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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Family physicians should be familiar with the acute management of atrial fibrillation and the initiation of chronic therapy for this common arrhythmia. Initial management should include hemodynamic stabilization, rate control, restoration of sinus rhythm, and initiation of antithrombotic therapy. Part II of this two-part article focuses on the prevention of thromboembolic complications using anticoagulation. Heparin is routinely administered before medical or electrical cardioversion. Warfarin is used in patients with persistent atrial fibrillation who are at higher risk for thromboembolic complications because of advanced age, history of coronary artery disease or stroke, or presence of left-sided heart failure. Aspirin is preferred in patients at low risk for thromboembolic complications and patients with a high risk for falls, a history of noncompliance, active bleeding, or poorly controlled hypertension. The recommendations provided in this article are consistent with guidelines published by the American Heart Association and the Agency for Healthcare Research and Quality.
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PMID:Acute management of atrial fibrillation: Part II. Prevention of thromboembolic complications. 1272 47

Atrial fibrillation is a common arrhythmic disorder which is becoming increasingly prevalent among the elderly. Atrial fibrillation is an independent risk factor for ischaemic stroke. Patients with hypertension, heart failure, diabetes, age older than 65 years, previous thromboembolisms, left atrial enlargement and left ventricular dysfunction have an increased risk. Coumarins (with a target international normalised ratio (INR) of 2.0 to 3.0) are the treatment of first choice in patients with atrial fibrillation. In young patients without additional risk factors, acetyl salicylic acid provides sufficient protection. The management of anticoagulant therapy during electric cardioversion in the acute phase of an ischaemic stroke and during elective surgical interventions, is still a subject of clinical research.
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PMID:[Anticoagulant treatment of patients with atrial fibrillations: dependent on age and other risk factors for thromboembolism]. 1262 83

Incidence data on thromboembolism in patients with heart failure (which may include stroke, peripheral embolism, pulmonary embolism) are limited but provide a general population range from 1-5 cases per 1000 each year, increasing with age to more than 30 cases per 1000 each year among people aged 75 years or older. However, the incidence of thromboembolism varied depending very much on what was being investigated in each of these studies. Data from subgroup analysis of the larger heart failure trials would seem to support this incidence data, although there is very little true epidemiological data and no randomised, controlled trial has been designed to specifically investigate thromboembolism in patients with heart failure. The pathophysiology of heart failure is complex. There are many well recognised factors which are associated with thrombosis in heart failure patients, such as vascular abnormalities, increased coagulability and impaired blood flow. In the past 50 years many studies have been performed to investigate if oral anticoagulation is of benefit for the prevention of thromboembolism in patients with heart failure. The use of warfarin therapy for heart failure patients has been a controversial subject. Warfarin does have a role to play in patients with myocardial infarction and those with atrial fibrillation. Furthermore, in patients with congestive heart failure secondary to coronary artery disease, warfarin reduces the occurrence of nonfatal myocardial infarction and, therefore, may reduce the chances of progression to heart failure. It has also been shown that warfarin reduces the risk of thromboembolic strokes in patients recovering from myocardial infarction. At present, there is a lack of randomised data, and the incidence of bleeding complications in patients with heart failure has caused a decrease in the use of oral anticoagulants for the prevention of thrombosis. This review summarises the incidence, potential mechanism and therapeutic approaches for management of thromboembolism in heart failure.
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PMID:Blood coagulation in patients with chronic heart failure: evidence for hypercoagulable state and potential for pharmacological intervention. 1265 54

Our understanding of the pathogenesis of congestive heart failure (CHF) has improved remarkably in recent years. However, despite better knowledge and novel pharmaceutical strategies, this disease is still one of the most brutal killers in the Western world. The pathophysiology of CHF is complex, and much of our comprehension revolves strictly around the neurohormonal and mechanical mechanisms involved. It has been suggested that CHF is associated with altered hemostasis, but whether a prothrombotic state contributes to the pathogenesis and progression of the disease is still not well known. The purpose of this review article is to discuss our current knowledge of platelet activation in patients with CHF and the potential role of antiplatelet agents in preventing these hemostatic abnormalities. Clopidogrel is an established medication that reduces the incidence of stroke, myocardial ischemia, or vascular death. It is currently the drug of choice in the prophylaxis of subacute stent thrombosis and postischemic stroke treatment. Promising results of the most resent trials (Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events [CAPRIE] and Clopidogrel in Unstable angina to prevent Recurrent Events [CURE]) may expand future indications of this ADP receptor antagonist for prevention of thrombotic complications in the CHF population. Currently conducted clinical trials (Warfarin and Antiplatelet Therapy in Chronic Heart Failure [WATCH] and Plavix Use for Treatment of Congestive Heart Failure [PLUTO-CHF] should clarify the role of clopidogrel in these patients.
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PMID:Platelet activation in patients with congestive heart failure: do we have enough evidence to consider clopidogrel? 1266 Jun 60

Recent observational data suggest that mild or moderate heart failure is associated with an annual risk of stroke of approximately 1.2%. Indeed, it is possible that the major cause of sudden death in chronic heart failure is not related to arrhythmias, but to vascular occlusion. Anticoagulation may reduce the rate of embolic events, but there is controversy about the mandatory use of antithrombotic therapy for all patients with ventricular dysfunction in sinus rhythm. At present antithrombotic therapy is indicated only in "high risk" subgroups of patients: atrial fibrillation, mobile/protruding/irregular thrombi, acute post-myocardial infarction thrombi or a recent history of thromboembolism. Actually there is no evidence to recommend the use of aspirin to prevent thromboembolism in patients with ventricular dysfunction in sinus rhythm. Further trials of both antiplatelet agents and anticoagulation are sorely needed and we are waiting for the results of large trials such as the WATCH trial (Warfarin and Antiplatelet Therapy in Chronic Heart Failure) and the WARCEF trial (Warfarin Versus Aspirin in Reduced Ejection Fraction). The future appears promising due to the advent of a new oral direct thrombin inhibitor, ximelagatran, with good efficacy and safety profile for the treatment and prevention of thromboembolism.
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PMID:[Antithrombotic prophylaxis in patients with ventricular dysfunction: critical review of the literature and new perspectives]. 1278 54

Venous thromboembolism, which is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE), represents a significant cause of death, disability, and discomfort. Two million people/year are affected by VTE, making it the third most common cardiovascular disease after coronary heart disease and stroke. The rationale for VTE prophylaxis stems from the clinically silent presentation of the disease and its prevalence among hospitalized patients. At greatest risk are patients undergoing major orthopedic surgery and those admitted to the intensive care unit with acute myocardial infarction, heart failure, ischemic stroke, respiratory disease, systemic infection, or other medical conditions that immobilize patients for 5 days or longer. Several anticoagulant regimens have been effective in reducing the risk of VTE after major orthopedic surgery. For patients undergoing total hip or knee replacement, treatment with adjusted-dose warfarin, low-molecular-weight heparins, or fondaparinux may be used. Warfarin, which has been around for more than 50 years, is the only oral anticoagulant available for VTE prophylaxis. Ximelagatran, a new low-molecular-weight oral prodrug of the direct thrombin inhibitor melagatran, has advantages over warfarin that may make it the drug of choice for prevention of VTE.
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PMID:The role of oral direct thrombin inhibitors in the prophylaxis of venous thromboembolism. 1562 37

A 40-year-old woman admitted with heart failure had undergone aortic valve replacement with a Model 2310 Starr-Edwards valve due to aortic regurgitation 33 years previously. She had been followed up for several years, but discontinued follow-up and medication (including Warfarin) for the past 25 years. Echocardiography demonstrated marked dilatation and thickening of the left ventricle, and the peak pressure gradient of the prosthesis was measured as 87.9 mmHg. Under the diagnosis of chronic aortic valve prosthesis-patient mismatch with subsequent severe left ventricular dysfunction, the Starr-Edwards valve was explanted and replaced with a 23 mm St. Jude Medical prosthetic valve. The removed valve showed minimal cloth wear except for a small part of the strut. The postoperative echocardiography demonstrated recovering of left ventricular function. To our best knowledge, this case presents the longest duration for a surgically explanted Starr-Edwards aortic prosthetic valve in Japan.
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PMID:Reoperation for a Starr-Edwards aortic prosthetic valve 33 years after initial implantation. 1582

Platelets play a pivotal role in the pathogenesis of atherothrombosis, believed to be integrally involved in both the development and progression of atherosclerotic heart disease, as well as in its acute thrombotic complications. Antiplatelet therapy constitutes the cornerstone in the management of patients with acute coronary syndromes and generally high-risk patients with atherothrombosis. Until recently, long-term antiplatelet therapy for the treatment and prevention of the complications of atherothrombotic disease was traditionally limited to aspirin. The availability of the thienopyridines, in particular clopidogrel, represents an important addition to the physician's armamentarium. Clopidogrel is currently one of the most widely prescribed drugs for the treatment of symptomatic coronary artery disease. Aspirin and clopidogrel interfere with platelet activation in complementary, but separate pathways. Aspirin irreversibly inhibits cyclooxygenase, thus preventing the production of thromboxane A(2), which is a prothrombotic and vasoconstrictive substance. Clopidogrel, a newer thienopyridine which has largely supplanted ticlopidine due to a more favorable safety profile, irreversibly prevents platelet activation by blocking one of the three known adenosine 5'-diphosphate (ADP) receptors (the P2Y(12) receptor) on the platelet surface, thus interfering with platelet activation, degranulation and aggregation. Both these antiplatelet agents have a potent protective effect against adverse vascular events, but the combination of these two agents has an even stronger antiplatelet effect translating into superior antithrombotic protection in coronary, cerebral or peripheral arterial disease, without an inordinate increase in bleeding complications. A number of seminal clinical trials have demonstrated and confirmed the incremental benefit and efficacy of the combination of clopidogrel and aspirin therapy above and beyond that of aspirin alone, with multiple other important large-scale clinical trials currently ongoing. Newer data are being accumulated from studies where indications for the use of clopidogrel and aspirin continue to expand into other patient groups, rendering this dual antiplatelet drug therapy a sweeping combination in Cardiology. However, important issues remain to be further and more thoroughly explored about the benefit of this antiplatelet drug combination in these other patient groups, such as in patients with heart failure, where preliminary data indicate a favorable effect on thrombotic vascular events, in patients with atrial fibrillation, where there is hope that this combination may replace or be an alternative treatment modality to coumadin in certain subpopulations, in patients undergoing demanding catheter ablation procedures, where data point to a protective effect from thromboembolic events. Another pertaining issue to be further investigated is the occurrence of drug-resistance observed in some patients for both these antithrombotic agents. This article is a comprehensive review of all these data and the landmark trials on the two antiplatelet agents, the issues involved and the current recommendations for their use in patients with atherosclerotic heart disease and other cardiovascular disorders and procedures.
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PMID:Aspirin and clopidogrel: a sweeping combination in cardiology. 1597 85

Chronic left ventricular systolic dysfunction is a well recognized problem with an increasingly significant impact on healthcare in the form of congestive heart failure (CHF). Advances in medicine have led to improved survival after myocardial infarction (MI) and as a result, an increased prevalence of left ventricular systolic dysfunction. An increased incidence of thromboembolism, especially stroke, in patients with left ventricular systolic dysfunction is also well recognized. Pharmacological strategies to prevent stroke have been proposed in numerous studies. For example, anticoagulation in patients with atrial fibrillation and heart failure has been shown to reduce mortality rates and the incidence of stroke; however, its role in patients with left ventricular dysfunction and normal sinus rhythm is unclear and utilization of anticoagulation in these patients varies widely. The role of aspirin to prevent thromboembolism in patients with CHF is controversial. The relatively new pharmacological agent ximelagatran, which has an advantage of unmonitored oral administration has the potential to change the anticoagulation strategy in patients with heart failure. Important trials to define optimal therapy for reducing the risk of thromboembolism and death in patients with left ventricular systolic dysfunction and sinus rhythm include the recently reported WATCH (Warfarin and Antiplatelet Therapy in Chronic Heart failure) trial and the WARCEF (Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction) trial, which is currently underway. The WATCH trial failed to outline significant differences between aspirin (acetylsalicylic acid), warfarin, and clopidogrel in the primary composite endpoint of all-cause mortality, nonfatal MI, and nonfatal stroke. Combined data from WATCH and WARCEF may provide sufficient statistical power to clarify outcomes such as stroke and death in patients with reduced cardiac ejection fraction. The pooled data may also help define optimal preventative measures for thromboembolism in patients with left ventricular systolic dysfunction and sinus rhythm.
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PMID:Pharmacological prevention of thromboembolism in patients with left ventricular dysfunction. 1648 47

HMR1766 is a new nitric oxide (NO)-independent activator of soluble guanylyl cyclase (sGC) in development for the treatment of cardiovascular diseases and chronic heart failure. A significant fraction of patients to be treated with HMR1766 is expected to be maintained on warfarin. Because HMR1766 is an inhibitor and warfarin a substrate of CYP2C9, the authors studied whether warfarin pharmacokinetics and pharmacodynamics are influenced by HMR1766. Eighteen healthy males were to receive a single oral dose of 20 mg warfarin each under steady-state conditions of HMR1766 or placebo. Plasma concentrations of HMR1766, (R)- and (S)-warfarin, and its 7-hydroxy-metabolites were determined using high-performance liquid chromatography and prothrombin time, and the international standardized ratio was determined by the nephelometric method. (S)-Warfarin AUC(inf) and t(1/2) were 106,471 h x microg/L and 82.92 hours versus 33,148 h x microg/L under HMR1766 and 31.72 hours under placebo, and the maximum decrease in prothrombin time values after warfarin dosing was 58.75% versus 39.94%. These data demonstrate a CYP2C9-mediated pharmacokinetic interaction with pharmacodynamic, clinically relevant consequences, which might require warfarin dose adjustment.
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PMID:Significant pharmacokinetic and pharmacodynamic interaction of warfarin with the NO-independent sGC activator HMR1766. 1719 4


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