[19-year-old asthma patient with pronounced eosinophilia and acute coronary syndrome]. / 19-jähriger Asthmatiker mit ausgeprägter Eosinophilie und akutem Koronarsyndrom.

Diagnosis of Churg-Strauss syndrome should be considered in young asthmatics with fatigue and eosinophilia. On the base of the etiopathology of a 19-year old man, who was initially admitted because of dyspnoea, fever and acute chest pain, we show that eosinophilia gives an important hint for further diagnostic and is the key trend parameter. Histologically an eosinophilic myocarditis could be shown in the myocardial biopsy. High dose prednisolone induced a clear improvement in symptoms, with decrease of the inflammatory signs and the eosinophilia and a clear improvement of the left ventricular function.

Ventricular oversensing in 518 patients with implanted cardiac defibrillators: incidence, complications, and solutions.

The present study evaluates the incidence of various complications in implanted cardiac defibrillators (ICD) therapy due to ventricular oversensing (VO) and its complications. From June 1998 to May 2005, we retrospectively screened 518 patients (1085.6 patient years) for the occurrence of VO episodes (441 male, 77 female). The overall incidence was 7.3% (n = 38) with inappropriate shock deliveries accounting for 2.3% (n = 12). All VO episodes were caused by either T-wave oversensing (n = 10), myopotentials (n = 8), electrode failure (n = 5), interference with electromagnetic fields (n = 3), double-counting (n = 4), pacemaker interactions (n = 2), or others (n = 2). There were five life-threatening events due to inappropriate ICD reaction. In eight (22%) cases, ICD reprogramming was able to avoid further oversensing episodes (e.g. adaptation of sensitivity, T-wave suppression feature), 13 (35%) patients had to undergo invasive procedures (e.g. electrode replacing) to suppress VO, 16 (43%) were told to avoid the trigger situation, and one demanded to deactivate all ICD therapies because of inappropriate shock delivery. Our data demonstrate that VO is a rare complication, but might lead to life-threatening events. In most cases, VO episodes could be prevented by appropriate ICD reprogramming or avoidance of the initiating trigger.

Scapulothoracic dissociation.

Scapulothoracic dissociation is a rare entity that consists of disruption of the scapulothoracic articulation. The mechanism of injury is probably traction caused by a blunt force to the shoulder girdle. This lesion is characterized by massive soft-tissue swelling of the shoulder; lateral displacement of the scapula, measured radiographically; an injury to bone (an acromioclavicular separation, a displaced fracture of the clavicle, or a sternoclavicular disruption); a severe neurovascular injury; and a variety of upper and lower-extremity fractures. We treated fifteen patients who had this lesion, most of whom had several associated injuries. Three patients died: two from exsanguination and one from a cardiac arrest. In most patients, the damaged artery was repaired and the brachial plexus was explored. All of the twelve patients who had a complete brachial-plexus injury were left with a flail upper extremity. Most patients refused amputation.

Reversible clopidogrel resistance due to right ventricular myocardial infarction: risk factor of recurrent stent thrombosis?

A 63-year-old male Patient was admitted to the intensive care unit due to acute inferior myocardial infarction with right ventricular dysfunction. He received a loading dose of clopidogrel (600 mg) and aspirin (500 mg) and was immediately revascularized by reopening of the proximal right coronary artery (RCA) and implantation of a bare metal stent. After primary successful intervention the patient suffered from thoracic pain on day 5 of admission. The ECG indicated reinfarction. The proximal RCA was again re-opened by PTCA alone. The following day the patient suffered again from thoracic pain with ST-elevation in the inferior leads, this time complicated by additional total AV-blockade. The angiography showed another time a thrombotic occlusion of the initially implanted stent. He received another intervention with implantation of additional two bare-metal stents, an aortic counter-pulsation and a temporary two-chamber pace maker. Tirofiban was administered for 24 h and the IABP was withdrawn after 60 h. The patient was discharged on Aspirin 300 mg/d, Clopidogrel 150 mg/d and Enoxaparin 40 mg/d. Six weeks later the patient demonstrated an improved right ventricular function (TAPSE 18 mm), liver enzymes were normal, and inhibition of platelet aggregation by clopidogrel (150 mg/d) was sufficient. In conclusion this implies that the reversible "clopidogrel-resistance" might have been due to congestion and reduced metabolism due to right ventricular infarction.

Expression of alpha 2-adrenergic receptor genes in rat tissues.

Alpha-2 adrenergic receptor subtypes are coded for by three genes. Pharmacologically alpha 2 adrenergic receptors can be classified into four subtypes: alpha 2A, alpha 2B, alpha 2C, and alpha 2D. Although pharmacologically distinct, the amino acid sequences of the alpha 2A and alpha 2D subtypes are approx 90% identical and have not been detected in a single species. Thus, they should be considered species orthologs and may be referred to as alpha 2A/D. The tissue distribution of the mRNAs for the rat alpha 2A/D, alpha 2B, and alpha 2C was analyzed utilizing RNase protection assays with probes directed to the third cytoplasmic loops. Alpha-2 adrenergic receptor mRNA was found in all tissues tested. Kidney, brain, and spinal cord had transcripts for all three subtypes. Only one mRNA subtype was detected in several tissues. Aorta and spleen had only alpha 2A/D mRNA, whereas heart and liver had only alpha 2B mRNA. All other tissues had two alpha 2 adrenergic subtype transcripts present. In contrast to the rat CNS, which contains predominantly alpha 2A/D and alpha 2C mRNA with little alpha 2B mRNA, peripheral tissues contain predominantly alpha 2A/D and alpha 2B mRNA with little alpha 2C mRNA.

The cloning and expression of an OK cell cDNA encoding a 5-hydroxytryptamine1B receptor.

Serotonin (5-hydroxytryptamine or 5-HT) is an important biogenic amine that functions as both a neurotransmitter and a hormone in the central nervous system (CNS) and the periphery. We report here the isolation of a cDNA from the OK cell that encodes a serotonin receptor (OKc1). When expressed in cultured cells, it displayed the pharmacological profile and negative coupling with adenylyl cyclase characteristic of a 5-HT1B receptor subtype. Similar to the cloned rodent 5-HT1B receptors, it had high affinity for the beta-adrenergic ligand [125I]iodocyanopindolol, because of the presence of an asparagine instead of a threonine residue in the seventh transmembrane region. The ligands used displayed the following rank order of potencies: cyanopindolol > RU24969 > methiothepin > serotonin > sumatriptan > methysergide > 8-OH-DPAT > isoproterenol. This profile correlates well (r = 0.97) with the native OK cell 5-HT1B receptor. When OKc1 is compared to the rat, mouse, and human 5-HT1B receptors, it has an amino acid sequence identity of 82%, but it is only 54% identical to the human 5-HT1D receptor.

Cloning and expression of the alpha 2C-adrenergic receptor from the OK cell line.

The alpha 2-adrenergic receptors have been divided into four pharmacological subtypes, alpha 2A, alpha 2B, alpha 2C, and alpha 2D. The OK cell line, a cell line derived from an opossum kidney, expresses the alpha 2C-adrenergic receptor and is the prototypical cell line for the alpha 2C receptor subtype. The cloned human alpha 2C-C4 and rat RG10 receptors have been shown to express alpha 2C pharmacology. Here we report the cloning and expression of the OK alpha 2C-adrenergic receptor, OKc2. The receptor has 64% deduced amino acid identity and 21% similarity to the alpha 2-C4 receptor, giving an overall similarity of 85%. The clone, expressed in Chinese hamster ovary cells, has a pharmacology that correlates very well (r = 0.97) with that of the native OK cell alpha 2C-adrenergic receptor, and it is negatively coupled to adenylyl cyclase.