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Aggrenox (Acetylsalicylic Acid + Dipyridamole)
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Aggrenox

Generic Aggrenox is an effective preparation which is taken in struggle against pain, fever, and inflammation. Generic Aggrenox is also used to keep platelets in your blood from sticking together to form clots. Generic Aggrenox consists of aspirin and dipyridamole combination. Generic Aggrenox is also taken to protect from the risk of stroke in people who have had blood clots or a "mini-stroke" (transient ischemic attack or TIA).

Other names for this medication:

Similar Products:
Aspirin, Dipyridamole

 

Also known as:  Acetylsalicylic Acid + Dipyridamole.

Description

Generic Aggrenox is developed by medical scientists to relieve pain, fever, and inflammation. Also it keeps platelets in your blood from sticking together to form clots.

Generic Aggrenox is also created for people who have had blood clots or a "mini-stroke" (transient ischemic attack or TIA) to protect from possible risk of stroke.

Generic Aggrenox consists of aspirin (25 mg) and dipyridamole (200 mg).

Aspirin is in a group of drugs called salicylates. Aspirin works by reducing hormones that cause inflammation, fever and pain in the body.

Dipyridamole operates by keeping platelets in your blood from sticking together to form clots.

Dosage

Take capsules orally with a full glass (8 ounces) of water.

It is possible to take Generic Aggrenox with or without food.

Remember to swallow the capsule whole without any tries to crush, chew, break, or open it.

Remember that taking Generic Aggrenox is not the same as taking each of the medications (aspirin and dipyridamole) separately.

If you want to achieve most effective results do not stop using Generic Aggrenox suddenly.

Overdose

If you overdose Generic Aggrenox and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Aggrenox overdosage: feeling light-headed, or fainting, warmth or tingly feeling, sweating, restlessness, dizziness, weakness.

Storage

Store at a room temperature between 4 and 30 degrees C (39 and 86 degrees F) away from moisture, light and heat. Throw away the after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Aggrenox are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not use Generic Aggrenox if you are allergic to Generic Aggrenox components.

Do not use Generic Aggrenox if you're pregnant or you plan to have a baby, or you are a nursing mother. It is not known whether Generic Aggrenox harms baby.

Do not use Generic Aggrenox with any other over-the-counter pain medication.

Do not give Generic Aggrenox to a child or teenager who has a fever, flu symptoms or chicken pox. Generic Aggrenox can cause a serious and sometimes fatal condition called Reye's syndrome in children.

Do not use Generic Aggrenox if you have a history of allergy to an NSAID (non-steroidal anti-inflammatory drug) such as Advil, Motrin, Aleve, Orudis, Indocin, Lodine, Voltaren, Toradol, Mobic, Relafen, Feldene, and others, asthma or nasal polyps.

Be careful with Generic Aggrenox if you are taking medicines such as acetazolamide (Diamox); diuretic (water pill) such as amiloride (Midamor, Moduretic), furosemide (Lasix), hydrochlorothiazide (HCTZ, HydroDiuril, Hyzaar, Lopressor, Vasoretic, Zestoretic), spironolactone (Aldactazide, Aldactone), triamterene (Dyrenium, Maxzide, Dyazide), and others; seizure medication such as carbamazepine (Carbatrol, Tegretol), phenytoin (Dilantin), or phenobarbital (Luminal, Solfoton); methotrexate (Rheumatrex, Trexall); diabetes medications that you take by mouth; Alzheimer medications such as donepezil (Aricept), galantamine (Reminyl), or rivastigmine (Exelon); beta-blocker such as atenolol (Tenormin), carvedilol (Coreg), esmolol (Brevibloc), metoprolol (Lopressor, Toprol), propranolol (Inderal, InnoPran), sotalol (Betapace), timolol (Blocadren), and others; aspirin or other NSAIDs (non-steroidal anti-inflammatory drugs) such as ibuprofen (Motrin, Advil), naproxen (Aleve, Naprosyn), indomethacin (Indocin), ketoprofen (Orudis), meloxicam (Mobic), nabumetone (Relafen), piroxicam (Feldene); gout medications such as probenecid (Benemid) or sulfinpyrazone (Anturane); ACE inhibitor such as benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), lisinopril (Prinivil, Zestril), quinapril (Accupril), ramipril (Altace), and others.

Be careful with Generic Aggrenox if you suffer from or have a history of kidney disease, stomach ulcers or bleeding, bleeding disorder such as hemophilia, low blood pressure, heart disease, congestive heart failure, or recent heart attack, liver disease.

Avoid alcohol.

It can be dangerous to stop Generic Aggrenox using suddenly.

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Among high vascular risk patients, acetylsalicylic acid (ASA) reduces the relative risk of serious vascular events by about one fifth. However, because ASA fails to prevent four fifths of serious vascular events, more effective, yet equally safe and affordable, antiplatelet regimens are desired. Compared with ASA, clopidogrel alone reduces the odds of serious vascular events by about 10%, and the combination of dipyridamole and ASA reduces the odds of serious vascular events by about 6%. Combining ASA with an orally administered platelet glycoprotein (GP) IIb/IIIa blocker is not effective, and indeed more hazardous than ASA alone. Among patients with non-ST-segment acute coronary syndromes (ACS), the addition of an intravenously administered GP IIb/IIIa receptor antagonist to ASA reduces the risk of vascular events by about 10% compared with ASA, and the addition of clopidogrel to ASA reduces the risk of vascular events by 20% compared with ASA alone. Among patients undergoing percutaneous coronary intervention (PCI), both the addition of an intravenously administered GP IIb/IIIa receptor antagonist to ASA, and the addition of clopidogrel to ASA reduce the risk of vascular events by 30% compared with ASA alone. The greater efficacy of the combinations of ASA with clopidogrel, and ASA with an intravenously administered GP IIb/IIIa receptor antagonist, in patients with ACS and those undergoing PCI has fostered several ongoing and planned trials of these regimens in the acute and long-term management of patients with ischaemic brain syndromes. The combination of ASA and clopidogrel is being compared with ASA alone within 12 h of onset of symptoms of TIA in two trials (FASTER, ATARI), and the use of an intravenously administered GP IIb/IIIa receptor antagonist is being compared with placebo within 6 h of onset of acute ischaemic stroke in two trials (AbESST, AbESST-2). Six trials are assessing the combination of clopidogrel and ASA in the long-term management of patients with ischaemic brain syndromes due to atherothrombosis (MATCH, CHARISMA, ARCH, CARESS, SPS3) or atrial fibrillation (ACTIVE). The MATCH trial of clopidogrel and ASA versus clopidogrel alone in patients with recent TIA or ischaemic stroke is the first which is likely to report its results - in mid 2004. The combination of dipyridamole and ASA is being compared with ASA in the ESPRIT trial and with the combination of clopidogrel and ASA in the planned PRoFESS trial. These ongoing and planned clinical trials of antiplatelet therapy promise to further define the role of combination antiplatelet therapy in the acute and long-term management of patients with ischaemic brain syndromes.

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Thrombotic thrombocytopenic purpura is a severe multisystemic disorder of unknown origin. The association of relapsing TTP with pregnancy is rare but well documented and high mortality rates of mothers and fetuses have been reported so far. Since the introduction of plasma therapy for treating the acute exacerbations of the disease, overall mortality rates have decreased significantly. It is now evident that the manifestations of the disease may reappear even after long disease-free intervals and as many as a third of the recovering patients may develop a relapse. Presented are two TTP patients with relapsing TTP complicating their pregnancies. Prophylactic treatment with aspirin and dipyridamole during their last three successful pregnancies prevented or minimized the severity of TTP relapses. The course of these pregnancies and the management of such patients is discussed.

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University department of cardiology.

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Angiotensin (ANG) II-induced relaxations in isolated dog renal and cerebral arteries are postulated to be mediated by the release of prostaglandin (PG) I2 from the arterial wall. In helical strips of dog renal arteries treated with dipyridamole, relaxations induced by ANG II (10(-7) M) and exogenously applied PGI2 (10(-8) M) were potentiated; the potentiation was appreciably greater in the ANG-induced relaxation. Treatment with phthalazinol did not alter the response to ANG II, but significantly potentiated the relaxation induced by PGI2. The ANG-induced relaxations were suppressed or reversed to contractions by aspirin or indomethacin. Combined treatment of dipyridamole with aspirin or indomethacin restored the relaxant response to ANG II, while phthalazinol in combination with aspirin did not restore the response. It may be concluded that the potentiation of responses to ANG II by dipyridamole is associated with increments in the release of PGI2 from the arterial wall and potentiations of the response of arterial smooth muscle to PGI2. Dipyridamole appears to increase the production of PGI2 even in the presence of PG synthesis inhibition by aspirin or indomethacin.

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Chang Gung Memorial Hospital.

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This is an update of our previous review; the goal was to create a valid synthesis of all available, methodologically sound data to further assess the safety and efficacy of combined oral anticoagulant and antiplatelet therapy versus oral anticoagulant monotherapy in patients with prosthetic heart valves.

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Twenty dogs with naturally occurring metastatic tumors were treated with anticoagulants (Warfarin) or platelet enzyme inhibitor drugs (dipyridamole, dipyridamole plus aspirin, RA233, sulfinpyrazone, or a combination of RA233 and sulfinpyrazone) to determine if tumor-related reductions in platelet survival and concentration could be reversed. Anticoagulation was ineffective, while platelet enzyme inhibitors were able to produce improvements in platelet survival. Of the 18 dogs with metastatic tumor treated with platelet enzyme inhibitors, only 5 (28%) showed a reduction in platelet survival during the first week of observation on therapy compared to their baseline survivals. This is significantly different than the decreases in platelet survivals observed in 8 of 10 untreated dogs (80%) with metastatic tumor observed for the same interval. Furthermore, 8 of the 18 treated dogs (44%) had platelet survivals within 2 standard deviations of normal, compared to only 1 of 10 untreated dogs. Of the 8 dogs with normal platelet survivals, 6 were treated with a combination of a phosphodiesterase inhibitor (RA233 or dipyridamole) and a cyclooxygenase inhibitor (sulfinpyrazone or aspirin). The combination of RA233 and sulfinpyrazone was the best drug program tested and resulted in normal platelet survivals in 63% and improved platelet counts in 75% of the animals treated. Thus, platelet enzyme inhibitors with different mechanisms of action may have a synergistic effect in reversing the abnormal platelet hemostasis found in a variety of spontaneously occurring canine neoplasms.

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The aim of this study was to assess whether triple antiplatelet therapy is superior to dual and mono therapy in attenuating platelet and leucocyte function. Aspirin (A), clopidogrel (C), and dipyridamole (D) were administered singly and in various combinations (A, C, D, AC, AD, CD, ACD), each for two weeks (without washout) to 11 healthy subjects and to 11 patients with previous ischaemic stroke in two randomised multiway crossover trials. At the end of each two-week period platelet aggregation, platelet-leucocyte conjugate formation and leucocyte activation were measured ex vivo blinded to treatment. Platelets were stimulated with collagen; additional measurements were made with adenosine diphosphate (ADP), platelet activating factor (PAF), adrenaline and the combination of, ADP, PAF and adrenaline. Results show that in the presence of collagen, ACD was superior to all antagonists or combinations, except AC, in reducing aggregation, platelet-leucocyte conjugate formation, and monocyte activation (all p<0.05). ACD was also more potent than other treatments, except AC, in inhibiting the aggregation and platelet-monocyte conjugate formation induced by the combination of ADP, PAF and adrenaline. The effects were similar in both volunteers and stroke patients. No serious adverse events or major bleeding events occurred. Triple antiplatelet therapy did not appear to be more effective than combined aspirin and clopidogrel in moderating platelet and leucocyte function. Any additional clinical benefit provided by dipyridamole may be through other mechanisms of action.

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The adherence of 51Cr-labeled platelets to the subendothelium of rabbit aortas was inhibited in vitro and in vivo by high concentrations of dipyridamole (100 microM in vitro, 2.5 or 12.5 mg/kg in vivo). Dipyridamole (100 microM) inhibited release of 14C-serotonin from platelets that adhered to the subendothelium or to a collagen-coated glass surface; lower concentrations of dipyridamole had only a slight inhibitory effect. Scanning electron microscopy showed that many of the platelets that adhered to the subendothelium were rounded, with few pseudopodia. The combination of dipyridamole with PGI2 was no more inhibitory of platelet adherence than either agent alone; however, this combination of inhibitors exerted synergistic inhibitory effects on aggregation and release of 14C-serotonin from platelets aggregated by collagen. The effects of dipyridamole on platelet adherence are a consequence of the action of dipyridamole alone and do not appear to result from its interaction with PGI2 formed by injured vessels in vivo, since the inhibitory effect is not influenced by aspirin inhibition of PGI2 formation, either at the shear rates in the in vitro studies or under the shear conditions found in rabbit aortas in vivo.

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We performed a study to evaluate the effect of acetylsalicylic acid (ASA) plus dipyridamole on the retinal vascular pattern over 3 months in rats with experimental diabetes mellitus. Rats treated with ASA alone showed a continuous vascular bed and less tortuous vessels than untreated diabetic rats. Rats treated with ASA plus dipyridamole showed a continuous vascular bed, scarce tortuous vessels and vascular diameters similar to those in nondiabetic control rats. The findings were related to aortic prostacyclin production: treatment with ASA alone produced a reduction in prostacyclin production, whereas treatment with ASA plus dipyridamole resulted in normal prostacyclin production. ASA alone or with dipyridamole inhibited collagen-induced aggregation in whole blood by 57% compared with the untreated diabetic rats.

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We included 17 trials with 42,234 participants (mean age 64.4 years, 65% male) and follow up ranging from 4 weeks to 3.5 years. Compared with placebo, any single antiplatelet agent was associated with a significant reduction in recurrence of any stroke (risk ratio [RR] 0.77, 0.62-0.97, 2 studies) and ischemic stroke (RR 0.48, 0.30-0.78, 2 studies), but not for the composite outcome of any stroke, myocardial infarction, or death (RR 0.89, 0.75-1.05, 2 studies). When other antiplatelet agents (ticlodipine, cilostazol, and dipyridamole) were compared with aspirin, there was no consistent reduction in stroke recurrence (RR 0.91, 0.75-1.10, 3 studies). Dual antiplatelet therapy did not confer clear benefit over monotherapy (any stroke RR 0.83, 0.68-1.00, 3 studies; ischemic stroke RR 0.80, 0.62-1.02, 3 studies; composite outcome RR 0.90, 0.80-1.02, 3 studies).

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New oral drugs are being tested; these may be as effective at reducing stroke risk as warfarin in patients with AF. Direct thrombin inhibitors such as ximelagatran are not inferior to warfarin and, based on results from the SPORTIF III and V trials, are perhaps safer, with no need for long-term monitoring and dose adjustment. However, the side-effect of raised amounts of the liver enzyme alanine amino-transferase in 6% of patients needs to be resolved. In the ACTIVE trial, the efficacy of a combination of antiplatelet drugs (aspirin plus clopidogrel) is being tested against dose-adjusted warfarin; and in AMADEUS, the factor-Xa inhibitor and pentasaccharide idraparinux is being assessed in a similar way. Several surgical procedures and devices are also being developed to control AF rhythm and prevent stroke. WHERE NEXT?: The place of these new drugs in the management of AF needs to be established. In the short term, it seems that ximelagatran will replace warfarin in patients for whom there is evidence of a favourable risk-to-benefit ratio. The SPORTIF population consists of patients with AF plus at least one risk factor. More information about the effect of raised liver enzymes will probably not be available until phase IV studies are completed. Combination antiplatelet drugs need to be tested further--perhaps even triple therapy with aspirin, clopidogrel, and dipyridamole--if the results of ACTIVE are encouraging. The place of surgical procedures and devices to control rhythm and prevent stroke is unclear. Whatever happens, there is a high probability that the days of warfarin are numbered.

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These results suggest that dipyridamole potentiates the antiplatelet effect of cilostazol without prolongation of the bleeding time, implying a potential novel combination antithrombotic therapy.

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Although patients treated with regimens 2 and 4 were more ill at presentation than those treated with regimens 1 and 3, respectively, the duration of fever was shorter in the former patient groups (P =.0013). Coronary aneurysms developed least frequently in patients treated with regimen 4 and less frequently with regimen 2 than with regimen 1 (P =.0730). Multiple regression analysis showed significant reductions of fever and coronary aneurysm incidence with prednisolone (P <.0001 and P =.0307, respectively).

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A total of 353 patients met inclusion criteria: 273 non-ACAP (77%) and 80 ACAP (23%). Upon exclusion of three patients taking a combination of agents, 350 were available for advanced analyses. ACAP status was significantly related to in-hospital mortality. After adjustment for patient and injury characteristics, anticoagulant users were more likely than non-ACAP patients to show progression of initial hemorrhage and develop a new hemorrhagic focus. However, compared with non-ACAP users, antiplatelet users were more likely to die in the hospital. Among survivors to discharge, anticoagulant users were more likely to be discharged to a care facility, but this finding was not robust to adjustment.

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We found that treatment with dipyridamole is associated with increased overall fracture risk, but not to the risk of osteoporotic fractures. In contrast, low-dose acetylsalicylic acid is associated to increased risk of overall fractures and fractures of the hip. Finally, in the current study clopidogrel is not associated with increased fracture risk.

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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.

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Published articles and abstracts were identified from a MEDLINE search (1966-December 1999) using the search terms dipyridamole, aspirin, antiplatelet, antiaggregation, and stroke prevention. Pertinent articles written in English were considered for review. Additional articles were identified from the references of retrieved literature.

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Stroke is a leading cause of death and the primary cause of serious, long-term disability in the United States. Joint guidelines from the American Heart Association (AHA) and American Stroke Association (ASA), as well as recent guidelines from the Eighth American College of Chest Physicians (ACCP) Conference on Antithrombotic and Antiplatelet Therapy, recommend aspirin, clopidogrel, or extended-release dipyridamole plus aspirin as acceptable first-line options for secondary prevention of ischemic events in patients with a history of ischemic stroke or transient ischemic attack (TIA). The ACCP strongly recommends the combination of extended-release dipyridamole plus aspirin over aspirin monotherapy (highest level of evidence) and suggests clopidogrel monotherapy over aspirin monotherapy (lower level of evidence). The AHA-ASA guidelines suggest that either extended-release dipyridamole plus aspirin or clopidogrel monotherapy should be used over aspirin monotherapy. Both guidelines recommend avoiding the combination of clopidogrel and aspirin for most patients with previous stroke or TIA. Results from recent trials evaluating combination antiplatelet therapy have been published that enhance the AHA-ASA recommendations and provide the foundation for the updated ACCP guideline. To identify pertinent combination antiplatelet trials, a MEDLINE search of the literature from 1967-2007 was performed. Two trials were identified--the European-Australasian Stroke Prevention in Reversible Ischemia Trial (ESPRIT) and Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance (CHARISMA). The ESPRIT compared aspirin monotherapy with the combination of aspirin plus extended-release dipyridamole for prevention of secondary ischemic events in patients with a history of TIA or minor stroke. The CHARISMA trial compared aspirin plus clopidogrel with aspirin alone in a population at high risk for atherothrombotic events using the composite outcome of myocardial infarction, stroke, and death from cardiovascular causes. Data from ESPRIT add to evidence that the combination of aspirin plus extended-release dipyridamole is superior to aspirin alone. The findings of the CHARISMA trial reinforce recommendations from both AHA-ASA and ACCP that the combination of aspirin and clopidogrel be reserved for special populations requiring this antiplatelet combination (e.g., those who have had coronary artery stenting).

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In total, 426 patients (7.5%) had mRS score of 4 or 5 at baseline. The risk of an outcome event increased with mRS score. The relative risk associated with the combination of aspirin and dipyridamole compared to aspirin alone in patients with mRS score 0 to 5 was 0.79 (95% confidence interval, 0.69-0.91). The relative risk according to mRS subcategory score 0 to 4 at baseline varied between 0.73 and 0.96 for vascular events and between 0.62 and 0.96 for stroke. The number of patients with mRS score 5 was too small for reliable estimates, but the data suggest a beneficial effect. There was no evidence of interaction between treatment effect and mRS score at baseline.

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To obtain, in a larger patient population, a more precise estimate of the possible differences in efficacy and safety between the two treatments.

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In the last ten years the relationship between the presence of lupus type anticoagulants in the blood and some obstetrical complications, in particular spontaneous abortions, repeated fetal deaths in utero and intra-uterine growth retardation, has been well documented. A study of the literature shows that there were only twenty live-born children out of 280 pregnancies in 71 women who had the lupus type anticoagulant factor. The presence of the factor in high levels in a pregnant woman was seen to be of poor prognostic significance for the obstetric outcome. Biologically the lupus type circulating anticoagulant should be suspected when there is a five to six seconds prolongation of clotting time and it is highly suspicious if the time is prolonged by more than seven seconds. Its presence should equally be suspected by testing for the activated partial thromboplastin time (APTT). It has been shown that early treatment directed to lessen the activity of the lupus type factor (the use of corticoid-immunosuppressors) and forestalling as far as possible placental insufficiency (by giving heparin, aspirin and dipyridamole) could help, thus enabling some women to have live children who would not otherwise be able to do so.

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Initial reduced dose treatment with ASA+MR-DP may cause fewer headaches than regular dosing, and seems better tolerated by those susceptible to phosphodiesterase inhibitor-induced headache.

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Blood samples were drawn from healthy volunteers and platelet-rich plasma specimens were prepared at a concentration of 4 x 10(8)/mL. Abdominal aorta segments were obtained from New Zealand rabbits, they being deprived of endothelium by alpha-chymotrypsin. Red cells and platelets were separately or conjointly treated on reconstituted whole blood using ASA and DIP at therapeutic doses, separately or in association. Perfusion experiences were carried out in Baumgartner's annular chamber. Upon finishing the studies, the aorta segments were morphometrically evaluated by an optic analysis system attached to a computer with an automatic image recognition programme. The statistical analysis was performed with Student's t test, differences between groups of p < 0.05 being assigned significance.

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Secondary pharmacological prevention of ischemic stroke or transient ischemic attack (TIA) is often provided with acetylsalicylic acid (ASA), dipyridamole (DP) or a combination of the two. A problem with DP is the occurrence of headache, sometimes leading to medication cessation. By using a titration regime of DP the incidence of headache gets lower. However, there are no studies on interindividual differences in the incidence of headache with regard to age, gender, localization of stroke and the number of days since stroke onset.

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The postulated importance of platelets in the pathogenesis of thromboembolic events has stimulated interest in drugs that inhibit platelet function. Clinical trials of antiplatelet agents in the secondary buy aggrenox prevention of myocardial infarction and transient ischaemic attacks have so far been inconclusive. In children antiplatelet drugs area used on the evidence of nothing but anecdote. Optimum drug or combination of drugs and dosage are still controversial. Possible fruitful applications of platelet modifying agents such as aspirin and dipyridamole in paediatric nephrology and cardiology await further evaluation in prospective trials.

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Angiographic internal mammary artery graft patency at 1 year was assessed in 494 patients who received both internal mammary artery and vein grafts. These patients were a subgroup of a prospective, randomized vein graft patency study in 948 buy aggrenox patients assigned to treatment with aspirin, aspirin plus dipyridamole, or oral anticoagulant agents. The design was double-blind for both aspirin groups and open for oral anticoagulant treatment. Dipyridamole (5 mg/kg body weight per 24 h intravenously, followed by 200 mg twice daily) and oral anticoagulant agents (prothrombin time target range 2.8 to 4.8 international normalized ratio) were started before operation, and low dose aspirin (50 mg/day) after operation. Clinical outcome was assessed by the incidence of myocardial infarction, thrombosis, major bleeding or death.

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To compare, using the best available evidence, the benefits and harms of antenatal antithrombotic therapy to improve maternal or Augmentin 875 Mg Twice Daily infant health outcomes in women considered at risk of placental dysfunction, when compared with other treatments, placebo or no treatment.

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A total of 163 patients having 175 Lasix 40 Mg Image surgical carotid endarterectomies.

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1. Antiplatelet drugs have been demonstrated to reduce the incidence of recurrent events in patients with symptomatic vascular disease. However, there is no experimental data indicating the effects of these agents when given together on platelets and leukocytes. We investigated the ability of aspirin (an inhibitor of cyclo-oxygenase), dipyridamole (an inhibitor of phospodiesterases and adenosine uptake) and AR-C69931 (a direct acting P(2T) antagonist with effects similar to those of clopidogrel which can be used in vitro) when used alone or in combination to inhibit platelet and leukocyte function. 2. Measurements of platelet and leukocyte function were performed in blood taken from normal volunteers, and the inhibitory effects of aspirin (100 micromol l(-1)), dipyridamole (10 micromol l(-1)) and AR-C66931 (100 nmol l(-1)) were determined. Platelet aggregation was induced by stirring blood with and without adenosine diphosphate (ADP) or platelet activating factor (PAF) and measured by platelet counting. Platelet P-selectin expression, platelet-leukocyte conjugate formation, and leukocyte activation were determined by flow cytometry. 3. Dipyridamole, AR-C69931, dipyridamole and AR-C69931, dipyridamole and aspirin, AR-C69931 and aspirin, and all three agents together inhibited platelet aggregation induced by Amaryl 15 Mg stirring, ADP and PAF (P<0.01). However, it was only the combination of all three agents inhibited P-selectin expression (P<0.01). Similarly, it was the combination of all three antiplatelet agents that most consistently inhibited platelet-monocyte and platelet-neutrophil conjugate formation and monocyte and neutrophil activation. 4. Since both platelets and leukocytes are thought to contribute to arterial thrombosis and atherosclerosis, it is possible that combinations of different antiplatelet agents with different mechanisms of action may afford better protection than individual or pairs of agents used on their own.

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Headache episodes, being mostly mild and transient, rapidly declined from 67% of the volunteers on the first day of treatment to 3% on the final days of treatment (days 4-5 of the second period). During the first days the prevalence of the headaches peaked 2-3 h after the morning administration, which coincided with the peak Singulair Tablets of the plasma concentrations of dipyridamole. The occurrence of headaches was not related to interindividual differences of the pharmacokinetic parameters.

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HF patients show an increase in inflammatory indices Trileptal Reviews Bipolar independently of underlying A therapy.

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To describe the pharmacology, Anafranil Drug Classification pharmacokinetics, efficacy, and safety of a fixed-dose combination of aspirin and extended-release (ER) dipyridamole indicated for the secondary prevention of stroke.

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This study evaluated the effects of an antiplatelet drug for the patients after open heart surgery. Dipyridamole (D), aspirin (A), ticlopidine (T) and sarpogrelate hydrochloride (S) were chosen as an antiplatelet drug. The 6 groups were devided into as G 1 with warfarin (W) and Cialis 80 Mg Dosage D, as G 2 with W alone, as G 3 with A and D, as G 4 with A alone, as G 5 with A and T, and as G 6 with A and S. The indices of anticoagulation and antiplatelet were as follows: TT, APTT, PT, D. Dimer, fibrinogen, TXB2, 6 kPGF1 alpha, beta TG, vWF and platelet aggregation with Grading Curve methods. The results showed that D.Dimer was beyond the normal range in G 1 and G 2. Thromboxane B 2 was increased markedly in G 1 and G 2 and showed under the normal range in G 3 and G 6. In all groups, 6 kPGF1 alpha showed low levels than normal. Activation of platelet causes the increased beta TG which was not suppressed with the antiplatelet drugs administered. The platelet aggregation was not suppressed in G 1 and G 2. Mild to moderate suppression was seen in G 3 and G 4 with no difference between the two group. Moderate to marked suppression was demonstrated in G 5 and G 6. This study demonstrated that dipyridamole had no effects as antiplatelet function. Aspirin showed antiplatelet effects and the combination of aspirin with the another antiplatelet drugs demonstrated the additional effects.

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Seventy-five patients with coronary stent were treated with one of two different antithrombotic protocols. A group comprised of 34 patients (group A) received sodium heparin and acenocoumarin, plus acetylsalicylic acid (325 mg) and dipyridamole (225 mg). The remaining 41 patients (group B) were given antiplatelet agents, namely ticlopidine (125-250 mg) and Aggrenox Online Pharmacy aspirin (125 mg).

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Despite improvements in treatment, stroke still carries a high death toll and disability in Asia. Extended-release dipyridamole (ER-DP) plus acetylsalicylic acid (ASA) has consistently been shown to be superior over conventional platelet inhibition by ASA Triphala User Reviews . ER-DP plus ASA is well established in the secondary prevention of stroke in a lot of countries including the USA and Europe. DP has an established benefit in the treatment of heart disease in Japan; however, for the prevention of stroke, the fixed-dose combination of ER-DP plus ASA has only been investigated in a small number of patients in Japan.

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The prevalence of ex vivo high on-treatment platelet reactivity (HTPR) to commonly prescribed antiplatelet regimens after transient ischemic attack (TIA) or ischemic stroke is uncertain.

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The Second European Stroke Prevention Study (ESPS2) was a randomized, placebo-controlled trial that investigated the efficacy of low-dose acetylsalicylic acid (ASA) and modified-release dipyridamole (DP), alone or in combination, in the secondary prevention of ischemic stroke. The trial demonstrated that the combination was significantly more effective than either agent used alone. The aim of the present study was to evaluate the influence of age on the efficacy of ASA and DP, alone or in combination, in the secondary prevention of stroke in the ESPS2 population.

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The patency rate and reocclusion incidence were studied in 97 patients following vascular surgery necessitated by occlusion in the aortoiliac or femoropopliteal regions or both. Forty-nine patients were treated orally with a combination of acetylsalicylic acid and dipyridamole (1050 mg + 150 mg/day) and 48 patients with the haemorheologically active agent pentoxifylline (1200 mg/day, Trental 400 tds.) for uniform periods of 6 months. Reocclusion occurred in 10 patients receiving ASAD and in 5 patients receiving pentoxifylline. Adverse reactions were recorded in 12 patients with ASAD (discontinuation in 11) and in 3 patients with pentoxifylline (discontinuation in 2). Patency and tolerability rate were significantly superior in those patients treated with pentoxifylline, suggesting that the combination of haemorheological effects with antihaemostaseological and antithrombotic properties offered by pentoxifylline may be of benefit in the prevention of reocclusion after vascular surgery.

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Aspirin, alone or in combination with dipyridamole, is known to prevent occlusion of aortocoronary vein grafts. The benefit of dipyridamole in addition to aspirin remains controversial, and the efficacy and safety of oral anticoagulants for prevention of vein-graft occlusion have not been established. We assessed one-year angiographic vein-graft patency after aortocoronary-bypass surgery in 948 patients assigned to receive aspirin, aspirin plus dipyridamole, or oral anticoagulants in a prospective, randomised trial. The design was double-blind and placebo-controlled for the aspirin groups, but open for oral anticoagulant treatment. Dipyridamole (5 mg/kg per 24 h intravenously for 28 h, followed by 200 mg twice daily) and oral anticoagulants (desired prothrombin time range 2.8-4.8 international normalised ratio) were started before surgery, and aspirin (50 mg per day) was started after surgery. Clinical outcome was assessed by the incidence of myocardial infarction, thrombosis, major bleeding, or death. Occlusion rate of distal anastomoses was 11% in the aspirin plus dipyridamole group versus 15% in the aspirin group (relative risk 0.76, 95% CI 0.54-1.05) and 13% in the oral anticoagulants group. Clinical events occurred in 20.3% of patients receiving aspirin plus dipyridamole compared with 13.9% of the aspirin group (relative risk 1.46, 95% CI 1.02-2.08) and 16.9% of the oral anticoagulants group. Our data provide no convincing evidence that addition of dipyridamole to 50 mg aspirin per day improves aortocoronary vein-graft patency. Moreover, there is evidence that the combination increases the overall clinical-event rate. Compared with aspirin, oral anticoagulants provided no benefit.

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Within a cross-sectional study, nested in a cohort we identified 931 patients with a recent ischemic stroke or TIA who were discharged with OAC or with one of the antiplatelet medications aspirin, clopidogrel, or the combination of aspirin and extended-release dipyridamole. By means of multivariate logistic regression analysis, we determined the influence of several clinical variables on the decision between OAC and overall antiplatelet therapy as well as on the decision between different antiplatelet therapies.

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Previous studies have suggested that pre-stroke treatment with low-dose aspirin (A) could reduce the severity of acute ischaemic stroke, but less is known on the effect of pre-stroke treatment with a combination of aspirin and dipyridamole (A + D) and post-stroke effects of these drugs. The aim of the present study was to evaluate the effect of this drug combination on acute and long-term prognosis of ischaemic stroke.

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This article reviews randomized control trials (RCT's) published in 2006 of various medications evaluated for stroke patients. These trials were primarily efficacy studies. These included aggrenox (an antiplatelet agent), magnesium (to treat arterial spasm after an aneurysmal subarachnoid hemorrhage), NXY (a free radical trapping agent) and albumin which were both tested as a neuroprotectant, amphetamine (to aid motor recovery), fluoxetine (an anti-depressant and anxiolytic) and low molecular weight heparin (for prevention of deep vein thrombosis post-stroke).

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The previously published meta-analysis of individual patient data was updated with data from ESPRIT (n = 2,739); trials without data on the comparison of A+D versus ASA were excluded.

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This study aimed to determine whether the PPI omeprazole influences the pharmacokinetic (PK) and pharmacodynamic (PD) behavior of ASA+ER-DP.

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were 16 male volunteers, aged 22-39 years, mean age, 26.6 years.

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This review investigates whether the addition of dipyridamole to ASA further reduces the risk of stroke recurrence.

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Most heart failure patients are older adults. Heart failure is the number one hospital discharge diagnosis of older Americans. The renin-angiotensin system plays a major role in the pathophysiology of heart failure, and ACE inhibitors play a pivotal role in the management of heart failure. Large-scale double-blind randomized trials have demonstrated the survival benefits of using ACE inhibitors in patients with heart failure associated with left ventricular systolic dysfunction. In addition to inhibiting the conversion of angiotensin I to angiotensin II, ACE inhibitors also decrease the breakdown of bradykinin. Bradykinin, a potent vasodilator, acts by stimulating formation of vasodilatory prostaglandins such as prostacyclin, whereas aspirin or acetyl salicylic acid inhibits the enzyme cyclooxygenase, which in turn decreases the production of the prostaglandins. Coronary artery disease and hypertension are the two major underlying causes of heart failure. Most heart failure patients are also on aspirin. There is evidence that aspirin at a daily dose of 80 to 100 mg prevents the synthesis of thromboxane A2 by platelets while relatively sparing the synthesis of prostacyclin in the vascular endothelium. Aspirin at a daily dose of 325 mg has significant inhibitory effects on the vasodilatory prostacyclin synthesis. Studies have demonstrated that, in heart failure patients, low-dose aspirin has no adverse effect on hemodynamic, neurohumoral, or renal functions. Whether the prostacyclin-inhibiting effects of aspirin attenuate some of the beneficial effects of ACE inhibitors mediated by prostacyclin stimulation in heart failure patients is currently unknown.

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Twenty-seven patients with peripheral atherosclerotic disease were randomized into two therapy regimens consisting of indobufen (Indo) (400 mg/day) and dipyridamole (Dip) (225 mg/day) plus acetylsalicylic acid (ASA) (1 g/day), respectively. Maximal walking distance (MWD) and ankle-arm systolic pressure ratios were measured before and after three and six months of therapy; bleeding time, beta-thromboglobulin (beta-TG), platelet factor 4 (PF4) and serum thromboxane B2 (TXB2) were also assessed. The two treatment groups showed a significant and progressive increase in pain-free walking distance at both three and six months of therapy, but patients taking indobufen showed a greater improvement. On the contrary, the pressure doppler ratio at rest was statistically improved only in the ASA plus Dip group. Basal beta-TG and PF4 levels were normal and no changes occurred during the study in either group, while in all patients bleeding times showed a significant increase above basal values and serum TBX2 decreased.

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The middle cerebral artery of C57BL/6 mice was occluded for 2.5-10min, followed by reperfusion periods of 1-28days. Intravital microscopy was used to monitor thrombus development in cerebral microvessels induced by light/dye photoactivation. Thrombosis was quantified as the time to platelet aggregation on the vessel wall and the time for complete blood flow cessation. While brief periods of cerebral ischemia were not associated with neurological deficits or brain infarction (evaluated after 1day), it yielded a pronounced and prolonged (up to 28days) acceleration of thrombus formation, compared to control (sham) mice. This prothrombotic phenotype was not altered by pre- and/or post-treatment of mice with either aspirin (A), clopidogrel (C), dipyridamole (D), or atorvastatin (S), or with A+D+S.

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In this study, 591 patients with recent cerebral ischemia of arterial origin were randomly allocated to treatment with aspirin 30 to 325 mg/d or with the combination of aspirin and dipyridamole 400 mg/d in the European/Australian Stroke Prevention in Reversible Ischemia Trial. In an on-treatment analysis, the change in blood pressure measurements from baseline to values after at least 6 months of follow up was assessed with linear regression analysis.

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A double-blind crossover study comparing low-dose aspirin (ASA) and dipyridamole (DPM) (100 mg ASA + 75 mg DPM, t.d.s.), high-dose ASA and DPM (300 mg ASA + 75 mg DPM, t.d.s.), and placebo on platelet deposition and thrombus formation on hemodialysis membranes was undertaken in 17 long-term dialysis patients. The high-dose combination significantly reduced the fall in platelet count during dialysis and also significantly increased postdialysis heparin concentrations. Scanning electron microscopy of the Cuprophan membranes showed a reduction in platelet deposition and fibrin formation during both treatment schedules, but this was most marked with the high-dose combination. The results of this study indicate that there is a graded response to combined ASA-DPM treatment and that this can significantly reduce platelet consumption and contact activation of fibrin during hemodialysis with Cuprophan membranes.

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Completed randomized controlled trials of dual versus mono antiplatelet therapy in patients with acute (≤3 days) ischemic stroke/transient ischemic attack were identified using electronic bibliographic searches. The primary outcome was recurrent stroke (ischemic, hemorrhagic, unknown; fatal, nonfatal). Comparison of binary outcomes between treatment groups was analyzed with random effect models and described using risk ratios (95% CI).

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Ex vivo dipyridamole 'non-responsiveness' has not been extensively studied in ischaemic cerebrovascular disease. Platelet surface marker expression, leucocyte-platelet complex formation and inhibition of platelet function at high shear stress as detected by the PFA-100® Collagen-Adenosine-diphosphate (C-ADP) and Collagen-Epinephrine cartridges was assessed in 52 patients within 4 weeks of transient ischaemic attack (TIA) or ischaemic stroke on aspirin, and then 14 d (14 d) and >90 d (90 d) after adding dipyridamole. A novel definition of 'Dipyridamole non-responsiveness' was used. The median C-ADP closure time increased following addition of dipyridamole, remained elevated at 90 d (P ≤ 0·03), and was unaffected by aspirin dose. 59% at 14 d and 56% at 90 d were 'dipyridamole non-responders' on the PFA-100. The proportion of non-responders at 14 and 90 d was similar (P= 0·9). Compared with baseline (4·6%), median monocyte-platelet complexes increased at 14 d (5·0%, P= 0·03) and 90 d (4·9%, P= 0·04). Low C-ADP closure times were associated with increased monocyte-platelet complexes at 14 d (r= -0·32, P= 0·02) and 90 d (r= -0·33, P = 0·02). Monocyte-platelet complexes increased in the subgroup of dipyridamole non-responders on the PFA-100 (P≤ 0·045), but not in responders (P ≥ 0·5), at 14 and 90 d versus baseline. Additional inhibition of platelet function has been detected with the PFA-100 when dipyridamole is added to aspirin. Elevated monocyte-platelet complexes may contribute to ex vivo dipyridamole non-responsiveness.

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This novel study in European TIA/ischaemic stroke patients, who were provided with a goal-directed secondary prevention plan, showed high rates of medication-continuation and self-reported adherence with prescribed treatment, associated with a low incidence of recurrent vascular events during a median follow up of 1.7 years.

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287 studies involving 135 000 patients in comparisons of antiplatelet therapy versus control and 77 000 in comparisons of different antiplatelet regimens.

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To measure the rate, extent, and time course of arterial mural thrombus formation in vivo and to assess the effects of antiplatelet therapy in that setting, we have studied autologous 111In-platelet deposition induced by experimental iliac artery aneurysms in baboons. Scintillation camera imaging analyses were performed at 1, 24, 48, and 72 hours after implantation of the device. Correction for tissue attenuation was determined by using a small, comparably located 111In source implanted at the time of surgery. In five animals, 111In-platelet activity accumulated progressively after device implantation, reaching a maximum after the third day. Repeat image analysis carried out 2 weeks after the surgical procedure also showed progressive accumulation of 111In-platelets over 3 days but at markedly reduced amounts as compared with the initial study. In five additional animals, treatment with a combination of aspirin and dipyridamole begun 1 hour after surgical implantation reduced 111In-platelet deposition to negligible levels by the third day. Although platelet survival time was shortened and platelet turnover was reciprocally increased in all operated animals, platelet survival and turnover were not affected by antiplatelet therapy. We conclude that, in contrast to platelet survival and turnover measurements, 111In-platelet imaging is a reliable and sensitive method for localizing and quantifying focal arterial thrombi and for assessing the effects of antiplatelet therapy.

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Early patency and late patency have consistently been better with single internal mammary artery grafts than with saphenous vein conduits. To determine the efficacy of these two types of grafts in sequential anastomoses, we performed sequential anastomoses of the left internal mammary artery to the left anterior descending and diagonal coronary arteries in 40 patients and compared the results with those in 58 patients who received sequential saphenous vein grafts. Treatment with dipyridamole (starting 48 hours before operation) and aspirin (added 7 hours after operation) was given to the 40 patients with internal mammary artery grafts and to 32 of the 58 patients in the saphenous vein group. After the bypass procedure, mean blood flows were as follows: 68 ml/min in patients with internal mammary artery grafts, 73 ml/min in patients who received saphenous vein grafts and a placebo, and 99 ml/min in those who received saphenous vein grafts, aspirin, and dipyridamole. Early patency of sequential internal mammary artery grafts to the diagonal and left anterior descending coronary arteries was comparable to that of sequential saphenous vein grafts. Because a substantial late reduction in patency has been noted in sequential saphenous vein grafts, sequential internal mammary artery grafts may be the preferred conduit for coronary artery revascularization.

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Between July, 2007, and February, 2009, 543 patients were treated: 283 received early aspirin plus extended-release dipyridamole and 260 received aspirin plus extended-release dipyridamole after 7 days on aspirin. At day 90, 154 (56%) patients in the aspirin plus early extended-release dipyridamole group and 133 (52%) in the aspirin plus later extended-release dipyridamole group had no or mild disability (tele-mRS 0 or 1; difference 4.1%, 95% CI -4.5 to 12.6, p=0.45). 28 patients in the early initiation group and 38 in the late initiation group reached the composite endpoint (hazard ratio 0.73, 95% CI 0.44-1.19 p=0.20).

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More and more patients receiving anticoagulant therapy or other drugs modifying the coagulation mechanism require dental or oral surgical treatment nowadays. The reason is that in Hungary the various forms of thrombosis are on the first place of morbidity and mortality lists. More than 50 per cent of all the mortality is due to thromboembolism. In view of all this it is not surprising that in the past years the indications, application and dosage of anticoagulant and platelet aggregation inhibitor drugs have changed. Decades-old principles have been modified. It is important for dentists and oral surgeons to know the risk of interventions in patients receiving anticoagulant or platelet inhibitory therapy.

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To obtain, in a larger patient population, a more precise estimate of the possible differences in efficacy and safety between the two treatments.