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PubMed1997

European stroke prevention study 2: dipyridamole and acetylsalicylic acid in the secondary prevention of stroke.

In 1988, an optimal antiplatelet regimen for secondary stroke prevention remained to be defined. We undertook a randomised, placebo-controlled, double-blind trial to investigate the safely and efficacy of low-dose acetylsalicylic acid (ASA), modified-release dipyridamole, and the two agents in combination. Patients with prior stroke or transient ischaemic attack (TIA) were randomised to treatment with ASA alone (50 mg daily), modified-release dipyridamole alone (400 mg daily), the two agents in a combined formulation, or placebo. Primary endpoints were stroke, death, and stroke or death. TIA and other vascular events were secondary endpoints. Patients were followed on treatment for two years. We concluded that dipyridamole, in a modified-release form, at a dose of 200 mg b.d. and ASA 25 mg b.d., have been shown to be equally effective in the secondary prevention of ischaemic stroke and TIA; that when co-prescribed, the protective effects are additive, the combination being significantly more effective than each agent prescribed singly; and that low-dose ASA does not eliminate the propensity for induced bleeding.

Aged↗

PubMed1993

Does low-dose acetylsalicylic acid prevent stroke after carotid surgery? A double-blind, placebo-controlled randomized trial.

BACKGROUND AND PURPOSE: The aim of this randomized double-blind, placebo-controlled trial was to evaluate whether neurological deficits could be prevented with low-dose acetylsalicylic acid (ASA) as an adjunct to carotid endarterectomy. METHODS: A total of 232 patients were randomized to two groups, 75 mg/d ASA starting preoperatively and continued for 6 months (n = 117) or placebo (identical tablets) (n = 115). The patients were followed up regularly for 1 year. RESULTS: The groups were well matched regarding laboratory data and indication for operation. The number of patients with intraoperative or postoperative stroke without complete recovery within 1 week were 0 and 2 at 30 days and 6 months, respectively, in the ASA group, compared with 7 and 11 in the placebo group (P = .01). Including all neurological events within 6 months, this was found in 15 patients in the ASA group compared with 24 in the placebo group (P = .12). Mortality was 0.8% and 3.4% at 30 days and 6 months, respectively, in the ASA group. In the placebo group, the corresponding figures were 4.3% and 6.0%, respectively (P = .12). The intraoperative bleeding did not differ between the groups nor did the number of reoperations due to bleeding or other complications related to pharmacology. CONCLUSIONS: This study indicates that low-dose ASA (75 mg/d) reduces the number of postoperative strokes without complete recovery within 1 week. Overall neurological events are insignificantly reduced, as also mortality. The use of low-dose ASA (75 mg) seems safe and effective in reducing cerebrovascular events after carotid endarterectomy.

Adult↗

PubMedDate not supplied

Triflusal versus acetylsalicylic acid: a double-blind study for the prophylaxis of deep vein thrombosis after hip surgery.

The authors report the results of a randomised double-blind study comparing the antithrombotic activity of a new anti-platelet drug (Triflusal) with that of acetylsalicylic acid (ASA). 99 patients who underwent hip surgery were included in the study (total hip replacement, osteosynthesis of a pertrochanter fracture or Moore's prosthesis for intracapsular fracture of the femoral neck). Of the 48 patients having received Triflusal, 7 (14.5%) developed deep vein thrombosis as indicated by 125I-fibrinogen isotopic scanning and confirmed by phlebography. Of the 51 patients treated with ASA, 11 (21.6%) presented the same complication as diagnosed by the same techniques. This difference is not statistically significant, considering the number of cases studied. Nevertheless, Triflusal appears to provide prevention of thromboembolic risk to patients who have undergone hip surgery, particularly total hip replacement.

Adult↗

PubMed2002

Helicobacter pylori and acetylsalicylic acid synergistically accelerate apoptosis via Fas antigen pathway in rabbit gastric epithelial cells.

The mechanism for gastric epithelial cellular apoptosis by both H. pylori and NSAIDs remains unknown. Normal gastric epithelial cells, collected from rabbit stomach, were cultured with viable H. pylori and/or an acetylsalicylic acid for 24 hr as an in vitro model of gastric epithelial cell injury. The Fas antigen expression rate in the gastric epithelial cells was measured using a FACScan. In group E, in which H. pylori inoculation of epithelial cells was followed by treatment with an NSAID, the rate of Fas antigen expression was significantly higher than the rate observed after treatment with either H. pylori or NSAID alone. Despite the fact that drug treatment alone did not significantly increase the Fas expression rate vs control cells. The results suggest that H. pylori and NSAID induce gastric cell injury as apoptosis via the Fas antigen pathway in a synergistic manner and that this effect is particularly strong when NSAID treatment follows H. pylori infection.

Animals↗

PubMed1985

Acetylsalicylic acid and dipyridamole improve the early patency of aorta-coronary bypass grafts. A double-blind, placebo-controlled, randomized trial.

A total of 125 patients undergoing aorta-coronary bypass grafting for disabling angina were randomized to receive either 330 mg of acetylsalicylic acid (aspirin) plus 75 mg of dipyridamole three times daily or a placebo for 6 months postoperatively. In addition, all patients were given warfarin for 3 months. Repeat angiography was performed at 6 months in 103 patients. In the treatment group 95 grafts were implanted in 48 patients, of which 87 were patent (91.6% patency rate). This figure compares with 88 grafts patent out of 118 implanted in 55 patients in the placebo group (74.6% patency rate) (p less than 0.01). We conclude that antiplatelet therapy improves the early patency of saphenous vein aorta-coronary bypass grafts.

Adult↗

PubMed1999

Efficacy and safety of intravenous acetylsalicylic acid lysinate compared to subcutaneous sumatriptan and parenteral placebo in the acute treatment of migraine. A double-blind, double-dummy, randomized, multicenter, parallel group study. The ASASUMAMIG Study Group.

Two-hundred-and-seventy-eight patients with acute migraine attacks with or without aura were treated in 17 centers with 1.8 g lysine acetylsalicylate i.v. (Aspisol; = 1 g acetylsalicylic acid), 6 mg sumatriptan s.c. or placebo using a double-blind, double-dummy, randomized, multicenter parallel group study design. Two-hundred-and-seventy-five of them fulfilled the criteria for efficacy analysis, corresponding to 119 patients treated with lysine acetylsalicylate (L-ASA), 114 with sumatriptan and 42 with placebo injections. Both treatments were highly effective compared to placebo (p < 0.0001) in decreasing headache from severe or moderate to mild or none (verbal rating scale, VRS, placebo = 23.8%). Sumatriptan showed a significantly (p = 0.001) better response (91.2%) compared to L-ASA (response 73.9%). Of the patients in the L-ASA-group, 43.7% were pain-free after 2 h; 76.3% after sumatriptan and 14.3% after placebo. It took patients on average 12.6 (L-ASA), 8.2 (sumatriptan), and 19.4 h (placebo) to be able to work again. There was no significant difference between treatment groups in recurrence of headache in responders within 24 h (18.2% L-ASA, 23.1% sumatriptan, 20% placebo). Accompanying symptoms (nausea, vomiting; photophobia, phonophobia, and visual disturbances) improved with both verum treatments to a similar extent. L-ASA was significantly better tolerated than sumatriptan (adverse events L-ASA 7.6%, sumatriptan 37.8%). In conclusion, subcutaneous sumatriptan and lysine acetylsalicylate i.v. are effective treatments for patients suffering from migraine attacks. Sumatriptan is more effective, but resulted in more adverse events.

Adult↗

PubMed1985

The effects on lipids, blood viscosity and platelet aggregation of combined use of niceritrol (Perycit) and a low dose of acetylsalicylic acid.

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.

Adult↗

PubMed2003

Acetylsalicylic acid and acetaminophen to combat elevated body temperature in acute ischemic stroke.

BACKGROUND: Because elevated body temperature (BT) in acute ischemic stroke is associated with poor outcome, it is currently recommended to maintain normothermia with antipyretics. Whether this can be achieved by the administration of acetylsalicylic acid (ASA) or acetaminophen is uncertain. METHODS: Over a period of 9 months, patients admitted with acute hemiparetic ischemic stroke were monitored for BT in the first 48 h. When BT rose >37.5 degrees C, patients were treated with either ASA 500 mg intravenously or acetaminophen suppository 1,000 mg. When 6 h later the BT was still or again >37.5 degrees C, patients were further treated with acetaminophen suppository 1,000 mg up to 4 times a day. Primary outcome measure was normothermia (BT </=37.5 degrees C) within respectively 1 and 3 h after intervention. Secondary outcome parameters were any decrease in BT and the mean decrease in BT. RESULTS: Of a total of 132 patients, 63 (48%) developed a BT >37.5 degrees C. The effects of 43 injections of ASA and 89 administrations of acetaminophen were studied. After 1 h, treatment with acetaminophen produced both significantly more reductions in BT and normothermia (respectively in 60 and 20%) than treatment with ASA (respectively in 37 and 5%). At 3 h, both interventions had a similar effect, with normothermia being achieved in only 37-38%. Fever (>38.0 degrees C) and evidence of an infection were related to unresponsiveness to treatment. CONCLUSIONS: In the majority of patients with acute ischemic stroke, ASA and acetaminophen are insufficient for reducing an elevated BT to a state of normothermia.

Acetaminophen↗

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↗

PubMed1998

Inhibition of PMN- and HOC1-induced vascular injury in isolated rabbit lungs by acetylsalicylic acid: a possible link between neutrophil-derived oxidative stress and eicosanoid metabolism?

Neutrophils are involved in the pathogenesis of acute lung injury. The neutrophil-derived enzyme myeloperoxidase (MPO) catalyzes the formation of the oxidant hypochlorous acid (HOCl). This study characterizes the effects of (A) continuous HOCl infusion, and (B) stimulated neutrophils on pulmonary circulation in an isolated rabbit lung model. Furthermore, the effect of cyclooxygenase inhibition by acetylsalicylic acid (ASA, 0.5 mM) on these effects was investigated. (A) Infusion of HOCl (in nmol min-1, groups: 0, 0+ASA, 1000, 1000+ASA, 2000, and 2000+ASA) into the isolated organ was started after a 45-min steady-state period (t=0). (B) Neutrophils (PMN group: 1480+/-323 and ASA group 1294+/-320 microliter-1) were added into the perfusate between (t=-45 min) and stimulated with FMLP (1 microM) after two 45-min steady-state periods (t=0). Perfusate MPO activity was measured at t=-90, -45, 0, 1, 2, 3, 5, 10, 15, 30, 60, and 90 min. For both groups, pulmonary artery pressure (PAP) and lung weight were continuously recorded and the capillary filtration coefficient (Kf,c in 10(-4) cm(3) s(-1) cm H2O(-1) g(-1) was calculated from the slope of weight gain after a hydrostatic challenge at t=-45, -15, 30, 60 and 90 min. (A) Continuous HOCl infusion (1000/2000 nmol min-1) evoked a significant increase in DeltaPAP and an up to 10-fold increase in Kf,c reaching the maximum extent of the observed effects significant earlier in the 2000 nmol min-1 group. ASA reduced DeltaPAPmax significantly to about 50% in corresponding groups and the increase in PAP and Kf,c occurred later in the ASA groups. (B) Neutrophil stimulation (PMN group/ASA group) evoked a rapid increase in DeltaPAP and MPO activity, while the changes in vascular permeability were rather moderate, but still significant. The release of MPO activity was similar in both groups. ASA significantly reduced the increase in DeltaPAP without affecting the release of MPO activity. Compared to baseline values, the preventive effects on vascular permeability increase reached level of significance as well. In summary, the described changes in pulmonary circulation caused by HOCl infusion or by neutrophil stimulation are significantly reduced by ASA. An involvement of cyclooxygenase products in the mediation of neutrophil-derived oxidative stress could be concluded.

Animals↗

PubMed1995

Involvement of brain serotonergic system in the antinociceptive action of acetylsalicylic acid in the rat.

The pain-threshold in the hot-plate test and serotonin (5-HT) receptor binding capacity in the cortex and pontine areas of rat brain were studied after intraperitoneal (ip) administration of acetyl salicylate of lysine equivalent to 400 mg/kg of acetylsalicylic acid (ASA). The antinociceptive activity of ASA was prevented by ip pre-treatment with Parachlorophenylalanine (PCPA) at the rate of 100 mg/kg/day for 4 days. PCPA pre-treatment increased the number of 5-HT receptors and abolished the ASA-induced reduction in 5-HT receptor binding capacity in the cortex but did not affect serum salicylate levels. These results provide support for the hypothesis that the antinociceptive action of ASA, at least in the hot-plate test, involves the central serotonergic system.

Analgesics↗

PubMed1984

[Inhalation provocation test with lysine acetylsalicylic acid (Aspisol)--a useful method for the diagnosis of analgesic asthma].

In patients with analgesics induced asthma (AIA) provocation tests by inhalation are less dangerous than oral provocation. Bianco et al. and Schmitz-Schumann et al. described an inhalation provocation test (IPT) with Lysine-acetylsalicylic-acid (Lys-ASA). We found analgesics induced asthma in 5 p.c. of our patients with bronchial asthma. The results of 41 IPT with Lys-ASA are reported. In 26 of 29 patients with analgesics intolerance in the history the test was positive after a threshold dose of 18,0 mg (9,3-53,3 mg) Lys-ASA. 3 patients believed to have analgesics intolerance. It could be excluded by negative IPT and following negative oral provocation. In a control group of 12 patients with intrinsic asthma, nasal polyps and sinusitis, but without analgesics intolerance in the history, the test was positive too in 2 patients. They didn't use analgesics in the past years. The diagnosis could be confirmed by oral provocation. In our opinion IPT with Lys-ASA is very useful to find an AIA or to exclude it. It is better controllable than oral provocation. The induced bronchospasm is good reversible by inhalation of beta-mimetics or injection of methylxanthines. Intraindividual variations of bronchial tolerance can be supposed. All patients with AIA tolerated oral provocation with salicyclamide.

Airway Resistance↗

PubMed1982

In healthy habitual smokers acetylsalicylic acid abolishes the effects of tobacco smoke on the platelet aggregate ratio.

After abstinence for at least 8 hours, 20 healthy habitual smokers smoked two unfiltered cigarettes during each of two 20-minute periods separated by 48 hours. They had taken one 0.32-g tablet of acetylsalicylic acid (ASA) the night before the second period. The mean platelet aggregate ratios in venous blood taken immediately before and after each period of smoking were 0.79 and 0.70 respectively when ASA had not been taken beforehand and 0.89 and 0.91 when it had. The mean after smoking was significantly higher when ASA had been taken beforehand. In conjunction with the previous finding that in nonsmokers ASA prevented a lowering of the platelet aggregate ratio by experimental smoking without affecting the ratio before smoking, the data from the present study suggest that ASA abolishes both acute and longer-lasting effects of tobacco smoke on the platelet aggregate ratio in healthy habitual smokers.

Adolescent↗

PubMed1993

Acetylsalicylic acid inhibits anticardiolipin antibody-induced platelet-activating factor (PAF) synthesis.

Enhanced endothelial cell PAF synthesis has been identified as a consequence of anticardiolipin antibody (ACA)-positive serum exposure. We proposed this observation as a contributing factor to thrombogenesis in women with the antiphospholipid syndrome. Since acetylsalicylic acid (ASA) is an accepted therapeutic alternative in these patients, we sought to determine if ASA would attenuate endothelial cell PAF production resulting from ACA exposure. Using primary, confluent monolayers of umbilical vein endothelial cells, experiments were performed to evaluate PAF synthesis after incubation with antibody-positive serum and ASA. Total PAF and its radyl-derivatives (1-alkyl- and 1-acyl-PAF) were quantified by tritiated acetate incorporation, phospholipid extraction, thin-layer chromatography and scintillation spectroscopy. ASA consistently decreased ACA-induced PAF synthesis (No ASA, 9573 +/- 443 vs 1mmol/L ASA, 4829 +/- 838 dpm/ml; p = 0.016) and the observed reduction was dose-dependent over a range of ASA concentrations (0.1, 1, 10 and 100 mmol/L; ANOVA, p = .00015). Reduced PAF synthesis was also observed in cultures exposed to ASA and incubated with antibody-negative serum. These observations suggest that in ACA-positive women, the antithrombotic effects of ASA may relate in part, to reduced endothelial cell PAF synthesis.

Antibodies, Anticardiolipin↗

PubMed2001

Acetylsalicylic acid inhibits the pituitary response to exercise-related stress in humans.

PURPOSE: Prostaglandins (PGs) modulate the activity of the hypothalamus-pituitary axis, and pituitary hormones are largely involved in the physiological responses to exercise. The purpose of this study was to analyze the effects of acetylsalicylic acid (ASA), an inhibitor of PGs synthesis, in the pituitary responses to physical stress in humans. METHODS: Adrenocorticotropin (ACTH), beta-endorphin, cortisol, growth hormone (GH), and prolactin (PRL) responses to exercise were evaluated after administration of either placebo or ASA. Blood samples for hormone evaluations before (-30, -15, and 0 pre) and after (0 post, +15, +30, +45, +60, and +90 min) a 30-min treadmill exercise (75% of .VO(2max)) were taken from 12 male athletes during two exercise trials. One tablet of ASA (800 mg), or placebo, was administered two times daily for 3 d before and on the morning of each exercise-test. RESULTS: The results clearly show that, compared with placebo, ASA ingestion significantly blunted the increased serum ACTH, beta-endorphin, cortisol, and GH levels before exercise (anticipatory response) and was associated with reduced cortisol concentrations after exercise. Furthermore, although no differences in the GH response to exercise were shown, a significantly reduced total PRL response to stress condition was observed after ASA. CONCLUSION: ASA influences ACTH, beta-endorphin, cortisol, GH, and PRL responses to exercise-related stress in humans (preexercise activation/exercise-linked response). Even though it is not possible to exclude direct action for ASA, our data indirectly confirm a role of PGs in these responses. We have to further evaluate the nature of the preexercise endocrine activation and, because of the large use of anti-inflammatory drugs in athletes, whether the interaction between ASA and hormones might positively or negatively influence health status, performance, and/or recovery.

Adrenocorticotropic Hormone↗

PubMed1998

Effect of roxatidine bismuth citrate (MX1) against acetylsalicylic acid- and indomethacin-induced gastric mucosal damage in rats.

We have studied the effect of the newly synthesized agent, roxatidine bismuth citrate (N-[3-(3-(1-piperidinyl-methyl)phenoxy)propyl]-hydroxyacetamide-2- hydroxypropane-1,2,3-tricarboxylate-bismuth(3+) complex), code name MX1, against acetylsalicylic acid (ASA)- and indomethacin-induced gastric mucosal damage in rats. Effects of MX1 (12.5, 50, 125, 184, 250 mg/kg) were compared to the effects of equimolar doses of roxatidine and bismuth subcitrate. Effect of MX1 (10(-6) M) on mucin biosynthesis measured by [3H] glucosamine incorporation in rat gastric corpus has been determined. MX1-pretreatment dose-dependently decreased the mean ulcer number and length in all doses used in an extent similar to that of roxatidine and more pronounced in comparison with bismuth subcitrate. The morphometrical results have been confirmed histomorphologically. The biosynthesis of mucin was found to be significantly enhanced after MX1 addition. The results of the present study suggest that MX1 has a gastroprotective effect against ASA- and indomethacin-induced ulcers which might be due both to its H2-blocking and mucus-stimulating activity.

Animals↗

PubMed1979

Effect of two prostaglandin synthesis inhibitors, indomethacin and acetylsalicylic acid, on plasma ACTH and cortisol levels in man.

The aim of this study was to investigate the possible role of prostaglandins (PG) in the control of the hypohtalamic-pituitary-adrenocortical axis in normal volunteers. Acute oral administration of 100 mg indomethacin (ID) or 1.5 g acetylsalicylic acid (ASA) did not alter ACTH and cortisol plasma levels. Administration of 300 mg daily ID for 4 days delayed the onset, but increased the magnitude, of the response of ACTH to insulin hypoglycaemia, while it blunted the cortisol response. Administration of 3.2 g ASA daily depressed ACTH response to hypoglycaemia leaving the cortisol response unchanged, except for a 15 min delay in onset. These results are interpreted assuming that ID and ASA chiefly acted at the pituitary and hypothalamic level, respectively, and that ID, but not ASA, interfered with adrenocortical cortisol production. Our findings support the concept, based on animal studies, that PG enhance hypothalamic CRF release and adrenocortical steroidogenesis and may restrain ACTH secretion in the pituitary.

Administration, Oral↗

PubMed1980

The German-Austrian aspirin trial: a comparison of acetylsalicylic acid, placebo and phenprocoumon in secondary prevention of myocardial infarction. On behalf of the German-Austrian Study Group.

In a multicenter clinical trial on the prevention of recurrent myocardial infarction, 946 patients who had survived a myocardial infarction for 30-42 days were randomly allocated to acetylsalicylic acid (ASA, 1.5 g/day) (317 patients), placebo (309 patients) or phenprocoumon treatment (320 patients) and were followed to determine the incidence of total mortality, coronary death and nonfatal recurrent myocardial infarction. The ASA and placebo groups were treated in double-blind fashion. The observation period for each patient was 2 years. Total mortality was lower in the ASA group (27 patients) than in the placebo (32 patients) and phenprocoumon groups (39 patients). There were 13 coronary deaths (fatal myocardial infarction and sudden death) in the ASA group, 22 in the placebo group and 26 in the phenprocoumon group. This represents a reduction rate of 42.3% in the ASA group compared with placebo (p less than 0.1) and of 46.3% in the ASA group with phenprocoumon (p approximately 0.07). Considering male patients alone, the difference regarding coronary death is significant between ASA vs placebo (p less than 0.05, reduction rate 56.4%) and ASA vs phenprocoumon (p less than 0.05, reduction rate 55.6%). Coronary events (coronary death and nonfatal recurrent myocardial infarctions) were lower in the ASA group (24 events) than in the placebo (37 events) (p less than 0.07) or phenprocoumon group (32 events).

4-Hydroxycoumarins↗