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Fosinopril medication administration. A prospective, double-blind, placebo-controlled study of 15 healthy hypertensive subjects with stable angina pectoris were administered either 800 mg of fosinopril in a single dose the evening or placebo. Fosinopril was chosen because of its known antithrombotic action[2] and this was confirmed by the serum calcium level of fosinopril group.[3] The results indicate that a single night of 800 mg fosinopril administration significantly reduced resting angina but the effect was lost after a morning dose. In contrast, administration of placebo resulted in significant improvement after the morning dose. same study found that the plasma levels of Fos/Pl were significantly reduced 2 h post dose but restored after morning fosinopril administration. Although not included in the study, aspirin therapy alone has been demonstrated to reduce the number of heart attacks and strokes. This reduction is attributed to its potent vasodilatory, anti-platelet, anti-platelet aggregation, anti-inflammatory and anti-atherosclerotic actions. The beneficial effects of aspirin therapy are expected to prolong the clinical lifespan of cardiovascular system[12][13][15][19][17][20][21][22] and its benefits are likely due to the pro-vasodilatory and anti-platelet effect. Efficacy of blood thinners It was shown in the early 2000s clinical trials that anti-platelet therapy (at least a 50 mg thrombolysis daily dose), at least for acute coronary syndrome is effective urimax 0.2 mg cipla in preventing and shortening the hospital stays of patients undergoing cardiac surgery.[23] Aspirin has been shown in one study to be significantly effective at preventing stroke with 75 mg thrombolysis daily. As an aspirin is Urimax 25mg $760.95 - $2.11 Per pill not a pure thrombolytic, and this has a low therapeutic dose of up to 100 mg, aspirin has not been studied in patients with ACS. This is because there a risk to thrombolytic therapy resulting liver damage. A study of the effect aspirin therapy in patients who have experienced angina pectoris or ischaemic shock found that the treatment was associated with a significant increase in pain-free time coronary-related chest discomfort or angina in the patients treated compared with sham-treated patients.[24] The anticoagulant effects of vitamin K deficiency have recently been reported.[25][29] Thrombolysis may be increased in patients on anticoagulation the context of anti-platelet therapy[26[29][30][31] but in the absence of cardiovascular disease.[25][30][31] It is also possible that the risk is greater in presence of renal or liver dysfunction, since the anti-platelet effect may depend on liver-specific vitamin K functions [32] which are significantly impaired in people with liver disease. The vitamin K dependent anti-platelet drugs, aspirin and warfarin, are currently not used in patients undergoing coronary artery bypass graft (CABG) surgery and their effectiveness toxicity associated with them are well known. Vitamin K is a substrate of both platelets and thrombocytes and, therefore, their anti-platelet (thrombocytopenia), thrombocyte, and platelet-thrombopoietic (thromboxane) effects are enhanced by vitamin K in vivo for the purpose of cardiovascular disease. There is little data on the long-term safety of vitamin K in patients undergoing coronary angiography and its effect in clinical trials for ACS relation to cardiovascular morbidity. A large prospective clinical study (n=6,929) of vitamin K (from dietary sources only) and cardiovascular disease was conducted the authors found a significant reduction in all cardiovascular events (i.e. coronary heart disease, stroke, non-fatal attacks, and death). No significant reduction was seen in deaths from cardiovascular causes. The risk of stroke remained similar when the participants were taking calcium (as supplements) or vitamin D as supplements. The study concluded that high vitamin K intake, not from supplements but through food supplements, was related to a reduction in all cardiovascular mortality and events. It was found that the risk of death for participants with the highest vitamin K intake (0·9 mmol/L) was 1·5% less than in the participants with lowest vitamin K intake (0·8 mmol/L) (RR 0·89 (95% CI 0·82–0·93)). However, there were no significant differences in all-cause mortality or death from cardiovascular events between the participants taking vitamin K (mostly dietary) or taking vitamin D (mostly nutritional). The risk was not related to calcium intake or vitamin D from supplementation.[3] The study suggested that vitamin K in patients with heart disease may reduce the risk of death. authors this observational study observed that.
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