Biomedical subjects
Publications and source records attributed to L Thuesen.
Percutaneous balloon valvuloplasty of mitral stenosis was described in 1984. The subsequent results were promising and the method appears to be capable of replacing surgical valvotomy. Mitral balloon valvuloplasty in a patient with non-calcified rheumatic mitral stenosis is described here.
A double-blind, placebo-controlled, crossover study on the effects of 4 months' growth hormone (GH) treatment was carried out in 22 GH-deficient adults (8 women, 14 men; mean [SEM] age 23.8 [1.2] years). 1 patient was withdrawn because of oedema. Mean total body weight of the other 21 did not change, whereas mean muscle volume of the thigh, estimated by computerised tomography (CT), was significantly higher after GH than after placebo (70.0 [3.7] vs 66.3 [3.1] ml/0.8 cm cross-sectional slice). The mean adipose tissue volume of the thigh and subscapular skinfold thickness fell significantly during GH treatment. Growth hormone caused a small increase in the isometric strength of the quadriceps muscles and a significant rise in exercise capacity (60.8 [7.2] vs 54.2 [6.6] kJ). The heart rate both at rest and after maximum exercise was low during the placebo period and increased significantly during GH treatment. Blood pressure and echocardiographic wall mass of the left ventricle did not change during the study. Growth hormone increased both mean glomerular filtration rate and renal plasma flow from a subnormal level on placebo to a level comparable with that of an age-matched control group. The filtration fraction did not change. Urinary albumin excretion was in the low normal range and was not affected by GH treatment. Finally, GH treatment normalised mean circulating levels of insulin-like growth factor 1 (IGF-1), which were low after the placebo period (96 [9] micrograms/l placebo; 224 [28] micrograms/l GH). These findings suggest that GH, in a conventional replacement dose, has several potentially beneficial effects in GH-deficient adults and therefore encourage future long-term trials.
To evaluate whether the moderately elevated human growth hormone concentration, seen in insulin dependent diabetic patients, has any impact on lipoproteins, human growth hormone was given to nondiabetic persons in doses which would bring their plasma human growth hormone concentration up in the same level as seen in insulin dependent diabetic patients. After one week of treatment with human growth hormone we found total plasma triglyceride to be significantly raised (0.98 mmol/l +/- 0.28 mmol/l (mean +/- SD) before versus 1.27 mmol/l +/- 0.38 mmol/l (mean +/- SD) after treatment). Very low density lipoprotein (VLDL) was separated into two fractions (VLDL-1 and VLDL-2) of which VLDL-2 is regarded as a VLDL-remnant which is suggested to be of importance for development of atherosclerosis. After one week of human growth hormone treatment there were no changes in VLDL-1 concentrations whereas a significant raise in VLDL-2 triglyceride and VLDL-2 cholesterol was seen.
Nine acromegalic patients were treated by the somatostatin analogue SMS 201-995 octreotide (Sandostatin (octreotide), Sandoz, Basle, Switzerland] 250 micrograms/day in 4 divided s.c. injections (50 + 50 + 50 + 100 micrograms) for 1 month, 250 micrograms/24 has continuous s.c. infusions for another month and thereafter 200 micrograms three times daily as s.c. injections. Echocardiography was performed before the treatment, following 1 month of octreotide s.c. infusion/injection and after 6 and 12 months of octreotide treatment. No differences in serum growth hormone, heart rate, blood pressure, cardiac contractility or left ventricular wall mass or wall thickness were found between the infusion and the injection periods. As compared to the pretreatment levels serum growth hormone decreased by 62 and 66% respectively following 6 and 12 months octreotide treatment. The heart rate per minute (+/- SD) decreased from the pretreatment level of 75 +/- 12 to 63 +/- 13 (P less than 0.007) at month 12. The systolic and the diastolic blood pressure decreased from the pretreatment level of 121 +/- 8 and 79 +/- 5 mmHg respectively to 108 +/- 7 (P less than 0.0007) and 71 +/- 7 mmHg (P less than 0.0001) respectively at month 12.(ABSTRACT TRUNCATED AT 250 WORDS)
Seventy-nine patients admitted for VVI pacemaker treatment were randomly given a Siemens-Elema 412 S endocardial electrode (tip material vitreous carbon, tip area 12 mm2) (41 patients) or a Siemens-Elema 415 S endocardial electrode (tip material platinum, tip area 12 mm2) (38 patients). The groups did not differ in age, sex, magnitude of intracardiac signal or indication for pacemaker treatment. Pacing threshold was measured by the vario technique at 3 and 15 months after the implantation. In the group of carbon-tip electrodes and in the group of platinum-tip electrodes stimulation thresholds at implantation were 0.49 +/- 0.10 V and 0.54 +/- 0.14 V (ns), at months 31.40 +/- 0.45 V and 1.57 +/- 0.53 V (ns), and at months 15 1.12 +/- 0.33 V and 1.37 +/- 0.38 V (P = 0.003), respectively. After 1 year, 88% of the patients in the carbon-tip group and 66% (P = 0.04) in the platinum-tip group fulfilled our criteria for reducing pacemaker output from 5.0 V to 2.5 V. In comparable platinum-tip and carbon-tip pacing electrodes, the chronic stimulation threshold was lower in the carbon-tip than in the platinum-tip electrode.
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Cardiac function was studied by echocardiography in 12 patients with active acromegaly and in 12 age- and sex-matched healthy control subjects. None of the patients had cardiovascular diseases or other endocrine diseases than acromegaly. The patients had a mean age of 39 +/- 5 years and were short-term acromegalic with a mean duration of disease of 6 +/- 3 years. Mean left ventricular mass was 163 +/- 43 g/m2 in the acromegalic group versus 120 +/- 24 g/m2 in the control group. Preload (the diastolic diameter of the left ventricle) was within normal limits, while afterload (end-systolic meridional wall stress) was significantly decreased in the acromegalic group. Myocardial contractility assessed as fractional shortening of the left ventricle was 39.9 +/- 3.6% in the acromegalic group versus 32.9 +/- 5.1% in the control group, and cardiac output was increased by 52% in the acromegalic group because of increased heart rate and stroke volume. We suggest that augmented peripheral blood flow is responsible for the condition of cardiac hyperkinesia in short-term acromegaly and involved in the development of hypertension, which is a frequent complication of long-term acromegaly.
Left ventricular wall mass, thickness and movement were investigated by echocardiography in 80 insulin-dependent diabetic patients with no signs of ischaemic heart disease and in 40 healthy controls. In diabetics with a disease duration of greater than 30 yr, urinary albumin excretion rate greater than 200 micrograms/min (clinical nephropathy), proliferative retinopathy or autonomic neuropathy, both the posterior wall thickness and the septal thickness were increased compared to controls. The posterior wall thickness and the septal thickness were positively correlated to blood pressure (p less than 0.001), disease duration (p less than 0.001), urinary albumin excretion rate (p less than 0.001), and negatively correlated to the heart variation during deep respiration (p less than 0.01). The left ventricular wall mass was correlated to both blood pressure (p less than 0.01) and urinary albumin excretion rate (p less than 0.01). By multiple regression analysis urinary albumin excretion rate, disease duration and heart rate variation during deep respiration did not add significantly to the correlation between left ventricular wall mass/wall thickness and blood pressure. The septal movement was reduced in diabetics with proliferative retinopathy or clinical nephropathy. In conclusion, left ventricular wall thickness and wall mass were closely related to blood pressure in insulin-dependent diabetics. Signs of impaired cardiac function, such as reduced septal movement, were seen only in patients with severe microvascular disease.
Cardiac function was studied by echocardiography in 80 insulin-dependent diabetic patients with no signs of ischemic heart disease and in 40 healthy control subjects. Echocardiographic findings were related to the urinary albumin excretion rate (UAE). In the diabetes group, fractional shortening of the left ventricle (FS) was 37.3% versus 34.3% (P less than .01) in the control group, whereas indices of preload and afterload were at the same levels as in control subjects. In diabetic patients with preclinical nephropathy (UAE 20-200 micrograms/min), FS was 41.1% compared to 37.0% (P less than .002) in patients with no signs of nephropathy (UAE less than 20 micrograms/min) and 34.8% (P less than .001) in patients with clinical nephropathy (UAE less than 200 micrograms/min). Furthermore, in patients with preclinical nephropathy, afterload was significantly decreased, whereas preload was at the same level as in the other two groups of UAE. In conclusion, a condition of cardiac hyperfunction has been found in diabetic patients with no signs of ischemic heart disease and seems pronounced in diabetic patients developing microvascular disease (patients with preclinical nephropathy), probably secondarily to a condition of hyperperfusion in these patients.
In order to investigate the pathophysiological background for the increased cardiac performance described in short-term insulin-dependent diabetes, we infused glucagon intravenously in 8 healthy men at a dose of 5 ng/kg/min for 1 h and at a dose of 10 ng/kg/min for a further hour. Heart rate and blood pressure were measured and myocardial contractility assessed by echocardiography as the fractional shortening of the left ventricle and as the mean circumferential shortening velocity before the glucagon infusion (first base-line level), after the first glucagon infusion period, after the second glucagon infusion period and at 1 h after stopping the glucagon infusion (second base-line level). Plasma levels of glucagon were 79 +/- 15 ng/l, 123 +/- 76 ng/l, 381 +/- 179 ng/l and 77 +/- 22 ng/l, respectively. Heart rate decreased significantly during the first (8%, p less than 0.05) and second (6%, p less than 0.01) glucagon infusion period compared to the mean of the first and the second base-line value. Mean arterial blood pressure, fractional shortening of the left ventricle and mean circumferential shortening velocity were unchanged. We conclude that increments in plasma concentrations of glucagon to levels seen in poorly controlled diabetes does not change myocardial contractility in normal man.
On two occasions eight insulin-dependent diabetic patients were connected to an artificial beta-cell, and insulin was administered by continuous intravenous infusion at a rate of 2 mU/kg/min, producing a moderate hyperinsulinaemia (mean 116 microU/ml). At random, blood glucose was kept constant by concomitant glucose infusion, or allowed to decrease to a mean value of 5.3 mmol/l. M-mode echocardiography was performed before, at 90 and at 180 min of insulin infusion. Following the euglycaemic insulin infusion periods, the fractional shortening of the left ventricle increased from 38.2% to 41.0 and 40.2%, respectively (p less than 0.02). The diastolic diameter (pre-load) and end-systolic meridional wall stress (after-load) remained constant in this experiment. In contrast, no change in fractional shortening could be demonstrated during falling blood glucose, possibly because pre-load was altered to a significant degree during this experimental condition. In conclusion, concomitant infusion of insulin and glucose, producing an euglycaemic hyperinsulinaemia, is followed by increased myocardial contractility.
Cardiac function was studied by echocardiography in 11 normal subjects before subcutaneous growth hormone administration (first control), after one week of subcutaneous growth hormone administration and at one week after stopping subcutaneous growth hormone administration (second control). Plasma growth hormone was 1.4 ng/ml and 4.5 ng/ml, respectively, at the first two examinations. Compared to the first and second control situations heart rate increased by 9% (p less than 0.1) and 15% (p less than 0.01), fractional shortening of the left ventricle by 8% (p less than 0.02) and 9% (p less than 0.01), and mean circumferential shortening velocity by 10% (p less than 0.05) and 14% (p less than 0.01) respectively. Mean arterial blood pressure was unchanged. Thus, in normal man an increase in plasma growth hormone up to levels comparable to those seen in type 1 diabetics during conditions of poor metabolic control seems to be followed by enhancement in myocardial contractility. Therefore we suggest that growth hormone might contribute to the increase of myocardial contractility earlier described in type 1 diabetic patients with no clinical signs of microvascular disease.
Left ventricular wall mass and thickness were investigated by echocardiography in 80 insulin dependent diabetic patients with no signs of ischaemic heart disease and in 40 healthy controls. In diabetics with duration of disease greater than 30 years, with urinary albumin excretion rate greater than 200 micrograms/min (clinical nephropathy), with proliferative retinopathy or with autonomic neuropathy both the posterior wall thickness and the septal thickness were increased compared to controls. The posterior wall thickness and the septal thickness were positively correlated to blood pressure (p less than 0.001), duration of disease (p less than 0.001), urinary albumin excretion rate (p less than 0.001) and negatively correlated to the heart rate variation during deep respiration (p less than 0.01). The left ventricular wall mass was correlated to both blood pressure (p less than 0.01) and to urinary albumin excretion rate (p less than 0.01). By multiple regression analysis urinary albumin excretion rate, duration of disease and heart rate variation during deep respiration did not add significantly to the correlation between left ventricular wall mass/wall thickness and blood pressure. In conclusion, left ventricular wall thickness and wall mass were related to blood pressure in insulin dependent diabetics.
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The response to prolonged hyperventilation (HVT) was evaluated by electrocardiography (HVT-ECG) and thallium-201 myocardial scintigraphy (HVT-Tl-Sc) in 40 patients suspected of vasospastic angina. Both tests showed ischaemic changes in 16 patients and no changes in 20 patients. Two patients had abnormal HVT-ECG and normal HVT-Tl-Sc, and the reverse combination was found in two patients. Prolonged HVT was performed in 14 patients during coronary angiography (CAG). Nine developed transient total or subtotal occlusion in one of the major coronary arteries, all of whom had ischaemic HVT-ECG and eight had abnormal HVT-Tl-Sc. In the five patients without spasm at CAG four had normal HVT-ECG and all five normal HVT-Tl-Sc. Our data suggest that HVT-ECG and HVT-Tl-Sc have essentially the same sensitivity and specificity in detecting vasospastic angina.
Cardiac function during acute hyperglycaemia was investigated by means of echocardiography in eight insulin-dependent (type 1) diabetic patients without microvascular or cardiac disease. Blood glucose was raised from 5.1 +/- 0.8 to 13.0 +/- 0.9 mmol/l for 1 h and then to 20.1 +/- 1.2 mmol/l for 1 h. A saline control study was performed to obtain an equal amount of plasma volume expansion. The left ventricular end-diastolic diameter increased significantly in both studies, however, significantly more following glucose infusion (3.3% at blood glucose of 13.0 mmol/l, 5.4% at blood glucose of 20.1 mmol/l versus 2.7% after both saline infusions). At the blood glucose level of 20.1 mmol/l, fractional shortening of the left ventricle and cardiac output were increased as compared with the baseline level and the level during moderate hyperglycaemia, and also increased compared with values of non-diabetics. In conclusion acute hyperglycaemia is followed by increased myocardial performance, probably as a consequence of increased peripheral blood flow.