H D Bruhn

Christian-Albrechts-Universität zu Kiel, Kiel, Schleswig-Holstein, Germany

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Publications (61)75.2 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: □ HintergrundPatienten mit koronarer Herzerkrankung sind durch thromboembolische Ereignisse besonders gefährdet. Eine Steigerung der Gerinnungsativierung, wie sie durch körperliche Aktivität hervorgerufen werden kann, läßt das Risiko für ein solches Ereignis ansteigen. Die Frage, ob die bei diesen Patienten häufig durchgeführte Fahrradergometrie mit einem erhöhten thromboembolischen Risiko verbunden ist, soll in der vorliegenden Arbeit betrachtet werden. □ Patienten und Methodik49 Patienten (Gruppe 1: mittleres Alter 59 Jahre; 42 Männer, sieben Frauen) mit angiographisch bekannter koronarer Herzerkrankung und 51 Patienten (Gruppe 2: mittleres Alter 53 Jahre; 44 Männer, sieben Frauen) ohne koronare Herzerkrankung wurden einer standardisierten Fahrradergometrie unterzogen. Vor und nach Belastung wurden Parameter der Blutgerinnung und der Fibrinolyse bestimmt. □ ErgebnisseZwischen beiden Gruppen fanden sich für alle vor und nach Belastung bestimmten Parameter keine signifikanten Unterschiede. Allerdings zeigten drei Parameter signifikante Änderungen innerhalb der Gruppen: Faktor VIII erhöhte sich in Gruppe 1 von 132 auf 156% und in Gruppe 2 von 106 auf 136%. Der von-Willebrand-Faktor stieg in Gruppe 1 von 230 auf 249% und in Gruppe 2 von 228 auf 24% an. Als Zeichen einer gesteigerten Fibrinolyse fand sich eine Steigerung des plasminogen-α2-antiplasmin-Komplexes in Gruppe 1 von 251 auf 401 μg/l und in Gruppe 2 von 247 auf 350 μg/l. □ SchlußfolgerungDiese Befunde unterstreichen, daß von der Fahradergometrie, durchgeführt in standardisierter Form und in aerober Stoffwechsellage, kein erhöhtes thromboembolisches Risiko für Patienten mit koronarer Herzerkrankung gegenüber Patienten ohne koronare Herzerkrankung ausgeht. □ BackgroundPhysical exercise leads to an elevated coagulation activity with a possibly disturbed hemostatic balance. Therefore patients with coronary heart disease have a potentially increased risk of thromboembolic events after a bicycle exercise tolerance test, that is frequently performed for diagnostic reasons. □ Patients and MethodsPatients with angiographically known coronary heart disease (Group 1: n=49; age 59 years; male=42, female=7) were investigated in comparison to a healthy cohort (Group 2: n=51; age 53 years; male=44, female=7) to study the influence of a standardized exercise tolerance test on hemostatic variables. Blood samples were taken before and after exercise. □ ResultsNo significant changes were found for any investigated parameter between both groups. However, 3 parameters did change significantly within the groups: factor VIII rose in Group 1 from 132 to 156% and in Group 2 from 106 to 136% and the von Willebrand factor rose in Group 1 from 230 to 249% and in Group 2 from 228 to 247%. An elevated fibrinolytic potential was found with an increase of plasminogen-α2-antiplasmin in Group 1 from 251 to 401 μg/l and in Group 2 from 247 to 350 μg/l. □ ConclusionThe findings underline the clinical presumption that exercise tolerance test does not increase the risk for thromboembolic complications in patients with coronary heart disease in comparison to patients without coronary heart disease, as long as the exercise tolerance test is performed in a standardized way and under aerobe conditions.
    05/2012; 95(1):14-19.
  • Hans Dietrich Bruhn
    DMW - Deutsche Medizinische Wochenschrift 09/2003; 128(33):1730-1. · 0.65 Impact Factor
  • Thrombosis Research 12/2002; 108(2-3):191-4. · 3.13 Impact Factor
  • H H Seydewitz, J Gram, H D Bruhn, I Witt
    Hamostaseologie 06/2002; 22(2):7-10. · 1.59 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Physical exercise leads to an elevated coagulation activity with a possibly disturbed hemostatic balance. Therefore patients with coronary heart disease have a potentially increased risk of thromboembolic events after a bicycle exercise tolerance test, that is frequently performed for diagnostic reasons. Patients with angiographically known coronary heart disease (Group I: n = 49; age 59 years; male = 42, female = 7) were investigated in comparison to a healthy cohort (Group 2: n = 51; age 53 years; male = 44, female = 7) to study the influence of a standardized exercise tolerance test on hemostatic variables. Blood samples were taken before and after exercise. No significant changes were found for any investigated parameter between both groups. However, 3 parameters did change significantly within the groups: factor VIII rose in Group 1 from 132 to 156% and in Group 2 from 106 to 136% and the von Willebrand factor rose in Group 1 from 230 to 249% and in Group 2 from 228 to 247%. An elevated fibrinolytic potential was found with an increase of plasminogen-alpha 2-antiplasmin in Group 1 from 251 to 401 micrograms/l and in Group 2 from 247 to 350 micrograms/l. The findings underline the clinical presumption that exercise tolerance test does not increase the risk for thromboembolic complications in patients with coronary heart disease in comparison to patients without coronary heart disease, as long as the exercise tolerance test is performed in a standardized way and under aerobe conditions.
    Medizinische Klinik 02/2000; 95(1):14-9. · 0.34 Impact Factor
  • Medizinische Klinik - MED KLIN. 01/2000; 95(1):14-19.
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    ABSTRACT: Anticoagulant fucoidan fractions of different molecular weight and sulfate content were prepared and investigated for their effects on platelet function in vitro. The fucoidan fractions were incubated with human platelet rich plasma (PRP) at concentrations of 5, 10 and 50 micrograms/ml. Platelet activation was subsequently studied by a standard aggregation assay and flow cytometric determination of the activation dependent platelet-surface markers CD62p (P-selectin, GMP-140) and CD63 (GP53). All fucoidan fractions induced irreversible platelet aggregation in a dose-dependent manner. Comparing fractions of identical molecular weight (100 kDa) the low sulfate content fucoidan FF5 (S = 7.6%) exerted a significantly greater effect than the highly sulfated fucoidan FF7 (S = 10.2%) over the whole concentration range (n = 5, P < 0.05). Among fractions of identical sulfate content fucoidan-induced platelet aggregation was also found to depend on the molecular weight of the fucoidan. At concentrations of 10 and 50 micrograms/ml the high molecular weight fraction FF7/1 (150 kDa) showed a significantly greater effect than the 50 kDa fraction FF7/3 (24.8 +/- 6.7 vs. 7.0 +/- 3.5 and 54.6 +/- 13.5 vs. 15.0 +/- 9.0%, respectively; mean +/- SD, n = 5, P < 0.05). The molecular weight dependence of the fucoidan effect was also reflected by the flow cytometric data. Coincubation of FF7/1 and FF7/3 (10 micrograms/ml) with PRP increased the number of CD62p and CD63 positive platelets by 9.0 +/- 3.3 vs. 2 +/- 1.9 and 7.1 +/- 2.4 vs. 3.2 +/- 2.6% over control values, respectively (n = 5, P < 0.05). In conclusion, our results show that the low molecular weight fucoidan FF7/3 combines potent anticoagulant and fibrinolytic properties with only minor platelet activating effects and is therefore a suitable substance for further pharmacological studies.
    Thrombosis Research 04/1997; 85(6):479-91. · 3.13 Impact Factor
  • H D Bruhn
    DMW - Deutsche Medizinische Wochenschrift 03/1997; 122(7):210. · 0.65 Impact Factor
  • M Lins, K H Zurborn, B Pries, H D Bruhn
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    ABSTRACT: Inflammatory reactions are taken to be nonspecific defensive measures of the organism and are associated with complex changes at cellular and humoral level. Activation of blood coagulation plays an important part in this, especially as it is accompanied by an increased risk of thromboembolism. It was the aim of this investigation to assess this risk by measuring sensitive markers of coagulation activation. Biochemical markers of coagulation activation (prothrombin-fragment F1 + 2 and thrombin-antithrombin III complex [TAT]) and fibrin formation (D-dimer) were measured in 130 patients (61 men, 69 women; mean age 56.9 [20-89] years). 44 had pneumonia, 44 bronchitis and 42 urinary tract infections. A healthy control group for comparison consisted of 11 men and 15 women (mean age 48.7 [23-79] years). F1 + 2, TAT and D-dimer were significantly increased, compared with the controls, in all three patient groups (P < 0.01). The greatest rises occurred in the patients with pneumonia: F1 + 2: median 1.2 vs 0.6 nmol/I, TAT: 6.2 vs 2.1 micrograms/l and D-dimer 2476 vs 223 ng/ml. These findings underline the importance of consistent thrombosis prophylaxis in patients with inflammatory disease, especially those at an increased risk.
    DMW - Deutsche Medizinische Wochenschrift 07/1996; 121(27):855-9. · 0.65 Impact Factor
  • M. Lins, K. H. Zurborn, B. Pries, H. D. Bruhn
    DMW - Deutsche Medizinische Wochenschrift 01/1996; 121(27):855-859. · 0.65 Impact Factor
  • H D Bruhn, K H Zurborn
    DMW - Deutsche Medizinische Wochenschrift 11/1995; 120(42):1441-4. · 0.65 Impact Factor
  • H D Bruhn, K H Zurborn
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    ABSTRACT: In comparison to a control group of 47 healthy, non-anticoagulated persons, 164 patients under stable oral anticoagulation therapy showed significant reduction in the plasma level of the prothrombin fragment F1+2 (p < 0.0005). Even with low intensity anticoagulation (INR < 2.0), F1+2 levels were reduced to within the normal range (0.32 - 1.2 nM/l) in all patients. The reduction in the plasma level of prothrombin fragment F1+2 is directly dependent on the intensity of oral anticoagulation therapy and provides a means of monitoring the anticoagulation effect achieved. Clinical studies are required to assess the practicality of using F1+2 for monitoring anticoagulation and in particular to assess the usefulness of low levels in predicting bleeding risk and high levels in predicting thrombotic risk during treatment.
    The Journal of heart valve disease 04/1995; 4(2):138-40. · 1.07 Impact Factor
  • H. D. Bruhn, K.-H. Zurborn
    Deutsche Medizinische Wochenschrift - DEUT MED WOCHENSCHR. 01/1995; 120(42):1441-1444.
  • H D Bruhn, K H Zurborn
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    ABSTRACT: It was the aim of this study to ascertain whether the plasma level of prothrombin fragment F1+2 is a suitable indicator of the anticoagulant effect of coumarin derivatives. The F1+2 levels were measured in 164 patients (100 women, 64 men; mean age 63.3 [34-83] years) in whom stable anticoagulation had been achieved with phenprocoumon, comparing the results with those obtained in healthy subjects (28 women, 19 men; mean age 54.6 [25-72] years) without anticoagulation. There was a significant reduction (P < 0.0005) in F1+2 plasma levels with oral anticoagulation (0.45 + 0.23 vs. 0.67 + 0.32 nmol/l). Even on a low degree of anticoagulation (international normalized ratio [INR] < 2.0) the F1+2 value was reduced to within the normal range (0.32-1.2 nmol/l). These results indicate that changes in the plasma level of prothrombin fragment F1+2 are directly dependent on the degree of oral anticoagulation and that this measure seems suitable for the monitoring of the anticoagulant effect. This is also true for oral anticoagulation of mild degree (INR < 2.0) in which the effect cannot be satisfactorily measured by the thromboplastin time (Quick test).
    DMW - Deutsche Medizinische Wochenschrift 08/1993; 118(26):967-70. · 0.65 Impact Factor
  • H D Bruhn, J Liebsch, C Wagner
    Thrombosis Research 12/1992; 68(3):317-9. · 3.13 Impact Factor
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    ABSTRACT: A multicenter study of a recently developed ELISA for the determination of prothrombin fragment F1+2 was performed in order to evaluate analytical and clinical aspects. Mean intra-assay and inter-assay reproducibility were found to be 11.0 and 12.6%, respectively. The measuring range covered by the calibration curve reaches from 0.04 to 10.0 nM/l F1+2. Testing 133 healthy subjects a reference range of 0.37 to 1.11 nM/l F1+2 (2.5-97.5 percentile) with a median of 0.66 nM/l F1+2 was calculated. Minor difficulties with blood sampling (venous occlusion for 2 min) did not affect F1+2 plasma concentrations. Significantly increased F1+2 levels were measured in patients with leukemia (p < 0.0001), severe liver disease (p < 0.005) and after myocardial infarction (p < 0.01). Elevated F1+2 concentration before the beginning of heparin therapy (1.25 nM/l) decreased to 0.77 nM/l (p < 0.0001) after 1 day of therapy. For patients in the stable phase of oral anticoagulant therapy decreasing F1+2 concentrations were measured with increasing INR. F1+2 levels were already significantly reduced in patients with INR < 2.0 (0.56 nM/l; p = 0.0005). Thus F1+2 determination may be helpful in identifying activation processes as well as in monitoring anticoagulant therapy.
    Thrombosis and Haemostasis 10/1992; 68(4):413-7. · 5.76 Impact Factor
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    ABSTRACT: Monitoring of anticoagulant treatment is not yet satisfactory. Otherwise optimal treatment control in special situations as low dose heparin prophylaxis in hip surgery or high dose anticoagulant treatment in patients after coronary stent implantation may be desirable. Recently available thrombin markers were analyzed in 51 patients under low dose (group 1) and 30 patients under high dose therapy with unfractionated heparin (group 2a and b) as well as in controls (n = 26). Before therapy these parameters were significantly elevated in both patient groups. Elevated thrombin-antithrombin III-complexes (TAT) despite adequate prolongation of aPTT under high dose heparin in 38.2% of patients indicate that therapeutic concentrations of heparin in these cases are insufficient for depressing this parameter completely. During low dose therapy only prothrombin fragment (F1 + 2) significantly decreased. This may be explained by catalytic induction of TAT-complex formation by heparin. Decrease of D-Dimer under heparin therapy in both groups does not parallel with TAT and F1 + 2 but was more prolonged. This can be explained by dependence of the D-Dimer level on spontaneous fibrinolytic activity and by a longer plasma half-life as well as a chronic and continuous fibrinolytic process in an older thrombus. In conclusion, thrombin markers seem to be helpful in estimating anticoagulant treatment efficacy. As a consequence, anticoagulant treatment has to be intensified in high-risk patients for complete depression of these markers. Whether the benefit of higher heparin doses is worth the risk of drug-induced hemorrhage, however, remains to be clarified in clinical studies.
    Thrombosis Research 06/1992; 66(2-3):121-31. · 3.13 Impact Factor
  • J Gram, H Duscha, K H Zurborn, H D Bruhn
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    ABSTRACT: We studied the activation of coagulation and fibrinolysis in the blood of patients with compensated (n = 25) and decompensated (n = 25) liver cirrhosis. We observed increased blood concentrations of thrombin-antithrombin III (TAT) complexes (p less than 0.001) and of D-dimer (p less than 0.001) in both groups of patients compared with healthy volunteers (n = 25). The blood levels of tissue-type plasminogen activator (t-PA) activity (p less than 0.001) and the concentrations of t-PA antigen (p less than 0.001) were also significantly raised in both groups of patients compared with controls, whereas plasminogen activator inhibitor did not deviate. There were no significant differences in the determined variables between the two groups of patients except that the concentrations of D-dimer were significantly higher (p less than 0.001) in patients with decompensated liver cirrhosis. The ratio between D-dimer and TAT did not deviate between patients with compensated liver cirrhosis and healthy volunteers but was significantly increased in patients with decompensated liver cirrhosis. These observations indicate that efflux from the extravascular space (for example, ascitic fluid) contributes to the high concentrations of fibrin degradation products (D-dimer) in patients with decompensated liver cirrhosis. In addition, we conclude that patients with liver cirrhosis have an enhanced activation of both coagulation and fibrinolysis but that the balance between these two systems is not significantly displaced compared with healthy volunteers.
    Scandinavian Journal of Gastroenterology 12/1991; 26(11):1173-8. · 2.33 Impact Factor
  • H H Seydewitz, J Gram, H D Bruhn, I Witt
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    ABSTRACT: A congenital fibrinogen variant in a German family is described which has been identified as a substitution of His in position 16 of the A alpha-chain for Arg, manifested over three generations in heterozygous form. The characterization is based on the reaction of the variant fibrinogen with thrombin and reptilase, on the HPLC-chromatographic properties and the amino acid composition of the abnormal fibrinopeptide A. Clinical observations in the affected family members (neither haemorrhagic nor thrombophilic tendencies), the results of routine coagulation tests (normal global clotting tests, prolonged thrombin and thrombin-coagulase time, decreased fibrinogen concentration in functional as opposed to immunological tests), and the autosomal co-dominant modus of inheritance of the fibrinogen variant are all in complete agreement with other reports in the literature concerning the same amino acid exchange. The results of our experiments with fibrinogen Kiel allow no definite conclusion regarding the question of whether it consists of pure homodimers or as of a mixture of homo- and heterodimers.
    Blood Coagulation and Fibrinolysis 09/1991; 2(4):501-6. · 1.25 Impact Factor
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    ABSTRACT: Cytostatic therapy is known to aggravate tumor-induced coagulopathy. Therefore, we have studied the effect of different chemotherapeutic regimens on the activation of coagulation and fibrinolysis in patients with non-Hodgkin's lymphomas or acute leukemias. In non-Hodgkin's lymphoma patients treated with an aggressive protocol (COL-BLAM) and in leukemia patients (TAD-9) fibrinopeptide A, prothrombin fragment (F1 + 2) and thrombin antithrombin III complexes (TAT) increased (Tables 4 and 6), while D-dimer did not deviate significantly. The ratio D-dimer/TAT consequently showed a significant decrease, indicating increased formation of thrombin after release of procoagulant factors, which is not paralleled by an activation of fibrinolysis. Both these groups were also characterized by an increase in uric acid and in C-reactive protein and plasminogen-activator inhibitor, two acute-phase reactants. In contrast, patients with non-Hodgkin's lymphomas treated with a less aggressive protocol (COP) showed no significant changes in hemostatic variables, uric acid, or acute-phase reactants. The release of procoagulant factors relates to the cytostatic sensitivity of the tumor and to a high tumor-cell destruction. Our results further emphasize the need for large-scale studies on antithrombotic prophylaxis in patients undergoing cytostatic treatment.
    European Journal Of Haematology 08/1991; 47(1):55-9. · 2.55 Impact Factor

Publication Stats

324 Citations
75.20 Total Impact Points

Institutions

  • 1989–2012
    • Christian-Albrechts-Universität zu Kiel
      • Institut für Medizinische Klimatologie
      Kiel, Schleswig-Holstein, Germany
  • 2003
    • Universitätsklinikum Schleswig - Holstein
      Kiel, Schleswig-Holstein, Germany
  • 1992
    • HELIOS Klinik Kiel
      Kiel, Schleswig-Holstein, Germany
  • 1991
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany