Effect of non-surgical periodontal therapy on glycemic control in patients with type 2 diabetes mellitus.
These studies describe experimental conditions where aspirin is less effective than other antiplatelet and anticoagulant drugs in inhibiting acute arterial thrombosis. External electrolytic injury of the rat carotid artery was used to induce occlusive thrombi in 97% of vehicle-treated rats. Thrombi were revealed by light and electron microscopy to be comprised primarily of platelets enmeshed in a fibrin network. The thrombin inhibitor D-phenylalanyl-L-prolyl-L-arginyl chloromethylketone (PPACK; 6 mg/kg, i.v.) decreased thrombus weight by 90%. Aspirin alone (1, 10 and 30 mg/kg, i.v.), dipyridamole alone (5 mg/kg i.v.) and aspirin (1 and 10 mg/kg, i.v.) in combination with dipyridamole (5 mg/kg, i.v.) did not inhibit thrombosis. The platelet-activating factor (PAF) antagonist, WEB 2086, (1 mg/kg i.v.) was also ineffective. Other drugs had intermediate activity. Thrombi were decreased 56% by the thromboxane receptor antagonist, BMS 180,291, either alone (5.8 mg/kg i.v.) or in combination with aspirin (10 mg/kg, i.v.). Heparin (900 U/kg, i.v.), warfarin (0.25 mg/kg, p.o. once daily for 3 days) and ticlopidine (200 mg/kg, p.o. once daily for 3 days) reduced thrombus weight by 63, 73 and 43% respectively. Reductions in thrombus weight were always associated with improvements in either average blood flow or vessel patency.
In diabetic patients platelet abnormalities and hemostatic dysfunction have been reported and may play a role on the development of retinopathy. It has been shown that aspirin and dipyridamole modify platelet functions in vitro and in vivo. The aim of this multicenter controlled clinical trial was to investigate the effect of aspirin and aspirin + dipyridamole on the evolution of background retinopathy. In this paper are described the main clinical characteristics of the 450 patients included in the study, the protocol and the major end-points. Patient recruitment started in 1977 and was completed in 1981. Compliance to the protocol is satisfactory, side effects have been minimal and the number of patients lost to follow up is small.
This study clearly demonstrates that combination therapy with DP and ASA is superior to either agent used alone in the secondary prevention of ischemic stroke, irrespective of the age of the patient.
The study cohort comprised 283 patients with [corrected] IE. Twenty-eight patients (24.1%) who received prior continuous antiplatelet therapy developed a symptomatic embolic event compared with 66 (39.5%) who did not receive such treatment. After adjusting for propensity to treat, the effect of antiplatelet therapy on embolic risk was not statistically significant (odds ratio, 0.71; 95% confidence interval [CI], 0.37-1.36; P=.30). Only 14 patients (18.2%) who received prior continuous statin therapy developed a symptomatic embolic event compared with 80 (39.4%) of the 203 patients who did not. After adjusting for propensity to treat with statin therapy, the benefit attributable to statins was significant (odds ratio, 0.30; 95% CI, 0.14-0.62; P=.001). The 6-month mortality rate of the entire cohort was 28% (95% CI, 23%-34%). No significant difference was found in the propensity-adjusted rate of 6-month mortality between patients who had and had not undergone prior antiplatelet therapy (P=.91) or those who had and had not undergone prior statin therapy (P=.87).
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.
Platelets play a much more important role in myocardial ischemia than in cerebral ischemia, because atherothrombosis - the underlying cause of the vast majority of myocardial infarcts - is responsible for only 25-30% of cerebral infarcts. Aspirin is the only effective antiplatelet drug for primary prevention of ischemic events, especially those affecting the heart. For secondary prevention of cerebral infarction, clopidogrel and the combination of aspirin with extended-release dipyridamole are both marginally better than aspirin alone, but aspirin remains the gold standard worldwide because of its remarkable cost/benefit/tolerability ratio. The clopidogrel-aspirin combination is to be avoided because of the risk of hemorrhage, particularly in the brain and gastrointestinal tract. Revascularization strategies and the choice of antiplatelet drugs for the acute phase of myocardial and cerebral ischemia are very different, consisting of endovascular treatment and aggressive platelet inhibition for coronary infarcts, versus intravenous thrombolysis and / or aspirin for cerebral infarcts. None of the new antiplatelet drugs used in acute coronary syndromes has so far been studied in acute cerebral ischemia.