Antithrombotic Management in Patients with Prosthetic Valves

Butchart, Eric G.; Caterina, Raffaele De

doi:10.1002/9781118410875.ch17

Cited by 4 publications

(3 citation statements)

References 124 publications

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“…Only a limited number of case series have been published, and these provide inconclusive information on the pattern of use and optimal antithrombotic regimen for patients with prosthetic heart valves (88). European (89) and North American guidelines (90) differ on the recommendations for prescribing anticoagulants without (89) or with aspirin (90), respectively, likely reflecting different patterns of simultaneous use of VKA and aspirin in different parts of the world (see [91] for an in-depth discussion).…”

Section: Prosthetic Heart Valvesmentioning

confidence: 99%

General mechanisms of coagulation and targets of anticoagulants (Section I)

Caterina¹,

Husted²,

Wallentin³

et al. 2013

Thromb Haemost

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162

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Contrary to previous models based on plasma, coagulation processes are currently believed to be mostly cell surface-based, including three overlapping phases: initiation, when tissue factor-expressing cells and microparticles are exposed to plasma; amplification, whereby small amounts of thrombin induce platelet activation and aggregation, and promote activation of factors (F)V, FVIII and FXI on platelet surfaces; and propagation, in which the Xase (tenase) and prothrombinase complexes are formed, producing a burst of thrombin and the cleavage of fibrinogen to fibrin. Thrombin exerts a number of additional biological actions, including platelet activation, amplification and self-inhibition of coagulation, clot stabilisation and anti-fibrinolysis, in processes occurring in the proximity of vessel injury, tightly regulated by a series of inhibitory mechanisms. "Classical" anticoagulants, including heparin and vitamin K antagonists, typically target multiple coagulation steps. A number of new anticoagulants, already developed or under development, target specific steps in the process, inhibiting a single coagulation factor or mimicking natural coagulation inhibitors.

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Section: Prosthetic Heart Valvesmentioning

confidence: 99%

General mechanisms of coagulation and targets of anticoagulants (Section I)

Caterina¹,

Husted²,

Wallentin³

et al. 2013

Thromb Haemost

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162

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“…(c) wherever a higher intensity VKA therapy is used, specifically in some settings of mechanical valve antithrombotic prophylaxis (e.g., with an unfavorabletricuspid, mitral or pulmonarymechanical valve position, in the presence of a medium-or high-thrombogenicity mechanical valve, or in the presence of comorbidities), its rationale is relatively weak 18,49 , and indeed not adopted in the ACC/AHA Guidelines 50 ;…”

Section: Problems With the Use Of Vitamin K Antagonists In Areas Of Tmentioning

confidence: 99%

Non-vitamin K antagonist oral anticoagulants in atrial fibrillation accompanying mitral stenosis: the concept for a trial

Caterina

2015

Europace

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Patients at thromboembolic risk with non-valvular atrial fibrillation (AF) can now be managed either with a vitamin K antagonist (VKA) or with a fixed dose of a non-VKA oral anticoagulant (NOAC), while patients with valvular AF have been restricted to VKAs on the basis of a potentially higher risk and different mechanism of thrombosis, and the lack of sufficient data on the efficacy of NOACs. The terms 'non-valvular AF' and 'valvular AF' have not been however consistently defined. 'Valvular' AF has included any valvular disorder, including valve replacement and repair. In AF with rheumatic mitral disease, observational studies strongly suggest that VKA treatment is valuable. These patients have not been included in NOAC trials, but there is also no stringent argument to have excluded them. This is at sharp variance from patients with mechanical valves, also excluded from the pivotal Phase III trial comparing warfarin with NOACs, but in whom a single Phase II trial of dabigatran etexilate against VKA treatment was stopped prematurely because of increased rates of thromboembolism as well as increased bleeding associated with dabigatran. Until more data are available, such patients should be therefore managed with VKAs. We here propose an open-label randomized trial of one of the NOACs against the best of treatment available in regions of the world in which rheumatic heart disease is still highly prevalent, aiming at showing the superiority of the NOAC used against current standard treatment.

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“…The recommended intensity of oral anticoagulation with VKAs has been therefore adjusted in recent ESC guidelines (162,163) to lower levels compared with previous statements. Intensity of anticoagulation in such cases is adjusted according to the thrombogenicity of the prosthesis, the position (aortic vs mitral/tricuspid/pulmonary), and associated thromboembolic risk factors, as summarised in ▶ Table 6 (164,165). The post-operative anticoagulant therapy should be started during the first days.…”

Section: Prosthetic Mechanical Valvesmentioning

confidence: 99%

Vitamin K antagonists in heart disease: Current status and perspectives (Section III)

Caterina¹,

Husted²,

Wallentin³

et al. 2013

Thromb Haemost

316

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Oral anticoagulants are a mainstay of cardiovascular therapy, and for over 60 years vitamin K antagonists (VKAs) were the only available agents for long-term use. VKAs interfere with the cyclic inter-conversion of vitamin K and its 2,3 epoxide, thus inhibiting γ-carboxylation of glutamate residues at the amino-termini of vitamin K-dependent proteins, including the coagulation factors (F) II (prothrombin), VII, IX and X, as well as of the anticoagulant proteins C, S and Z. The overall effect of such interference is a dose-dependent anticoagulant effect, which has been therapeutically exploited in heart disease since the early 1950s. In this position paper, we review the mechanisms of action, pharmacological properties and side effects of VKAs, which are used in the management of cardiovascular diseases, including coronary heart disease (where their use is limited), stroke prevention in atrial fibrillation, heart valves and/or chronic heart failure. Using an evidence-based approach, we describe the results of completed clinical trials, highlight areas of uncertainty, and recommend therapeutic options for specific disorders. Although VKAs are being increasingly replaced in most patients with non-valvular atrial fibrillation by the new oral anticoagulants, which target either thrombin or FXa, the VKAs remain the agents of choice for patients with atrial fibrillation in the setting of rheumatic valvular disease and for those with mechanical heart valves.

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Antithrombotic Management in Patients with Prosthetic Valves

Cited by 4 publications

References 124 publications

General mechanisms of coagulation and targets of anticoagulants (Section I)

General mechanisms of coagulation and targets of anticoagulants (Section I)

Non-vitamin K antagonist oral anticoagulants in atrial fibrillation accompanying mitral stenosis: the concept for a trial

Vitamin K antagonists in heart disease: Current status and perspectives (Section III)

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