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Biomedical subjects

H Stormorken

Publications and source records attributed to H Stormorken.

At least 37 records · Page 2Linked to original sources
PubMed1995

Contrast media effects on hemostatic and thrombotic parameters. Possible consequences for practical techniques and prophylactic measures.

This paper reviews the basic mechanisms of the thrombohemorrhagic balance and ways in which contrast media (CM) influence these processes. Coagulation and platelet functions are strongly inhibited by ionic CM, but weakly so by nonionic CM, whereas the former are more detrimental to endothelium, and thus thrombogenic in this sense. Some observations indicate a lower rate of thromboembolic events with the ionic CM in percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass grafting (CABG), but this purported difference does not effect mortality or frequency of re-PTCA and emergency CABG. Thus, to challenge these events, strong acting antithrombotics, which also, unlike heparin, inactivate fibrin-bound thrombin, are necessary. Aggressive anti-atherogenic prophylaxis may hamper both thrombosis and reocclusion. The ideal antithrombotic in this setting is yet to be found.

Angioplasty, Balloon, Coronary↗
PubMed1995

Studies on the haemostatic defect in a complicated syndrome. An inverse Scott syndrome platelet membrane abnormality?

The Stormorken syndrome is a multifacetted syndrome including a bleeding tendency. No deviations were found in the coagulation- or fibrinolytic systems. Platelet number was low normal, and size abnormal, whereas EM findings were unremarkable. Survival time was half normal. Clot retraction was initially rapid, but clearly decreased, whereas prothrombin consumption was also initially rapid, but complete. Membrane GP's were normal, so was AA metabolism, PI-cycle, granule storage and secretion, and c-AMP function, whereas 5-HT uptake and storage was decreased. Optical platelet aggregation was low normal with all physiological agonists. The only clearly abnormal finding was that coagulant activity was present on non stimulated platelets at the same level as kaolin-stimulated normal platelets. This indicated a platelet abnormality which should lead to a thrombogenic, not to a haemorrhagic trait. This paradox may have its origin in rheology, because when challenged with in vivo shear rates in an ex vivo perfusion chamber, platelet cohesion was abnormally low. Further studies to better delineate the membrane abnormality are underway.

Blood Platelet Disorders↗
PubMed1994

Reduced thrombus formation in native blood of homozygous factor VII-deficient patients at high arterial wall shear rate.

Inhibition of thrombin formation in flowing native blood reduces thrombus formation on subendothelium, dacron, or collagen fibrils at arterial wall shear rates of 450 to 650 s-1. In the present study, we have investigated the role of low levels of factor VII (FVII) in thrombus formation on collagen fibrils at arterial wall shear rates of 650 s-1 (coronary arteries), 2,600 s-1 (mildly stenosed arteries), and 10,510 s-1 (severely stenosed arteries) in parallel-plate perfusion chambers. In the perfusion chamber with the highest wall shear rate, thrombus formation took place at the apex of an eccentric stenosis, which reduced the cross-sectional area of the blood flow channel by 80%, thus simulating thrombus formation at an atherosclerotic plaque rupture. Native blood from 21 healthy volunteers and 12 homozygous FVII-deficient patients was drawn by a pump directly from an antecubital vein over a surface of fibrillar collagen positioned in the respective perfusion chambers. The patients had FVII coagulant activities ranging from 1.3% to 4.5% and FVII antigen levels of 16% to 23% of normal. Immunoaffinity purification of the patients' FVII followed by electrophoresis (sodium dodecyl sulfate-polyacrylamide gel electrophoresis [SDS-PAGE]) and immunoblotting showed a protein with similar molecular mass as normal FVII. In the perfusion studies, a reduction in thrombus volume of 54% of normal (P < .007) at 10,510 s-1 was observed. The deposition of fibrin on the thrombogenic surface and the plasma level of fibrinopeptide A (FPA) in blood samples collected distal to the perfusion chamber were concomitantly reduced (P < .002 and P < .04, respectively). The plasma FPA level was also reduced at 2,600 s-1 (P < .04), but not at 650 s-1. However, at the lower shear conditions, the thrombus volume and the fibrin deposition were within the ranges observed in normal blood. The platelet-collagen adhesion was not affected at any of the three shear conditions. Thus, low plasma levels of FVII result in significantly less formation of thrombin and fibrin in and around growing platelet masses at high shear condition. This may weaken the thrombus stability and reduce platelet recruitment, thereby lowering thrombus volume. In support of this theory, one patient with afibrinogenemia had an 83% reduction in thrombus volume at this high shear condition.

Afibrinogenemia↗
PubMed1994

[Month of birth and prevalence of fibromyalgia].

We have studied the possible influence of season of birth on prevalence of fibromyalgia. Data from the Norwegian Fibromyalgia Association, where diagnosis is compulsory, were compared with mean figures for 1936-65 from the National Register of Births. Figures for 8,125 patients were correlated with figures for two million persons from the register. Unlike other musculoskeletal diseases, which are more prevalent in summerborn persons, and certain mental diseases, which are more prevalent in winterborn persons, no such association was found for fibromyalgia.

Adult↗
PubMed1993

Haematocrit: a predictor of cardiovascular mortality?

OBJECTIVES: The main purpose of the study was to assess a possible association between haematocrit (Hct) and long-term cardiovascular disease (CVD) mortality. DESIGN: An extensive examination programme was carried out in 2014 men, defined as apparently healthy, during the period 1972 to 1975, including Hct measurements in a 25% random subsample. Sequential, cause-specific mortality was followed prospectively over a period of 16 years. SETTING: The survey was conducted at Medical Department B, Rikshospitalet, Oslo, Norway. SUBJECTS: The participants represented 86% of all eligible apparently healthy men working in five preselected companies in Oslo. INTERVENTIONS: No intervention was given by the study group during follow-up. MAIN OUTCOME MEASURES: Complete, cause-specific mortality figures after 8-16 years were obtained from the Norwegian Central Bureau of Statistics. RESULTS: Hct measures were obtained in 488 men (24.2%). Mean Hct was 47.2% (SD 2.9%). After correcting for differences in age, plasma cholesterol, systolic blood pressure, erythrocyte sedimentation rate and smoking habits (Cox proportional hazards model), an increase in Hct by 2 SDS was associated with an increase in CVD mortality by a factor ranging between 2.9 at 10, and 1.9 at 16 years (P < 0.05). A similar increased risk was observed earlier during follow-up but the number of deaths was too small for meaningful statistical analysis. No association was found between Hct and non-CVD mortality. CONCLUSIONS: Our data show that increased Hct is associated with an increased risk of dying from CVD--independent of conventional CVD risk factors.

Adult↗
PubMed1992

Concomitant occurrence of mucopolysaccharidosis IIIB and Glanzmann's thrombasthenia. Further evidence of a hyperactive alpha-N-acetylglucosaminidase-producing allele.

A daughter of first cousins had two extremely rare, recessive disorders: thrombasthenia (Glanzmann's disease, glycoprotein IIb/IIIa deficiency) and mucopolysaccharidosis IIIB, (Sanfilippo B syndrome, alpha-N-acetylglucosaminidase (NAG) deficiency). Normal alpha-N-acetylglucosaminidase activity was observed in two obligate heterozygotes (the proband's father and her maternal grandmother), suggesting that in addition to the normal and defective alleles, a third, hyperactive allele is also present in this family. Such a hyperactive allele seems to be quite prevalent in our area, and makes the biochemical identification of heterozygotes impossible if no extensive family surveys provide additional clues. There was no linkage between the two diseases, nor between any of them and several blood-groups and HLA-antigens tested for.

Acetylglucosaminidase↗
PubMed1992

A new hereditary syndrome with a bleeding tendency, extreme miosis, spasms, dyslexia, thrombocytopathia etc. Pupillometric, evaporimetric, and ophthalmological observations.

A recently described familiar syndrome consists of the following components: A bleeding tendency with thrombocytopathia, miosis, muscular weakness and spasms, ichthyosis, asplenia, dyslexia, and headache. Four definite and 2 probable patients have been identified in 4 generations. In the present study, the pupillary behaviour was scrutinized in two 'definite' cases with the infrared, binocular pupillometer. The forehead sweating pattern was also investigated with an Evaporimeter. The basal pupillary widths were: 1.25-1.75 mm. Only minor responses were noted upon topical stimulation with an indirectly acting pupillodilating agent (OH-amphetamine). A directly acting sympathicomimetic drug (phenylephrine) exerted a more marked influence on the pupil, indicating a relative supersensitivity. The evaporimetric pattern in the forehead seemed to be within reference limits, at variance with what is the case in Horner's syndrome. Further findings were: the orbit seemed to be smaller than normal; a bilateral VI. cranial nerve palsy was identified, and a marked upward gaze palsy coexisted with pupils with Argyll Robertson's traits. There is no readily acceptable explanation for the ocular abnormalities. The disorder underlying the pupillary abnormality may possibly be located in the upper mesencephalon.

Adult↗
PubMed1991

X-linked thrombocytopenia and thrombocytopathia: attenuated Wiskott-Aldrich syndrome. Functional and morphological studies of platelets and lymphocytes.

Detailed studies on the rare disorder X-linked thrombocytopenia showed that it resembles the Wiskott-Aldrich syndrome (WAS) in inheritance, clinical bleeding tendency, platelet morphology, marked thrombocytopenia and microplatelets. The calculated platelet mass was 5% of normal. Functional and biochemical studies indicated qualitatively normal aggregation and release mechanisms, whereas a moderate storage pool defect was present. The classical platelet membrane glycoproteins and lymphocyte sialophorin (CD 43) were normal. The reason for the bleeding tendency was concluded to be deficient hemostatic plug formation resulting from the low platelet mass and a moderate storage pool defect. The only clear distinction from WAS was the normal immunofunctional tests, the moderate tendency to infections and the absence of eczema. We therefore consider the trait as an attenuated form of WAS. That women are affected may indicate a particular variant.

Adenosine Diphosphate↗
PubMed1991

Blood platelet count and function are related to total and cardiovascular death in apparently healthy men.

BACKGROUND: Experimental animal and clinical studies indicate that blood platelets have an important role in atherosclerosis and formation of thrombi. Prospective studies presenting evidence of an association between blood platelet count and cardiovascular mortality have not been performed. METHODS AND RESULTS: From 1973 to 1975, blood platelets were counted, and their responsiveness to aggregating agents was studied in healthy middle-aged men. The aim was to assess the possible association between these variables and coronary heart disease. At 13.5 years of follow up, a significantly higher coronary heart disease mortality was observed among the 25% of subjects with the highest platelet counts. Platelet aggregation performed in a random subsample (150 of the 487 men), moreover, revealed that the 50% with the most rapid aggregation response after ADP stimulation had significantly increased coronary heart disease mortality compared with the others. These associations could not be explained by differences in age, lipids, blood pressure, or smoking habits. CONCLUSIONS: The present study is the first to present conclusive, prospective evidence of an association between platelet concentration and aggregability and long-term incidence of fatal coronary heart disease in a population of apparently healthy middle-aged men.

Adenosine Diphosphate↗
PubMed1990

A new case of total kininogen deficiency.

Six families with total kininogen deficiency have been described in the literature. We report herein an additional case in a Pakistanese woman. The defect was discovered accidentally due to lack of normal clot formation in a preoperative routine blood sample. She had a borderline prolonged bleeding time, and reported occasional hematuria, but was otherwise without symptoms. Absence of both kininogen species was proven by functional and immunological methods, and by lack of kinin formation both by plasma kallikrein and hog pancreas kallikrein. Prekallikrein was reduced, probably because the main part circulates complexed to high molecular kininogen. Activation of intrinsic fibrinolysis was grossly hampered, and cold activation of coagulation absent with epsilonaminocaproic acid and greatly retarded by dextran sulfate, kaolin and ellagic acid. Together with other evidence the findings indicate the following order of importance for contact activation in plasma--F.XII, high molecular weight kininogen, prekallikrein.

Adult↗
PubMed1990

Polymorphism of a platelet polypeptide.

Polymorphism of a platelet protein is described. The gene products are represented by two peptides of MW around 30 kD. The allele frequency was estimated to 0.85 and 0.15, the common variant being of slightly higher MW and about 2 charge units more acidic than the other. The peptides were neither released nor phosphorylated, and subcelluar fractionation indicated localization to the cytosol. Attempts to raise antibodies failed, and further characterization could not be done, but the peptides seem to differ from all reasonably well characterized platelet proteins so far.

Alleles↗
PubMed1990

[Acetylsalicylic acid in the prevention of arterial thrombosis. Dosage problems in general and in the authors' experiment].

Acetylsalicylic acid is now accepted as a clinically useful drug for secondary prophylaxis against several thromboembolic complications, but there is still much controversy about the dosage. We discuss this problem, in the light of data from newly published clinical trials and of results from a pharmacological study performed by ourselves. All in all it seems reasonable to recommend 100-150 mg acetylsalicylic acid per day for prophylaxis after acute myocardial infarction. As for cerebrovascular indications, no clinical data available so far justify a dose reduction below 300 mg.

Adult↗
PubMed1990

Adenine nucleotides, serotonin, and aggregation properties of platelets of blue foxes (Alopex lagopus) with the Chediak-Higashi syndrome.

Bleeding times, concentrations of serotonin in whole blood, and concentrations of adenine nucleotides as well as aggregation properties of platelets were examined in 18 blue foxes with Chediak-Higashi-like syndrome (CHS) and 16 controls. A claw of each ketamine-sedated fox was cut until bleeding started and the bleeding time was recorded as the time from the first to the last drop. The bleeding time was greatly increased in CHS foxes. Platelet counts of CHS foxes were normal, but aggregation induced by adenosine diphosphate (ADP), serotonin, collagen, and arachidonate was impaired. Adrenaline and serotonin was impaired. Adrenaline and serotonin potentiated the aggregatory effect of ADP on control as well as on CHS platelets. The mean concentration of ADP in CHS platelets was about one-third that in controls, whereas adenosine triphosphate (ATP) was approximately one-half that in controls. Serotonin could not, in most cases, be detected in blood of CHS foxes. These findings suggest that the prolonged bleeding time in the CHS foxes is, at least partly, due to a storage pool deficiency. The drastically reduced, and in some cases absent, aggregation of CHS platelets in response to arachidonate suggests that defective arachidonate metabolism contributes to the impaired hemostasis.

Adenine Nucleotides↗