[Treatment reality of aortic diseases in Switzerland]. / Versorgungsrealität von Aortenerkrankungen in der Schweiz.

BACKGROUND: Due to the federally organized healthcare system in Switzerland, aortic interventions are performed in many different hospitals, presumably sometimes with a very small number of cases per institution. The aim of this study was to present the treatment reality of aortic diseases based on the aortic interventions recorded in Switzerland's vascular registry Swissvasc. METHODS: All interventions on the aorta that were carried out between January 2018 and December 2020 in Switzerland and entered in the Swissvasc registry were included in this overview. Interventions for the treatment of isolated pathologies of the iliac vessels as well as interventions on the ascending aorta and the proximal aortic arch were excluded. RESULTS: Open aortic surgery was performed in 28 hospitals and endovascular aortic repair (EVAR) in 33. Just under half of these hospitals achieved the recommended minimum number of cases for abdominal aortic aneurysms (AAA) of 30 open and endovascular interventions per year, which are currently discussed in the literature. In line with the literature 67% of the elective treatments for AAA were performed by EVAR. Corresponding to the current literature, 11% of the AAA were ruptured in the 3­year observation period. In contrast to the recommendations of the current guidelines almost 60% of the ruptured AAA were treated by open repair. There was a certain tendency for a spontaneous centralization in the treatment of thoracic aortic pathologies as 87% of the interventions were carried out in only 5 hospitals. CONCLUSION: This study shows that many clinics in Switzerland treat aortic pathologies, some with a very small caseload. Further investigations of the quality of care in the treatment of aortic pathologies are urgently needed.

[Combined dorsal and palmar plate osteosynthesis for intraarticular distal radius fractures]. / Kombinierte dorsale und palmare Plattenosteosynthese bei distalen intraartikulären Radiusfrakturen.

BACKGROUND: Complex comminuted intraarticular fractures of the distal radius require anatomic restoration. In rare cases, this aim can only be achieved by a combined dorsal and volar plate fixation despite increasing experience with volar locking compression implants. This retrospective quality control study investigated functional, radiological and subjective outcomes of patients treated with this technique. METHODS: Between March 1999 and January 2003, 30 out of 360 patients who were operated on for an unstable distal radius fracture with complex C2/C3 type distal radius fractures at the Division of Trauma Surgery of the University Hospital Zurich, had been treated with a combined dorso-palmar plate fixation (dorsal two 1/4 tubular plates, volar 3.5 mm T-plate) and were included in this study (9 female, 21 male, mean age 52 years). Of the 30 patients 25 could be evaluated at an average of 29 months after injury. RESULTS: Anatomic reconstruction could not be achieved in all cases, 56% showed mild and 28% explicit signs of arthrosis. Flexion reached 66% and extension 75% of the contralateral wrist, whereas pronation reached 98% and supination 91%, respectively. Grip strength achieved 75% of that of the contralateral side and 10 patients (40%) developed a complex regional pain syndrome (CRPS). Return to work was possible 120 days after the injury. CONCLUSION: With the dorso-palmar plate fixation joint reconstruction in complex intraarticular distal radius fractures can be achieved with a satisfactory subjective, functional, and radiologic result, although additional soft tissue injury was caused by the bilateral approach. The patient has to be informed of the high rate of CRPS and the long period of disability.

[Complex fracture of the proximal humerus in the elderly. Locking plate osteosynthesis vs hemiarthroplasty]. / Komplexe proximale Humerusfraktur beim alten Menschen. Winkelstabile Plattenosteosynthese vs. Hemiarthroplastik.

BACKGROUND: The purpose of the present study was a direct comparison of fixed-angle plate fixation (FAPF) and shoulder hemiarthroplasty (SHA) for complex fractures of the proximal humerus in the elderly. PATIENTS AND METHODS: A single-institution case series of 52 consecutive geriatric patients (age > or =70 years) treated with FAPF for three- and four-part fractures of the proximal humerus between 2003 and 2005 was analysed 1 year after surgery. The analysis included Constant Score (CS), Oxford Shoulder Score (OSS), and radiological evaluation. Outcome was compared with a similar historic group of patients (n=59) who received SHA in an earlier period (1995--1997). RESULTS: The patient groups showed no differences in age, gender, or fracture type. Median CS was significantly better for FAPF (71 vs 41). Evaluation of pain demonstrated no differences between the two treatment modalities in the OSS. Revision surgery was performed more often in the FAPF group (25% vs 2%). CONCLUSION: Compared to SHA, functional outcome was superior with FAPF. However, this was associated with a higher rate of revision surgery. Most patients were still able to live independently in their original environment, regardless of the type of surgery.

Increased expression of endothelin-1 and inducible nitric oxide synthase isoform II in aging arteries in vivo: implications for atherosclerosis.

We here report that aging increases expression of endothelin-1 and NO synthases in the vasculature and kidney of normotensive rats in vivo. Expression of preproendothelin-1 mRNA was quantified by RT-PCR and in situ hybridization, and endothelin-1 protein was determined by radioimmunoassay/HPLC. Vascular mRNA expression of NO synthase isoforms II and III was analyzed by RT-PCR. In young animals, vascular endothelin-1 protein was differentially expressed (aorta < renal artery < carotid artery) and increased with aging in all vascular beds (P < 0.05). In the intact aorta of aged rats, mRNA expression of preproendothelin-1, "inducible" NO synthase II, and endothelial cell NO synthase III gene was up-regulated (P < 0.05). Moreover, preproendothelin-1 mRNA expression increased in glomeruli and tubulointerstitial cells (P < 0.05). To our knowledge this is the first study demonstrating local vascular up-regulation of the trophic factor endothelin under physiological conditions. Activation of vascular endothelin and NO synthases may be important, pressure-independent factors contributing to structural and functional abnormalities of age-dependent diseases, including atherosclerosis.

Inverse regulation of endothelin-1 and nitric oxide metabolites in tissue with aging: implications for the age-dependent increase of cardiorenal disease.

Aging is an independent risk factor for cardiovascular and renal disease. The study reported here investigated whether aging affects endothelin-1 (ET-1) and tissue levels of the nitric oxide metabolites nitrite/nitrate in the kidney of rodents. Blood pressure was measured by the tail-cuff method, ET-1 protein was determined by radioimmunoassay/high-performance liquid chromatography (RIA/HPLC) and nitrite/nitrate was measured by ion-pairing chromatography. Compared to young male Wistar Kyoto rats (3 months of age), renal ET-1 protein levels in whole kidneys increased 3.6-fold at 24 months of age (from 70 +/- 9 to 253 +/- 43 pg/g tissue, p < 0.05, n = 6 each group). Similarly, renal ET-1 protein increased 1.7-fold in 18-month-old C57BL/6J mice as compared to 8-month-old adult animals (from 188 +/- 18 to 319 +/- 14 pg/g tissue, p < 0.05, n = 5-7). In female RoRo-Wistar rats (6, 18 and 33 months of age), tissue nitrite/nitrate levels in whole kidneys decreased with increasing age (from 232 +/- 25 to 130 +/- 6 micromol/l/g tissue, p < 0.05). Thus, aging in healthy rodents is associated with a marked upregulation of renal ET-1 protein content and a decrease in tissue nitrite/nitrate levels in whole kidneys, independent of blood pressure. Activation of the ET pathway with aging may promote the development of age-dependent diseases such as glomerulosclerosis, hypertension and atherosclerosis.

Endothelin regulates angiotensin-converting enzyme in the mouse kidney.

Using the orally active endothelin-A- (ET(A)) receptor antagonist LU135252, we determined whether endothelin-1 (ET-1) and/or dietary fat may be involved in angiotensin-converting enzyme (ACE) regulation in vivo. In C57BL6/J mice, renal and pulmonary tissue ACE activity (nmol/l His-Leu/mg protein) was measured and ACE mRNA expression, tissue ET-1 protein content and nitrite/nitrate level were measured in the kidney. Western-type diet increased renal ACE activity by 70% (55 +/- 4 vs 33 +/- 3 nmol/l His-Leu/mg protein, p < 0.05) and increased renal ET-1 levels (267 +/- 19 pg/g vs 190 +/- 18, p < 0.05). Chronic LU135252 treatment completely prevented activation of renal ACE activity (13.3 +/- 0.3 His-Leu/mg protein nmol/l, p < 0.05) independent of ACE mRNA expression or renal ET-1 protein levels. Thus, dietary fat activates renal ACE activity and ET-1 is involved in regulation of tissue ACE activity in vivo independently of ACE mRNA expression.

Obesity is associated with tissue-specific activation of renal angiotensin-converting enzyme in vivo: evidence for a regulatory role of endothelin.

In the C57BL/6J mice model, we investigated whether obesity affects the function or expression of components of the tissue renin-angiotensin system and whether endothelin (ET)-1 contributes to these changes. ACE activity (nmol. L His-Leu. mg protein(-1)) was measured in lung, kidney, and liver in control (receiving standard chow) and obese animals treated for 30 weeks with a high-fat, low cholesterol diet alone or in combination with LU135252, an orally active ET(A) receptor antagonist. ACE mRNA expression was measured in the kidney, and the effects of LU135252 on purified human ACE were determined. Aortic and renal tissue ET-1 protein content was measured, and the vascular contractility to angiotensin II was assessed. Obesity was associated with a tissue-specific increase in ACE activity in the kidney (55+/-4 versus 33+/-3 nmol/L) but not in the lung (34+/-2 versus 32+/-2 nmol/L). Long-term LU135252 treatment completely prevented this activation (13.3+/-0.3 versus 55+/-4 nmol/L, P<0.05) independent of ACE mRNA expression, body weight, or renal ET-1 protein but did not affect pulmonary or hepatic ACE activity. Obesity potentiated contractions in response to angiotensin II in the aorta (from 6+/-2% to 33+/-5% KCl) but not in the carotid artery (4+/-1% to 3.6+/-1% KCl), an effect that was completely prevented with LU135252 treatment (6+/-0.4% versus 33+/-5% KCl). No effect of LU135252 on purified ACE was observed. Thus, obesity is associated with the activation of renal ACE in vivo independent of its mRNA expression and enhanced vascular contractility to angiotensin II. These effects are regulated by ET in an organ-specific manner, providing novel mechanisms by which ET antagonists may exert organ protection.