Biomedical subjects
Publications and source records attributed to J Videbaek.
The pacemaker syndrome is a frequently occurring and frequently overlooked syndrome which can, as a rule, be treated. The diagnosis is often overlooked on account of the diffuse symptoms together with the frequency of symptoms in elderly patients. The temporal connection with VVI pacing is often, but not always, helpful in establishing the diagnosis. Three case histories with various manifestations of the syndrome are reviewed.
In connection with screening for risk factors for ischaemic heart disease in Bispebjerg Hospital, we have assessed three different models for calculation of the risk, employed on our own material. A total of 462 persons participated in the screening and 275 of these were under the age of 65 years. Out of these 275, 92 had plasma cholesterol values over or equal to 7.0 mmol/l and or smoked over 20 gram tobacco daily. On comparison between three models for calculation of the risk: one American, one British and one Swedish, moderate agreement was observed: the correlation coefficients varied between 0.75 and 0.89. The reason for this may be that the models for calculation of the risk are constructed on the basis of statistics already described from epidemiological investigations in which coincidence is demonstrated between selected observable factors and ischaemic heart disease. It is thus possible that the factors which we measure and possibly attempt to influence are not pathogenetic. We consider, therefore, that risk scoring should be employed with caution. As causal connection between ischaemic heart disease and cholesterol and smoking, respectively, have been demonstrated with reasonable certainty, we consider that it is reasonable to screen and intervene for these factors alone.
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Twenty-two patients with mild or moderate mitral or aortic incompetence were randomly assigned to treatment with either hydralazine (mean 127 mg/day, range 37-225) or placebo. Eight patients in the hydralazine group and ten patients in the placebo group completed the study. Two of the patients in the hydralazine group and one patient in the placebo group were withdrawn because of suspected side effects. One patient dropped out because of influenza. Over a period of seven weeks the patients were monitored clinically as well as non-invasively with echocardiography and exercise testing. The systolic blood pressure fell from 152 +/- 10 to 135 +/- 9 mm Hg (mean +/- s.e.m.) (17%, P less than 0.01). The diastolic blood pressure fell from 63 +/- 8 to 58 +/- 8 mm Hg (5%, P = 0.09). The heart rate was unchanged. Left ventricular internal diameter in systole decreased from 49 +/- 3 to 45 +/- 3 mm (9%, P = 0.05) and in diastole from 73 +/- 4 to 70 +/- 3 mm (4%, P = 0.03). Left ventricular systolic wall tension fell from 200 +/- 16 to 152 +/- 18 mm Hg (24%, P less than 0.01). Left ventricular shortening fraction increased from 32 +/- 3 to 36 +/- 3% (12%, P less than 0.01). Maximal exercise capacity improved from 3200 +/- 800 to 3800 +/- 700 kpm (19%, P = 0.02). No significant responses were observed in the placebo group. Oral hydralazine reduces left ventricular internal diameters, improves left ventricular performance, presumably at a lower level of oxygen consumption, and improves exercise capacity in patients with modest mitral or aortic incompetence.
Changes in myocardial performance after administration of gallamine 1.5 mg kg-1 and pancuronium 0.1 mg kg-1 were investigated in hypercapnic (PaCO2 = 7.08 kPa) and hypocapnic (PaCO2 = 2.74 kPa) dogs anaesthetized with thiopentone, nitrous oxide and halothane. Administration of pancuronium during hypocapnia caused a decrease of 25% in dP/dt max (corrected for changes in preload, afterload and heart rate). This change was not seen during hypercapnia, probably because of the associated sympathetic stimulation. By contrast, gallamine was without effect on dP/dt max in both groups. The increase in heart rate and cardiac output caused by the atropine-like action of both groups. The increase in heart rate and cardiac output caused by the atropine-like action of these relaxant drugs differed in the hypercapnic and hypocapnic group of dogs, with the more pronounced response in the latter group. The duration of the chronotropic changes was the same in both groups.
The results of a one to 19 year follow-up study of 9 children with supraventricular tachycardia of more than one month's duration are reported. The ECG diagnosis of tachycardia was made before birth in one patient and between the ages of 8 months and 12 years in 8. Four had sustained and 4 had repetitive tachycardia, while one patient had both patterns at different times. Reciprocal rhythm was diagnosed in 3 patients and exit block in 2. Severe symptoms had occurred in 2 patients, but as a rule symptoms were mild or absent. No treatment abolished the arrhythmias but digitalis reduced the overall ventricular rate in 6 patients. After a duration of 1-7 years, 3 patients still had tachycardia at the follow-up. In the remaining 6 patients the tachycardia had subsided 7 months to 10 years after the onset.
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Blood glucose, glucose tolerance, serum insulin, free fatty acids in serum, plasma noradrenaline, and plasma adrenaline were measured in 10 patients with acute myocardial infarction (AMI) as well as in healthy subjects. Both noradrenaline and adrenaline in plasma were elevated in patients with AMI, the level being fairly constant in the individual patients and dependent on their degree of illness. In the fasting state, blood glucose, serum insulin, and free fatty acids were elevated in patients with AMI. Plasma noradrenaline showed a highly significant correlation with the fasting blood glucose concentration, but not with serum insulin or free fatty acids. The concentration of free fatty acids in serum could be predicted only if both plasma noradrenaline and the basal insulin concentration were known. Intravenous glucose tolerance was reduced in patients with AMI, especially in patients with high plasma noradrenaline and a low initial rise in insulin. There was a significant negative correlation between the initial rise in insulin expressed in percentage of the basal insulin concentration and the plasma noradrenaline level. The statistical effects of serum insulin and plasma noradrenaline on the glucose tolerance could not be separated from each other. The decline in free fatty acids after intravenous injection of glucose showed a negative correlation with plasma noradrenaline and a positive correlation with the initial rise in insulin. Plasma adrenaline did not correlate with any of the metabolic parameters mentioned above. The plasma noradrenaline concentration was elevated to such a degree in patients with AMI that the observed changes in metabolism might have been caused directly by the circulating noradrenaline. During the glucose tolerance tests, the effects of noradrenaline was probably carried out indirectly via a suppression of insulin secretion. It is conceivable that any effect of plasma noradrenaline on the basal insulin secretion was neutralized by the fasting hyperglycemia.
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