[Hypertrophic obstructive cardiomyopathy (author's transl)]. / Die hypertrophische obstruktive Kardiomyopathie

The course of hypertrophic obstructive cardiomyopathy is characterized by a slow progressiveness. The degree of clinical severity can therefore not seldom be unchanged over 10 years and more. Even today, no therapy is known that will guarantee a confirmed improvement in the prognosis of the disease. The symptoms and discomforts can be favorably influenced in many cases by conservative measures. Compared with the conservatively treated patients the favorable results are in the surgically treated group.

[Course observations of hypertrophic obstructive myocardiopathy]. / Verlaufsbeobachtungen der hypertrophischen obstruktiven Myokardiopathie (HOCM)

The course of HOCM is characterized by a slow progression. Symptoms can often be influenced favourably by medical treatment. Altogether there is some difference between the course of untreated and the propranolol-treated patient groups which is, however, not statistically significant. Furthermore, the rate of sudden death is uninfluenced. Comparing clinical and haemodynamic results in medicically treated patients we find a reduction of the outflow tract obstruction in case with clinical improvement but not a reduction of the enddiastolic pressure. Independent on the clinical course there was a significant increase of the enddiastolic pressure after 5.5 years. We may conclude that there is a progredient process of hypertrophy which is uninfluenced by the obstruction and by conservative management. The best results are obtained in the operated group. According to our results a surgical intervention should possibly be considereed more generously.

[Indication for coronary surgery with special reference to hemodynamic results]. / Indikation zur Koronarchirurgie unter Berücksichtigung hämodynamischer Resultate

An analysis is made whether and how far the aims of coronary artery bypass surgery improvement or relief of angina, improvement of the physical working capacity, improvement of the oxygen supply of ischemic myocardium, improvement of the myocardial function, improvement of longevity, can be attained. 48 percent of 87 patients had complete subsidance of angina pectoris after operation. There was a considerable improvement in 32 percent, no change in 14 percent, and a deterioration in 6 percent. After operation, the working capacity was improved in 73 percent of our patients significantly, in some cases nearly unlimited. By a comparison between loss of complaints and bypass function (open or closed) we found a good correlation between functioning bypasses and complaints. But there are some cases without complaints in spite of a closure of the bypass. Also the reverse, unchanged complaints in spite of an open bypass, was seen. A normalisation of preoperative disturbed myocardial function can be attained. Significant improvements, but also deteriorations can be found. Generally, there is a good correlation between improved myocardial function and improvement of the working capacity. Yet there is not rarely a discrepancy between a significant improvement of the working capacity and the left ventricular function. The explanation may be a loss or a postoperative augmented threshold for anging pectoris. Comparing the groups of patients with conservative and surgical treatment, the superiority of surgical treatment cannot be proved as yet. An exception seems to be the stenosis of the left main coronary artery. With this exception, prognostic considerations cannot play a role for the indication of a coronary bypass operation. Aspects for the indication of coronary surgery are untractable or disabling angina pectoris and the consideration how impending complications can be prevented.

The effects of hypoxia, hypertrophy, and diet on rat myocardial ornithine decarboxylase activity.

We have shown that there is a highly significant difference between right and left ventricular ornithine decarboxylase activity. The left ventricle had a much higher activity compared with the right ventricle. A restricted diet caused a decrease in ornithine decarboxylase activity after 24 hr. Hypoxia caused a depression of the ornithine decarboxylase activity during the first 2 days of the experiment. In the hypertrophied right ventricle there was an initial decrease in ornithine decarboxylase after 24 hr and then a gradual increase in ornithine decarboxylase activity during the 7 days of the experiment. The increase in ornithine decarboxylase activity became significant when an increase in tissue weight became apparent.

Some properties of rat myocardial ornithine decarboxylase and the in vitro effects of nucleotides.

Myocardial ornithine decarboxylase appears to have characteristics similar to those of enzymes isolated from other tissues. Ornithine decarboxylase activity decreased very rapidly after the death of the animal. Storage of the cell sap fraction at 0 degrees C or -15 degrees C, however, led to only a small decrease in the enzyme activity up to 3 days after preparation. Pyridoxal phosphate at an optimum of 50 muM was essential for full enzyme activity. Thiol compounds did not increase the myocardial ornithine decarboxylase enzyme activity. The subcellular distribution of the enzyme in the myocardium was found to be different from that reported in other tissues. A partial purification of the enzyme was possible using the proteins precipitated at pH 5 from a cell-soluble fraction or by passing a soluble fraction through a Sephadex G 100 gel column. ATP, ADP, and AMP inhibited ornithine decarboxylase at high concentrations (5 mM), but GTP, CTP, and ITP inhibited at a 1 mM concentration and above.