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Biomedical subjects

P Fitscha

Publications and source records attributed to P Fitscha.

At least 109 records · Page 6Linked to original sources

[Defects in the prostaglandin system. V. Inherited (?) disorder of prostacyclin degradation in the plasma (Wien-Döbling defect)].

The case report is presented of a woman of child-bearing age who developed myocardial infarction. An extremely shortened in vitro half-life of PGI2 in plasma was detected in this patient. This new familial defect "Wien-Döbling", in the prostaglandin system might affect an essential coregulator of haemostatic balance in man. It is not known whether this short half-life of PGI2 in vitro is due to accelerated degradation or a failure in stabilization of this biologically active compound.

Adult↗

[Accelerated degradation of prostacyclin in diabetic plasma--a further factor in the impairment of hemostatic balance?].

Prostacyclin is degraded in human plasma in vitro with an average half-life of 10 minutes. The degradation in plasma of patients suffering from type II diabetes mellitus is significantly enhanced. However, the inactivation of prostacyclin in plasma in patients with clinical manifestations of atherosclerosis, such as peripheral vascular disease, is unchanged. Methodological studies reveal that storage of plasma at various temperatures up to investigation, repeated freezing and thawing, as well as the addition of thromboxane-synthetase inhibitors do not exert any effect on plasmatic degradation of PGI2. In addition, no differences are found in plasmatic degradation in diabetics in accordance with the mode of treatment. The presence of a factor in human plasma in diabetics capable of increasing PGI2 degradation or the loss of a possible stabilizer could be one further important parameter, amongst others responsible for the development of either macro- or microangiopathy in diabetes mellitus.

Aged↗

Platelet sensitivity to antiaggregatory prostaglandins (PGE1,D2,I2) in patients with peripheral vascular disease.

Platelet sensitivity to antiaggregatory prostaglandins (PGI2, PGE1, PGD2) was studied in 143 patients (122 male) with angiographically proven peripheral vascular disease and compared with age-matched clinically normal controls. Patients had a significantly lower platelet sensitivity to PGI2, PGE1, and PGD2 than controls. Clinical stages had no significant influence on the platelet sensitivity to PGI2 and PGE1. Patients with stage IIa had a lower sensitivity to PGD2 than patients with stage IV, the difference not being significant. Analyzing the influence of risk factors like diabetes, hyperlipoproteinemia, or smoking, there seemed to be an inverse relation between risk factors and platelet sensitivity to PGI2 and PGE1. Smokers especially, together with smokers exhibiting an additional risk factor, exhibited the highest prostaglandin consumption (PGI2, PGE1) and therefore the lowest platelet sensitivity. However, it has to be emphasized that the differences were not significant. There was a significant correlation between platelet sensitivity to PGI2 and PGE1, whereas this was not the case between the respective sensitivities to PGI2 and PGD2. This supports the hypothesis that both these prostaglandins (PGI2, PGE1) share the same receptor on the platelet surface, whereas PGD2 has its own receptor.

Adenosine Diphosphate↗

The prostacyclin synthesis stimulating plasma factor is unchanged during acute angina pectoris.

Earlier studies have demonstrated that the levels of prostacyclin synthesis stimulating plasma factor are changed during various clinical situations thus leading to disturbances in hemostatic balance. Therefore, we studied the plasma factor in 20 patients undergoing acute anginal attacks in order to see whether there is any influence or a timedependent change after the event. The patients were subdivided into males or females as well as into those with or without maturity onset diabetes and who were smokers or no-smokers. As in-vitro test systems the rat abdominal aorta, human coronary artery and cultured endothelial and smooth muscle cells obtained from minipigs were used. Our findings demonstrate that incubating the different tissue samples in plasma leads to a significant increase of prostacyclin formation or of its stable breakdown 6-oxo-PGF1 respectively, in comparison to buffer control incubation. However, in none of the groups was a change observed during an anginal attack or in rate 60 and 120 minutes thereafter. These findings suggest that the prostacyclin synthesis stimulating plasma factor is not involved in hemostatic dysregulation, which has been observed to occur during and immediately after a coronary anginal attack.

Adult↗

Detection of aneurysms by gamma-camera imaging after injection of autologous labelled platelets.

Autologous platelet labelling was used to calculate platelet half-life in 860 patients with symptoms of coronary heart disease and/or peripheral vascular disease. Abnormal platelet deposition indicating an abdominal aortic aneurysm was found in 21 by gamma-camera imaging after reinjection of autologous indium-111 labelled platelets. Aneurysms detected by imaging were confirmed by angiography, computer tomography, and at subsequent surgery.

Adult↗

[Long-term ECG in clinical practice].

Long-term ECG monitoring is one of the greatest advances in clinical cardiology over the past 15 years. The recording examination including Holter technology is described. The clinical value of long-term ECG monitoring is compared with routine ECG and exercise testing. A survey on normal population data is made. Major indications for long-term ECG monitoring are detection of occult arrhythmias, evaluation of subjective symptoms such as palpitations, dizziness or syncope, recognition of pacemaker dysfunction, identification of high-risk patients with coronary heart disease and both evaluation as well as monitoring of drug therapy.

Arrhythmias, Cardiac↗

Is gamma-camera imaging of platelet deposition useful to assess the effectiveness of prostacyclin treatment?

Platelet labeling with 111-In-oxinesulfate allows visualization of platelet deposition in the vascular bed. Scintigraphic studies were performed in 6 patients with "active" (PUR greater than 1.20) and 8 patients with "inactive" (PUR less than 1.20) atherosclerotic lesions of the femoral artery. Platelet deposition was also studied in 11 patients with implanted prosthetic vascular grafts and in 21 patients with an abnormal aneurysm of the aorta. Infusing 5 ng/kg/min PGI2 during 6 hours for 5 days into patients with "active"-atherosclerosis and aneurysms of the aorta resulted in a significant decrease of platelet deposition even after having stopped the infusion. There was no influence of PGI2 on PUR in patients with "inactive" lesions. The group of patients with implanted prosthetic grafts demonstrated also a significant decrease of PUR values during the PGI2-infusion, but reached baseline values soon after stopping the infusion. When platelet deposition is increased gamma-camera imaging provides valuable date on the influence of any kind of therapy on the in-vivo platelet function.

Aorta, Abdominal↗

[Acute myocardial infarction in patients over 70].

History and clinical course were studied in 299 patients with acute myocardial infarction. 133 patients aged 70 and older (group 2) were compared to 166 patients under 70 (group 1). Hospital mortality of the total group was 23%. The mortality rate among the older patients (31%) was significantly higher than among the younger patients (17%) (p less than 0.01). The major cause of death in both groups was cardiogenic shock. It is noteworthy that in eight cases from group 2 pulmonary embolism was diagnosed at autopsy in spite of the fact that the patients were receiving prophylactic antithrombotic therapy. Analyzing the histories, it was noticed that group 2 had a significantly higher percentage of hypertension and left heart failure, whereas in group 1 significantly more smokers and hyperlipidemics were found. During hospitalization left ventricular enlargement and insufficiency were diagnosed more often in the elderly. It may be assumed that this fact is one of the reasons for the increased mortality of group 2.

Adult↗