Biomedical subjects

H B Ravn

Publications and source records attributed to H B Ravn.

36 records · Page 2Linked to original sources

PubMed1999

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.

Animals↗

PubMed1999

Inhibition of nitric oxide synthesis improves left ventricular contractility in neonatal pigs late after cardiopulmonary bypass.

BACKGROUND: Following neonatal open heart surgery a nadir occurs in left ventricular function six to 12 hours after cardiopulmonary bypass. Although initiated by intraoperative events, little is known about the mechanisms involved. OBJECTIVE: To evaluate the involvement of nitric oxide in this late phase dysfunction in piglets. DESIGN: Piglets aged 2 to 3 weeks (4-5 kg) underwent cardiopulmonary bypass (1 h) and cardioplegic arrest (0.5 h) and then remained ventilated with inotropic support. Twelve hours after bypass, while receiving dobutamine (5 microg/kg/min), the left ventricular response to non-selective nitric oxide synthase inhibition (l-N(G)-monomethylarginine (l-NMMA)) was evaluated using load dependent and load independent indices (E(es), the slope of the end systolic pressure-volume relation; M(w), the slope of the stroke work-end diastolic volume relation; [dP/dt(max)](edv), the slope of the dP/dt(max)-end diastolic volume relation), derived from left ventricular pressure-volume loops generated by conductance and microtip pressure catheters. RESULTS: 10 pigs received 7.5 mg l-NMMA intravenously and six of these received two additional doses (37.5 mg and 75 mg). E(es) (mean (SD)) increased with all three doses, from 54.9 (40.1) mm Hg/ml (control) to 86.3 (69.5) at 7.5 mg, 117.9 (65.1) at 37.5 mg, and 119 (80.4) at 75 mg (p < 0.05). At the two highest doses, [dP/dt(max)](edv) increased from 260.8 (209.3) (control) to 470.5 (22.8) at 37.5 mg and 474.1 (296.6) at 75 mg (p < 0.05); and end diastolic pressure decreased from 16.5 (5.6) mm Hg (control) to 11.3 (5.0) at 37.5 mg and 11.4 (4.9) at 75 mg (p < 0. 05). CONCLUSIONS: In neonatal pigs 12 hours after cardiopulmonary bypass with ischaemic arrest, low dose l-NMMA improved left ventricular function, implying that there is a net deleterious cardiac action of nitric oxide at this time.

Animals↗

PubMed1999

Intravenous magnesium reduces infarct size after ischemia/reperfusion injury combined with a thrombogenic lesion in the left anterior descending artery.

Experimental studies have demonstrated that intravenous magnesium (Mg) can protect the ischemic myocardium and has an antithrombotic effect. In patients with myocardial infarction, the reperfusion injury is complicated by the presence of a thrombogenic area in the affected coronary artery that may cause repetitive thrombus formation and embolization. We investigated the effect of Mg on infarct size in a randomized study in pigs. Myocardial infarction was induced by a 50-minute mechanical occlusion of the left anterior descending artery combined with an arterial injury, which stimulated a dynamic thrombus formation with emboli shedding on reperfusion. Magnesium sulfate (6 mmol/20 min plus 3 mmol/h) or saline was started at 30 minutes after coronary occlusion. Real-time ventricular pressure-volume loops were generated from the left ventricle by using a microtip pressure manometer and a conductance catheter. Platelet accumulation in the myocardium was evaluated by using 111In-labeled platelets. After 4 hours of reperfusion, the infarct size/area at risk ratio in the placebo group was 46+/-0.06% (n=8) compared with 22+/-0.07% (n=6) in the Mg-treated animals (P=0. 03). Ejection fraction decreased significantly in the control group but not in the Mg-treated animals (P=0.03). Platelet accumulation in the myocardium did not change significantly between the Mg- and placebo-treated animals (placebo group, 191+/-19%; Mg group, 177+/-29%; NS). The present study demonstrates that intravenous Mg infusion is able to reduce infarct size by >50% and preserve the ejection fraction in this model where ischemia/reperfusion injury was evaluated in the presence of a thrombogenic area in the nutrient artery.

Animals↗

PubMed1999

Plaque pathology and coronary thrombosis in the pathogenesis of acute coronary syndromes.

Coronary atherosclerosis is by far the most frequent cause of ischemic heart disease and plaque disruption with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden coronary death. Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why, after years of indolent growth, it suddenly becomes complicated by life-threatening thrombosis. Therefore, we have to focus on plaque composition and vulnerability to rupture and plaque thrombogenicity rather than on plaque size and stenosis severity. The risk for plaque disruption depends more on plaque vulnerability (plaque type) than on degree of stenosis (plaque size). Lipid-rich and soft plaques are more vulnerable and prone to rupture than collagen-rich and hard plaques. They are also highly thrombogenic after disruption because of high content of tissue factor. There seems to be three major determinants of a plaque's vulnerability to rupture: 1) the size and consistency of the lipid-rich atheromatous core, 2) the thickness of the fibrous cap covering the core, and 3) ongoing inflammation and repair processes within the fibrous cap. Lipid accumulation, cap thinning, lack of smooth muscle cells (smc), and macrophage-related inflammation destabilize plaques, making them vulnerable to rupture. In contrast, smc-related healing and repair processes stabilize plaques, protecting them against disruption. Plaque size or stenosis severity tell nothing about a plaque's vulnerability. Many vulnerable plaques are invisible angiographically due to their small size and compensatory vascular remodeling.

Acute Disease↗

PubMed1999

Pharmacological effects of magnesium on arterial thrombosis--mechanisms of action?

At present no consensus exists on the role of magnesium in acute myocardial infarction and this is primarily due to conflicting results from recent clinical trials. The ISIS-4 trial clearly showed that magnesium infusion is without benefit when given after thrombolysis or many hours after symptom onset. In contrast, the LIMIT-2 study provided strong evidence that early magnesium administration, given before any thrombolytic therapy protects the myocardium and improves long-term survival. Debate on the interpretation of the trial results is still ongoing, and is particularly focused on the time-dependency of magnesium, which has emerged from recent experimental studies. Candidate mechanisms, by which magnesium might modify the outcome of acute myocardial infarction, includes antiarrhythmic properties, improved coronary perfusion and haemodynamics, protection of the ischaemic myocardium, and an antithrombotic effect. So far animal models have shown a time-dependent effect of magnesium when given for both myocardial protection in experimental ischaemia-reperfusion injury and for antithrombotic purposes. Additional clinical trials are warranted and these must be carefully designed and implemented in the light of the laboratory evidence now available. In the present review magnesium's antithrombotic properties is discussed with respect to its effect on platelets, coagulation, fibrinolysis, and endothelial mediators with vasodilating and antithrombotic qualities. Observations from studies in patients with preeclampsia, another clinical condition where platelet hyperreactivity is well-recognized and where magnesium therapy is well-established, are briefly discussed in the present paper.

Animals↗

PubMed1998

Atherosclerosis and acute coronary events.

Without thrombosis, coronary atherosclerosis is generally benign. It is plaque disruption, or fissuring, and subsequent thrombosis that make coronary atherosclerosis dangerous. Small ruptures often remain clinically silent, whereas more extensive plaque rupture may cause the development of unstable angina, myocardial infarction, and sudden death. The risk of plaque disruption depends more on plaque type (composition) than on plaque size and stenosis severity. Both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption. The resultant thrombotic response, which affects the clinical presentation and outcome, is partly determined by the reactivity of the circulating platelets and the balance between the coagulation and fibrinolytic systems. To prevent and treat life-threatening coronary thrombosis, the medical community should seek new ways to identify and treat dangerous, vulnerable plaques and to optimize antithrombotic treatment.

Acute Disease↗

PubMed1998

[Increased concentration of Na,K-pumps in skeletal muscles of patients with chronic obstructive lung disease. Significance of magnesium depletion and treatment with glucocorticoids].

Patients with COLD may develop Mg depletion due to inadequate nutrition or treatment with diuretics and beta 2-agonists. In 36 consecutive COLD patients skeletal muscle concentrations of Mg and K were reduced by 22% and 14%, respectively, compared to 23 age- and sex-matched controls (p < 0.001). Patients receiving diuretics showed a further reduction of muscle Mg (-31%) and K (-27%) compared to controls. The mean concentration of Na,K pumps was increased by 31% (p < 0.001), while a more pronounced increase (+61%) was seen in 12 intensive care patients receiving high dosages of glucocorticoids. Thus muscle concentrations of Mg and K are reduced in COLD patients and are associated with an upregulation of the Na,K-pump concentration. It is plausible that this upregulation may be caused by glucocorticoid treatment. The clinical benefits of glucocorticoids may therefore in part be due to an increased activity and capacity of the Na,K-pump and thereby in a possible enhancement of muscle force.

Adult↗

PubMed1998

The effect of changing excitation frequency on parallel conductance in different sized hearts.

OBJECTIVE: An important component of the ventricular volume measured using the conductance catheter technique is due to parallel conductance (Vc), which results from the extension of the electric field beyond the ventricular blood pool. Parallel conductance volume is normally estimated using the saline dilution method (Vc(saline dilution)), in which the conductivity of blood in the ventricle is transiently increased by injection of hypertonic saline. A simpler alternative has been reported by Gawne et al. [12]. Vc(dual frequency) is estimated from the difference in total conductance measured at two exciting frequencies and the method is based on the assumption that parallel conductance is mainly capacitive and hence is negligible at low frequency. The objective of this study was to determine whether the dual frequency technique could be used to substitute the saline dilution method to estimate Vc in different sized hearts. METHODS: The accuracy and linearity of a custom-built conductance catheter (CC) system was initially assessed in vitro. Subsequently, a CC and micromanometer were inserted into the left ventricle of seven 5 kg pigs (group 1) and six 50 kg pigs (group 2). Cardiac output was determined using thermodilution (group 1) and an ultrasonic flow probe (group 2) from which the slope coefficient (alpha) was determined. Steady state measurements and Vc estimated using saline dilution were performed at frequencies in the range of 5-40 kHz. All measurements were made at end-expiration. Finally, Vc was estimated from the change in end-systolic conductance between 5 kHz and 40 kHz using the dual frequency technique of Gawne et al. [12]. RESULTS: There was no change in measured volume of a simple insulated cylindrical model when the stimulating frequency was varied from 5-40 kHz. Vc(saline dilution) varied significantly with frequency in group 1 (8.63 +/- 2.74 ml at 5 kHz; 11.51 +/- 2.65 ml at 40 kHz) (p = 0.01). Similar results were obtained in group 2 (69.43 +/- 27.76 ml at 5 kHz; 101.24 +/- 15.21 ml at 40 kHz) (p < 0.001). However, the data indicate that the resistive component of the parallel conductance is substantial (Vc at 0 Hz estimated as 8.01 ml in group 1 and 62.3 ml in group 2). There was an increase in alpha with frequency in both groups but this did not reach significance. The correspondence between Vc(dual frequency) and Vc(saline dilution) methods was poor (group 1 R2 = 0.69; group 2 R2 = 0.22). CONCLUSION: At a lower excitation frequency of 5 kHz a smaller percentage of the electric current extends beyond the blood pool so parallel conductance is reduced. While parallel conductance is frequency dependent, it has a substantial resistive component. The dual frequency method is based on the assumption that parallel conductance is negligible at low frequencies and this is clearly not the case. The results of this study confirm that the dual frequency technique cannot be used to substitute the saline dilution technique.

Animals↗

PubMed1997

Insights into the pathophysiology of unstable coronary artery disease.

Coronary atherosclerosis without thrombosis is, in general, a benign disease. However, plaque disruption, or fissuring, with superimposed thrombosis, frequently complicates the course of coronary atherosclerosis. Small ruptures often remain clinically silent, whereas more extensive plaque rupture may cause the development of unstable angina, myocardial infarction, and sudden death. The risk of plaque disruption depends more on plaque type (composition) than on plaque size and stenosis severity. Major determinants of a plaque's vulnerability to rupture are: the size and consistency of the lipid-rich atheromatous core; the thickness of the fibrous cap covering the core; and ongoing inflammation and repair within the cap. Both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption. The former predisposes the plaque to rupture whereas the latter may precipitate it. The resultant thrombotic response, which is important for the clinical presentation and outcome, is portly determined by the reactivity of the circulating platelets and the balance between the fibrinolytic and coagulation systems. New ways of identification and treatment of the dangerous vulnerable plaques responsible for infarction and death, and optimization of antithrombotic treatment, are highly warranted in order to prevent and treat life-threatening coronary thrombosis.

Coronary Artery Disease↗

PubMed1997

The concentration of sodium, potassium pumps in chronic obstructive lung disease (COLD) patients: the impact of magnesium depletion and steroid treatment.

OBJECTIVES: To evaluate the concentrations of magnesium (Mg), potassium (K) and sodium,potassium pumps (Na,K pumps) in skeletal muscle in patients with chronic obstructive lung disease (COLD) treated with or without diuretics. DESIGN: An open cross-sectional study. SETTING: COLD patients admitted to the Medical Department of Vejle Hospital, Denmark. SUBJECTS: Thirty-six consecutive COLD patients and 23 age- and sex-matched controls. MAIN OUTCOME MEASURES: Biopsies of skeletal muscle were performed in patients and controls for measurements of Mg, K and Na,K pumps. In a parallel animal experiment the influence of medical treatment on the concentration of Na,K pumps in skeletal muscle was evaluated by infusing 10-week-old rats for 14 days with vehicle, terbutaline, or dexamethasone. RESULTS: In the patients, mean muscle Mg and K concentrations were reduced by 22 and 14% respectively (P < 0.001), but in those patients who received diuretics muscle Mg and K were further reduced (by 31 and 27%, respectively, of the control values). The concentration of Na,K pumps was increased by 31% (P < 0.001), with a maximum increase of 61% (P < -0.001) in 12 intensive care patients receiving high dosages of glucocorticoids. Linear regression analysis showed a positive correlation between daily glucocorticoid intake and the concentration of Na,K pumps in the biopsy specimens from each patient (r = 0.38, P = 0.02). In the experimental study, dexamethasone induced 27-34% increase in the concentration of Na,K pumps (P < 0.01) in three different muscles, whereas there was no significant change following terbutaline infusion. CONCLUSIONS: COLD patients show reduced concentrations of Mg and K in skeletal muscle, associated with an upregulation of the Na,K pump concentration. It is plausible that this upregulation may be caused by glucocorticoid treatment. The clinical benefits of glucocorticoids may in part be due to an increase in the activity and capacity of the Na,K pump and thereby in a possible enhancement of muscle force.

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

[Resistance to activated protein C. The most common cause of familial thrombophilia].

Resistance to activated protein C (APC) is caused by the most prevalent single gene defect associated with thromboembolic disease so far described. The majority of cases are caused by a single point mutation in the Factor V gene, which predicts replacement of Arg506 in the APC-cleavage site with a Gln. APC resistance is found in 20-60% of patients with venous thrombosis and in 3-10% of the normal population among Caucasians. In its heterozygous state, the mutation is associated with a 5-10-fold increased risk of thrombosis. Homozygosity is associated with more severe APC resistance, and a higher risk of developing thrombosis. By the age of 33 years, 8% of normals, 20% of heterozygotes, and 40% of homozygotes have had manifestations of venous thrombosis. APC resistance has been described in 60% of women with thromboembolic complications during pregnancy and in approximately 30% of women with thromboembolic complications using oral contraceptives. Development of clinical episodes of thrombosis in patients with APC resistance is likely to occur on a multifactorial basis. Hypercoagulable states may result from multigene interactions, and prothrombotic insults in patients with an inherited predisposition may precipitate thrombotic complications. In this review we present and discuss results from the recent medical literature.

Anticoagulants↗

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↗

PubMed1990

[Hallucinogenic psilocybine containing mushrooms. Toxins contained in Danish wild mushrooms].

A number of the wild Danish mushrooms contain the hallucinogenic agent psilocybin which resembles LSD in many ways. The commonest of these are the "liberty cap" or "magic mushrooms" (Psilocybe semilanceata). On the basis of experience from USA and western Europa, increase in employment of this mushrooms as a hallucinogenic intoxicant may be anticipated in Denmark. The history, epidemiology, botany and pharmacology of the mushroom are reviewed. Clinical pictures and treatment are described for: 1) Acute poisoning with psilocybin-containing fungi, 2) Late sequelae of consumption of psilocybin-containing fungi and 3) Poisoning with more poisonous fungi on account of incorrect identification. General practitioners, duty roster doctors, doctors in casualty departments and in acute psychiatric departments should be aware of these problems. Intoxication with psilocybin may be confused with panic anxiety or euphoria in persons with mydriasis and other sympathomimetic symptoms. The possibility of more serious mushroom poisoning on account of incorrect identification should be borne in mind.

Denmark↗