[Modern treatment options for Zenker's diverticulum: indications and results]. / Aktuelle Behandlungskonzepte des Zenker-Divertikels--Indikationen und Ergebnisse.

Conventional transcervical therapy of Zenker's diverticulum comprises diverticulectomy, invagination, diverticulopexy and myotomy, which may be combined with the aforementioned methods. Transoral diverticuloesophagostomy is performed by diathermy, lasers or staplers through a rigid esophagoscope, or more recently by diathermy applied via a flexible endoscope. Morbidity of transcervical procedures ranges between 3 (myotomy) and 23 % (diverticulectomy + myotomy). The percentage of patients with at least significantly improved symptoms is 92 % or more, while recurrences occur in 5.7 (diverticulectomy alone) to 21 % (invagination). Transoral procedures have a morbidity of 9 (stapler) to 26 % (Laser), while symptoms improve in 91 (diathermy through rigid esophagoscope) to 99 % (diathermy via flexible endoscope), however in up to 64 % of patients reoperations are necessary. Small diverticula (Brombart I/II) can be treated by diverticulectomy (with/without myotomy) or flexible endoscopy, larger diverticula in general by all methods. Patients younger than 60 years should undergo diverticulectomy, elderly multimorbid patients should be treated by transoral procedures.

Copper-induced inflammatory reactions of rat carotid arteries mimic restenosis/arteriosclerosis-like neointima formation.

The pathogenesis of arteriosclerosis and of restenosis after angioplasty is linked with an inflammatory and fibroproliferative response of the arterial tissue. We have induced a non-infectious inflammation by implanting a silicon-copper cuff around rat carotid arteries. The copper ions released from the oxidized copper initiate and mimic all morphological features of post-angioplasty restenotic and arteriosclerotic lesions. The copper-induced lesions were analyzed by electron and light microscopy, immunohistochemical methods and quantified by morphometry. During the first phase of copper-induced tissue reaction (3 days), macrophages and polymorphonuclear leucocytes invaded through the endothelium, accumulated in the subendothelial space and triggered the proliferation of smooth muscle cells which then migrated from the tunica media through the lamina elastica interna into the intima. Within 3 weeks, the accumulated smooth muscle cells, macrophages, leucocytes and newly synthesized extracellular matrix formed a circular mostly eccentric fibrotic thickening that narrows the vessel lumen by 30-40%. The accompanying structural disorganization of the medial layer led to focal rupture and aneurysm-like dilatation of the vessel wall in 3 of 11 animals between day 20 and 43. The neointima progressively increased in thickness over time leading to corresponding reduction of the vessel lumen. The carotid arteries of control animals and animals treated with copper-free silicon cuffs showed no abnormal pathological appearance. Our results show that inflammation-inducing agents can contribute to and simulate restenosis- and arteriosclerosis-like lesions and that the copper-cuff model may be useful in the exploration of new approaches to intervention.