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Biomedical subjects

E Nylander

Publications and source records attributed to E Nylander.

54 records · Page 3Linked to original sources
PubMed1990

The value of exercise test, Holter monitoring, and programmed electrical stimulation in detection of ventricular arrhythmias in patients with hypertrophic cardiomyopathy.

To determine the best way to detect serious ventricular arrhythmia in patients with hypertrophic cardiomyopathy (HCM), 15 patients with HCM performed an exercise test, had Holter monitoring during 24 hours, and programmed electrical stimulation (PES) in a randomized order, and the presence and type of ventricular arrhythmia was noted. During exercise testing, only one patient demonstrated ventricular tachycardia (VT) just prior to the test. By Holter monitoring, four patients had short episodes of asymptomatic VT. PES, using up to three extrastimuli induced VT or ventricular fibrillation (VF) in ten patients including those with VT during exercise testing and Holter monitoring. There were no differences between patients with and without ventricular arrhythmia during PES regarding age, left ventricular outflow obstruction, thickness of interventricular septum, interventricular septum/posterior wall thickness ratio, corrected QT interval, or the amplitude of the R wave in lead aVR in electrocardiography. Our results indicate that inducible VT/VF during PES is a common finding in patients with HCM. Twenty-four hour Holter monitoring was superior to exercise testing in revealing serious ventricular arrhythmia in those patients.

Cardiac Pacing, Artificial↗
PubMed1989

Arm and ankle blood pressure response to treadmill exercise in normal people.

Nineteen healthy volunteers, 10 men and nine women (mean age 38 and 30 years), exercised on a treadmill. The systolic blood pressure (BP) was measured at the ankle and in the arm after submaximal (8 min with a final load of 2 W kg-1 body weight) and maximal exercise. The BP was measured for 10 min after exercise, or until the elimination of a negative pressure difference between ankle and arm. The pre-study resting systolic arm and ankle pressures were 122 +/- 11 and 144 +/- 13 mmHg. One minute after submaximal exercise, arm and ankle BP were 147 +/- 18 and 159 +/- 19 mmHg (ankle-arm pressure difference 12 +/- 13 mmHg); 1 min after maximal exercise the corresponding figures were 182 +/- 26 and 153 +/- 35 mmHg (ankle-arm pressure difference -29 +/- 33 mmHg). We conclude that maximal exercise, but not an appropriately chosen submaximal exercise level, causes a negative BP difference between ankle and arm in normal people.

Adolescent↗
PubMed1989

Influence of long-term prenalterol treatment on the heart rate and the beta-adrenoceptor binding-sites in rat myocardium.

The density of beta- adrenoceptors has been determined on membranes prepared from rat myocardium. Long-term administration of prenalterol resulted in an increase in the density of receptors, without any change in affinity. The average heart rate increase induced by intravenous prenalterol administration to denervated rats was, however, similar in the prenalterol pretreated and the control groups. We conclude that long-term treatment with a partial beta1-adrenoceptor agonist lead to an increased beta-adrenoceptor density in the myocardium.

Animals↗
PubMed1988

Long-term efficacy of flecainide in paroxysmal atrial fibrillation.

The efficacy and safety of flecainide for long-term prevention of paroxysmal atrial fibrillation (AF) were studied in an open trial. Twenty patients with very frequent attacks (mean 13 per month) of paroxysmal AF for many years (mean 8 years) participated. Before inclusion, the patients had unsuccessfully been treated with an average of 3.3 antiarrhythmic drugs. Efficacy was jugded from a carefully kept diary in which the patients made daily notes of any AF attacks and possible side-effects from 1 month before treatment until the end of a follow-up period of 6 months. Twelve patients (60%) were completely free from AF and 11 of these are still successfully treated with flecainide after 11-38 months (mean 24 months). Flecainide plasma levels did not differ between responders and non-responders. Eleven patients (55%) had adverse effects but these were usually mild and well tolerated, necessitating withdrawal or dose reduction resulting in relapse of AF only in three patients (15%). No proarrhythmic events were seen.

Adult↗
PubMed1988

Selenium and vitamin E treatment of Duchenne muscular dystrophy: no effect on muscle function.

16 boys with Duchenne muscular dystrophy (DMD) were treated with sodium selenite and vitamin E for one year. One group of patients (10 boys) was examined using a battery of tests to assess muscular strength and function and cardiopulmonary function, and by CT scanning of 2 muscle groups over the 4 years prior to treatment. Six boys with DMD entered the study when the treatment was begun. Tests of muscular force and function, cardiopulmonary tests and CT-scanning were performed at the onset of treatment, and after 6 and 12 months. No beneficial effect on either muscular force or function was found during the treatment period. It is concluded that selenium and vitamin E in high doses do not improve muscle function in DMD.

Adolescent↗
PubMed1987

Cold sensitivity after replantation in relation to arterial circulation and vasoregulation.

Cold intolerance is a common problem after injuries to the hand. To elucidate the mechanism of this cold sensitivity, eight patients with successful replantations of amputations of the thumb or index finger were studied one and half years later. In six patients the Doppler signal from the anastomosed arteries was normal and in two patients signs of mild stenosis were found. All patients had normal or slightly reduced basal finger systolic pressure in the replanted finger. Six had signs of marked vasospasm. Alpha-receptor blockade had no effect on the cold-induced decrease in finger systolic pressure in the replanted finger. It is concluded that cold intolerance after hand injuries results from a defect in vasoregulation and is not caused by organic insufficiency of the circulation.

Adult↗
PubMed1987

Use of vectorcardiography in determination of the left ventricular muscle mass.

Many studies have investigated different ECG and vectorcardiographic (VCG): criteria for diagnosis of left ventricular hypertrophy (LVH). In some investigations VCG was more sensitive than ECG in this respect. This study was performed to elucidate whether it is possible also to determine the degree of LVH using VCG. Eighty cardiovascularly healthy subjects aged 15-39 were investigated with ECG, VCG (Frank system) and echocardiography. The echocardiographic left ventricular (LV) mass has been shown by others to correlate closely to the anatomical and the angiographically determined LV mass and was used as reference standard. Thirty-eight of the subjects were endurance sportsmen and had a LV mass above standard reference limits. The measured ECG variables were R-amplitude in a VL, I, V5, V6, S-amplitude in V1 and SV1 + RV5/V6 and the VCG variables were QRS spatial area and circumference and left maximal spatial vector. The sensitivity and specificity of single criteria tested were similar for ECG and VCG in the quantitative determination of LVH. The correlations between ECG-amplitudes and the magnitude of the LV mass were weak. The correlations were higher with the VCG-variables, QRS spatial circumference being superior to the others, but not good enough to permit an estimation of the LV mass in individual subjects. In conclusion, normal VCG variables were highly specific for a normal LV mass but in individuals with LVH, VCG was not useful for the estimation of the LV mass.

Adolescent↗
PubMed1986

Severe aortic stenosis in elderly patients.

Clinical and non-invasive findings were compared with catheterisation data in 91 elderly patients (mean 65 years, range 52-78) with suspected severe aortic stenosis requiring operation. Heart catheterisation showed that forty nine patients had a valve area of less than or equal to 0.6 cm2, 36 had a valve area of 0.7 - 1.0 cm2, and six an area of greater than or equal to 1.1 cm2. Coexistent aortic regurgitation was found in 85% of the cases, but severe regurgitation was found in only one patient (1%). Seventy seven per cent of patients had chest pain, 74% had dyspnoea, and 46% had exertional vertigo or syncope. Coronary angiography, which was performed in 77 patients, showed coronary artery disease in 24% of those with a history of angina pectoris and in none of those without. All patients had echodense valves; aortic valve calcification was shown by x ray in 76% and in all but one by cineradiography. The peak of the systolic murmur was delayed in 98% of the patients. Although a prolonged left ventricular ejection time was characteristic of severe aortic stenosis, a normal value did not exclude this diagnosis. Most patients (84%) had increased QRS amplitude on the electrocardiogram. Echocardiography showed an increased left ventricular wall thickness in 90% of the patients in whom it was possible to define the myocardial borders. There was an inadequate blood pressure increase in response to exercise in 82%. In about 25% of the patients the exercise test was at variance with the New York Heart Association classification. Findings suggesting severe aortic stenosis resembled those reported for younger age groups. When most findings point to severe aortic stenosis, the absence of a single symptom or non-invasive sign does not exclude severe aortic stenosis.

Aged↗
PubMed1985

Training-induced bradycardia in rats on cardioselective and non-selective beta receptor blockade.

After 12 weeks of treadmill training 10 Sprague-Dawley rats got a significant bradycardia at exercise of submaximal intensities compared to 10 sedentary controls. Twenty rats were subjected to the same training programme during oral treatment with the cardioselective beta receptor blocker metroprolol (10 rats) or propranolol (non-selective, 10 rats). Both treated groups developed a training-induced bradycardia at submaximal exercise of the same magnitude as the trained untreated group. It is concluded that the stimulation of cardiac beta receptors or the heart rate increase during exercise are not critical for the development of training bradycardia and that in this respect the effects of cardioselective and non-selective beta receptor blockade were not significantly different.

Adrenergic beta-Antagonists↗
PubMed1984

Influence of long-term beta receptor stimulation with prenalterol on intrinsic heart rate in rats.

Previous studies have shown that the intrinsic heart rate (IHR) may undergo changes, e.g., decrease after long-term endurance training. The mechanism for this adaptation is not known. In this study, rats were subjected to long-term oral treatment with the beta receptor stimulating drug prenalterol. During the treatment period heart rates at rest and during submaximal exercise were measured. Heart rate after 30 min rest and also 2 min after exercise was higher in the treated animals, due to the beta stimulation. The treated rats had a significantly lower heart rate increase during exercise than untreated controls, consistent with a partial beta-blocking effect of the drug in states with a high endogenous sympathetic activity. Therefore, the animals were not trained but only exposed to the increased stimulation of cardiac beta receptors accomplished by the drug while at rest. After 25 weeks, prenalterol was withdrawn and the IHR was measured in situ after a denervation procedure. The treatment with prenalterol had not altered the IHR. Our previous results from training studies indicate that a heart rate increase above a certain level or the stimulation for a lower setting of the IHR as seen after endurance training. In this study chronic beta receptor stimulation with prenalterol did not influence the IHR, which supports that hypothesis.

Adrenergic beta-Agonists↗
PubMed1983

Effect of increased blood oxygen affinity on skeletal muscle surface oxygen pressure fields.

A chronic left displacement of the blood O2 dissociation curve (ODC) was achieved in rats by administering cyanate over a period of 14 days. Control rats received NaCl. An acute left displacement of the ODC was achieved by exchange transfusion with bisulfite-treated erythrocytes. Control rats for this series received an exchange transfusion with fresh heparinized blood. In both series, skeletal muscle surface O2 pressure fields (expressed as PO2 histograms) were measured with the rats anesthetized, curarized, and artificially ventilated. The animals with chronically left-shifted ODC had normal PO2 histograms (for definition see DISCUSSION) when breathing air; during hypoxia (FIO2 0.12) four of the eight experimental and three of the seven control animals developed abnormal histograms, and all animals had normal histograms on return to air breathing. The majority, but not all, of the animals that were to receive exchange transfusions of left-shifted ODC blood had normal histograms before the transfusion, which caused some to become abnormal and others to become normal. Similar results were obtained in the control animals that received normal blood. The results do not provide evidence for an adverse effect of a left-shifted ODC on muscle tissue oxygenation.

Animals↗
PubMed1982

Training-induced bradycardia and intrinsic heart rate in rats.

After 10 weeks of treadmill training, female Sprague-Dawley rats had developed a bradycardia at exercise on submaximal work loads. This bradycardia was also present after autonomic denervation and in isolated perfused heart preparations. The heart weight/body weight ratio was increased in these trained animals compared to untrained littermates. Sympathectomized, trained rats developed the same degree of cardiac hypertrophy, but their heart rate after denervation and in the isolated heart was the same as in sympathectomized, untrained rats. It is concluded that the bradycardia of trained and thereafter denervated animals seen in this and a previous investigation represents an adaptation within the heart itself, since it was present in the isolated heart. These results thus provide further evidence for a non-neural component in training-induced bradycardia. Since the trained sympathectomized rats had a cardiac hypertrophy but no reduction of intrinsic heart rate, it seems likely that the myocardial mass is of minor importance for the level of intrinsic heart rate.

Adaptation, Physiological↗
PubMed1982

New aspects on training bradycardia.

Rats were trained by treadmill running after chemical sympathectomy with 6-hydroxy-dopamine or during chronic beta receptor blockade. Contrary to untreated trained animals, sympathectomized rats did not get a reduction of the intrinsic heart rate after training despite an increased heart weight. In contrast, no cardiac hypertrophy occurred after training during beta adrenergic blockade but the heart rate during exercise was reduced in these animals. It is concluded that the training-induced bradycardia contains a lowering of the intrinsic heart rate and that this is not dependent on the stimulation of cardiac beta receptors or the magnitude of heart rate increase during exercise. The results also indicate that there is not a causal relationship between the training-induced bradycardia and cardiac hypertrophy. The latter conclusion is supported by an echocardiographic study in humans where no correlation was found between IHR and cardiac dimensions.

Adult↗
PubMed1981

Effect of beta-adrenergic receptor blockade on development of training-induced bradycardia in rats.

Metoprolol-treated and untreated rats were subjected to the same treadmill running program for 12 weeks. After training and withdrawal of metoprolol, the treated rats had a more pronounced bradycardia during submaximal exercise than non-treated rats, although they had a lower heart weight/body weight ratio. The intrinsic heart rate (IHR) was slightly but not significantly lower in trained than in untrained untreated animals. The IHR was not altered by a period of metoprolol treatment neither alone nor in combination with training. It is concluded that chronic cardioselective beta-blockade during training augments the training-induced bradycardia but may impair the development of cardiac hypertrophy. The training-induced bradycardia is thus not related to the degree of heart rate increase during exercise for its development.

Adrenergic beta-Antagonists↗
PubMed1980

Non-autonomic component in bradycardia of endurance trained men at rest and during exercise.

Autonomic nervous alterations have generally been held responsible for the bradycardia of the endurance athlete. In order to determine whether there is also a non-autonomic component in the bradycardia of long-term training, we compared the intrinsic heart rate (HR) of highly trained bicyclists (heart volume: 995 +/- 155 ml) with that of untrained men (heart volume: 805 +/- 195 ml) at rest and during bicycle ergometer exercise at 50, 75 and 100% of maximal oxygen uptake (VO2 max.) Intrinsic HR was achieved by combined vagal and beta-adrenergic blockade with atropine and propranolol or metoprolol (cardioselective) injected intravenously. Intrinsic HR was significantly lower in trained (T) than in untrained (UT) at rest and at all levels of exercise. The chronotropic reserve from resting HR to maximal HR was identical in the two groups. Nearly identical intrinsic HRs were achieved with atropine and either beta-adrenergic antagonist. HR differences between T and UT were very similar in magnitude--approximately 13 beats/min--at rest and during exercise at a given percentage of VO2 max, with and without autonomic blockade. Evidence is thus provided for a non-autonomic component in the bradycardia of well-trained men which may be responsible for a parallel downward shift in the relationship between HR and percentage of VO2 max. The lower intrinsic HR in well-trained men might be explained by, i.a. the cardiac enlargement.

Adult↗