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J Stalke

Publications and source records attributed to J Stalke.

3 recordsLinked to original sources

[Hemobahn endoprosthesis: experience with percutaneous placing in the arteria femoralis superficialis].

The self-expanding Polytetrafluoroethylene-lined nitinolstent Hemobahn offers from its design a prophylaxis for re-occlusion after angioplasty of long femoral artery occlusions. During the last two years we placed in 33 patients at 35 extremities a total of 53 Hemobahns. Fontaine's clinical stages were: 30 x IIb, 1 x III and 4 x IV. The treated lesions were femoral stenoses (3x) and occlusions (32x with mean distance 12 cm). Follow-up-visits were after 3, 6 and 12 months. The mean ankle-brachial-index changed from 0.49 to 0.85, post-interventional Fontaine's stages were: 24 x I, 5 x IIa, 2 x IIb and 4 x IV. The primary inhospital patency rate was 91%. After 3 months all primary/secondary patency rates were: 77%/87%, after 6 months 62%/85% and after 1 year 40%/67%. Causes for re-occlusions were a poor "run off", calcifications and multiple vessel lesions. The results for "ideal indications" were much better. Such "ideal indications" applied to: > or = 1 cm "healthy" proximal and distal vascular segments, missing lesions in the popliteal artery, at least one open lower leg vessel and no severe calcifications. The primary/secondary patency rate was inhospital 100% (n = 23), after 3 months 95/100%, after 6 months 85/100% and after 1 year 80/100%. Side effects were local haematoma, pain in the prosthesis and temporarily temperature reactions. Sonographically no re-stenoses at the limb ends were observed. Hemobahn-endoprostheses are suited for therapy of long femoral artery occlusions. The medium patency rate of "ideal indications" is higher than that of angioplasty with or without uncovered stents.

Aged↗

Changes of fluid-dynamic parameters in peripheral stenoses with transcutaneous interventions.

UNLABELLED: Peripheral vessels provide a useful in vivo haemodynamic model allowing evaluation of local intravascular fluid dynamics. Velocity measurements using a 0.018 inch Doppler-tipped angioplasty guidewire, quantitative angiography and laboratory data were gathered from 45 patients with a total of 48 percutaneous transluminal laser assisted angioplasties (PTLA) in the superficial femoral, in the iliac, in the popliteal artery and in the peroneal artery. From these data, blood flow, whole blood viscosity, Reynold's numbers, Womersley numbers and shear stress were calculated, evaluated as to their changes post PTLA and correlated with clinical improvement at early follow-up. The clinical result was quantified as categorial improvement according to the American Heart Association guidelines. The primary angiographic results of angioplasty were satisfactory in all patients. Clinically 17/45 patients showed a marked, 6/45 a moderate, 18/45 a minimal, and 4/45 no improvement. The mean values of maximal peak velocity at stenosis decreased from 235 +/- 28 cms-1 to 84 +/- 8 cms-1 after PTLA (P < 0.01). The minimal intrastenotic cross section increased from 7.7 +/- 0.9 to 21.9 +/- 1.6 mm2 (P < 0.01). Mean trans-stenotic flow increased after intervention by about 50% (P < 0.01) and improved further by 135% after administration of adenosine triphosphosphate i.a. (P < 0.01). Reynold's numbers were elevated intrastenotically (1285 +/- 198) pre-intervention as compared to values proximal (564 +/- 81) and distal (449 +/- 66) to the stenosis and were reduced significantly (P < 0.05) at stenosis by PTLA, whereas values proximally and distally increased significantly (P < 0.01) post PTLA (proximal 829 +/- 84, intra 773 +/- 107, distal 676 +/- 98). Shear stress, reflecting mechanical interaction between flow and vessel wall, was elevated at stenosis pre-intervention to 44 +/- 8.9 Pa and reduced at post-stenoric vessel sites to 2.4 +/- 0.5 Pa. PTLA caused a decrease in stenosis to 6.3 +/- 1 Pa (P < 0.01) and an increase distally to 4.6 +/- 1 Pa (P < 0.01). Whereas in single stenoses removal of the obstruction was associated with a significant (P < 0.05) increase in trans-stenotic flow and shear stress distally, there was only auenuated increase in trans-stenotic flow in multiple lesions despite an angiographically good PTLA result. Shear stress distally remained low in those patients. Velocities and Reynold's numbers were lower in these vessels even pre PTLA. Residual flow, Reynold's number and minimal cross-section pre-intervention correlated significantly with clinical outcome. Pooling cases with no or minimal, as opposed to those with marked or moderate improvement, 81% of patients were correctly classified using the Reynold's numbers pre- and post-PTLA. CONCLUSION: Peak velocity monitoring is feasible and safe during angioplasty. Velocity provides clinically relevant physiological information in addition to angiography. Combining quantitative angiography, velocity measurements and laboratory data allow the calculation of blood flow, Reynold's numbers and shear stress, thereby providing complex fluid dynamic information. Thus the evaluation of haemo-dynamics in single and multiple obstructions before and after intervention is improved. Fluid dynamic parameters pre-and post-PTLA are significantly correlated with clinical short-term result.

Adult↗

The role of vasopressin in the nicotine-induced stimulation of ACTH and cortisol in men.

Experimental evidence indicates that arginine vasopressin (AVP) contributes to the release of ACTH under certain conditions. The present study investigates the role of vasopressin as a secretagogue of ACTH during cigarette smoking or nicotine infusion with additional injection of corticotropin releasing hormone (CRH) and using the specific AVP antagonist d(CH2)5Tyr(Me)-AVP. We first tested the effect of the AVP antagonist (10 micrograms/kg body weight i.v.) on ACTH and cortisol release following cigarette smoking in 15 healthy young male smokers. Smoking led to marked increments in plasma nicotine and to a small rise in plasma ACTH and cortisol. Mean plasma ACTH and cortisol levels were at no time significantly altered by the antagonist. This might be due to a slight agonistic effect of the AVP antagonist, to high interindividual variability of the ACTH and cortisol responses after smoking or to a negligible role of AVP in smoking-induced ACTH release. In a second study we performed the following tests in six healthy male non-smokers: (1) nicotine infusion (1.0 micrograms/kg body weight per min); (2) CRH i.v. (100 micrograms); (3) AVP antagonist i.v. (5 micrograms/kg); (4) nicotine infusion plus CRH i.v.; (5) nicotine infusion plus AVP antagonist i.v.; (6) nicotine infusion plus CRH and AVP antagonist i.v.; and (7) sham infusion. Nicotine infusion led to greater increments of AVP, ACTH and cortisol than smoking without causing nausea. Peak nicotine levels after nicotine infusion were lower than after smoking. The AVP antagonist in the reduced dosage given alone had no effect on hormone levels. However, it slightly attenuated the effect of nicotine on ACTH and cortisol (P less than 0.05, ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗