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Biomedical subjects

S E Husted

Publications and source records attributed to S E Husted.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Percutaneous transluminal coronary angioplasty in acute myocardial infarction. A prospective controlled study].

In the present study we compared the outcome of primary percutaneous coronary angioplasty (PTCA) (PTCA without prior or concomitant administration of thrombolytic drugs) in 82 consecutive patients with acute myocardial infarction (AMI) with the outcome of 82 AMI patients, who were treated with intravenous thrombolysis. The thrombolysis patients were prospectively matched to the angioplasty patients regarding age, sex, duration of symptoms and infarct localisation. The in-hospital mortality was 3.7% in the PTCA group versus 4.9% in the thrombolysis group. Thrombolysis-treated patients had increased use of diuretics and ACE-inhibitors as compared to PTCA-treated patients. The mean ejection fraction was 52 +/- 11% in the PTCA group versus 47 +/- 10% (p = 0.01) in the thrombolysis group. We conclude that initial Danish experience with primary PTCA is promising, and that this treatment may favourably affect the outcome of acute myocardial infarction.

Aged↗
PubMed1998

[From paroxysmal to chronic atrial fibrillation].

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.

Atrial Fibrillation↗
PubMed1998

Thrombotic complications in coronary angioplasty--ionic versus non-ionic low-osmolar contrast media.

It has been suggested that the potential for thrombo-embolic complications is greater with the use of non-ionic contrast agents than with ionic contrast agents. The increasing use of interventional therapy in patients with acute coronary disease makes the discussion of a possible relationship between thrombo-embolic complications and use of non-ionic contrast media pertinent. It has been shown that ionic contrast media have a marked effect on the coagulation system and platelet function. The non-ionic contrast media have a less pronounced effect on the coagulation system and platelet function although there is no evidence of a thrombogenic effect. The anticoagulant effect observed with ionic contrast media in connection with coronary angiography or angioplasty (PTCA) is short and disappears as soon as the medium is excreted. Therefore an effective antithrombotic treatment in relation to the procedure is necessary. Larger randomized clinical studies need to be performed with effective antithrombotic regimens in order to clarify any difference in thrombo-embolic complications from the different contrast media. Until then, the non-ionic contrast media should be preferred to the ionic contrast media in high-risk PTCA, owing to their overall lower toxicity and fewer adverse reactions.

Animals↗
PubMed1997

Early administration of intravenous magnesium inhibits arterial thrombus formation.

An antiplatelet effect of magnesium has been demonstrated in vitro and ex vivo, and this effect may be advantageous in patients with acute myocardial infarction to inhibit reocclusion after coronary angioplasty or thrombolysis. We investigated the antithrombotic in vivo effect of intravenous magnesium in a placebo-controlled, blinded study in 46 male Wistar rats. Thrombus formation was induced by standardized arteriotomy of the femoral artery and partial inversion of the vessel wall to produce a thrombogenic area. The vessel was transilluminated and visualized dynamically by in vivo microscopy. Thrombus area was measured every minute for 30 minutes after removal of the vessel clamp by image analysis techniques, and the number of visible emboli was registered. Animals were randomized into three groups: groups 1 and 2 received saline (control group, n = 15) or MgSO4 (Mg-early group, n = 15), respectively, during the entire infusion period. In group 3 intravenous saline was given during preparation of the arteriotomy followed by infusion of MgSO4 (Mg-late group, n = 16) from 10 minutes after removal of the vessel clamp. Thrombus area was significantly reduced by 75% in the Mg-early group (P < .005) but not in the Mg-late group compared with the control group. Mean number of emboli was reduced during magnesium infusion. The serum magnesium level increased to 2.2 (2.1 to 2.5) and 3.5 (3.0 to 4.2) mmol/L after infusion in the Mg-late and the Mg-early group, respectively. In the present study, intravenous infusion of MgSO4 significantly reduced thrombus formation in vivo but only when it was given before reperfusion. The antithrombotic effect of magnesium may be utilized in patients with acute myocardial infarction to reduce the rate of reocclusion. Magnesium infusion may also be of value in elective arterial angioplasty, but this option has not been investigated in clinical trials. However, correct timing of magnesium administration is critical to obtain an efficient antithrombotic effect.

Animals↗
PubMed1996

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.

Aspirin↗
PubMed1996

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.

Adult↗
PubMed1996

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.

Adult↗
PubMed1995

[Anticoagulant and thrombolytic therapy in deep venous thrombosis and pulmonary embolism].

During the last 10 years anticoagulant (AC) therapy and thrombolytic treatment of venous thromboembolism (VT) have been evaluated in randomized studies. Adjusted subcutaneous (s.c.) heparin and low molecular weight heparin (LMWH) are found at least as effective as intravenous (i.v.) infusion of heparin in deep venous thrombosis (DVT) without an increased bleeding risk. In pulmonary embolism (PE) randomized trials assessing the efficacy of s.c. heparin and LMWH are missing. Oral AC-treatment can be initiated from the first or second day in VT. The recommended duration is three months for medical patients, and 4 weeks seem appropriate for surgical patients that are completely mobilized and without persisting predisposing factors. Long-term efficacy of thrombolytic treatment of DVT has only been assessed in small trials showing a trend towards reduced risk of developing chronic venous insufficiency. Short-term thrombolytic treatment of DVT is evaluated in ongoing trials. In the treatment of PE short-term thrombolysis with either t-PA or urokinase is found to be as effective as long-term thrombolytic treatment with a reduced bleeding risk. Thrombolytic therapy rapidly reduces embolic mass and stabilizes haemodynamics, but mortality and long-term efficacy of thrombolysis and AC-treatment versus AC-treatment alone in PE are being assessed in ongoing studies.

Anticoagulants↗
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↗
PubMed1994

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.

Administration, Oral↗
PubMed1994

Observer variation in the interpretation of ventilation-perfusion lung scintigraphy.

The diagnosis of pulmonary embolism (PE) remains one of the most difficult in clinical medicine, and the diagnostic value of lung scintigraphy has been questioned. To evaluate the observer variation in the interpretation of ventilation-perfusion lung scanning in the diagnosis of PE, 87 lung scintigrams from consecutive patients with phlebography-proven deep venous thrombosis and without clinical signs of PE were randomly mixed with 50 reference lung scintigrams from patients with PE symptoms. The scintigrams were reevaluated blind by two experienced clinical physiologists. Each observer evaluated each lung scintigram twice and recorded whether the lung scan was normal or abnormal. If it was abnormal, the location and number of segment defects were registered. The intraobserver agreement, including number and location of segments, ranged from 0.77 to 0.85 and for the diagnosis of PE from 0.88 to 0.92 with a kappa of 0.80-0.84. The values for the interobserver agreement for the diagnosis of PE were 0.73-0.80 with a kappa of 0.56-0.67. It is concluded that in the interpretation of ventilation-perfusion lung scintigraphy the use of a simple scheme-deciding whether there is segmental ventilation-perfusion mismatch or not-has a good reproducibility with a high kappa for inter- and intraobserver variation and can serve as a simple routine method for diagnosing PE.

Double-Blind Method↗
PubMed1994

Silent pulmonary embolism in patients with deep venous thrombosis. Incidence and fate in a randomized, controlled trial of anticoagulation versus no anticoagulation.

OBJECTIVES: A high frequency of asymptomatic pulmonary embolism (PE) in patients with deep venous thrombosis (DVT) has been reported, but information about the outcome of the patients with PE remains sparse. The aims of the present study were to assess the prevalence of silent PE in patients with symptomatic, venographically proven DVT, and to evaluate the natural history of silent PE. DESIGN: Consecutive patients from one centre of primary care were included in a randomized, open study with blinded control. All patients gave written, informed consent. SUBJECTS: Eighty-seven consecutive patients with venographically proven DVT and with a perfusion-ventilation lung scintigraphy performed within 48 h of the DVT diagnosis were included. On the 10th and 60th days the lung scintigraphy was repeated in 80 and 60 patients, respectively. All the patients were followed for 3 months in the out-patient clinic. INTERVENTIONS: All patients were ambulated from the first day and were allocated randomly to no anticoagulant (non-AC) therapy or to AC therapy with intravenous heparin infusion for at least 6 days and oral AC therapy for 3 months. RESULTS: Forty-three of these patients had a high probability lung scintigraphy for PE. Distal vein and femoral vein thrombosis embolized in 33 and 53% of patients, respectively. The progression rate after 60 days was 3% in both the AC and the non-AC group and after 10 days the rates were 13 and 8%, respectively. CONCLUSIONS: A high frequency of silent PE in patients with DVT both above and below the knee is demonstrated. AC treatment did not influence the resolution rate of PE or the rate of clinical PE in a 3-month follow-up period.

Adolescent↗
PubMed1994

Low dose acetylsalicylic acid in the antithrombotic treatment of patients with stable angina pectoris and acute coronary syndromes (unstable angina pectoris and acute myocardial infarction).

Acetylsalicylic acid has an antithrombotic effect by inhibition of thromboxane A2 synthesis in platelets. Thromboxane A2 is a potent stimulator of platelet aggregation and vasoconstriction and synthesis may be completely inhibited by a single oral dose of 150 mg acetylsalicylic acid or an intravenous dose of 100 mg. A daily maintenance dose of 75 mg acetylsalicylic acid is sufficient to effectively inhibit thromboxane A2 synthesis in long-term treatment. Acetylsalicylic acid therapy reduces acute myocardial infarction and sudden death in patients with stable angina pectoris and the drug is equally effective in patients with symptomatic and 'silent' angina pectoris. Early intervention with acetylsalicylic acid in patients with unstable angina pectoris reduces the risk of acute myocardial infarction and death. In patients with acute myocardial infarction, acute therapy with acetylsalicylic acid significantly reduces mortality both in monotherapy and in combination with thrombolytics. In the secondary prophylaxis following acute myocardial infarction, acetylsalicylic acid reduces the incidence of reinfarction and coronary death. Treatment of 100 patients with acute coronary syndrome (unstable angina pectoris or acute myocardial infarction) for 2 years may hinder the development of 3-4 fatal and 4 non-fatal vascular events. The risk of gastrointestinal side-effects and bleeding during acetylsalicylic acid therapy is dose-dependent and the incidence is low with a daily dose of 75-150 mg.

Administration, Oral↗
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↗