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Biomedical subjects

B O Olofsson

Publications and source records attributed to B O Olofsson.

At least 19 recordsLinked to original sources
PubMed1991

Tissue plasminogen activator and other risk factors as predictors of cardiovascular events in patients with severe angina pectoris.

The value of measurements of the fibrinolytic factors, tissue plasminogen activator and plasminogen activator inhibitor, for predicting death and non-fatal cardiovascular events was studied in 213 consecutive patients with angiographically documented coronary artery disease. In the course of 4-year follow-up, 47 patients (22.1%) had at least one cardiovascular event. We found the incidence of cardiovascular events to be positively associated with high tissue plasminogen activator antigen concentration, in addition to previous myocardial infarction, low ejection fraction, hypertension, high body mass index and high triglyceride levels. Cholesterol was not found to be associated with cardiovascular events. A high concentration of tissue plasminogen activator antigen thus implies an increased risk of cardiovascular events in patients with severe angina pectoris.

Adult↗
PubMed1991

Assessment of hypothalamic-pituitary function in patients with familial amyloidotic polyneuropathy.

This study was performed to evaluate hypothalamic-pituitary hormone regulation in patients with familial amyloidotic polyneuropathy. Twenty-two patients without clinically overt endocrinological dysfunction were studied. A thyrotropin-releasing hormone test revealed abnormal growth hormone regulation in 9 of 17 (53%) patients, and abnormal prolactin regulation in 9 of 18 (50%) patients. Abnormalities in either growth hormone or prolactin regulation were found in 12 of 17 (71%) patients. Serum somatomedin C levels were normal in all 22 patients. In 3 of 18 (17%) patients the plasma arginine vasopressin levels were low relative to the serum osmolality levels. Thus abnormalities in hypothalamic-pituitary hormone regulation may be common in familial amyloidotic polyneuropathy.

Amyloidosis↗
PubMed1990

Assessment of autonomic nerve function in myotonic dystrophy.

The function of the autonomic nervous system was studied in 23 patients with myotonic dystrophy, from a defined population in northern Sweden with an extremely high prevalence of this disease. Heart rate variability tests showed only minor signs of parasympathetic dysfunction. Blood pressure and plasma noradrenaline measurements in recumbent and upright positions showed no signs of sympathetic neuropathy. Increased plasma levels of noradrenaline was an unexpected finding. Our study does not support the hypothesis that cardiac arrhythmias, orthostatic hypotension, gastrointestinal motility disturbances and urinary bladder dysfunction in myotonic dystrophy are caused by autonomic neuropathy, and we believe that these symptoms should rather be ascribed to a defective function of the target organs.

Adolescent↗
PubMed1990

Cardiac involvement in congenital myotonic dystrophy.

Seven young patients (mean age 19 years 8 months) with congenital myotonic dystrophy and with defined symptoms at birth were investigated by electrocardiography and echocardiography. None had cardiovascular symptoms. Electrocardiograms or echocardiograms or both were abnormal in all patients. Atrioventricular and intraventricular conduction defects were the most common electrocardiographic abnormalities and were seen in five patients. The echocardiographic examinations showed impaired left ventricular systolic function in one patient. Other echocardiographic findings were a small left ventricle and atrium, minor valve defects, and mitral valve prolapse. This study shows that the heart is often affected in young patients with congenital myotonic dystrophy. The specialised conduction system is often affected and so too is the myocardium, causing impaired systolic function.

Adolescent↗
PubMed1990

Reduced levels of tissue plasminogen activator and plasminogen activator inhibitor in plasma of patients with familial amyloidotic polyneuropathy.

Tissue plasminogen activator (tPA) antigen levels and plasminogen activator inhibitor (PAI) activity were measured in the plasma from 23 patients with familial amyloidotic polyneuropathy. Both tPA levels and PAI activity were reduced to about half normal, even when the effects of patient age and body mass index were taken into account. There were higher mean tPA levels and PAI activity in patients with mild disability than in those with moderate or severe disability, but these differences were not statistically significant. There were normal tPA levels after venous occlusion of the upper arm, indicating a normal capacity of vascular endothelium to release tPA. This is the first reported disorder with reduced rather than increased basal tPA and PAI levels. The pathogenetic and clinical significances of these disturbances so far remain obscure.

Adult↗
PubMed1989

Evidence for increased levels of plasminogen activator inhibitor and tissue plasminogen activator in plasma of patients with angiographically verified coronary artery disease.

We studied 234 consecutive patients who underwent coronary angiography because of severe angina pectoris. Tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI), and lipoprotein Lp(a) were measured in citrated plasma samples. The 214 patients showing significant coronary artery stenosis (greater than 50% reduction of luminal area in any of the great coronary arteries) had higher mean levels of tPA (P less than 0.001) and PAI (P less than 0.01) than a random population sample of similar age. PAI and tPA levels were higher in smokers than in either non-smokers or ex-smokers, and in patients with hypertension tPA was increased. Subjects with blood group A had a higher mean Lp(a) level than subjects with blood group O. There were positive correlations of PAI and tPA levels with serum triglycerides and with body mass index; Lp(a) correlated weakly with plasma fibrinogen concentrations. The findings suggest an impairment of the fibrinolytic system in patients with coronary artery disease, which offers a link between established risk factors and a plausible pathophysiological mechanism, namely thrombus turnover.

Adult↗
PubMed1989

Assessment of thyroid and adrenal function in patients with familial amyloidotic polyneuropathy.

This study was performed to evaluate thyroid and adrenal function in patients with familial amyloidotic polyneuropathy. Twenty-four patients without any clinical overt endocrinological dysfunction were studied. None of the patients showed laboratory evidences of hypo- or hyperthyroidism. A short ACTH-stimulation test was performed in 17 of the patients. A low cortisol response to ACTH stimulation, suggesting adrenocortical insufficiency, was found in four (24%) of the patients, and an intermediate response interpreted as suspected hypofunction was found in three (18%) patients. Low serum dehydroepiandrosterone sulphate levels, suggesting adrenal hypofunction, were found in six (25%) of the patients. We believe that the possibility of glucocorticoid insufficiency should always be considered in patients with familial amyloidotic polyneuropathy.

Adrenal Cortex↗
PubMed1989

Autonomic neuropathy in familial amyloidotic polyneuropathy. A clinical study based on heart rate variability.

Familial amyloidotic polyneuropathy (FAP) is characterized by both sensimotor and autonomic dysfunction. Autonomic disturbance involving the gastrointestinal tract, the urinary bladder, the cardiac conduction system, and the peripheral circulation has been described. In this study simple, non-invasive tests of autonomic function based on heart rate variability were applied to 12 patients with FAP and 12 healthy volunteers. The heart rate variation during normal breathing, deep breathing and during tilt from recumbent to standing position was measured. All tests showed significantly less heart rate variation in patients than in controls and the heart rate variation decreased with increasing severity of neurological disability, but the small number of patients in our study does not allow any further comparison between subgroups. Our study thus indicates impaired cardiovascular autonomic function in patients with FAP and we believe that these findings might also be of importance in other forms of systemic amyloidosis.

Adult↗
PubMed1988

Propafenone versus disopyramide for treatment of chronic symptomatic ventricular arrhythmias. A multicenter study.

The efficacy and safety of propafenone, 150 mg four times daily, were compared with those of disopyramide, 100 mg four times daily, in a randomized single-blind, cross-over study in 38 patients with symptomatic premature ventricular complexes (PVCs). The 24-hour ambulatory ECG, employed for assessing antiarrhythmic efficacy, was analyzed blindly. The median reduction in the number of PVCs was higher with propafenone than with disopyramide (91.4% vs. 63.5%, respectively, p less than 0.01). A reduction of at least 80% was achieved by propafenone in 22 (59%) and by disopyramide in 16 patients (43%) (NS). Ventricular tachycardias (VTs) were abolished by propafenone in eight out of 11, and by disopyramide in five out of nine patients with VTs (NS) a possible proarrhythmic effect was seen in three patients during disopyramide and in one patient during propafenone treatment. Micturition disturbances (p less than 0.001) and a dry mouth (p less than 0.01) were more commonly associated with disopyramide than with propafenone. In conclusion, in the given dosages, propafenone was superior to disopyramide in suppressing PVCs and had fewer side-effects.

Adult↗
PubMed1988

Electrocardiographic findings in myotonic dystrophy.

Sixty five patients with myotonic dystrophy, from a defined population in northern Sweden with an extremely high prevalence of this disease, were examined by electrocardiography. The patients were subdivided into three groups according to the severity of the disease. Abnormal electrocardiograms were found in 6 (35%) patients with mild disease, 12 (50%) patients with moderate disease, and 23 (96%) patients with severe disease. First degree atrioventricular block and left anterior hemiblock were the most commonly encountered abnormalities in patients with mild and moderate disease, whereas atrial fibrillation and flutter, abnormal Q waves, and repolarisation abnormalities were more common in patients with severe disease. This study shows that the heart is often affected by myotonic dystrophy. These effects can be detected by electrocardiography in early and mild forms of the disease. The effect on the heart is progressive and clinically important atrial arrhythmias and electrocardiographic abnormalities which are useful in differential diagnosis are common in severe forms of the disease.

Adolescent↗
PubMed1988

24-hour electrocardiographic study in myotonic dystrophy.

Thirty-eight consecutive adult patients with myotonic dystrophy were included in a study with electrocardiography at rest and 24-hour ambulatory electrocardiography. The patients were subdivided into three groups according to the severity of the disease. The prevalence of abnormal electrocardiograms at rest was 31, 50 and 100% in patients with mild, moderate and severe disease, respectively. The main characteristics observed at ambulatory electrocardiography were a high frequency of sinus bradycardia (58%) and intermittent atrioventricular block II (8%). These bradyarrhythmias were not correlated to the severity of the disease. Sustained atrial fibrillation or flutter was found in 3 patients (8%), all with the most severe form of the disease. Ambulatory electrocardiography should be used deliberately in the evaluation of patients with myotonic dystrophy and symptoms compatible with cardiac arrhythmias.

Adolescent↗
PubMed1987

Cardiac stimulation threshold in familial amyloidosis with polyneuropathy.

It has been suggested that a higher cardiac stimulation threshold reduces the applicability of pacemaker therapy in cardiac amyloidosis. We therefore reviewed threshold data in patients with familial amyloidosis with polyneuropathy (FAP), which is an inherited type of systemic amyloidosis, invariably involving the heart. Fourteen FAP patients treated with a pacemaker were studied. The mean (+/- SD) voltage stimulation threshold during implantation was 1.0 +/- 0.5 V, and noninvasive follow-up 6 months later revealed a mean Vario threshold of 1.9 +/- 0.5 V. Beyond this time, the threshold tended to be stable, and high threshold exit block did not occur in any patient. Several FAP patients did show a moderately elevated threshold, and a multiprogrammable pulse generator with a high output capability is recommended when pacemaker therapy is considered in these patients.

Adult↗
PubMed1987

Prealbumin: its association with amyloid.

In recent years prealbumin has been shown to be a major component of two forms of systemic amyloid, senile systemic amyloid (SSA), and familial amyloidotic polyneuropathy (FAP). Despite the fact that the amyloid fibril proteins associated with these two forms of amyloid, designated ASc1 and AF, respectively, share many similarities the clinical features of the two diseases are remarkably different. To understand better this paradox the clinical, histochemical, immunological and biochemical features of SSA and FAP were reviewed.

Adult↗
PubMed1987

Prealbumin variants in the amyloid fibrils of Swedish familial amyloidotic polyneuropathy.

Amino-acid sequence analysis of an amyloid fibril protein from a patient with Swedish familial amyloidotic polyneuropathy showed homology with prealbumin but with heterogeneous N-terminal deletions. One-third of the molecules had the same amino acid substitution, methionine for valine in position 30, as in familial amyloidosis of Portuguese, Japanese and Swedish-American type. A protein with the same antigenic properties and size was found in the fibrils of two other patients with Swedish FAP while the amyloid fibrils in two further patients predominantly contained a smaller prealbumin-derived protein. Cyanogen bromide cleavage of this protein revealed no evidence for a methionine residue in position 30.

Aged↗
PubMed1987

Differentiation of cardiac amyloidosis and hypertrophic cardiomyopathy. A comparison of familial amyloidosis with polyneuropathy and hypertrophic cardiomyopathy by electrocardiography and echocardiography.

The clinical and echocardiographic features of cardiac amyloidosis may closely resemble those of hypertrophic cardiomyopathy, and the disorders may thus be mixed up. The present study was undertaken in an attempt to identify features separating the two conditions by analysis of electro- and echocardiographic findings in patients with familial amyloid polyneuropathy and hypertrophic cardiomyopathy. Twenty-nine patients with familial amyloidosis and 22 with hypertrophic cardiomyopathy were studied. Particular attention was given to the sum of the S wave in V1 and R wave in V5 or V6, the echocardiographic left ventricular mass and cross-sectional area, the presence or absence of asymmetrical septal thickening, granular and sparkling myocardial appearance, thickened heart valves, systolic anterior motion of the mitral valve, and pericardial effusion. A granular and sparkling appearance of the myocardium and thickened heart valves were found to be the best predictors of cardiac amyloidosis, while low QRS amplitudes in relation to echocardiographic left ventricular mass and a pericardial effusion seemed less important. The presence of systolic anterior movement of the mitral valve, a large left ventricular mass and a sum of S in V1 and R in V5 or V6 greater than 35 mm indicated hypertrophic cardiomyopathy. When the four strongest predictors (left ventricular mass, thickened heart valves, a granular sparkling myocardial appearance, and systolic anterior movement of the mitral valve) were used to reclassify the present patients, 28 of 29 amyloidosis patients and 21 of 22 patients with hypertrophic cardiomyopathy were correctly categorized. Noninvasive methods may thus be useful for detecting the myocardial infiltrative process, and cardiac amyloidosis may be confidently diagnosed by typical noninvasive findings together with histopathological documentation of amyloid in an organ other than the heart.

Adult↗
PubMed1986

Heart valve involvement in familial amyloidosis with polyneuropathy.

Involvement of the heart is common in the various types of amyloidosis. Little attention has, however, been paid to the presence and significance of amyloid in cardiac valves. We examined the heart valves of twelve autopsy cases with familial amyloidosis with polyneuropathy. All leaflets showed more or less abundant amyloid infiltration with significant valvular aortic stenosis due to degenerative calcification in two cases. In familial amyloidosis with polyneuropathy, amyloid deposits are thus invariably present in the valves, but the valvular function is often preserved. Amyloid may, however, produce hemodynamically significant valvular lesions, and the importance of valvular involvement in the various types of amyloidosis may still be underestimated.

Adult↗