Improved nutritional status in elderly patients 6 months after stroke.

INTRODUCTION: Nutritional status among stroke patients has received limited attention despite the fact, that it may have an influence on clinical outcome. Previous studies have estimated that 15-20 % of patients suffer from malnutrition in the acute phase of stroke, but so far no studies have focused on the late rehabilitation phase after stroke in the patients own home, where the attention on nutrition may be reduced. AIMS: To determine the prevalence of malnutrition during 6 months of stroke rehabilitation, and to investigate the association between nutritional status, functional recovery, length of stay in hospital and infectious complications. SUBJECTS AND METHODS: 89 patients with ischemic stroke consecutively admitted to a geriatric stroke rehabilitation unit had their nutritional status evaluated in the hospital at 1 week and 5 weeks after stroke, and in their own home at 3 months and 6 months. Nutritional status was evaluated by body weight, body mass index (BMI), mid upper arm circumference (MAC), triceps skinfold thickness (TSF) and serum concentrations of albumin and transferrin. Malnutrition was defined if the patients had 2 or more abnormal nutritional variables. RESULTS: We found a significant increase in albumin from 1 week to 6 months (P < 0.0001), and a significant increase in transferrin form 5 weeks to 6 months (P < 0.05). There was no significant change in weight or BMI from 1 week to 6 months. The number of patients with 2 or more abnormal nutritional variables was 31 (35 %) at 1 week and was reduced to 20 (22 %) at 6 months. CONCLUSION: 35 % of elderly patients with ischemic stroke admitted to a geriatric rehabilitation unit were malnourished 1 week after stroke. Particularly serum proteins and body fat were affected. Follow-up of nutritional variables showed improvement for serum proteins, and 22 % of the patients were malnourished 6 months after stroke.

Magnesium inhibits platelet activity--an in vitro study.

The in vitro effect of magnesium (Mg) on platelet aggregation and platelet release function was evaluated in healthy volunteers. Platelet aggregation was induced with collagen, ADP, or thrombin after incubation of the sample with saline or increasing concentrations of magnesium sulphate (MgSO4) (0.5-8.0 mM). Mg showed a dose-dependent inhibition of platelet aggregation in whole blood, platelet rich plasma and washed platelets. An antiaggregatory effect was also present with low Mg concentrations. Statistically significant inhibition of the mean aggregation response was obtained in 83% of the different media and agonists tested following the addition of 1.0 mM Mg. The remaining 17% were significantly inhibited with the addition of 2.0 mM Mg. The platelet synthesis of thromboxane A2 and release of beta-thromboglobulin were also inhibited by Mg, in a dose-dependent manner. In order to evaluate if any of these effects were modified by conventional antithrombotic treatment with low-dose acetylsalicylic acid (ASA), volunteers were asked to meet on two consecutive days. On day 2 the participants were given 300 mg ASA orally, one hour prior to blood sampling. The Mg mediated effects were present independent of this pretreatment with ASA. Following stimulation with collagen a synergistic effect of Mg and ASA was demonstrated on platelet aggregation. The platelet inhibiting effect demonstrated in this study may in part explain the beneficial effect of Mg infusion in some patients with acute myocardial infarction. The effect of Mg infusion, given alone or administered simultaneously with ASA, should also be evaluated in other arterial thrombotic disease states.

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)

Magnesium inhibits platelet activity--an infusion study in healthy volunteers.

Magnesium (Mg) has shown the ability to inhibit arterial thrombus formation in some experimental animal studies. This effect may be due to an inhibition of platelet reactivity as in vitro studies have demonstrated that Mg inhibits platelet aggregation. In order to evaluate the in vivo effect of Mg in humans measurements of platelet activity, fibrinolytic activity, as well as measurements of prostacyclin (PGI2), and nitric oxide (NO) release were performed after infusion of magnesium sulphate (MgSO4) in healthy volunteers. In a placebo controlled, cross-over study in 14 healthy male subjects, 8 mmol MgSO4 was given as an intravenous bolus over 15 min followed by 3 mmol MgSO4/h. The mean S-Mg concentration increased from 0.85 to 1.50 mM during the Mg infusion period. A transient decrease in blood pressure was observed during the initial bolus infusion of Mg. Haemodynamic parameters were otherwise unstable. The bleeding time increased by 48% during the Mg infusion (p < 0.005), and in accordance with this, ex vivo platelet aggregation in platelet rich plasma was significantly inhibited, both following collagen (p = 0.02) and ADP (p = 0.04) stimulation. There were no significant changes in plasma beta-thromboglobulin concentration or the excretion of 2,3-dinor-thromboxane B2 in the urine. Neither tissue plasminogen activator (t-PA)activity, tissue plasminogen activator (t-PA)antigen nor plasminogen activator inhibitor (PAI)antigen changed during the Mg infusion period. There was no sign of increased release of PGI2 from the vessel wall as judged by urinary concentration of 2,3-dinor-6-keto-prostaglandin F1 alpha. Nor was there any sustained increase in the release of NO, measured as nitrate concentration in urine. However, a transient increase in NO release was observed during one sample period. In conclusion a reduced platelet activity and increased bleeding time, was found during Mg infusion in healthy volunteers. Fibrinolytic activity showed no changes. An anti-platelet effect may in part be responsible for the beneficial effect of Mg, described in patients with acute myocardial infarction (MI) and preeclampsia.

Plasma thromboxane B2 as an early marker of acute graft rejection after heart transplantation: preliminary report.

Six patients undergoing heart transplantation were followed up by serial endomyocardial biopsies to detect signs of graft rejection and the plasma level of thromboxane B2 was measured at the same time. During the operative procedure and concomitant with histologic signs of acute graft rejection, the plasma level of thromboxane B2 significantly increased. After immunosuppressive treatment with steroids and either antithymocyte globulin or monoclonal antibody, regression of the histologic signs of rejection and a significant fall in the level of thromboxane B2 were documented. We conclude that the plasma level of thromboxane B2 may be useful as an early marker of acute graft rejection after heart transplantation.

Incomplete thromboxane inhibition with 100 mg of intravenous acetylsalicylic acid in patients with acute ST elevation myocardial infarction: a placebo-controlled pilot trial.

BACKGROUND: Acetylsalicylic acid (ASA) is now a standard treatment of acute myocardial infarction (AMI). ASA inhibits thromboxane A(2) (TXA(2)) production by blocking the constitutive cyclooxygenase (COX)-1 enzyme, but only to a small degree the inducible COX-2. COX-2 is induced by increased concentrations of cytokines, which is related to an enhanced inflammatory response. Previously, we have found a complete inhibition of TXA(2) synthesis in healthy volunteers after intravenous administration of 50 mg of ASA. We measured in a randomized, placebo-controlled pilot trial the effect of 100 mg of ASA injected intravenously on TXA(2) synthesis in AMI patients treated with streptokinase. METHODS AND RESULTS: Nineteen patients with AMI treated with streptokinase were randomized to 100 mg of ASA or placebo injected intravenously. Se-TXB(2) and bleeding time were measured before and after drug administration. One hundred and eighty minutes after intravenous ASA administration, treatment with oral ASA was initiated. We found a significant decrease in serum concentrations of TXB(2) after 30, 60 and 180 min following ASA injection compared to placebo, but in none of the patients was complete inhibition of TXA(2) production achieved. No significant change in bleeding time could be demonstrated. CONCLUSION: Intravenous ASA in a dosage of 100 mg did not completely prevent TXA(2) production in AMI patients treated with streptokinase. This may be due to synthesis of TXA(2) by the inducible COX-2 enzyme and/or to a transcellular metabolism in platelets of prostanoids generated by endothelial cells.

Anticoagulant therapy in deep venous thrombosis. A randomized controlled study.

Ninety patients with venographically proven deep venous thrombosis(DVT) but without clinical signs of pulmonary embolism(PE) were randomized into two different treatment regimens to compare the safety and efficacy of continuous intravenous heparin and oral anticoagulant(AC) treatment versus non-AC treatment. All patients in the two treatment groups were actively mobilized from the day of admission and wore graduated compressing stockings. In the non-AC-group the patients were treated with phenylbutazone for ten days. Treatment with heparin was maintained for 6 days and oral AC treatment was given from the third day and continued for 3 months. Venography was repeated after 30 days. A perfusion-ventilation lung scan was performed on day 1-2, 10 and 60. In fifty-nine patients a revenography was performed, twenty nine in the AC-group and thirty in the non-AC group. For distal veins regression was found in nine and eight respectively (4.4% in favour of AC, 95% confidence limit 27.5% to -18.7%) and in proximal veins regression was found in five and eight, respectively (10.9% in favour of AC, 95% confidence limit 32.0% to -10.1%). No difference in lung scans was found after 10 days (0.8% in favour of AC, 95% confidence limit 21.5% to -19.9%) or after 60 days (3.3% in favour of non-AC treatment, 95% confidence limit 21.8% to -28.5%). In the AC group the incidence of bleeding complications was 8.3%. No side-effects of phenylbutazone was found. The present controlled clinical study demonstrated no effect of AC-treatment on DVT progression in actively mobilized patients wearing graduated compressing stockings when compared to a non-AC treated group receiving analgetic therapy with phenylbutazone. However, the patient population of the study is relatively small with wide confidence intervals for differences between groups. Before more general recommendations can be made, a large scale placebo-controlled study is needed to evaluate the possible effect of AC-treatment in DVT patients, who can be mobilized from the first day.

Dietary fish oil reduces microvascular thrombosis in a porcine experimental model.

Microvascular thrombosis plays a significant role in the pathophysiology of ischaemic reperfusion injury. A fish oil-supplemented diet containing n-3 polyunsaturated fatty acids (PUFA) reduces thromboxane A(2) (TxA(2)) synthesis and, thus, vasoconstriction and platelet aggregation. The aim of this study was to elucidate whether n-3 PUFA in a porcine model of ischaemia and reperfusion injury 1) inhibit accumulation of platelets and fibrinogen in ischaemia-reperfusion injured tissue, 2) prolong the bleeding time, and 3) inhibit TxA(2) synthesis. Nine pigs were fed a standard diet supplemented with 7 g n-3 PUFA/day for 3 weeks. Nine pigs on the standard diet served as controls. Unilateral myocutaneous flaps were exposed to ischaemia for a period of 6 hours. Contralateral flaps were nonischaemic. Tissue contents of radioactive-labelled platelets and fibrinogen were measured after 4 hours of reperfusion. Platelet count, serum TxB(2), and the cutaneous bleeding time were measured before and after 3 weeks of diet. In the fish oil group, the accumulation of platelets was significantly reduced in all the myocutaneous flaps, except in the ischaemic skin part, when compared to control animals. Fibrinogen was significantly reduced in nonischaemic flaps, but not in ischaemic flaps. After the feeding period, the level of TxB(2) was significantly lowered in the fish oil group (p<0.01). No difference in the bleeding time was observed. Thus, dietary supplementation with n-3 PUFA inhibits the formation of microvasculatory thrombosis in this model.

Bepridil versus verapamil in stable angina pectoris--a controlled clinical trial.

The calcium antagonist bepridil (bepridil monohydrochloride monohydrate, Org 5730, Cordium) was investigated in comparison with verapamil in a double-blind cross-over design in patients with angina pectoris. Exercise parameters, frequency of anginal attacks, consumption of nitroglycerin and subjective preference were analysed for 36 patients. The exercise capacity, estimated by exercise time and total work load during standard bicycle testing, was significantly more improved with bepridil treatment than with verapamil treatment. No significant differences were observed in frequencies of anginal attack, consumption of nitroglycerin and subjective preference. Side effects were mild and equally divided over both treatment groups.

Magnesium inhibits human platelets.

Magnesium (Mg) may inhibit experimental arterial thrombus formation by inhibition of platelet activity. However, inhibition of platelet aggregation has mainly been shown with high concentrations of magnesium ( > 2 mM). To test the effects of Mg in more clinically relevant concentrations, an in vitro study was performed where platelets were incubated with MgSO4 in the concentration range of 0.5-8.0 mM. Healthy volunteers participated on 2 consecutive days. On Day 2 the volunteers ingested 300 mg of acetylsalicylic acid (ASA) 1 h before blood sampling. Blood was anticoagulated with hirudin and platelet aggregation was performed in platelet-rich plasma (PRP) after incubation with saline or MgSO4 for 5 min. Platelets were stimulated with threshold concentrations of collagen or ADP or a fixed high concentration of collagen (5 micrograms/ml) on both days. A concentration dependent inhibition of platelet aggregation was found after addition of MgSO4. A statistically significant inhibition (P < 0.05) was present at 0.5-1.0 mM MgSO4. The effect of Mg was independent of pretreatment with ASA. Following maximal stimulation with collagen in PRP, a synergistic inhibition of ASA and Mg on platelet aggregation was demonstrated. Administration of MgSO4 in clinically relevant concentrations showed a dose-dependent inhibition of platelet aggregation. Platelet inhibition also occurred after ASA administration and concomitant medication induced a synergistic effect.

Intravenous acetylsalicylic acid, magnesium and their combination in experimental arterial thrombosis in rats.

Intravenous acetylsalicylic acid (ASA) and magnesium (Mg) both possess antiplatelet properties and are thus potential inhibitors of the formation of arterial thrombi. Their effect on the dynamic aspects of arterial thrombus formation was investigated following intravenous administration of both substances alone and in combination. A blinded, placebo-controlled, in-vivo study was performed in 71 rats. Thrombus formation was induced by a standardized arteriotomy in the right femoral artery with inversion of the vessel wall during subsequent closure. Thrombus formation was recorded on video tapes and analysed off-line for 30 min. Animals were randomly assigned to one of four groups: 20 mg bolus of ASA followed by 0.3 mmol/h Mg (ASA/Mg group); NaCl followed by 0.3 mmol/h Mg (Mg group); 20 mg bolus of ASA followed by NaCl (ASA group); or NaCl throughout the experiment (control group). In the ASA-treated groups, serum levels of thromboxane B2 were reduced significantly, and the Mg-treated groups reached a serum level of Mg just above 2.0 mmol/l. No significant differences were observed in initial or maximum thrombus area or in mean thrombus area during the study period. In the ASA/Mg group, a trend towards reduced thrombus formation was observed (P = 0.06). In the same group, seven of 22 animals developed an occlusive thrombus (P < 0.01), an unexpected adverse event possibly related to the combined administration of ASA and Mg.

Targeting treatment for optimal outcome.

Rapid assessment of patients presenting with acute chest pain is essential, in order to distinguish between those who have a life-threatening condition, such as myocardial infarction or unstable angina, and the substantial proportion who do not have an acute coronary syndrome. It is thus of vital importance that reliable techniques are available to facilitate rapid risk stratification, as an aid to both clinical diagnosis and management strategy decisions. Assessments based on clinical findings, electrocardiographic monitoring, symptom-limited exercise testing, and biochemical marker measurements, used either singly or in various combinations, can fulfill this role. The present paper reviews some of the recent data that demonstrate the value of these techniques. Very few studies allow conclusions to be drawn about optimal treatment strategies in relation to groups stratified according to prognostic markers, and the question of whether intense medical treatment or early invasive intervention is most beneficial is one that clinical trials have yet to address adequately. In the recently completed Fragmin and Fast Revascularization during InStability in Coronary artery disease (FRISC II) study, comparisons were made of clinical outcomes achieved with early invasive versus noninvasive (i.e., medical) management strategies, and with short-term versus prolonged anticoagulation with dalteparin sodium (Fragmin), in patients with unstable coronary artery disease. All study participants underwent symptom-limited exercise testing and provided blood sample for measurements of biochemical markers; continuous electrocardiography monitoring and echocardiography were also performed in a high proportion of patients. Data from the FRISC II trial thus shed further light on the issue of risk stratification and its use to determine optimal treatment strategies.

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.

[Fibrinolytic agents in acute myocardial infarction. Reperfusion--a two-edged sword? Advantages and disadvantages of various preparations]. / Fibrinolytika ved akut myokardieinfarkt. Reperfusion--et tveaegget svaerd? Fordele og ulemper ved de enkelte praeparater.

An account is presented of the problems which occur on reperfusion of the myocardium in connection with fibrinolytic treatment and the present day possibilities for reducing the complications. Restenosing is mentioned in particular. The advantages and disadvantages of the individual fibrinolytic preparations are illustrated. The clinical investigations available demonstrate that the higher frequencies of reperfusion for "fibrin selective" plasminogen activator are observed mainly in patients with durations of AMI symptoms for more than three hours before the commencement of thrombolytic treatment. In a comparison between t-PA and streptokinase investigations regardless of the time of inclusion no difference could be demonstrated in the effect on the left ventricular function, lethality after 12 months and the risk of haemorrhage. Employing APSAC and streptokinase, significant reduction in the one year lethality was found and, where streptokinase was concerned, on treatment up to 24 hours after the commencement of symptoms. Acetylsalicylic acid has an additive effect, possibly as a result of the reduced risk for rethrombosing among other things. The current data provide, however, no final explanation of the relative efficacy of the individual fibrinolytic drugs because the various investigations have had different forms of selection of patients, initiation of treatment and parallel medication. Attempts will be made to elucidate these in future investigations where ISIS-3 compares t-PA, streptokinase and APSAC while GISSI-2 will compare t-PA and streptokinase. Simultaneously, the value of heparin will be investigated in connection with fibrinolytic therapy.

[Tirofiban (Aggrastat). A non-peptide glycoprotein IIb/IIIa receptor inhibitor]. / Tirofiban (Aggrastat). En non-peptid glykoprotein IIb/IIIa-receptorhaemmer.

Platelet aggregation and thrombus formation on a ruptured atherosclerotic plaque plays an important role in the pathogenesis of acute coronary syndromes. Activation of glycoprotein IIb/IIIa receptors (GP-receptors) on the surface of platelets is the final common pathway which leads to the binding of fibrinogen and crosslinking of platelets to form the white thrombus. Antiplatelet therapy reduces the risk of ischaemic complications in patients with acute coronary syndromes. Recently, the GP-receptor antagonists have been introduced. They inhibit the binding of fibrinogen to the GP-receptors and thus prevent platelet aggregation. Tirofiban is a low molecular, intravenously administered GP-receptor antagonist, which in combination with unfractionated heparin in several controlled studies has been shown to decrease morbidity and mortality in patients with unstable angina pectoris and non-Q-wave infarction and, in patients subsequently undergoing percutaneous coronary intervention.

[Tennis leg--a differential diagnosis in deep vein thrombosis]. / Tennisben--en differentialdiagnose til dyb venøs trombose.

A case of pulmonary embolism in a healthy young man aged 22 years which was caused by prolonged air travel is reported. The patient developed deep thrombophlebitis in the left lower limb and pulmonary emboli in the left lung.

[Apical hypertrophic cardiomyopathy]. / Apikal hypertrofisk kardiomyopati.

Apical hypertrophic cardiomyopathy is a subtype of non-obstructive hypertrophic cardiomyopathy characterized by a unique spade-like configuration and apical obliteration in the left ventriculogram as well as in the long axis two-dimensional echocardiogram. The symptoms and electrocardiographic findings in apical hypertrophic cardiomyopathy are quite similar to ischemic heart disease and confusion of the two diseases is obvious. An illustrative case, in which ventriculographic and echocardiographic findings were diagnostic for apical hypertrophic cardiomyopathy, is presented.

[Acetylsalicylic acid in the treatment of arterial thromboembolic diseases. 1. Pharmacologic aspects]. / Acetylsalicylsyrebehandling ved arterielle trombo-emboliske sygdomme. 1. Farmakologiske aspekter.

The possible antithrombotic potential of acetyl salicylic acid (ASA) has been established in recent years and the preparation has been employed extensively in ischaemic cardiac disease and cerebrovascular conditions. The inhibiting effect of ASA on platelet function by means of blocking of cyclo-oxygenase is mentioned and, similarly, the presumed role in thrombosis development and atherogenesis is mentioned. ASA's pharmacokinetics are illustrated with emphasis on optimal anti-thrombotic ASA dosage, in particular, in relation to the effects of the preparation on the thromboxan A2 (TxA2)/prostacyclin (PGI2)-ratio. This is probably best achieved by means of low oral dosage in the form of sustained-release ASA formulation where the inhibition of platelet function probably occurs mainly in the presystemic circulation. It is concluded that a daily dosage of 80-100 mg ASA ensures effective and rapid inhibition of TxA2 production. Administration of 30-50 mg ASA daily results in a corresponding blockage of TxA2 production but not until after treatment for three to four days.

[From paroxysmal to chronic atrial fibrillation]. / Fra paroksystisk til kronisk atrieflimren.

Chronic atrial fibrillation is by definition always preceded by paroxysmal atrial fibrillation. The electropathophysiological mechanisms underlying paroxysmal atrial fibrillation are reviewed: atrial electrophysiological inhomogeneity, atrial ectopic activity, and cardiac autonomic dysfunction. Safe and effective interventions that prevent the progression from paroxysmal into chronic atrial fibrillation have not yet been developed. Such developments should be given high priority, as the consequences of chronic atrial fibrillation--stroke and heart failure--are unacceptable.

[Acetylsalicylic acid in the treatment of arterial thromboembolytic diseases. 2. Clinical documentation]. / Acetylsalicylsyrebehandling ved arterielle tromboemboliske sygdomme. 2. Klinisk dokumentation.

A review of the literature is undertaken to account for the current status of acetylsalicylic acid (ASA) in the treatment of patients with arterial thrombo-embolic conditions. Employment of ASA monotherapy has been documented to be effective in clinically controlled investigations in patients with unstable angina pectoris, transient cerebral ischaemia, coronary by-pass and femoro-popliteal endarterectomy and introduction of vascular prostheses and, in addition, in primary and secondary prophylaxis of acute myocardial infarction (AMI). In combination with dipyridamol, ASA has been found to be effective in secondary AMI prophylaxis, coronary by-pass operation and in peripheral arteriosclerosis. In patients with cardiac valvular prostheses, conventional anticoagulation therapy must still constitute the basic treatment but dipyridamol may be employed to increase the antithrombotic efficacy of the treatment. The dosage of ASA in the majority of works has been about 1,000 mg daily while isolated investigations have shown good effect from doses as low as 60 mg daily. It appears to be important for the efficacy of the treatment with platelet inhibitors in the above-mentioned conditions that treatment is instituted rapidly and, in connection with operative intervention, preferably preoperatively. In other clinical conditions such as preeclampsia, hypertension in pregnancy, diabetic angiopathy and nephropathy, membranoproliferative glomerulonephritis and arterio-venous shunts with haemodialysis, treatment with ASA appears to be effective but documentation in extensive clinically-controlled investigations is not yet available. The duration of treatment with ASA in arterial thrombo-embolic disease does not appear to be illustrated unanimously in the articles published but, as the atherosclerotic lesion is not influenced by ASA, there are indications for life-long therapy.