA) is offered only reluctantly to elderly patients, as the general conviction is that this invasive form of treatment carries a substantial risk whilst offering only modest benefits [1, 5, 6]. However, in the last few years interventional techniques have improved and stents have become more widely used, and it is especially in elderly patients that success rates have risen and complication rates fallen [3, 4]. The effectiveness of PTCA is seen in angiographic and functional results, improvements in clinical symptoms and quality of life and finally also in cost [2].

Background-Increased thrombogenicity and smooth muscle cell proliferative response induced by the metal struts compromise the advantages of coronary stenting. The objective of this randomized, multicenter study was to assess whether a reduced strut thickness of coronary stents is associated with improved follow-up angiographic and clinical results.Methods and Results-A total of 651 patients with coronary lesions situated in native vessels >2.8 mm in diameter were randomly assigned to receive 1 of 2 commercially available stents of comparable design but different thickness: 326 patients to the thin-strut stent (strut thickness of 50 mum) and 325 patients to the thick-strut stent (strut thickness of 140 mum). The primary end point was the angiographic restenosis (greater than or equal to 50% diameter stenosis at follow-up angiography). Secondary end points were the incidence of reinterventions due to restenosis-induced ischemia and the combined rate of death and myocardial infarctions at 1 year. The incidence of angiographic restenosis was 15.0% in the thin-strut group and 25.8% in the thick-strut group (relative risk, 0.58; 95% CI, 0.39 to 0.87; P=0.003). Clinical restenosis was also significantly reduced, with a reintervention rate of 8.6% among thin-strut patients and 13.8% among thick-strut patients (relative risk, 0.62: 95% CI, 0.39 to 0.99, P=0.03). No difference was observed in the combined 1-year rate of death and myocardial infarction.Conclusions - The use of a thinner-strut device is associated with a significant reduction of angiographic and clinical restenosis after coronary artery stenting. These findings may have relevant implications for the currently most widely used percutaneous coronary intervention.

Coronary stent embolization is an uncommon but potentially hazardous complication of percutaneous transluminal coronary angioplasty (PTCA). Previous small-sized clinical studies reported incidence rates ranging from 0.9% to 8.4%.(1-5) In this study we report the incidence, management, and hospital follow-up of a large, consecutive series of patients with coronary stent embolization.

The objective of the study was to identify the relative importance of erythrocyte flow resistance and aggregation in acute and chronic coronary syndromes. 117 subjects in five groups were studied: (1) 34 patients shortly after acute myocardial infarction (AMI) before reperfusion therapy; (2) 27 patients with unstable and (3) 21 with stable angina pectoris (AP); (4) 14 age-matched control patients and (5) 21 healthy volunteers. Single erythrocyte transit times were measured using the Cell Transit Analyser. Shear dependent elongation and aggregation was measured by a modified computerized Myrenne aggregometer. Leukocyte count was increased in coronary artery disease (CAD), especially in acute syndromes (mean +/- SD for groups 1-5): 12.2 +/- 4.5; 10.0 +/- 5.4; 8.0 +/- 2.0; 8.0 +/- 3.7; 7.0 +/- 2.0 (pl(-1))). Platelets, hematocrit, fibrinogen, alpha(2)-macroglobulin did not differ between the groups. Plasma viscosity (mPa s) was elevated in AMI and stable AP: 1.34 +/- 0.10; 1.30 +/- 0.09; 1.32 +/- 0.08; 1.27 +/- 0.07; 1.27 +/- 0.05. Erythrocyte filtrability was not different as was the shear dependent deformation. Aggregation parameters such as gamma T-min were elevated in CAD: 180 +/- 70; 159 +/- 60; 166 +/- 59; 115 +/- 43; 113 +/- 51 (s(-1)). Erythrocyte deformability, measured with two independent methods, does not appear to contribute to the pathophysiology of acute coronary syndromes. Erythrocyte aggregation and plasma viscosity were again found increased both in unstable and stable coronary disease. It is unlikely that increased red cell aggregation contributes to emergence of AMI.