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Biomedical subjects

W Mäurer

Publications and source records attributed to W Mäurer.

At least 19 recordsLinked to original sources
PubMed1992

[The therapy of the heparin-induced thrombosis-thrombocytopenia syndrome with immunoglobulins].

A 51-year-old obese woman who had just undergone a second osteotomy for arthrosis of the hip joint was given unfractionated heparin, 7,500 IU subcutaneously three times daily, as thrombosis prophylaxis. Signs of fulminant pulmonary embolism occurred on the 16th postoperative day with a platelet count of 33,000/microliters. Suspected heparin-induced thrombocytopenia and thrombosis (HITT) was confirmed by platelet tests. When heparin had been discontinued immunoglobulin G was administered, seven times 5 g intravenously, in view of the immunological genesis of HITT. In addition thrombolysis treatment with streptokinase combined with phenprocoumon was undertaken, until satisfactory anticoagulation was achieved after 4 days. Platelet count rose to 136,000/microliters within 20 hours of the first immunoglobulin dose. Complete clinical normality was restored, scintigraphy showed no perfusion deficit in the lungs.

Blood Cell Count↗
PubMed1990

[Fulminant venous and arterial thromboses under heparin therapy].

A deep-vein thrombosis developed in a 71-year-old patient on the eleventh day of heparin treatment (25,000 U intravenously over 24 hours) given because of a nontransmural anterior-wall infarct. Subsequently there occurred a unilateral and then bilateral thrombotic occlusion of the femoral arteries and thrombosis of the infrarenal artery with occlusion of the right renal artery which necessitated operative thrombectomy. Platelet count, initially 370,000/microliters, fell to 34,000/microliters. No source of emboli was found either echocardiographically or by thoracic and abdominal computed tomography. After heparin administration had been discontinued on the 15th day, platelet count quickly returned to normal. Rapidly progressing demarcation necessitated amputation of both legs. The patient died on the 23rd hospital day. The reported findings indicate a heparin-induced thrombosis-thrombocytopenia syndrome.

Acute Disease↗
PubMed1979

[Catecholamines for treatment of severe heart failure (author's transl)].

In patients with severe heart failure there is increased sympathetic-adrenergic activity functioning as a compensatory mechanism. Despite of increased plasma catecholamine levels myocardial sensivity to catecholamines administered for therapeutic reasons is not diminished. The positive inotropic effect of catecholamines is more pronounced as compared to digitalis glycosides. The therapeutic efficacy of catecholamines, particularly their capability to increase cardiac output, is strongly dependent on their action on alpha- and beta2-receptors. In order to enhance cardiac performance, catecholamines are mainly used under three clinical settings: 1. severe heart failure and cardiogenic shock secondary to acute myocardial infarction, 2. 'Low cardiac output syndrome" following cardiac surgery, and 3. chronic congestive heart failure refractory to therapy with glycosides and diuretics. The use of catecholamines in the presence of acute myocardial infarction may be hazardous due to the accompanying increase of myocardial oxygen consumption. Among the available catecholamines, clinical interest recently focused on dopamine and dobutamine. Particularly with the primarily cardioselective beta-stimulating agent dobutamine a marked positive inotropic effect can be achieved in a range of dosage not significantly affecting heart rate and peripheral resistance. Positive inotropic agents may be even more effective when used in combination with vasodilators, which decrease impedance to left ventricular ejection.

Catecholamines↗
PubMed1979

[Coronary reserve, left ventricular function, and coronary risk factors in patients with myocardial infarction, but normal coronary arteries (author's transl)].

In 5 patients with angiographically normal coronary arteries and previous myocardial infarction (left ventricular a- or dyscinesia), measurement of coronary reserve revealed normal values. On average, patients with myocardial infarction and normal coronary arteries were younger than patients with angiographically proven obstructive coronary lesions (p less than 0,001), and did not exhibit a rise in coronary risk factors. These results suggest that in some cases myocardial infarction is due to acute, completely reversible occlusion or severe stenosis of larger coronary arteries without morphological or functional defects of coronary arteries detectable later on.

Adult↗
PubMed1978

[The effect of etilefrine and dihydroergotamine on sympathetic nervous system activity when standing up (author's transl)].

Systolic blood pressure, heart rate and concentrations of adrenaline, noradrenaline and dopamine as well as plasma dopamine-beta-hydroxylase (DBH) were measured in 22 subjects in recumbency and on standing up. Six subjects each had previously been given intravenously dihydroergotamine (0.5 mg) or etilefrine (0.25 mg/min) or a placebo. It was demonstrated that orthostasis leads to an increased activity of the sympathetic nervous system and the adrenal system. After administration of dihydroergotamine there was a diminished reaction of the sympathetic nervous system with an increase of venous tone which counteracted the decrease in cardiac output. Etilefrine, on the other hand, inhibited the sympatho-adrenal reaction on orthostasis and decreased the liberation of adrenaline. It acts directly via stimulation of alpha-and beta-receptors and is thus predominantly indicated if there is insufficient response of the baroreceptor reflex at its efferent limb.

Adult↗
PubMed1977

[Functional assessment of coronary-artery stenosis (author's transl)].

Left-ventricular angiography was performed in 28 patients after measuring ascending aortic and left ventricular pressures and during isometric exercise (hand grip, 0.3-0.4 kg/cm2 for 3 min). In 13 patients coronary blood flow was measured at rest and during hand-grip exercise by means of the argon method. Eight patients without heart disease served as controls. In 14 patients with coronary heart disease abnormal left-ventricular kinetics, demonstrated already at rest, got worse during hand-grip exercise. In five patients with normal left-ventricular angiograms at rest hypokinesia and dyskinesia occurred during isometric exercise. The coronary artery supplying the abnormal ventricular wall had a 50-75% decrease in diameter. One patients with isolated 25% stenosis had normal left-ventricular kinetics both at rest and on hand-grip exercise. In all patients coronary blood flow rose by 60-90% during isometric exercise. It iducing a significant rise in myocardial oxygen demand and increased coronary blood flow.

Angiography↗
PubMed1976

[Congestive cardiomyopathy (author's transl)].

Congestive cardiomyopathy principally affects adolescent young men. The prognosis is very serious, mortality is almost 50%. Symptomatology, clinical and radiological findings are chiefly determined by signs of cardiac insufficiency. The ECG almost always shows a pathological but not a pathognomonic finding. If ventricular dilation is marked, left ventricular function is partly extremely limited. As causes of congestive cardiomyopathy, inflammatory changes, autoimmunological processes and metabolic disorders are discussed.

Adult↗
PubMed1976

[Urinary excretion of the catecholamines adrenaline, noradrenaline and dopamine as well as the derivatives metanephrine and normetanephrine in heart disease patients].

In 20 normal persons and in 57 patients with heart diseases with functional class I-IV (according to the classification of the New York Heart Association) the 24 hour urinary excretion of the catecholamines adrenaline, noradrenaline and dopamine and of the O2-methylated degradation products metanephrine and normetanephrine was determined. The 3 catecholamines and the 2 O-methylated derivatives were measured simultaneously using chromatographic extraction and purification (Bio-Rex 70) and selective flurometric determination. The following results could be obtained: 1. The urinary excretion of noradrenaline increased with increasing severity of the heart disease. 2. In patients with severe congestive heart failure (functional class IV) in addition the adrenaline excretion in addition the adrenaline excretion increased significantly. 3. There was no relationship between the urinary excretion of dopamine and the severity of the heart disease. 4. The ratio of noradrenaline excretion to dopamine excretion increased with increasing severity of the heart disease, indicating an increased activity of dopamine-mu-hydroxylation in patients with congestive heart failure. 5. The excretion of the O-methylated degradation products metanephrine and normetanephrine in normal persons and in patients with heart diseases paralleled the excretion of the corresponding catecholamines adrenaline and noradrenaline. This indicates, that increased excretion of noradrenaline and adrenaline (Class IV) in patients with heart failure was not due to impaired catecholamine-degradation but indead to increased catecholamine-release indicating increased sympatho-adrenergic activity. These results show in addition that also in patients with heart failure O-methylation represents still the main degradation step for the inactivation of the circulating catecholamines. 6. The relationship of toal excretion of 0-methylated derivates to total excretion of adrenaline and noradrenaline, however, decreased with increasing severity of heart disease, indicating a relative impairment of O-methylation under the condition of severe congestive heart failure.

Adult↗