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T Kunz

Publications and source records attributed to T Kunz.

18 recordsLinked to original sources

[Non-surgical therapy of iatrogenic false aneurysms].

SUMMARY: False aneurysms occur after 0.1 - 1.5 % of all diagnostic and up to 6 % of all therapeutic percutaneous interventions. Surgery used to be the treatment of choice in symptomatic patients. But two non-invasive measures of treatment gain more attention: ultrasound guided compression (UGC) and ultrasound guided thrombin injection (UGTI). UGC with compression times from 30 - 120 min is effective in 80 % of patients without anticoagulation. However, UGC is often painful and results in prolongation of in-hospital time. UGTI is effective in 95 % of patients. Usually, 100 - 2000 U of thrombin are injected into the false aneurysm. UGTI is also effective in the presence of anticoagulation or antiplatelet therapy. UGTI is not indicated in patients with a large communication with the native vessel and in arterio-venous-fistulas. In patients with large haematomas, ongoing bleeding, damage of the native vessel, compression of arteries, veins or neurological deficits, or with infections, early surgical repair is still the treatment of choice.

Aneurysm, False↗

A prospective study on ultrasound-guided compression therapy or thrombin injection for treatment of iatrogenic false aneurysms in patients receiving full-dose anti-platelet therapy.

BACKGROUND: False aneurysms (FA) develop at the puncture site in up to 6% of percutaneous cardiovascular procedures. Previous management included surgery or manual compression. Recently, selective injection of thrombin has been proposed as an alternative. However, there has been no direct comparison of thrombin injection to manual compression. AIM: To study the effectiveness of manual compression compared to that of thrombin injection in patients with false aneurysms on full-dose aspirin and clopidogrel. METHODS AND PROTOCOL: All patients with a clinically suspected FA after percutaneous invasive procedures were recruited for the study. The patients were examined with color ultrasound (7.5 MHz transducer). The minimum and maximum diameters of the false aneurysm and the distance between the surface and the false aneurysm were measured online. Under local anesthesia, manual compression was applied under sonographic guidance in all patients. If compression stopped flow into the false aneurysm, manual compression was applied for a maximum of 40 min followed by compression bandage for a minimum of 12 hours. If compression failed, thrombin was injected under ultrasound guidance. RESULTS: Thirty-six patients had a FA. Their age ranged from 58 to 90 years (mean 71+/-9 years). All patients were taking aspirin (median dose 100 mg per day) and clopidogrel (median dose 75 mg per day). Additionally, 24 patients had received subcutaneous heparin (7500 to 12 500 units) or enoxaprin (0.4-1.0 ml) 3 to 12 hours before treatment. The mean width of the false aneurysm was 22.1+/-3 mm, mean length 33.6+/-35.4 mm, and mean depth 19.5+/-8.2 mm. In six patients (17%), ultrasound-guided manual compression was tolerated, succeeding after 5 to 31 minutes. Thirty patients received thrombin injections (100-1800 units, mean 880+/-470 units, median 800 units). Complete thrombosis occurred in 28 patients (93%). Surgery was performed in the other two patients. The thrombin injection was not associated with any complications. In particular, there were no peripheral vascular complications. CONCLUSION: In patients with FA taking aspirin and clopidogrel, selective thrombin injection is more effective than manual compression.

Aged↗

Nimesulide aggravates kainic acid-induced seizures in the rat.

Treatment of rats with kainic acid (10 mg/kg, intraperitoneally) triggers limbic seizures. Cyclooxygenase-2 mRNA is expressed in the hippocampus and cortex after 8 hr and marked cell loss occurs after 72 hr in the CA1-CA3 areas of the hippocampus. We examined the effect of the cyclooxygenase-2 inhibitor, nimesulide (N-(4-nitro-2-phenoxyphenyl)-methanesulfonamide), on kainate-induced seizures and delayed neurotoxicity. Nimesulide (10 mg/kg, intraperitoneally) was well tolerated given alone or 6-8 hr after kainate. However, pretreatment with nimesulide augmented seizures and increased the mortality rate from approximately 10% to 69%. We examined the effect of nimesulide on delayed cell loss after 72 hr in the surviving animals with histological staining. Cell loss did not seem to be reduced in animals treated with nimesulide 6-8 hr after kainate, but in the surviving animals pretreated with nimesulide less cell loss occurred. We conclude that nimesulide should be used with caution as an antiinflammatory drug in patients with convulsive disorders.

Animals↗

The selective cyclooxygenase-2 inhibitor rofecoxib reduces kainate-induced cell death in the rat hippocampus.

Treatment of male Sprague-Dawley rats with kainic acid (10 mg/kg, i.p.) triggered limbic seizures in 60% of the animals starting within 30 min and lasting for about 6 h. Cyclooxygenase-2 (COX-2) mRNA was strongly induced in the pyramidal cells of the hippocampus, in the amygdala and the piriform cortex after 8 h, as shown by in situ hybridization, and returned to control levels after 72 h. At this time marked cell loss occurred in the CA1-CA3 areas of the hippocampus. We hypothesize that rofecoxib, a selective COX-2 inhibitor, might abbreviate the late neurotoxicity, possibly associated with COX-2 induction. Animals which developed seizures were treated for 3 days with rofecoxib (10 mg/kg, i.p., n = 12) starting 6 or 8 h after kainic acid injection. Histological staining of viable cells confirmed that rofecoxib treatment selectively diminished cell loss in the hippocampus. The TdT-mediated dUTP nick end labelling (TUNEL) technique was used to estimate delayed cell death. Abundant TUNEL-positive cells were detected in seizure rats 72 h after kainic acid injection in pyramidal cells of the hippocampus (CA1-CA3), in cells of the thalamus, the amygdala and the piriform cortex. Treatment with rofecoxib selectively and significantly (P < 0.05) attenuated the number of TUNEL-positive cells in the hippocampus, whereas the cells of the thalamus, amygdala and piriform cortex were not protected. Therefore we conclude that COX-2 might contribute to cell death of pyramidal cells of the hippocampus as a consequence of limbic seizures.

Animals↗

Comparison of primary angioplasty with conservative therapy in patients with acute myocardial infarction and contraindications for thrombolytic therapy. Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) Study Group.

The benefit of primary angioplasty in patients with acute myocardial infarction (AMI) and contraindications for thrombolysis compared to a conservative regimen is still unclear. Out of 5,869 patients with AMI registered by the MITRA trial, 337 (5.7%) patients had at least one strong contraindication for thrombolytic therapy. Out of these 337 patients 46 (13.6%) were treated with primary angioplasty and 276 (86.4%) were treated conservatively. Patients treated conservatively were older (70 years vs. 60 years; P=0.001), had a higher rate of a history with chronic heart failure (14.8% vs. 4.4%; P=0.053), a higher heart rate at admission (86 beats/min vs. 74 beats/min; P=0.001), and a higher prevalence of diabetes mellitus (27.1% vs. 12.8%; P=0.056). Patients treated with primary angioplasty received more often aspirin (91.3% vs. 74.6%; P=0.012), beta-blockers (60.9% vs. 46.1%; P = 0.062), angiotensin converting enzyme (ACE) inhibitors (71.7% vs. 44%; P=0.001), and the so-called optimal adjunctive medication (54.4% vs. 32.3%; P=0.004). Hospital mortality was significantly lower in patients who received primary angioplasty (univariate: 2.2% vs. 24.7%; P=0.001; multivariate: OR=0.46; P=0.0230). In patients with AMI and contraindications for thrombolytic therapy, primary angioplasty was associated with a significantly lower mortality compared to conservative treatment. Therefore, hospitals without the facilities to perform primary angioplasty should try to refer such patients to centers with the facilities for such a service, if this is possible in an acceptable time.

Aged↗

Differences in patients with acute myocardial infarction treated with primary angioplasty or thrombolytic therapy. Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) Study Group.

BACKGROUND: Little is known about the differences in patients with acute myocardial infarction (AMI) treated with primary angioplasty or intravenous thrombolysis in clinical practice. METHODS: In all, 5,906 patients with AMI were registered by the Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) study. Of these, 491 (8.3%) patients were treated with primary angioplasty and 2,817 (47.7%) with intravenous thrombolysis. RESULTS: There were only minor differences in baseline characteristics between the two groups. Prehospital delay time (median) was longer in the angioplasty group than in the thrombolysis group (161 vs. 120, p = 0.001), as was door-to-treatment time (88 vs. 30 min; p = 0.001). Patients treated with primary angioplasty more often had contraindications for thrombolytic therapy (12.9 vs. 6%, p = 0.001) and received beta blockers (65 vs. 58.1%, p = 0.004), heparin (98.2 vs. 91.6%, p = 0.001), angiotensin-converting enzyme (ACE) inhibitors (64.8 vs. 50%, p = 0.001) and "optimal" concomitant medication (56.4 vs. 42.9%, p = 0.001) more often. Univariate analysis showed a significant lower incidence of heart failure (5.3 vs. 16.5%, p = 0.001), postinfarct angina (7.3 vs. 16.4%, p = 0.001), in-hospital death (7.9 vs. 11.7%, p = 0.015) and the combined end point (21.6 vs. 40.3%, p = 0.001) in these patients. Stepwise logistic regression analysis revealed optimal concomitant medication [odds ratio (OR) = 0.94, 95% confidence interval (CI): 0.89-0.98) and the type of revascularization (OR = 0.65, 95% CI: 0.58-0.73) to be associated with a significant reduction in the incidence of the combined end point. Similar results were obtained in all predefined subgroups. CONCLUSIONS: In clinical practice, patients treated with primary angioplasty are more often treated with beta blockers and ACE inhibitors than patients treated with intravenous thrombolysis. Thus, the selection of patients and the type of revascularization contributes to the reduction in mortality, overt heart failure, and postinfarct angina in these patients.

Angioplasty, Balloon, Coronary↗

Daytime and nighttime differences in patterns of performance of primary angioplasty in the treatment of patients with acute myocardial infarction. Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) Study Group.

BACKGROUND: Concern exists regarding the results of primary angioplasty for acute myocardial infarction when the procedure is performed during night hours. METHODS AND RESULTS: Between June 1994 and January 1997, 491 patients with acute myocardial infarction who underwent primary angioplasty procedures were consecutive registered in the Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) study. Three hundred seventy-eight patients (77%) were treated during the day and 113 (23%) at night. Baseline characteristics showed no major differences between the 2 groups. Prehospital delay time was 60 minutes shorter during the night (median value 180 minutes for day, 120 minutes for night, P =.005), and in-hospital time to treatment was 9 minutes longer (median value 85 minutes day, 94 minutes night, P =.037). Patients treated during the night more often received angiotensin-converting enzyme blockers (61.4% day, 76.1% night, P =.004) and the so-called optimal adjunctive therapy (54% day, 64.6% night, P =.045). There were no differences concerning clinical events between the 2 groups. Hospital mortality was 8.7% during the day and 5.3% during the night (univariate analysis P =.238; logistic regression P =.653). CONCLUSIONS: In a clinical setting, primary angioplasty for acute myocardial infarction can be performed safely during the night with a clinically insignificant prolongation of in-hospital time to reperfusion compared with practice during the day.

Aged↗

Cytochromes P450 with bisallylic hydroxylation activity on arachidonic and linoleic acids studied with human recombinant enzymes and with human and rat liver microsomes.

Bisallylic carbons of polyunsaturated fatty acids can be hydroxylated in NADPH-dependent reactions in liver microsomes. Human recombinant cytochromes P450 and human and rat liver microsomes were assayed for bisallylic hydroxylation activity. CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC. Both substrates were also converted to many other metabolites. CYP2C9 appeared to form 12R-HETE and 13-HETE, whereas CYP2C8 formed 13-HETE, 11-HETE and 15-HETE as main monohydroxy metabolites. Fetal human liver microsomes metabolized linoleic acid to 11-HODE as a major hydroxy metabolite, whereas arachidonic acid appeared to be hydroxylated at C13, C20 and, to some extent, at C10, C19 and C7. Fetal liver microsomes mainly formed 13R-HETE, whereas adult human liver microsomes and CYP1A2 mainly formed 13S-HETE. 7,8-Benzoflavone (5 microM) and furafylline (20 microM), two inhibitors of CYP1A2, reduced the bisallylic hydroxylation activity of adult human liver microsomes. Treatment of rats with erythromycin or dexamethasone induced bisallylic hydroxylation of linoleic acid to 11-HODE in liver microsomes by 2- and 10-fold, respectively. The biosynthesis of 11-HODE by microsomes of dexamethasone-treated rats was inhibited by troleandomycin (ED50 = 1 microM) and by polyclonal antibodies against CYP3A1, suggesting that CYP3A1 could catalyze bisallylic hydroxylations in the dexamethasone-treated rat. We conclude from steric analysis of 13-HETE and the effects of CYP inhibitors on adult human liver microsomes that CYP1A2 might contribute to its bisallylic hydroxylation activity.

Animals↗

Aromatase inhibition with 4-hydroxyandrostenedione in the treatment of postmenopausal patients with advanced breast cancer: a phase II study.

Estrogen deprivation by aromatase inhibition is an effective treatment in breast cancer. Between October 1986 and March 1988, 91 postmenopausal patients with advanced breast cancer entered a phase II study performed jointly in three center to investigate the new aromatase inhibitor 4-hydroxyandrostenedione. Patients received 500 mg 4-hydroxyandrostenedione intramuscularly (IM) every 2 weeks for 6 weeks, and 250 mg every 2 weeks thereafter. There were two complete (CRs) and 19 partial remissions (PRs) (response rate, 23%). Disease stabilization (no change; NC) was seen in 26 patients, and in 44 patients (48%), disease progression occurred. Duration of the CRs is 20+ months, median durations of PR and NC are 13+ and 8 months, respectively. Receptor status, relapse-free interval, and sites of metastatic lesions did not appear to influence treatment results. However, efficacy of previous tamoxifen treatment favorably predicted response to 4-hydroxyandrostenedione. Serum estradiol levels decreased significantly in patients after 2 weeks of treatment. Side effects were mostly nonspecific and of low degree, requiring discontinuation of treatment in only 3% of the patients. We conclude that aromatase inhibition with 4-hydroxyandrostenedione is efficacious in the treatment of postmenopausal breast cancer.

Adult↗

Lesions of the basal ganglia, thalamus, and deep white matter: differential effects on language functions.

Forty-five patients with unilateral demarcated vascular lesions in the basal ganglia, the thalamus and the deep white matter were investigated with an "aphasia battery." Patients with basal ganglia lesions performed worse than both other groups in tests of articulation, syntax, and lexical functions. The deficit of patients with basal ganglia lesions on all expressive language modalities was lateralized to the left hemisphere. Patients with left thalamic lesions showed impairments of speech fluency and in the Token Test. Patients with white matter lesions alone showed no effect of laterality in tests of language functions. The results are discussed on the basis of a recent theory of the participation of the deep nuclei in language processing.

Adult↗

Neuropsychological deficits associated with small unilateral thalamic lesions.

Neuropsychological deficits resulting from small, well demarcated, unilateral thalamic lesions were investigated in 13 right-handed patients. Fourteen patients with deep white matter lesions and 12 normal subjects served as controls. The performance of thalamic patients was generally worse than that of normals and patients with white matter lesions, although the lesions in the latter were significantly larger. There was no clear indication of a dichotomous lateralization of function at the level of the thalamus, although patients with left-sided lesions performed less well in almost all tests. There was some evidence of a rostrocaudal dichotomy, rostral thalamic lesions leading to memory deficits and caudal lesions to impairments of 'abstraction' and 'categorization'.

Adult↗