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Biomedical subjects

H Linderholm

Publications and source records attributed to H Linderholm.

At least 19 recordsLinked to original sources
PubMed1995

Comparison of some criteria for diagnosing a myocardial infarction after aorto-coronary bypass grafting (CABG).

The incidence of myocardial infarction during a 1-year follow-up period after coronary bypass surgery (CABG), i.e. a recent myocardial infarction (RMI), was studied in 86 patients. Different criteria for the diagnosis of a RMI were compared. Clinical observation, including ECG and serum enzyme analysis, diagnosed RMI in 8% of patients. Specific ECG changes indicating RMI (ECGsp) occurred in 12% of cases, and if less specific ECG changes were also taken into account (ECGsp+nonsp) RMI was found in 30% of cases. Asynergy, detected by two-plane ventriculography, indicated RMI in 24% of the patients, and was probably the most valid of the criteria examined. The differences in diagnostic accuracy of the various criteria highlight the importance of defining diagnostic criteria.

Adult↗
PubMed1995

Hereditary myopathy with lactic acidosis, succinate dehydrogenase and aconitase deficiency in northern Sweden: a genealogical study.

A hereditary myopathy with lactic acidosis during physical exercise, low physical work capacity, and paroxysmal myoglobinuria (HML), called "Myopathy with deficiency of succinate dehydrogenase and aconitase" (McKusick 255125) has been described in 19 members of nine families who lived in two geographically separate areas in northern Sweden. By using the unique Swedish historical archives, including Catechetical Meeting Records from a number of northern Swedish parishes, it has been possible to trace ancestors of the nine families including all known 19 cases back in time to some key couples, who lived up to 300 years ago (that is seven to ten generations). No common single couple or common links between families in the past was found in these registers as a support for a single or several mutations that had developed far back in time. The mode of inheritance in this family is most likely autosomal recessive. This material will be used for the chromosomal localisation of the gene.

Acidosis, Lactic↗
PubMed1992

Dependence of maximum performance time on work intensity in patients with a hereditary myopathy with succinate dehydrogenase deficiency.

Patients with a hereditary mitochondrial myopathy with succinate dehydrogenase (SDH) deficiency and abnormal lactacidosis during physical exercise have a low work capacity when exercising for about 10-15 min. Their maximum voluntary muscular strength is fairly normal. The relationship between the time (t) and a constant workload (N) that a healthy subject can maximally sustain can be expressed as: log t = beta + alpha log N. For normal subjects the constant alpha is approximately -5 and the constant beta has a large interindividual variation. Of four myopathy patients alpha was determined from two or three maximum bicycle exercise tests of different duration (including ramp- and steady-state tests using a new application of the method of adding submaximal loads to the final maximum workload). The value of alpha varied between -1.0 and -1.81 and beta had low values, both significantly different from those of healthy subjects. The alpha values explain the divergent results that may be obtained with different types of exercise tests in some of these patients, i.e. a normal or moderately reduced capacity in exercise tests of short duration (for example a short Tornvall or a ramp type of test) and a very low exercise capacity in tests of longer duration (for example a steady state type of test with workloads chosen to allow at least two loads). The low absolute value of alpha may be related to the abnormally increased anaerobic metabolism of these patients during exercise, caused by the SDH deficiency.

Acidosis, Lactic↗
PubMed1991

Reaction of patients with effort angina to cold exposure during exercise.

An attempt has been made to characterize so-called "responders" to cold among patients with effort angina. Forty-nine such patients, unselected with regard to their history of reactions to cold, who showed ST depressions during and after exercise, were examined. They worked on a bicycle ergometer close to their maximum capacity, Wmax, at room temperature (about 23 degrees C) and in a cold room (-15 degrees C). ECG was recorded and a rating scale was used to estimate the perceived exertion during exercise (RPE). The presence of angina pectoris during exercise and its duration after exercise was recorded by an EA score. An EA/W index was used to estimate the severity of the effort angina. In the whole group, the mean Wmax decreased and the mean ST depressions, RPE, and EA/W index (but not EA score) increased on exposure to cold. The changes in these variables due to exposure to cold were all associated (but not the EA score). Criteria requiring a decrease in Wmax or increase in ST depression, RPE or EA/W index on cold exposure identified 53 to 63 percent of the patients. By combining the criteria, the number of patients, who were identified, decreased. If all the criteria were applied, about 30 percent of the patients were identified as "responders" to cold and they showed the most marked responses. Thus several exercise ECG test parameters may be used to reliably define "responders" to cold exposure. This may enhance future studies of the response reaction.

Adult↗
PubMed1990

Low succinate dehydrogenase (SDH) activity in a patient with a hereditary myopathy with paroxysmal myoglobinuria.

An unusual hereditary myopathy with paroxysmal myoglobinuria has been described previously. We have studied muscle biopsy specimens taken before and after exercise to exhaustion (24 min at 20-25 W) in a young woman with this condition. Marked glycogenolysis with lactate production and marked phosphagen breakdown (ATP + CP) were observed after exercise, and almost all type I fibres were found to be depleted of glycogen. Succinate dehydrogenase (SDH) activity was low, while the activities of 3-OH-acyl-CoA-dehydrogenase, phosphofructokinase, phosphorylase and lactate dehydrogenase were normal. On electron microscopy, the mitochondria showed abnormalities typical of mitochondrial myopathy. The findings in our patient suggest a limitation of mitochondrial function, probably related to SDH in the tricarboxylic acid cycle and complex II in the electron transport chain. This may explain the inability of ATP regeneration to keep pace with ATP utilization during exercise. Other metabolic defects may coexist.

Adult↗
PubMed1990

Clinical physiology: an accepted branch of physiology.

Clinical physiology is a branch of physiology particularly dealing with functional disturbances in disease (pathophysiology) and the integrated function of the human body in disease against the background of normal function in healthy subjects, suitable physiological methods for the study of patients--particularly for diagnostic purposes--as well as for research, and the education of medical students and laboratory assistants in these fields. Departments of clinical physiology in university hospitals form a bridge between basic physiology and many clinical specialties. Independent departments of clinical physiology developed early in Sweden due to the work of Professor Torgny Sjöstrand at the Karolinska Hospital in Stockholm, and have been models of research, teaching and hospital organization which have been followed in several other countries. The International Union of Physiological Sciences (IUPS) has recognized clinical physiology as a separate branch of physiology by approving a Commission of Clinical Physiology which has contributed to the programme of this and, we hope, future congresses, as well as promote the development of clinical physiology internationally.

Humans↗
PubMed1988

Arsenic and Raynaud's phenomenon. Vasospastic tendency and excretion of arsenic in smelter workers before and after the summer vacation.

Occupational and environmental exposure to inorganic arsenic is associated with the occurrence of Raynaud's phenomenon and objectively registered abnormal finger systolic blood pressure at local cooling (FSP). A subnormal FSP during cooling indicates a vasospastic tendency. It is not known whether these phenomena are related to recent or historical long-term exposure to arsenic. Twenty-one workers from a Swedish smelter were selected on the basis of exposure to arsenic dust for more than 14 years and a previously (three years earlier) recorded subnormal FSP during local cooling. The workers were examined before and after a 4 to 8 week summer vacation. After this intermission in arsenic exposure the urinary excretion of arsenic decreased to normal values, whereas the vasospastic reaction in the fingers remained. Thus the vasospastic tendency seems to be unrelated to the most recent urinary arsenic levels. FSP levels on cooling were significantly increased as compared with the measurements made three years earlier. This suggests a gradual improvement in finger blood circulation caused by decreased exposure to arsenic as evaluated over a time period of several years. The data thus indicate that peripheral vascular disturbances caused by arsenic are dependent on long-term arsenic exposures and are independent of short-term fluctuations in arsenic exposure.

Arsenic↗
PubMed1986

Vasospastic tendency and Raynaud's phenomenon in smelter workers exposed to arsenic.

The long-term drinking of water with a high content of inorganic arsenic can lead to Raynaud's phenomenon, acrocyanosis, and gangrene of the lower legs ("black foot disease"). We have measured the systolic blood pressure in the finger after local cooling in 47 workers from a copper smelter who were habitually exposed to moderate amounts of arsenic dust. The controls were 48 workers not exposed to arsenic. The concentration of inorganic arsenic including its metabolites in urine was determined. We found a difference between As-exposed workers and the controls in the finger systolic pressure at skin temperatures of 10 degrees C and/or 15 degrees C expressed as a percentage of the pressure at 30 degrees C (FSP%), P less than 0.01; and the prevalence of Raynaud's phenomenon, P less than 0.05. A low FSP% was taken to indicate vasospastic tendency. There was a covariation between the duration of exposure to arsenic and the decrease in finger systolic pressure between the measurements at 30 and 10 degrees C (P less than 0.05). The uptake of arsenic at the time of the study probably did not exceed 300 micrograms/day. This was confirmed by estimation of the urinary excretion. The average total arsenic uptake was estimated to be about 4 g over 23 years, which is less than the total uptake of 20 g of arsenic by subjects who developed black foot disease. Increased vasospastic reactivity in the fingers and Raynaud's phenomenon in smelter workers seems to be due to functional alterations in the vessels caused by inhalation of arsenic.

Adult↗
PubMed1986

A laser Doppler technique for measuring distal blood-pressure: a comparison with conventional strain-gauge technique.

Twenty-five patients with peripheral circulatory disorders were examined by laser Doppler and strain-gauge techniques to compare these methods of measuring distal systolic blood-pressure. The correlation coefficients for simultaneous measurement of toe and ankle systolic blood-pressures were high, 0.98 and 0.99 respectively. The correlation coefficient for successive measurements of toe pressure was lower, 0.83, probably because of a variation in blood-pressure with time. The laser Doppler method seems to be more sensitive than the strain-gauge method in the low-pressure range. The laser Doppler probe is easy to attach to most skin surfaces and the laser Doppler technique may be, therefore, an alternative and a complement to the strain-gauge method when the strain-gauge is difficult to use on damaged or ulcerous toes and feet.

Adult↗
PubMed1986

Cold hands after exposure to arsenic or vibrating tools: effects of ketanserin on finger blood pressure and skin temperature.

The effect of ketanserin, a serotonin 5-HT2 receptor inhibitor, on the cold-provoked vasospasm in arsenic workers was examined by measuring the finger systolic pressure (FSP). After injection of 10 mg ketanserin the skin temperature and the FSP of the cooled finger increased significantly. Prolonged oral treatment with ketanserin, 2 X 40 mg per day, did not significantly influence the skin temperature or FSP during local cooling in arsenic workers or patients with primary or vibration-induced Raynaud's phenomenon. The effect of ketanserin intravenously indicates that serotonin is involved in the mechanism behind vasospasm of arsenic workers in the same way as it is known to be in patients with primary and vibration-induced Raynaud's phenomenon.

Administration, Oral↗
PubMed1986

Comparative toxicity of gentamicin and cefotetan.

In a prospective, randomized, comparative study, the renal, hepatic and gastrointestinal toxicity and effects on the vitamin K dependent coagulation factors of gentamicin and cefotetan were compared. Gentamicin, which in all but one patient was combined with a penicillin, was found to cause a significant decrease of glomerular filtration rate (GFR) after 1 week of treatment. In 6/14 patients a further decrease of GFR was found during the week following the last treatment day. The renal proximal tubular cells were affected by gentamicin, as evident from significant increases in urinary activity of 2 tubular enzymes, alanine aminopeptidase (AAP) and N-acetyl-beta-D-glucosaminidase (NAG), as well as rises of urinary beta 2-microglobulin. Changes in GFR and tubular function were reversible. No statistically significant changes of these variables were seen with cefotetan. One cefotetan treated patient developed diarrhoea of moderate severity and 2 patients in the same group developed minor increases of liver transaminases. A small but statistically significant decrease of the activity of the vitamin K dependent coagulation factors occurred during cefotetan treatment. No gastrointestinal or hepatic adverse reactions were observed in the gentamicin treated patients.

Aged↗
PubMed1985

Detection of coronary artery disease by means of exercise ECG in patients with aortic stenosis.

In a preoperative evaluation, 35 consecutive patients with aortic stenosis were examined by means of exercise ECG, Doppler and direct manometric measurements of the pressure difference over the aortic valve (delta P) and angiocardiography. Coronary artery disease (CAD) was found in 43% of the patients. Those with CAD had a lower mean maximum physical performance expressed as a percentage of the normal value (Wmax%), larger ST depressions and a higher effort angina (EA) score at the exercise test than the non-CAD group. Mean delta P was equal in the two groups. A myocardial coronary obstruction score covariated positively with a coronary insufficiency index (CT index = 100 X STdepr/Wmax%) and the EA score. There was no correlation between delta P and the EA score or the CI index. A CI index less than 3 and an EA score less than 2 were found in 49% of the patients and excluded the presence of CAD with a predictive accuracy of 88%, a better diagnostic complement to coronary arteriography than a history of EA.

Aged↗
PubMed1985

Phrenic nerve stimulation (diaphragm pacing) in respiratory paralysis.

Phrenic nerve stimulators (diaphragm pacers) were implanted in 16 patients with partial or total respiratory insufficiency due to high cervical medullary lesions and brain stem lesions (14 cases) or central hypoventilation syndrome (2 cases). At 5-72 months' follow-up (M = 35) 12 patients are entirely independent of conventional respirator, 2 of them after 8 years of total respirator dependency. Two patients are dead and the final 2 cases had limited help from diaphragm pacing.

Adolescent↗
PubMed1985

Arsenic exposure to smelter workers. Clinical and neurophysiological studies.

Forty-seven copper smelter workers, exposed to airborne arsenic for 8-40 years, were examined clinically with electromyography, and the motor and sensory conduction velocities in their arms and legs were determined. Fifty age-matched industrial workers not exposed to arsenic formed a reference group. The level of arsenic in the air at the smeltery was estimated to be below 500 micrograms/m3 before 1975 and approximately 50 micrograms/m3 thereafter. Urine analyses of arsenic showed a mean value of 71 micrograms/l (1 mumol/l) in the exposed group; this value is lower than that found in earlier studies reporting clinically detectable neuropathy. Only minor neurological and electromyographic abnormalities were found. A slightly reduced nerve conduction velocity in two or more peripheral nerves was more common among the arsenic workers than the referents, and a statistically significant correlation between cumulative exposure to arsenic and reduced nerve conduction velocity in three peripheral motor nerves was found. This occurrence was interpreted as a sign of slight subclinical neuropathy. In conclusion the risk of clinically significant neuropathy is small when exposure is kept below 50 micrograms/m3 in workroom air. The subclinical findings may be of interest in relation to the prevention of early adverse health effects from arsenic exposure.

Adult↗
PubMed1983

Restrictive ventilatory dysfunction in stroke: its relation to locomotor function.

Static and dynamic lung volumes, maximum respiratory pressures and lung compliance and resistance were registered in 54 subjects with hemiplegia or hemiparesis after stroke. These measures of ventilatory function were related to the degree of motor impairment and to the interval between stroke and investigation. In general ventilatory function, particularly parameters depending upon expiratory force, was restricted. This was most pronounced in subjects with severe hemiplegia while those with hemiparesis had only small changes. Since dynamic lung volumes (corrected for volume loss), lung compliance and resistance were all normal, it is evident that intrinsic lung function was unaffected. Inspiratory capacity - but no other measured variables of respiratory function - was lower six months after the stroke than earlier. It is suggested that expiratory muscle dys-coordination and weakness caused expiratory dysfunction while the less pronounced inspiratory restriction may be caused by muscular dysfunction and, as time goes by, by rib cage contracture.

Adult↗