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S D Kristensen

Publications and source records attributed to S D Kristensen.

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

[Interaction between thrombocytes and blood vessel wall--significance for acute ischemic coronary syndromes].

Intracoronary thrombus formation is the essential pathogenic substrate for the development of the acute ischaemic coronary syndromes (unstable angina pectoris (UAP), acute myocardial infarction (MI) and sudden cardiac death). Rupture of an atherosclerotic plaque has been shown to be of major importance for initiation of the thrombogenic process, but the reactivity of the circulating platelets and their interaction with the coronary vessel wall are also important for the formation and propagation of the intracoronary thrombus. The evidence favouring the role of platelets is: 1) the aggregability of platelets is increased in the morning where the incidence of MI and sudden cardiac death has been shown to be high, 2) shortened bleeding time and increased mean platelet volume in the acute phase of MI, 3) the synthesis of proaggregatory thromboxane A2 is increased in the acute phase of MI and in UAP, 4) a high platelet count and an increased ADP-induced platelet aggregation predispose to MI and death in healthy males, 5) high mean platelet volume and increased spontaneous platelet aggregation are risk factors for MI and death in patients with a recent MI, 6) the platelet inhibitor, acetylsalicylic acid, has been shown to reduce the incidence of MI and mortality in patients with silent myocardial ischaemia, stable and unstable angina pectoris and in patients with MI.

Angina, Unstable↗
PubMed1995

n-3 polyunsaturated fatty acids: update 1995.

Epidemiologic and biochemical studies have suggested an anti-inflammatory effect of n-3 fatty acids. Beneficial therapeutic effects reported from small patient groups need to be confirmed in large-cohort controlled clinical trials. There is a growing number of clinical trials of n-3 fatty acid supplementation in disease. Clinical benefits have been moderate in patients with rheumatoid arthritis and with arterial hypertension. Clearly negative results have been reported during the past 2 years for patients with lupus nephritis and for patients with psoriasis or with atopic dermatitis. Such trials have now been completed. For patients with coronary artery disease following coronary angioplasty, earlier results of a large meta-analysis, could not be confirmed. For patients with IgA-nephropathy and for patients following kidney transplantation, a clear benefit was seen in patients receiving fish oil. These promising results are currently pursued in follow-up phase III clinical trials.

Animals↗
PubMed1994

n-3 fatty acids and renal diseases.

There are numerous biologic rationales for the use of n-3 fatty acids in renal diseases, including a possible increase in the renal vasodilatory capacity by a rearrangement of renal prostanoid production, a reduction in the production of proinflammatory leukotrienes, a reduction in the transcapillary escape rate of albumin, and actions limiting cyclosporine-related nephrotoxicity. Studies of animal models of renal disease, mostly of immune-renal disease, support the idea of the possible usefulness of these compounds. The most promising areas of clinical investigation include the reduction of proteinuria in some chronic glomerular diseases, the treatment of immunoglobulin A nephropathy, and the prevention of cyclosporine-induced nephrotoxicity. However, the results of larger clinical studies, some of which are ongoing, are necessary to support the use of n-3 fatty acids in human renal diseases.

Animals↗
PubMed1993

The effects of n-3 fatty acids on plasma lipids and lipoproteins and other cardiovascular risk factors in patients with hyperlipidemia.

This review discusses the effects of dietary n-3 fatty acids on the plasma concentrations and metabolism of lipoproteins with a particular focus on work in human subjects. The influence of dietary n-3 fatty acids on the concentrations of plasma lipoproteins are affected by the amount of n-3 fatty acids as well as by the lipoprotein phenotype in the patients under investigation. On the basis of the observed changes in lipoproteins, dietary n-3 fatty acids exert the greatest effects on the concentrations of triglyceride-rich lipoproteins; their therapeutic potential is greatest in patients with hypertriglyceridemia. In addition to their effects on plasma lipoproteins, dietary n-3 fatty acids have been reported to exert potentially favorable effects on blood pressure, platelet function and viscosity. These effects may justify the use of supplements of dietary n-3 fatty acids in selected patients with hypertriglyceridemia to reduce the risk of atherosclerosis; however, the benefits of such therapy remain to be demonstrated.

Cardiovascular Diseases↗
PubMed1993

Platelet-derived growth factor release and antiplatelet treatment with low-dose acetylsalicylic acid.

Platelet-derived growth factor (PDGF) and beta-thromboglobulin (beta-TG) are released from alpha granules during platelet activation. PDGF may play a role in the development of atherosclerosis and the late restenosis after percutaneous transluminal coronary angioplasty (PTCA). The effect of acetylsalicylic acid (ASA) on PDGF release was studied in healthy volunteers before and twelve hours after ingestion of 300 mg ASA. PDGF, beta-TG, and thromboxane B2(TxB2) were measured by radioimmunoassay (RIA) in serum and in platelet rich plasma (PRP) after submaximal stimulation with collagen. TxB2 decreased significantly from 0.9 +/- 0.3 ng/(mL x 10(6) platelets) to 0.006 +/- 0.005 ng/(mL x 10(6) platelets) (mean +/- SD) in serum after ASA ingestion while PDGF and beta-TG remained unchanged. Measurements in PRP after stimulation with collagen showed a significant decrease in PDGF (from 21.5 +/- 1.4 pg/(mL x 10(6) platelets) to 1.8 +/- 4.1 (pg/mL x 10(6) platelets), in beta-TG (from 21.0 +/- 13.3 ng/(mL x 10(6) platelets) to 2.2 +/- 1.4 ng/(mL x 10(6) platelets)) and in TxB2 (from 143.6 +/- 80.7 pg/(mL x 10(6) platelets) to 0.5 +/- 0.6 pg/(mL x 10(6) platelets)) after treatment with ASA. In conclusion low-dose ASA inhibits collagen-induced release of both beta-TG and PDGF in PRP and TxB2-synthesis in PRP and serum.

Adult↗
PubMed1992

Intravenous acetylsalicylic acid--dose-related effects on platelet function and fibrinolysis in healthy males.

Low-dose acetylsalicylic acid (ASA) has been shown to be beneficial in patients with acute myocardial infarction and unstable angina pectoris. Oral administration of ASA is difficult in the acute phase of these syndromes. In this study we evaluated the effect of 25 mg, 50 mg or 100 mg of ASA given as an intravenous bolus injection on platelet function and fibrinolysis in healthy males and related this to plasma concentrations of ASA. No adverse effects were found. A complete inhibition of serum thromboxane B2 synthesis was demonstrated 5 min after injection of 100 mg ASA intravenously. ASA disappeared from the circulation within 60 min after bolus injection and at this time thromboxane B2 synthesis was inhibited dose-dependently by 71%, 90% and 100% for doses of 25 mg, 50 mg and 100 mg, respectively. Inhibition of thromboxane B2 synthesis after 100 mg of intravenous ASA was still 96.5% at 24 h and 93.4% at 48 h after the injection. The bleeding time measured at 30 min after ASA administration was significantly prolonged on the average by 70 s, 144 s and 211 s after 25 mg, 50 mg and 100 mg of ASA, respectively. Minor, but significant changes were found in tissue plasminogen activator antigen and in plasminogen activator inhibitor within the first hour after injection of low dose ASA, but similar changes were found after injection of saline. No change in tissue plasminogen activator activity was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Enalapril and exercise-induced hyperkalemia. A study of patients randomized to double-blind treatment with enalapril or placebo after acute myocardial infarction.

During exercise a marked increase in plasma potassium in healthy subjects has repeatedly been demonstrated. In patients on treatment with angiotensin-converting enzyme inhibitors this may be further augmented. Therefore, the aim of present study was to evaluate the effect of enalapril on exercise-induced hyperkalemia. This was done in patients with acute myocardial infarction randomized to double-blind treatment with enalapril 10-20 mg per day (n = 7) or placebo (n = 6) within 24 h of onset of chest pain, and the results were compared with data from healthy control subjects (n = 11). Baseline plasma potassium did not differ between the three groups; i.e. 4.2, 4.0, and 4.1 mmol/l, respectively. An incremental, symptom-limited, bicycle exercise test was done one month after the myocardial infarction, and blood samples were taken for determination of plasma potassium. The exercise-induced increase in plasma potassium was not higher in the enalapril group as compared to the placebo and control groups, and there was no difference between the enalapril and placebo group, the specific values being 0.6 vs. 0.6 and 0.7 mmol/l, respectively. No difference was observed in the slope (dK/dt) between the 3 groups. In conclusion, enalapril at a dosage of 10-20 mg per day does not provoke any augmentation of the increase in plasma potassium during exercise.

Adult↗
PubMed1992

The relationship between increased platelet count and megakaryocyte size in bronchial carcinoma.

This study investigates megakaryocyte size in bronchial carcinoma and its relationship to platelet count, mean platelet volume and platelet function, the latter determined in vivo by measurement of the cutaneous bleeding time. Measurements were performed in 19 patients with bronchial carcinoma and 11 patients with a hiatus hernia (controls). Platelet count (335 +/- 123 v. 241 +/- 72 x 10(9)/l) and megakaryocyte total area (772 +/- 135 v. 666 +/- 105 microns 2) (mean +/- standard deviation) were both significantly increased in patients with bronchial carcinoma when compared to controls whilst the bleeding time was shorter in the patient group (253 +/- 116 v. 321 +/- 80 s). Patients with bronchial carcinoma were older (60.2 +/- 8.4 v. 48.8 +/- 13.2 years) and smoked more heavily (760 +/- 511 v. 92 +/- 175 cigarette years) than controls. Megakaryocyte size, platelet count and bleeding time all correlated with smoking habit (r = 0.395, P = 0.031; r = 0.622, P less than 0.001; r = 0.515, P = 0.004 respectively). There were no statistically significant differences between the groups with respect to gender or mean platelet volume. When considering all patients, significant correlations existed between platelet count and megakaryocyte area (r = 0.400, P = 0.029), and bleeding time and megakaryocyte area (r = -0.365, P = 0.047). The megakaryocyte nuclear and cytoplasmic areas were positively correlated (r = 0.855, P less than 0.001). This study suggests that the elevated platelet count in patients with bronchial carcinoma is mediated by an increase in the size of bone marrow megakaryocytes although the results are compounded by the association between smoking and megakaryocyte/platelet parameters.

Bleeding Time↗
PubMed1992

The platelet-vessel wall interaction in experimental atherosclerosis and ischaemic heart disease with special reference to thrombopoiesis.

Platelets and their interaction with the vessel wall play a role in atherogenesis and in the formation of the coronary thrombus. Supplementation of the diet with n-3 PUFA shifts the platelet-vessel wall interaction in anti-thrombotic direction in healthy persons and in patients with IHD. This is in part caused by an inhibition of Tx synthesis and also by an increased synthesis of PGI2 and PGI3 in the vessel wall. However, the clinical significance of these findings needs to be elucidated in clinical trials. Large, dense platelets are more reactive than small ones. Platelet size and density are determined at thrombopoiesis. Large, reactive platelets have in states with an increased platelet demand been shown to be produced from large, high-ploidy megakaryocytes. In patients with thrombopoiesis in steady-state an inverse relation between the bleeding time and both the DNA content and the size of the bone marrow megakaryocytes has been demonstrated. The bone marrow megakaryocytes in these patients were larger in men than in women, which may explain the sex difference in bleeding time observed by others. In experimental atherosclerosis changes in megakaryocyte size have been demonstrated. The significance of these changes are still unclear. In a single study stimulation of the platelet-megakaryocyte axis was associated with an acceleration of experimental atherosclerosis. This study suggests that large, high ploidy megakaryocytes may produce a large amount of atherogenic platelets that may be responsible for the increased formation of atheroma in this model. However, due to the complexity of the study design this hypothesis needs verification in other experimental and clinical studies. In patients suffering from an AMI the mean platelet volume is increased. The bleeding time is shortened at the time of infarction in these patients probably due to increased synthesis of TxA2, but an increased production of adrenaline may also be of importance. These large, reactive platelets present in AMI may be a reflection of an altered thrombopoiesis in these patients. It remains to be established whether these changes in platelet reactivity are present before the time of coronary thrombus formation.

Animals↗
PubMed1991

Finger clubbing.

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Blood Platelets↗
PubMed1990

Differences in bleeding time, aspirin sensitivity and adrenaline between acute myocardial infarction and unstable angina.

STUDY OBJECTIVE - The objective was to measure platelet function in vivo (as cutaneous bleeding time), the role of catecholamines, and the effect of inhibiting thromboxane synthesis on bleeding time, in patients with myocardial infarction, unstable angina, and non-cardiac chest pain. DESIGN - Haemotological variables and plasma catecholamines were compared between patient diagnostic groups using the Kruskal-Wallis test, Conover's multiple comparison test, and Wilcoxon paired rank sum test. PATIENTS - 49 patients entered the study and 45 were assigned to three groups: myocardial infarction (n = 26), unstable angina (n = 9), and non-coronary chest pain (control) (n = 10). There were no significant differences between groups for age or sex. Patients with myocardial infarction smoked more than others. MEASUREMENTS and RESULTS - Compared to the controls, bleeding time in patients with myocardial infarction was shortened, while in unstable angina it was normal. Plasma adrenaline and noradrenaline concentrations were higher in the myocardial infarction group than in the unstable angina and control groups, but were not correlated with bleeding time. Bleeding time was remeasured 2 h after ingestion of 300 mg aspirin and increased in all subjects, especially in those with myocardial infarction, but it remained significantly shorter in the infarct group than in the comparison groups. Plasma adrenaline was inversely correlated with the bleeding time after aspirin in the infarct group. CONCLUSIONS - The shortened bleeding time may be an indicator of an increased prethrombotic tendency present in patients with myocardial infarction but not in those with unstable angina. The effect appears to be mediated by both thromboxane A2 and adrenaline.

Aged↗
PubMed1990

Accelerated atherogenesis occurs following platelet destruction and increases in megakaryocyte size and DNA content.

Platelets and megakaryocytes have a role in atherogenesis. In this study the effect of platelet destruction, caused by injection of serum containing anti-platelet antibodies, on the development of atheroma and on megakaryocyte size and DNA content was studied in rabbits on a high cholesterol diet. Seven days after destruction of the circulating platelets a significant (150% and 300% in two separate studies) increase in the area of atheroma in the aorta was demonstrated. Histological examination revealed that large quantities of extracellular lipid and connective tissue were present in these plaques. The acceleration of atherogenesis in this model was found to be preceded by a significant increase in megakaryocyte size and in the frequency of megakaryocytes with a high DNA content. Platelets derived from large, high ploidy megakaryocytes may be of importance for the development of the atherosclerotic lesion. Neither the endothelial permeability as assessed by injection of Evans blue nor the prostacyclin production by the aorta of animals injected with anti-platelet serum were significantly different from the aortas of control animals.

Animals↗