Die Bedeutung des Thrombin-Antithrombin III-Komplexes in der Diagnostik der Lungenembolie und der tiefen Venenthrombose — Vergleich mit Fibrinopeptid A,Plättchenfaktor 4 und β-Thromboglobulin

Summary In 22 patients with suspected pulmonary embolism and 19 patients with suspected deep vein thrombosis, thrombin-antithrombin III complex (TAT) as an indicator of thrombin activation was measured using a newly developed ELISA. For comparison fibrinopeptide A (FPA), as a marker of an activated coagulation, as well as platelet factor 4 (PF4), and -thromboglobulin (-TG), as markers of platelet activation, were determined. In all patients in whom pulmonary embolism was confirmed by perfusion lung scan and in 15 of 16 patients in whom deep vein thrombosis was confirmed by phlebography, TAT exceeded the upper limit of normal (3.0 ng/ml). FPA was increased in 71% of the pulmonary embolism patients, PF 4 in 53%, and -TG in 59%. The data for the patients with deep vein thrombosis were comparable. PF 4 and -TG were increased in more than 25% of the normal controls, FPA in 17%, and TAT in 9%.TAT is very sensitive in detecting an activation of the coagulation system in patients with suspected thromboembolic events. The test, however, is not specific for thrombembolism; it only indicates an activation of the coagulation system. Acute pulmonary embolism or deep vein thrombosis would appear to be unlikely if TAT is normal. The measurement of TAT is easier and less susceptible to disturbances than that of FPA, PF4, and -TG.

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Abkürzungen FPA Fibrinopeptid A - LE Lungenembolie - PF 4 Plättchenfaktor 4 - TAT Thrombin-Antithrombin III-Komplex - -TG -Thromboglobulin (beta-Thromboglobulin) - VT tiefe Venenthrombose     

Entzündliche Herzerkrankungen

Ohne Zusammenfassung     

Serum nitrite sensitively reflects endothelial NO formation in human forearm vasculature: evidence for biochemical assessment of the endothelial L-arginine-NO pathway.

OBJECTIVE: A reduced bioactivity of endothelial nitric oxide (NO) has been implicated in the pathogenesis of atherosclerosis. In humans, the endothelial L-arginine-NO pathway has been indirectly assessed via the flow response to endothelium-dependent vasodilators locally administered into the coronary, pulmonary or forearm circulation. However, biochemical quantification of endothelial NO formation in these organ circulations has been hampered so far because of the rapid metabolism of NO. Therefore, we aimed to work out a reliable biochemical index to assess endothelial NO formation in human circulation. METHODS: In 33 healthy volunteers, forearm blood flow (FBF) was measured by standard techniques of venous occlusion plethysmography at rest, after local application of the endothelium-dependent vasodilator acetylcholine (ACH), the endothelium-independent vasodilator papaverine (PAP), the stereospecific inhibitor of endothelial NO synthase (eNOS) L-NMMA, and L-arginine (ARG), the natural substrate of eNOS. In parallel, nitrite and nitrate concentrations in blood samples taken from the antecubital vein were measured by HPLC using anion-exchange chromatography in combination with electrochemical and ultraviolet detection following a specific sample preparation method. RESULTS: ACH dose-dependently increased resting FBF (from 3.0 +/- 0.3 to 10.4 +/- 0.9 ml/min per 100 ml tissue) and serum nitrite concentration (from 402 +/- 59 to 977 +/- 82 nmol/l, both p < 0.05, n = 12). A significant correlation was observed between the changes in FBF and the serum nitrite concentration (r = 0.61, p < 0.0001). L-NMMA reduced resting FBF and endothelium-dependent vasodilation by 30% and this was paralleled by a significant reduction in serum nitrite concentration at the highest dose of ACH (n = 9, p < 0.001). PAP increased FBF more than fourfold, but did not affect serum nitrite concentration (n = 11), whereas ARG significantly increased both FBF and nitrite. Basal serum nitrate amounted to 25 +/- 4 mumol/l and remained constant during the application of ACH, PAP and L-NMMA. CONCLUSIONS: The concentration of serum nitrite sensitively reflects changes in endothelial NO formation in human forearm circulation. This biochemical measure may help to characterize the L-arginine-NO pathway in disease states associated with endothelial dysfunction and to further elucidate its pathophysiological significance for the development of atherosclerosis in humans.     

Epidemiologie und Ursachen von Vorhofflimmern

Zusammenfassung Vorhofflimmern ist die h?ufigste, behandlungsbedürftige Herzrhythmusst?rung mit einer altersabh?ngigen Pr?valenz von 0,4–10%. Aufgrund der noch immer geringen Effizienz medikament?ser Therapien zur Konversion und Erhalt eines stabilen Sinusrhythmus und des zunehmenden Anteils ?lterer Menschen in unserer Bev?lkerung kommt der Diagnostik und Therapie des Vorhofflimmerns eine betr?chtliche Bedeutung zu.    Vorhofflimmern stellt keine homogene Arrhythmie dar, sondern basiert vielmehr auf einem weiten Spektrum unterschiedlicher ?tiologischer Faktoren. H?ufig ist Vorhofflimmern somit nicht als eigenst?ndiges Krankheitsbild, sondern vielmehr als Symptom einer zugrundeliegenden Erkrankung anzusehen. Die dabei h?ufigsten kardialen Erkrankungen sind die Herzinsuffizienz, die koronare Herzerkrankung, das Cor hypertensivum und Herzklappenfehler. Jedoch auch postoperativ nach kardiochirurgischen Eingriffen ist das Vorhofflimmern von hoher Bedeutung.    Die Lebensqualit?t der Patienten mit Vorhofflimmern kann aufgrund zahlreicher klinischer Symptome deutlich reduziert sein. Komplizierend weisen Patienten mit Vorhofflimmern ein mit dem Alter zunehmendes Schlaganfallrisiko sowie eine erh?hte Mortalit?t auf.    Kontovers diskutiert wird die Frage, ob das Vorhofflimmern selbst die erh?hte Mortalit?t verursacht oder nicht vielmehr die zugrundeliegenden Erkrankungen sowie die begleitenden Komplikationen hierfür verantwortlich sind, denn das Auftreten von Vorhofflimmern ist h?ufig Ausdruck einer fortgeschrittenen Herzinsuffizienz oder einer schweren koronaren Herzerkrankung.    Die Diagnostik und Therapie des Vorhofflimmerns sollte sich daher in erster Linie auf die Erkennung und Behandlung der m?glicherweise urs?chlichen Grunderkrankung sowie die Pr?vention assoziierter Komplikationen stützen. Eingegangen: 5. Mai 2001 Akzeptiert: 15. Mai 2001     

Restenosis after elective coronary balloon angioplasty in patients with end stage renal disease: a case-control study using quantitative coronary angiography

Objective—To assess the rate of angiographic restenosis in patients with end stage renal disease after elective coronary angioplasty.
Design—A retrospective case-control study of 20 patients with end stage renal disease and 20 sex and age matched controls without renal disease, who had undergone primarily successful coronary angioplasty. Control coronary angiography was performed regardless of worsening or renewed incidence of anginal symptoms.
Main outcome measures—Group comparison of coronary morphology, as evaluated by quantitative coronary angiography, and of cardiovascular risk factors.
Results—The rate of angiographic restenosis was 60% in patients with renal disease and 35% in controls. In patients with end stage renal disease the following differences (mean (SD) were found versus controls: raised plasma fibrinogen (483 (101) v 326 (62) mg/dl, p < 0.001); raised plasma triglyceride (269 (163) v 207 (176) mg/dl, p < 0.01); smaller diameter of the coronary reference segment (2.59 (0.87) v 2.90 (0.55) mm, p < 0.10); smaller minimum luminal diameter of the dilated stenosis (0.77 (0.46) v 0.97 (0.27) mm, p < 0.05). Discriminant analysis showed that minimum luminal diameter before angioplasty (r = −0.79) and fibrinogen (r = +0.34) had the highest statistical association with restenosis.
Conclusions—The high rate of angiographic restenosis in patients with end stage renal disease seems to be related to the size of the vessel dilated and to an increased prothrombotic risk, as indicated by higher fibrinogen concentrations.

Keywords: renal disease;  coronary artery disease;  coronary angioplasty;  restenosis     

Non-invasive assessment of graft patency using transcutaneous Doppler echocardiography for the validation of functional improvement after PTCA of the LAD via internal thoracic artery graft

Percutaneous transluminal coronary angioplasty (PTCA) of a native coronary artery via internal thoracic artery (ITA) graft after bypass surgery is a relatively rare procedure. Our current study evaluates the flow velocity patterns of the graft before and after PTCA. After intervention the mean diastolic flow velocity increased under rest and stress conditions. In addition, the graft patency was proved not before control angiography after 6 months. It could be verified that the measurement of flow velocity patterns under rest and stress conditions is a useful non-invasive procedure for monitoring long-term patency and PTCA-results of this vessel.     

Vorhofflimmern

Atrial fibrillation represents the arrhythmia that most frequently leads to hospital admission. Due to the age structure of our population and the increasing morbidity and comorbidity, one has to assume that this arrhythmia will reach an even higher prevalence. The therapeutic successes are often insufficient. First of all, it is important to diagnose and treat the underlying disease. Secondly, antiarrhythmic therapy has to be considered in symptomatic patients. In those patients and in the case of a persistent form, electrical cardioversion should be performed. Repetitive cardioversions in asymptomatic patients yield no advantage for mortality. Antiarrhythmic therapy consists of drugs of the classes Ia, Ic, and III. Concomitant anticoagulation is necessary; ASS in indicated only in patients without structural heart disease and lacking thromboembolic risk factors. If risk factors are present, effective therapy with coumarin derivatives is required. Therapy with ACE inhibitors and AT blockers leads to an advantage in patients with arterial hypertension and/or heart failure concerning the stability of sinus rhythm after cardioversion and the incidence of arrhythmia. Newer medications for anticoagulation and newer antiarrhythmic drugs raise the hope of a future therapy with higher efficacy and lower rate of side effects.     

Percutaneous peripheral laser angioplasty: initial clinical results

Laser angioplasty has developed as a new method for the treatment of peripheral arterial occlusive disease. In 19 patients with high grade stenoses or obstructions of the superficial femoral, popliteal or posterior tibial arteries (Fontaine stage IIa-IV) percutaneous transluminal laser angioplasty was performed using a novel laser catheter system. The laser catheter itself is made of polyethylene. Its distal tip is formed ovally and marked X-ray densely. A silica fiber (core diameter 0.6 mm) for delivering the laser energy is inserted into the laser catheter. Through a sheath with hemostatic valve, laser catheter and silica fiber are introduced into the artery and then advanced to the stenosis over a guide wire. During laser angioplasty, laser catheter and silica fiber are rotated around the guide wire. We use a cw-Nd: YAG laser with a wavelength of 1064 nm. The mean degree of stenosis decreased from 92 +/- 12% before to 31 +/- 19% after laser angioplasty. By conventional balloon angioplasty a further reduction of the degree of stenosis down to 15 +/- 20% was achieved. The mean systolic Doppler ankle-arm pressure ratio improved from 0.56 +/- 0.25 before laser angioplasty to 0.89 +/- 0.24 after combined laser and balloon angioplasty. In seven patients, clinically non-significant distal embolization occurred. In no patient there was a perforation of the arterial wall. Up to now, digital subtraction angiography 3 months after laser angioplasty has been performed in five patients and showed patency of all lesions. The mean systolic Doppler ankle-arm pressure ratio was 0.84 +/- 0.20.