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O Hansen

Publications and source records attributed to O Hansen.

At least 109 records · Page 6Linked to original sources

The clinical outcome of acute myocardial infarction is related to the circadian rhythm of myocardial infarction onset.

In order to study whether the circadian rhythm of acute myocardial infarction (AMI) onset has any impact on the clinical outcome, in terms of enzymatically estimated infarct size, circulatory arrest from ventricular tachyarrhythmias, and in-hospital mortality, the authors studied a representative population of 10,791 AMIs treated in the same center between 1973 and 1987. In 6,763 cases (63%) the time of symptom onset was known. In these cases a major peak in AMI incidence was observed between 7:01 AM and 10:00 AM, and minor peaks at 12:01 noon, 3:01 PM-4:00 PM, and 8:01 PM-9:00 PM. In a set of multivariate analyses including several clinical characteristics, symptom onset between 6:00 AM and 12:00 noon significantly predicted a greater infarct size, and symptom onset between 12:00 AM and 6:00 AM was associated with a significantly lower risk of circulatory arrests from ventricular tachyarrhythmias. The time of symptom onset was not significantly associated with in-hospital mortality after adjustment for other clinical characteristics, including infarct size. The authors suggest that the time of day has an impact, not only on the incidence, but also on the severity of AMI and that the ability of beta blockers to blunt the morning increase in AMI incidence may possibly contribute to the beneficial secondary preventive effects of such drugs after AMI.

Aged↗

Benefits of non-selective versus cardioselective beta-blockers in acute myocardial infarction in hypertensive patients.

AIM: To evaluate the effect of current treatment with non-selective or cardioselective beta-blockers on the outcome of a first acute myocardial infarction in hypertensive patients. OUTCOME MEASURES: Peak aspartate aminotransferase was measured as an indirect estimate of infarct size, the occurrence of circulatory arrest from ventricular tachyarrhythmias and in-hospital mortality. DESIGN: A retrospective analysis was performed on data collected in a continuously operating register of all hospitalized acute myocardial infarctions in Malmö, Sweden. PATIENTS: A total of 2114 hypertensive patients were admitted to hospital with a first acute myocardial infarction. Of these patients, 323 were treated with a non-selective beta-blocker on admission and 338 with a cardioselective beta-blocker. RESULTS: In patients given a non-selective beta-blocker the mean peak aspartate aminotransferase was 3.02 +/- 0.15 mukat/l, which was significantly lower than the peak (3.78 +/- 0.35 mukat/l) recorded in the patients given a cardioselective beta-blocker. In a multiple regression analysis, treatment with a non-selective beta-blocker was significantly and inversely related to peak aspartate aminotransferase after adjustment for several clinical characteristics. Age, anterior myocardial infarction, peak aspartate aminotransferase, serum potassium and treatment with a cardioselective beta-blocker were significantly and independently associated with the occurrence of circulatory arrest due to ventricular tachyarrhythmias. The relative risk of circulatory arrest in patients taking cardioselective beta-blockers was 1.73 (95% confidence interval 1.16-2.58) and in patients taking non-selective beta-blockers 1.02 (95% confidence interval 0.64-1.66). Advanced age, a history of diabetes mellitus, a history of stroke, anterior myocardial infarction, a high serum potassium level and a high peak aspartate aminotransferase level significantly predicted in-hospital mortality. The relative risk of in-hospital mortality in patients taking non-selective beta-blockers was 0.92 (95% confidence interval 0.64-1.30), and in patients taking cardioselective beta-blockers 0.84 (95% confidence interval 0.59-1.19). CONCLUSIONS: The study suggests that current treatment with non-selective beta-blockers may have reduced the enzymatically estimated infarct size and the occurrence of circulatory arrest due to ventricular tachyarrhythmias. Both non-selective and cardioselective beta-blockers may also have reduced the in-hospital mortality in this population of hypertensive patients suffering a first acute myocardial infarction. In a clinical study using with adrenaline infusions in healthy volunteers, we found that beta 2-receptor blockade improved potentially arrhythmogenic variables, such as hypokalemia and hypomagnesemia, but the adrenaline-induced reduction in diastolic blood pressure was reversed. Pretreatment with the new beta-blocker carvedilol preserved the beneficial electrolyte effects without increasing blood pressure during the adrenaline infusion.

Adrenergic beta-Antagonists↗

[Possible prognostic criteria for the evaluation of the susceptibility to septic diseases increased by stress in swine].

A test to assess leukocyte function developed in our laboratory and based on effector mediated alterations in the cell volume was applied to study the effect of stress on the immune status of pregnant pigs. Effectors selected were prolactin, opsonized particles (Zymosan) and Zymosan together with the autologous plasma. The pigs were exposed to two stress situation: 1. fixation for an ear vein catheterization and 2. injuries by laparotomy. The investigations demonstrated that--following the stress situation 1--the effector induced alterations in the cell volume gave an indication of the susceptibility to septic inflammatory processes subsequent to the laparotomy (stress situation 2) which was carried out about 1 week after the fixation (stress situation 1). Measuring the humoral immunocompetence CRP, C3c, alpha-2-macroglobulin levels in the blood plasma had no or little prognostic value concerning the susceptibility to or the onset of the disease.

Animals↗

Circadian distribution of onset of acute myocardial infarction in subgroups from analysis of 10,791 patients treated in a single center.

A circadian variation of symptom onset in acute myocardial infarction (AMI) with an increased frequency in the late morning and possibly also in the evening has been found in several studies. It has been suggested that different circadian rhythms may exist in various subgroups of patients. This possibility was examined in a population of 10,791 patients collected between 1973 and 1987 in a continuously operating register of patients with AMI in Malmö, Sweden. In 6,763 patients (63%) in whom a distinct symptom onset could be established, symptom onset occurred with an increased frequency between 6:01 A.M. and 12:00 noon (30.6%) and between 6:01 P.M. and 12:00 midnight (26.9%). Similar bimodal circadian rhythms were seen in patients aged greater than 70 years (n = 2,923), less than or equal to 70 years (n = 3,840), men (n = 4,528), women (n = 2,235), smokers (n = 2,458), hypertensives (n = 1,999), diabetics (n = 653), patients with (n = 1,872) and without (n = 4,891) a history of previous AMI, and in patients with recent non-Q-wave AMI (n = 333). In 455 patients receiving cardioselective beta blockers the circadian distribution did not differ from a random, whereas in patients taking nonselective beta blockers or calcium antagonists significant bimodal rhythms were found. Statistically significant interactions were found between symptom onset and age dichotomized at 70 years, and between patients with and without a history of previous AMI. In a multivariate analysis only these variables age less than or equal to/greater than 70 years; +/- history of a previous AMI) were found to modify the circadian rhythm of symptom onset in the population.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Ca(2+)-ATPase and Na(+)-K(+)-ATPase content in skeletal muscle from malignant hyperthermia patients.

The purpose of this study was to determine the concentration of Ca(2+)-ATPase and Na(+)-K(+)-ATPase in biopsies from vastus lateralis muscle of 24 patients, who underwent a diagnostic contracture test for susceptibility to malignant hyperthermia (MH). Ca(2+)-ATPase was quantified as the Ca(2+)-dependent 32P incorporation in whole muscle homogenates. Na(+)-K(+)-ATPase was quantified as the [3H]ouabain-binding capacity in intact muscle samples. These methods avoid isolation of membranes, a procedure that may influence the results due to interindividual variation in recovery. The results show that both enzymes can be determined in (frozen) muscle biopsies weighing 50 mg. Neither the concentration of Ca(2+)-ATPase nor that of Na(+)-K(+)-ATPase differed in biopsies from subjects diagnosed as susceptible (MHS) or nonsusceptible (MHN) to MH. Our data support the view that changes in the concentration of Ca(2+)-ATPase and/or Na(+)-K(+)-ATPase do not play a primary role in the pathogenesis of MH.

Adult↗

Effects of hydrochlorothiazide, amiloride, and lisinopril on the metabolic response to adrenaline infusions in normal subjects.

Twelve healthy male volunteers were given adrenaline infusions, 0.05 microgram/kg body weight/min over 120 minutes in order to achieve serum adrenaline concentrations comparable with those seen in acute myocardial infarction. The infusions were given on four occasions, at intervals of at least 4 weeks. Before the infusions the subjects were given, in random order, 14 days of pretreatment with placebo, hydrochlorothiazide 50 mg once daily, amiloride 10 mg once daily, or lisinopril 20 mg once daily. The adrenaline infusion induced a drop in serum potassium of the same magnitude in all four groups, with the lowest absolute value after hydrochlorothiazide because of the lowest pre-adrenaline level. The infusion-induced decreases in serum calcium and magnesium were of the same magnitude in all groups, with the absolute calcium being least low in the hydrochlorothiazide group because of the highest preinfusion value. Preinfusion serum urate was highest after hydrochlorothiazide and fell during the adrenaline infusion in all groups, although not significantly. Blood glucose increased during the adrenaline infusion in all groups, but significantly more after hydrochlorothiazide and amiloride than after lisinopril. Heart rate increased during the adrenaline infusion in all groups but least after lisinopril. QTc preinfusion was longer after hydrochlorothiazide than after amiloride and placebo, but the infusion-induced prolongation of QTc was of the same magnitude in all pretreatment groups. Since our results were obtained in short-term experiments in normal subjects, their clinical relevance is questionable, but they support the view that ACE inhibitors may have certain metabolic advantages over diuretics.

Adult↗

Geographical variation and time trends in the attack rate of coronary heart disease in five Swedish cities.

Based upon community myocardial infarction (MI) records in five Swedish cities, geographical variation and time trends in the attack rate of fatal and non-fatal MI have been evaluated. During the study period 1975-1982, a total of 7699 events were registered among men and 1823 events among women. The mean annual mortality was highest in the north, and a declining gradient in mortality was observed from the northern to the southern part of the country. The out-of-hospital death rate was highest in the north, while no difference in in-hospital mortality was observed. However, the geographical variation in the morbidity of MI was less consistent. Changes over time generally followed the same pattern in all cities. The attack rate of fatal and non-fatal MI tended to decline among women and men aged 60-64 years. The pattern was less consistent among younger men. Among women aged 50-59 years the mortality remained unchanged, but the attack rate of non-fatal MI increased in all cities. This increase was not explained by inclusion of less severe infarctions. A considerable proportion, about 85%, were recorded as primary events, emphasizing the possible role of primary prevention in obtaining a decrease in the incidence of the disease. The results of this study support previous findings of an important regional difference in the mortality of MI in Sweden. However, the magnitude of the regional variation in the incidence of coronary heart disease might be overestimated if only the mortality pattern is studied.

Adult↗

Clinical outcome of acute myocardial infarction in patients on treatment with beta-blockers or calcium antagonists. A study of 7,922 hospitalized first myocardial infarctions.

To assess the effects of current treatments with beta-blockers or calcium antagonists on the clinical outcome of acute myocardial infarction (MI), enzymatically estimated infarct sizes, circulatory arrests from ventricular tachyarrhythmias, ventricular tachycardia (VT)/ventricular fibrillation (VF), and in-hospital mortality were analyzed retrospectively from 7,922 citizens of Malmö, Sweden, hospitalized due to a first MI between 1973 and 1987. Of these patients, 296 were on treatment with calcium antagonists, 393 on treatment with a beta 1-selective beta-blocker, 482 with a nonselective beta-blocker, and 95 on combined treatment with beta-blockers and calcium antagonists at the time of admission to hospital. In a set of multivariate analyses including several clinical characteristics, patients on treatment with a nonselective beta-blocker had a significantly lower peak aspartate aminotransferase (ASAT; difference -0.70 mukat/l, 95% CL: -1.24 to -0.16), whereas no significant relations between peak ASAT and treatment with cardioselective beta-blockers or calcium antagonists were found. Treatment with cardioselective beta-blockers or calcium antagonists, in contrast to treatment with a nonselective beta-blocker, were significant predictors of the occurrence of circulatory arrests from VT/VF. The relative risk of VT/VF in patients on cardioselective beta-blockers was 1.51 (95% CI: 1.12-2.03), and in patients on calcium antagonists 1.44 (95% CI: 1.03-2.02). None of the treatments were significantly associated with in-hospital mortality. In patients on beta-blockers or calcium antagonists when suffering their first MI, nonselective beta-blockade may reduce infarct size. Treatment with beta-blockers or calcium antagonists identified patients with an increased risk of circulatory arrests from VT/VF, but neither of the treatments were significantly associated with in-hospital mortality. We suggest that only minor differences exist between the effects of chronic treatment with beta-blockers and calcium antagonists on the outcome of an acute MI.

Adrenergic beta-Antagonists↗

Heterogeneity of Na,K-ATPase from kidney.

Na,K-ATPase was purified from pig and mink kidney. Enzyme batches of high specific activity apparently contained only alpha- and beta-peptides, judging from the SDS-gel-electrophoretic pattern. Careful determinations of the ouabain-binding capacity and binding kinetics were carried out. The question whether the functional unit is an alpha beta-protomer, a diprotomer or even a polymer was analysed from the binding stoichiometry and the binding pattern at nonsaturating ouabain concentrations. The binding capacity exceeded half of the theoretical maximum value for exclusively alpha beta-promoters. A half-of-the-sites reactivity of a diprotomer thus seems less likely, though nearly half of the protein is not accounted for in its absence. When ouabain binding took place in the presence of Na+, at least two binding components were noticed. Most probably the two components are not of equal size, thus excluding a co-operative diprotomer construction of the active ouabain-binding units. If the co-operativity model has to be abandoned, the phenomenon could be due to two or more isozymes exhibiting different Na(+)-affinities. Isoforms of the hydrolytic alpha-peptide were analysed by an ELISA technique and on blots of Na,K-ATPase peptides utilizing commercial isoform-specific antibodies. Though not absolutely specific, the individual antibodies were assumed to be monospecific with respect to the single isoforms of the alpha-peptide. In that case, data were consistent with a significant contribution of alpha 2- and alpha 3-isoforms (about 15%), in addition to the predominant alpha 1-isoform in kidney Na,K-ATPase.

Animals↗

Nursing sickness in lactating mink (Mustela vison). I. Epidemiological and pathological observations.

In a retrospective survey, the epidemiological characteristics of nursing sickness in Standard Black and Pastel mink (Mustela vison) were examined in a Danish fur research farm. Based on the clinical diagnosis of the disease, the overall morbidity in a total of 1774 lactating females amounted to 14.4% and the case fatality rate to 7.8%. Apparently healthy females weaned an average of 5.0 kits per litter, while dams suffering from nursing sickness raised and weaned an average of 5.4 kits per litter (p less than 0.01). Based on logistic regression analysis, the increasing age of the lactating dam, followed by littersize and female weight loss, appeared to be major determinants for the development of nursing sickness. The impact of additional covariates such as litter weight gain and female color type were remarkably low. At weaning (day 43) the mean individual live weight of the kits of either sex did not differ between healthy and sick dams. In Standard Black, the total biomass of the offspring raised by sick dams was significantly larger than that of the healthy controls (p less than 0.01). During the final two weeks of lactation, apparently healthy dams lost on average 14% of their body mass, whereas those affected by nursing sickness had a mean weight loss of about 31% (p less than 0.001). Postmortem examination of 25 dams with severe nursing sickness verified the clinical findings of progressive dehydration and emaciation. The gastrointestinal tract was empty and gastric ulcers and melaena were frequently present. Other common findings included small livers,enlarged adrenals and pitted kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Nursing sickness in lactating mink (Mustela vison). II. Pathophysiology and changes in body fluid composition.

An investigation of the pathophysiological characteristics of nursing sickness in mink was carried out as a follow-up study of a previous epidemiological survey at a Danish fur research farm during the 1989 breeding season. In a total of 48 nursing females of the Standard Black and Pastel type, concentrations of several pertinent biochemical constituents of whole blood, plasma, urine and skeletal muscle were determined in order to identify nutritional and metabolic factors involved in the origin and development of the disease. Compared to the reference data obtained in 17 apparently normal lactating dams the findings in 31 females suffering from nursing sickness presented varying clinical and biochemical signs of progressive dehydration and emaciation: aldosteronism, hypovolemia, hyponatremia, hyperkalemia (in the face of muscle potassium depletion), hyperglycemia and azotemic acidemia. Neither ketosis nor severe lactacidemia was observed. The urine was almost devoid of sodium and chloride, and urinary potassium concentration diminished by approximately 50%. The concentrating ability of the kidneys was reduced to less than one third of the maximum value. The results were consistent with severe dehydration and emaciation due to heavy losses of energy, water and body mass along with increasing milk production. The progressive nature of the disease supported the hypothesis that nursing sickness is due to the combined effects of heavy milk production and excessive tissue catabolism along with reduced or ceased dietary intake, and maybe increasing environmental stress. In the advanced stage of the disease coma and death appear to be the inevitable outcome of the metabolic strains for continuing milk production.

Acid-Base Equilibrium↗

Epidemiologic aspects of coronary heart disease in Malmö, Sweden, 1935-1988.

Mortality from coronary heart disease has declined for more than 20 years in several industrialized countries. Partly because of a lack of morbidity data, the reasons for the decline are not satisfactorily established. This community-wide survey of coronary heart disease morbidity and mortality in Malmö, Sweden, showed declining mortality rates beginning in the mid-1970s. Between the 3-year intervals 1975-1977 and 1984-1986, coronary heart disease mortality declined by 17% (2,610/100,000 inhabitants in 1984-1986) in men aged greater than or equal to 70 years and by 8% (938/100,000 inhabitants in 1984-1986) in men aged 60-69 years, while coronary heart disease mortality in men aged 50-59 years increased by 7% (355/100,000 inhabitants in 1984-1986). In women aged greater than or equal to 70 years, coronary heart disease mortality decreased by 12% between 1975-1977 and 1984-1986 (1,609/100,000 inhabitants in 1984-1986), while the decrease in women aged 60-69 years was 5% (242/100,000 inhabitants in 1984-1986). The decline in mortality was associated with a decline in both incidence rates and in-hospital case fatality rates for myocardial infarction. The authors suggest that the declining coronary heart disease mortality in Malmö was due partly to prevention of coronary heart disease but that improved medical care for acute and chronic coronary heart disease may also have contributed.

Adult↗