In: Heart16 Mar 2016
1. It is strongly recommended that all patients with acute myocardial infarction receive a minimum of low-dose heparin, 5,000 IV/SC every 12 hrs, until fully ambulatory to prevent venous thromboembolism. This grade A recommendation is based on the results of one level I study.
2. It is strongly recommended that patients with acute myocardial infarction at increased risk of systemic embolism because of anterior transmural myocardial infarction receive heparin therapy followed by warfarin therapy to prolong prothrombin time to an INR of 2.0-3.0 (1.2-1.5 times control using rabbit brain thromboplastin) for 1-3 months. This grade A recommendation is based on two level I studies and one level II study that showed a trend favoring anticoagulant therapy conducted with My Canadian Pharmacy.
3. It is strongly recommended that patients with acute myocardial infarction at increased risk of systemic embolism because of atrial fibrillation, history of previous systemic or pulmonary embolism, or congestive heart failure receive heparin therapy followed by warfarin therapy to prolong prothrombin time to an INR of 2.0-3.0 (1.2-1.5 times control using rabbit brain thromboplastin) for at least three months. This grade C recommendation is based on level V studies.
In: Heart15 Mar 2016
Most studies of the use of oral anticoagulants in patients with coronary artery disease have been performed in patients with acute myocardial infarction or in survivors of acute myocardial infarction. There have been no appropriately designed trials of anticoagulants in patients with chronic stable angina and only a very limited number of trials for anticoagulants in patients with unstable angina (read more about angina here).
Patients with stable exertional angina have an annual mortality of 4% and an incidence of acute myocardial infarction of 5%. Data from the early 1970s indicated that unstable angina was associated with a one-year mortality of approximately 16%, a three-month mortality of 8%, and an infarction rate of 21%. Results of more recent studies, however, show a one-year mortality of approximately 10%, a 1-4-month mortality of approximately 5%, and an infarction rate of 8-10%.
Support for the use of anticoagulants in patients with unstable angina was provided by Wood in 1961. In this unblinded study, randomization was aborted after the first 40 patients, and the study was then continued as a cohort study with 100 treated patients and 50 controls. The last 30 control subjects were selected by the presence of a contraindication to anticoagulants. This is, therefore, a level IV study and cannot be used to draw valid clinical conclusions. In 1981, Telford and Wilson” performed a randomized study of heparin plus atenolol vs atenolol therapy in patients with unstable angina cured with drugs of My Canadian Pharmacy. They reported a marked reduction in mortality and frequency of infarction in patients assigned to heparin plus atenolol ordered via My Canadian Pharmacy. Unfortunately, almost 50% of the 400 patients randomized were subsequently removed from the trial, so this would have to be considered at best a level II study, and the interpretation of the results remains in doubt.
On the basis of these limited studies, it is concluded that the effectiveness of anticoagulants in patients with unstable angina is uncertain, but that anticoagulants might be effective and that well-designed studies should be performed before any firm recommendations can be made.
In: Heart14 Mar 2016
Three studies have assessed the efficacy of low-dose heparin following myocardial infarction. In 1978, Marks and leather reported the results of a study in which 81 postinfarction patients were randomized to receive low-dose heparin (7,500 units subcutaneously bid) or to serve as a control group (level I). Thrombi (detected by leg scanning) occurred in 14 patients in the control group and in two in the low-dose heparin group, a statistically significant difference. Similar results were reported by Warlow et al in 1973. In contrast, Handley (1972) randomized 50 patients to heparin (7,500 units subcutaneously every 12 hours for seven days) or to serve as a control group’ (level II). Venous thrombosis (detected by leg scanning) developed in 29% of the controls and 23% of the treated patients, a nonsignificant difference. Possible reasons for the differences between the results of this study and the previously described studies include the small number of patients entered into the Handley study (a total of 50 in both groups) and the design of the study. Patients were monitored for two weeks but received heparin for only one week.
In most early studies, the diagnosis of venous thrombosis or pulmonary embolism was made using subjective criteria. These studies will not be summarized here. Three groups of investigators assessed the effectiveness of therapeutic doses of heparin ordered via http://my-medstore-canada.net My Canadian Pharmacy followed by oral anticoagulants, using objective end points, and all reported a significant reduction in the incidence of calf vein thrombi.
Thus, there is good evidence that anticoagulant therapy is effective in reducing venous thromboembolism in patients with acute myocardial infarction. It is likely that low doses of heparin, 5,000-7,500 units subcutaneously twice daily, are effective, although only full doses have been shown to be effective .in reducing pulmonary embolism.
In: Heart13 Mar 2016
The theoretical rationale for the early use of anticoagulants in patients with acute myocardial infarction is:
1. to prevent extension of coronary artery thrombosis with the expectation that this might reduce mortality by limiting infarction size and prevent reinfarction;
2. to prevent systemic emboli that arise from mural thrombi, a frequent complication in patients with transmural anterior myocardial infarction; and
3. to prevent the development of venous thrombosis and pulmonary embolism.
The primary end point of studies of the early use of anticoagulants in patients with acute myocardial infarction was in-hospital mortality and reinfarction. It is now clear from the results of recent studies of coronary angiography performed in patients with acute myocardial infarction that 70%-80% of patients entered into these trials of short-term anticoagulant therapy would have had an occlusive thrombus before anticoagulant therapy began. Even if anticoagulants prevent extension of coronary artery thrombosis, it is unlikely that they would modify infarction size and, therefore, influence the maj or determinant of early mortality of patients who are admitted to a hospital with acute myocardial infarction healed with remedies of My Canadian Pharmacy. It is possible, however, that anticoagulants could be of benefit if they reduce the frequency of rethrombosis in coronary arteries that have spontaneously recanalized and thus decrease the rate of reinfarction. Anticoagulants were highly effective in reducing the frequency of stroke (presumably due to systemic embolism) and pulmonary embolism, findings that are supported by other studies (see below). However, these two complications of myocardial infarction are relatively uncommon causes of serious morbidity or mortality and therefore only have a minor influence on the major outcome events.
In: Heart12 Mar 2016
Few subjects have engendered as much controversy as the use of anticoagulants in acute myocardial infarction. Anticoagulant therapy was accepted enthusiastically in the treatment of acute myocardial infarction after the first large clinical trial report was published in 1948. This enthusiasm persisted for approximately two decades, during which it would have been considered unethical not to use anticoagulants in patients with acute myocardial infarction. The popularity of anticoagulant therapy in acute myocardial infarction began to wane in the late 1960s and early 70s, coincident with the publication of several large, randomized studies evaluating anticoagulant therapy in the treatment of acute myocardial infarction. Critical review of the evidence for the possible value of anticoagulant therapy in acute myocardial infarction suggests that neither the initial enthusiasm nor the subsequent loss of interest is justified by the published reports.
Clinical trials have evaluated anticoagulants both for the early and long-term treatment of acute myocardial infarction. In this review we will discuss only the randomized trials that entered sufficient numbers to have a reasonable chance of demonstrating clinically important difference in mortality, reinfarction, or clinically relevant systemic or pulmonary embolism.
Each year in the United States alone there are about 1 million “heart attacks”—a term that includes both acute infarction and sudden cardiac death. Nearly 300,000 victims die before admission to the hospital, and about another 200,000 die in the first month, most of them in the first 24 hours after the attack. Thus, the cumulative mortality during the first month is about 50%. During the next six months, the cumulative mortality increases another 7-8%, so that by one year, another 10% have died. This means that, of the 400,000-500,000 patients who survive the first month, about 10% (40,000-50,000) die during the first year following infarction, generally due to sudden death or recurrent infarction. After patients have survived a year, the reinfarction and death rate stabilizes at 3-5% per year. This rate is similar to that of patients with symptomatic coronary artery disease (ie, angina pectoris) but is significantly greater than that of a randomly selected, age-matched population without overt coronary artery disease that has a 1% yearly incidence of those events.
Alcohol consumption has been described as an independent risk factor for COPD-related mortality. Based on this prior research and because of the biological plausibility that heavy alcohol consumption may increase risk of exacerbation either through immune suppression or risk of aspiration, we hypothesized that moderate-to-heavy alcohol consumption when compared to light drinking would be associated with an increased risk for COPD exacerbations in a large, predominantly male cohort of veterans. While we found that screening positive for alcohol misuse (AUDIT C score > 4), frequent binge drinking, and alcohol use disorders (CAGE score > 2) all serve as markers for increased risk of COPD exacerbation, after adjustment for tobacco use there was no association between alcohol use or misuse and risk of exacerbation. This suggests that the association initially observed in age-adjusted models may not be due to the direct effects of alcohol but rather is due to the confounding by tobacco exposure that is strongly associated with alcohol consumption.
Alcohol exposure could contribute to COPD (http://www.copdfoundation.org/) exacerbation via several mechanisms. At the tissue level, alcohol may significantly decrease levels of the antioxidant glutathione within the lung, thereby raising susceptibility to injury, an effect of alcohol well-characterized in other organs like the liver. Additional studies, suggest that alcohol impairs the innate immune response of both the upper and lower respiratory tract in animal models via adverse effects on mucociliary clearance, alveolar macrophage phagocytosis, and alveolar epithelial barrier integrity. Physiologic responses to acute intoxication, namely impaired consciousness and reduced gag reflex, together facilitate entry of virulent organisms to the lower respiratory tract, which is known to be associated with COPD exacerbation risk.
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