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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.

The interference of various foodstuffs on methods to determine epinephrine (E), norepinephrine (NE), vanillylmandelic acid (VMA), metanephrines (MN), homovanillic acid (HVA), and 6-hydroxyindole acetic acid (5-HIA) in the 24 h urine for diagnosis of pheochromocytoma and carcinoid syndrome, respectively, was investigated. The foodstuffs included were: tea, coffee, almonds, pineapples, cheese, walnuts, vanilla pudding, bananas, tomatoes, and chocolate. Further, the interference of cigarette smoking on the determination of E, NE, VMA, and MN was also investigated. Walnuts caused a rather high elevation of 5-HIA in the urine. After eating bananas elevated excretion of E, NE, VMA, MN, and 5-HIA was observed. Small increases of the MN values were noticed after coffee and pineapples. Smoking of 20-30 cigarettes/day had no influence on the variables measured. If the methods described are used, thus, only bananas and walnuts have to be restricted some days before and during urine sampling, but not coffee and pineapples if consumed in the usual small quantities. There is no reason to insist on diet restriction except for bananas and walnuts.

It is possible to separate metanephrine and normetanephrine from urine for the automated fluorimetric routine determination by means of a combination of liquid-liquid partition with ethylacetate and clean-up of the extract through Amberlite XAD-4. The differentiated fluorimetric determination is based on the oxidation with potassium hexacyanoferrate (III) in the presence of zinc ions and different pH values in an autoanalyzer. No quenching effects were observed. The recovery yields were in the range of 60%, the relative standard deviation being less than 10%.

This study describes the secretion of cortisol, growth hormone, prolactin and catecholamines before, under, and following gynaecological surgery in electrostimulation anaesthesia combined with nitrous oxide (ESA). The hormonal stress reactions of ESA were compared to inhalation anaesthesia with enflurane-nitrous oxide ( EFL ). Twenty-two patients undergoing laparotomy were allocated evenly to one of these procedures. In both groups serum levels for cortisol, growth hormone, and prolactin increased during surgery. Growth hormone showed a considerably higher increase during ESA at the end of the operation, whereas prolactin was higher at all periods of surgery during EFL . Cortisol, however, was identical for both groups. Renal excretion rates of adrenaline and noradrenaline were not significantly different. During surgery more metanephrine and normetanephrine were excreted in the urine under ESA than under EFL . There is no advantage with ESA intra- or postoperatively as compared to other routine procedures of anaesthesia for abdominal gynaecological surgery with regard to the so-called stress hormones or sympathetic activity.

Between 1982 and 1984, 48 studies with 131I-meta-benzylguanidine were carried out in Erlangen in patients with suspected pheochromocytoma or neuroblastoma. Scintigraphy with MIBG was found to be highly specific. False positive findings can be avoided if with weak uptakes an exact correlation with the results of morphological studies such as CT or sonography is sought and if follow-up observations ensure that they are not caused by activity residues in the biliary, intestinal or urinary pathways. False negative findings are made in 5-10% of the investigations in pheochromocytoma and in 41% of those in neuroblastoma patients. In pheochromocytoma the uptake rates are generally low (1-2%), whereas in neuroblastoma they may reach 10% and more.

From 1949 to 1974, urine samples of 1669 patients with unclarified arterial hypertension were tested for non-conjugated catecholamines. Chromaffine tumours--among them one pheochromoblastoma and two families with inherited forms--were found in 1.1% of all cases. With the procedure applied, adrenergic alpha- and/or beta-mimetic actions on the circulation of cats can be identified when the excretion of total catecholamines is increased by the factor 1.5 to 2.0. Hence, chromaffine tumours with smaller excretion rates (about 200 mug/24 h) are also detectable, so in one case where the excretion of vanillyl-mandelic acid was normal. Thus all prerequisites concerning sensitivity and specificity of a screening method are fulfilled. The large variety of symptoms of chromaffine tumours becomes obvious from the catamnestic data of 19 patients indicating problems which may arise in differential diagnosis.

Investigations in 13 hospitalized patients with pheochromocytomata showed peculiar characteristics of heart rate variation at rest, when compared with normals. All patients were given alpha- and beta-sympatholytic drugs. In one case alpha-methyl-Tyrosine caused I-II degree AV blocks and a stable high frequency sinus rate without physiological variations. Resting heart rate in pheochromocytoma varied interindividually from 55-105/min, in the absence of clinical attacks of the underlying disease. The frequency profile was characterized in 12 patients by sudden and inadequate rises of heart rate (200%) of short duration, which were often recorded within 20 seconds of the onset of muscular activity. A similar but less pronounced heart rate modulation was found 1-2 weeks after operation in 3 cases. Our observations indicate that the heart rate profile described may be a sensitive parameter of dysfunction of the autonomous nervous system in pheochromocytoma. Whether the heart rate characteristics are of diagnostic value has to be assessed by further studies.

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.