UMLS:C0020538 - FACTA Search

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2 aspects of oral contraception (OC) were considered--the risk of arteriosclerotic cardiopathy and the interaction with other drugs. Opinions still diverge on the role of contraceptives in the etiology of myocardial infarction. In contrast to the British studies, the World Health Organization's (WHO) data and US statistics on death from cardiovascular diseases fail to show higher prevalence for OC users. Most likely the data of different countries cannot be compared due to the differing incidence of other cardiovascular morbidity and mortality risk factors such as hypertension, obesity, smoking, physical activity, and genetic predisposition. A recent study examined the prevalence of myocardial infarction in relation to the use of estroprogestinic contraceptives. Rosenberg et al. found that 156 out of 121,944 women (1.2%) had been hospitalized following myocardial infarction, and 23 of them used OCs. The authors concluded that OCs increased the risk of infarction by 1.8. Shapiro et al. studied 369 patients who suffered myocardial infarction and an adequate control group. The overall relative frequency was 4 times in OC users but it was 4.5 times in smokers and 3.9 times in nonsmokers. The smokers who did not use OCs showed a relative frequency of 7.8 times. The risk of arteriosclerotic cardiopathy depends upon the dose of both the estrogenic and progestinic components. When prescribing drugs, physicians should know whether their patients use OCs, since these hormonal steroids may interfere with the expected therapeutic effect. A phenomenon of enzymatic competition may occur which slows down the elimination of the drug, thus exposing the patient to a "relative overdose" despite the assumption of therapeutic doses. It has always been reported that the simultaneous administration of triacetiloleandomycin and OCs causes jaundice. Thus far 15 cases have been reported. OCs tend to enhance the effect of corticosteroids. Vitamin K antagonists, oral anticoagulants, are less effective in OC users. A research study conducted by Patwardhan et al. showed that caffeine is eliminated more slowly in OC users because of a mechanism of enzymatic competition with contraceptive steroids at the level of the hepatic oxygenase system linked to cytochrome P-450. ready been reported that the simultaneous administration of triacetiloleandomycin and OCs causes jaundice. Thus far 15 cases have been reported. OCs tend to enhance the effect of corticosteroids. Vitamin K antagonists, oral anticoagulants, are less effective in OC users. A research study conducted by Patwardhan et al. showed that caffeine is eliminated more slowly in OC users because of a mechanism of enzymatic competition with contraceptive steroids at the level of the hepatic oxygenase system linked to cytochrome P-450.
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PMID:Two problems in oral contraception: arteriosclerotic cardiopathy and drug interactions. 716 61

Anticoagulation with antivitamin K (AVK) is very effective for primary and secondary prevention of thromboembolic events. However, questions persist about the risks and management of over-anticoagulation. For reversal of excessive anticoagulation by warfarin, AVK withdrawal, oral or parenteral vitamin K administration, prothrombin complex or fresh frozen plasma may be used, depending on the excess of anticoagulation, the existence and site of active bleeding, patient characteristics and the indication for AVK. In over-anticoagulated patients, vitamin K aims at rapid lowering of the international normalized ratio (INR) into a safe range to reduce the risk of major bleeding and therefore improving patient outcome without exposing the patient to the risk of thromboembolism due to overcorrection, resistance to AVK, or an allergic reaction to the medication. The risk of bleeding increases dramatically when the INR exceeds 4.0-6.0, although the absolute risk of bleeding remains fairly low, <5.5 per 1000 per day. Patient characteristics, including advanced age, treated hypertension, history of stroke, and concomitant use of various drugs, affect the risk of bleeding. The absolute risk of thromboembolism associated with overcorrection appears to be in the same range as the risk of bleeding due to over-anticoagulation. The use of vitamin K in patients with warfarin over-anticoagulation lowers excessively elevated INR faster than withholding warfarin alone; however, it has not been clearly demonstrated that vitamin K treatment does, in fact, lower the risk of major hemorrhage. As vitamin K administration via the intravenous route may be complicated by anaphylactoid reactions, and via the subcutaneous route by cutaneous reactions, oral administration is preferred. A dose of 1-2.5mg of oral phytomenadione (vitamin K(1)), reduces the range of INR from 5.0-9.0 to 2.0-5.0 within 24-48 hours, and for an INR >10.0, a dose of 5mg may be more appropriate. Overcorrection of the INR or resistance to warfarin is unlikely if the above doses of vitamin K are used. Vitamin K is less effective for over-anticoagulation after treatment with acenocoumarol or phenprocoumon than after treatment with warfarin.
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PMID:The use of vitamin K in patients on anticoagulant therapy: a practical guide. 1496 65

Atrial fibrillation (AF) requires anticoagulation for prevention of arterial embolism, especially in the presence of defined risk factors summarized in the CHADS (2) score (congestive heart disease, hypertension, age >75 years, diabetes, history of ischemic stroke or transient cerebral ischemia). Vitamin K antagonists as drugs of choice have several limitations. International normalized ratio (INR) adjustment to 2.0 to 3.0 may be difficult to maintain, and doses vary widely between patients. Inherited variations of the vitamin K epoxide reductase C1 enzyme and of the cytochrome P450 2C9 system influence the dosage as well as exogenous factors such as food and drug intake or intercurrent diseases. Increasing age and risk of falling are the main factors behind the underuse of anticoagulation in AF. Anticoagulants with a lack of all or most of these characteristics and without need of regular monitoring for dose adjustment may improve the adherence to the indication for anticoagulation. Indirect systemic and oral direct factor Xa and oral direct thrombin inhibitors are currently being developed for the prevention of embolism in patients with AF.
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PMID:New anticoagulants in atrial fibrillation. 1978 62

Atrial fibrillation (AF) is the most commonly encountered arrhythmia in clinical practice and is associated with substantial morbidity and mortality. Its prevalence increases with age, affecting about 1% of patients aged <60 years and almost 10% of patients >80 years. AF is associated with a fivefold increasing risk of embolism or stroke with absolute risk ranging from less than 1% to 20% per year, depending on patient age and the presence of clinical risk factors including congestive heart failure, systemic hypertension, diabetes mellitus and prior history of cardioembolic events. Vitamin K antagonists (VKAs) and acetyl salicylic acid are currently the only licensed antithrombotic therapies for stroke prevention in patients with AF. Anticoagulants are very effective for stroke prevention in patients with AF, overall a 64% relative risk reduction. Nonetheless, approximately 50% of patients with AF who have an indication for VKA receive anticoagulant therapy, of which only 50% maintain adequate therapeutic ranges. Furthermore, 50% will discontinue VKAs within 3 to 5 years regardless of appropriate international normalized ratio control. Underutilization of VKAs is related, in part, to their numerous limitations and difficulty in maintaining adequate therapeutic control, prompting the development of new antithrombotic strategies that are equally effective and safer, and easier to manage than VKAs. This review focuses on new antithrombotic therapies for stroke prevention in patients with AF.
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PMID:New pharmacotherapy for stroke prevention in atrial fibrillation: update 2010. 2012 14

The growing incidence of Atrial Fibrillation (AF) induces an increasing morbimortality, particularly thromboembolism (TE). Vitamin K Antagonists (VKA) reduce of 62 % the stroke rate in case of AF and are more efficient with INR between 2 and 3 than aspirin or the association aspirin-VKA with INR<2. The only place for clopidogrel could be its association with aspirin if VKA are contra-indicated. But VKA increase of 1.4 to 3.36 %/year the major bleedings, whereas the risk with aspirin is less important. The TE risk factors validated in case of AF are: previous TE, heart failure, hypertension, age over 75, diabetes mellitus, rhumatismal valvulopathy or mechanical valvular prosthesis. Ischemic cardiomyopathy, age between 65 and 75 and the female gender represent intermediate risks. Guidelines suggest to anticoagulate patients with previous TE or CHADS(2) score > or = 2 and to discuss VKA for a score equal to 1. Lone AF must not be anticoagulated but the continuous follow-up of occurring risk factors remains essential. Paroxysmal and persistant/permanent AF present the same TE risk. VKA are preferable if patients are older than 75 unless a major bleeding risk is present. If AF occurs on an ischemic cardiomyopathy, VKA are often essential and reduce the total mortality even if they increase the bleeding risk due to the association with antiplatelet therapy. However no precise guidelines are available on this topic. After a successful AF ablation, guidelines recommend not to modify the antithrombotic strategy. The bleeding risk score called "HEMORR2HAGE" allows to establish an individual balance of risk/benefit of VKA. The utility of transoesophagial echocardiography could be recognized in case of intermediate TE risk to suggest VKA if thrombotic criteria are identified. At least, new antithrombotic therapy will probably modify our perception of the risk/benefit ratio.
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PMID:[Atrial fibrillation: who should be anticoagulated?]. 2047 91

Atrial fibrillation is the most frequent cardiac arrhythmia and its prevalence increases with age. It is essential to prevent the thromboembolic events, stroke in particular, considered as its most serious complication. Vitamin K antagonists are currently the most effective drugs to prevent them. However, despite their proven efficacy, they carry a risk of bleeding complications. Consequently, it is essential to balance individual thromboembolic risk with the hemorrhagic risk, taking into consideration age, cardiac diseases, hypertension, diabetes, history of cerebral vascular accident, history of hemorrhagic disease and also patient's compliance. The CHADS2 score is a stratification model for stroke risk in patients with non-valvular atrial fibrillation that is the easiest score to use in clinical practice and the most used one.
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PMID:[Which patients with atrial fibrillation need anticoagulation?]. 2096 18

The stroke rate in atrial fibrillation is 4.5% per year, with death or permanent disability in over half. The risk of stroke varies from under 1% to over 20% per year, related to the risk factors of congestive heart failure, hypertension, age, diabetes, and prior stroke or transient ischemic attack (TIA). Major bleeding with vitamin K antagonists varies from about 1% to over 12% per year and is related to a number of risk factors. The CHADS(2) index and the HAS-BLED score are useful schemata for the prediction of stroke and bleeding risks. Vitamin K antagonists reduce the risk of stroke by 64%, aspirin reduces it by 19%, and vitamin K antagonists reduce the risk of stroke by 39% when directly compared with aspirin. Dabigatran is superior to warfarin for stroke prevention and causes no increase in major bleeding. We recommend that all patients with atrial fibrillation or atrial flutter, whether paroxysmal, persistent, or permanent, should be stratified for the risk of stroke and for the risk of bleeding and that most should receive antithrombotic therapy. We make detailed recommendations as to the preferred agents in various types of patients and for the management of antithrombotic therapies in the common clinical settings of cardioversion, concomitant coronary artery disease, surgical or diagnostic procedures with a risk of major bleeding, and the occurrence of stroke or major bleeding. Alternatives to antithrombotic therapies are briefly discussed.
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PMID:Canadian Cardiovascular Society atrial fibrillation guidelines 2010: prevention of stroke and systemic thromboembolism in atrial fibrillation and flutter. 2132 65

Atrial fibrillation (AF) is the most common form of cardiac arrhythmia, and its incidence is rising as the population ages. AF is therefore a growing source of cardiovascular morbidity and mortality due to thromboembolic complications and heart failure. The risk of embolic stroke is multiplied by about 5.6-fold in non rheumatic AF and by 17.6-fold in rheumatic AF Strokes due to AF are often fatal or disabling. Paroxysmal and permanent fibrillation are associated with a similar thromboembolic risk. Embolic complications arise from the left atrium or the left atrial appendage. Known risk factors in patients with AF include a history of thromboembolism or stroke, age > 75 years, heart failure, rheumatic valve disease, mechanical prosthetic valves, arterial hypertension and diabetes mellitus. Ischemic cardiomyopathy, female gender and atherosclerotic vascular disease are associated with an intermediate risk of thromboembolism. Vitamin K antagonist therapy targeting an INR of 2 to 3 reduces the risk of stroke by two-thirds in patients with AF, and causes bleeding in 1.4 % to 3.6 % of patients. The bleeding risk can be evaluated with the CHADS2 scale. Aspirin (75/300 mg per day) reduces the risk of cerebral thromboembolism by about 21%. Current guidelines recommend vitamin K antagonist or dabigatran anticoagulation for patients with a CHADS2 score of 2. Patients with a score of 0 should receive either aspirin or no drug therapy, while patients with a score of 1 may receive either a vitamin K antagonist or aspirin. After successful AF ablation, the existing antithrombotic strategy should be pursued New strategies based on antithrombin or anti-Xa medications will probably have a better risk-benefit ratio.
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PMID:[Thrombotic risk factors and antithrombotic treatment in atrial fibrillation]. 2237 63

Rivaroxaban has been found to be noninferior to warfarin for preventing stroke or systemic embolism in patients with high-risk atrial fibrillation (AF) and is associated with a lower rate of intracranial hemorrhage. To assess the cost-effectiveness of rivaroxaban compared to adjusted-dose warfarin for the prevention of stroke in patients with AF, we built a Markov model using a United States payer/Medicare perspective and a lifetime time horizon. The base-case analysis assumed a cohort of patients with AF 65 years of age with a congestive heart failure, hypertension, age, diabetes, stroke (2 points) score of 3 and no contraindications to anticoagulation. Data sources included the Rivaroxaban Once-daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET-AF) and other studies of anticoagulation. Outcome measurements included costs in 2011 United States dollars, quality-adjusted life years (QALYs), and incremental cost-effectiveness ratios (ICERs). Patients with AF treated with rivaroxaban lived an average of 10.03 QALYs at a lifetime treatment cost of $94,456. Those receiving warfarin lived an average of 9.81 QALYs and incurred costs of $88,544. The ICER for rivaroxaban was $27,498 per QALY. These results were most sensitive to changes in the hazard decrease of intracranial hemorrhage and stroke with rivaroxaban, cost of rivaroxaban, and time horizon. Monte Carlo simulation demonstrated rivaroxaban was cost-effective in 80% and 91% of 10,000 iterations at willingness-to-pay thresholds of $50,000 and $100,000 per QALY, respectively. In conclusion, this Markov model suggests that rivaroxaban therapy may be a cost-effective alternative to adjusted-dose warfarin for stroke prevention in AF.
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PMID:Cost-effectiveness of rivaroxaban compared to warfarin for stroke prevention in atrial fibrillation. 2305 88

Vitamin K antagonists are advised in pulmonary arterial hypertension patients despite a lack of safety data. We reviewed major bleeding in three classes of pulmonary hypertension patients, all receiving vitamin K antagonists. Bleeding event rates were 5.4 per 100 patient-years for patients with idiopathic pulmonary arterial hypertension, 19 per 100 patient-years for connective tissue disease related pulmonary arterial hypertension patients and 2.4 per 100 patient-years for chronic thromboembolic pulmonary hypertension patients. Life tables analysis showed that event-free survival was worse in patients with connective tissue disease related pulmonary hypertension than in patients with idiopathic pulmonary arterial hypertension (Wilcoxon=12.8; p<0.001), and patients with chronic thromboembolic pulmonary hypertension (Wilcoxon=23.2; p<0.001). Patients with idiopathic pulmonary arterial hypertension suffered more events than patients with chronic thromboembolic pulmonary hypertension (Wilcoxon=7.2; p<0.01). Major bleeding was independent of age, sex, target international normalised ratio (INR) range, documented INR, vitamin K antagonist type, or right atrial pressure, but was associated with use of prostacyclin analogues. Major bleeding risk during vitamin K antagonist therapy differs among groups of patients with pulmonary hypertension. Further research regarding optimal anticoagulant therapy is needed, as well as risk-benefit analyses for pulmonary hypertension patients with a higher bleeding propensity.
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PMID:Major bleeding with vitamin K antagonist anticoagulants in pulmonary hypertension. 2354 44

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