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Antithrombotic therapy for surgical bioprosthetic valves and surgical valve repair

Antithrombotic therapy for surgical bioprosthetic valves and surgical valve repair
Literature review current through: Jan 2024.
This topic last updated: Jun 13, 2023.

INTRODUCTION — Surgical replacement of a diseased heart valve with a prosthetic valve aims to improve symptoms and prolong life but also exposes the patient to potential prosthesis-related complications. The frequency of serious complications depends upon the valve type and position and other clinical risk factors. Prosthetic valve complications include embolic events, bleeding, valve obstruction (due to thrombosis or pannus), infective endocarditis, structural deterioration (particularly for bioprosthetic valves), paravalvular or transvalvular regurgitation, hemolytic anemia, and patient-prosthesis mismatch. (See "Overview of the management of patients with prosthetic heart valves".)

This topic will review antithrombotic therapy following surgical bioprosthetic valve replacement or surgical valve repair [1,2]. Antithrombotic therapy refers to anticoagulation, antiplatelet therapy, or both.

The following related subjects are presented separately:

(See "Overview of the management of patients with prosthetic heart valves".)

(See "Transcatheter aortic valve implantation: Antithrombotic therapy", section on 'General approach'.)

Management of complications of bioprosthetic valves related to thrombosis or bleeding:

(See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

(See "Anticoagulation for prosthetic heart valves: Management of bleeding and invasive procedures".)

SURGICAL BIOPROSTHETIC VALVE

Risk of thrombotic complications with a surgical bioprosthetic valve — Complications caused by thrombus developing on a bioprosthetic valve include thromboembolic events and valve thrombosis (which may be obstructive or subclinical).

Thromboembolism — The term thromboembolism generally refers to clinical embolic events (including stroke, transient ischemic attack [TIA] or peripheral thromboembolism) ascribed to thrombus. For patients with a surgical bioprosthetic valve, the risk of thromboembolism varies depending upon time after implantation (risk is highest immediately after implantation and declines with time to a lower long-term risk after 90 days), valve position (higher risk with mitral versus aortic valves), and presence of risk factors such as atrial fibrillation (AF) or low left ventricular ejection fraction.

After surgical bioprosthetic valve replacement, the risk of thromboembolism is highest during the first three to six months (particularly the first 30 days) [1-5]; this applies even with exclusion of events in the first 24 hours [3,4]. The period of highest risk is relatively short, which limits the absolute risk of thromboembolism in the early postoperative period, as illustrated by the following studies:

Aortic valve – In an early series of 424 adults (mean age 64 years) undergoing bioprosthetic aortic valve replacement (approximately one-third treated postoperatively with vitamin K antagonist [VKA]), the rate of thromboembolic events during the first 10 days was 1.1 percent (a linearized rate of 41 percent per year), during days 11 to 90 the rate was 3.6 percent per year, and after 90 days the rate was 1.9 percent per year [3]. A high rate of thromboembolic events (5 percent) was also identified during the first 90 days in a later series of 861 adults (mean age 70 years) in sinus rhythm after bioprosthetic aortic valve implantation (with or without VKA therapy) [4].

A meta-analysis identified a long-term annual thromboembolic rate of 0.87 percent per year in 5837 adults (mean age 64.6 years) [6]. The long-term risk may be lower in a younger population, as suggested by a study with an incidence rate of 0.53 percent per year in a population of 2686 adults with mean age 50.7 years [7].

Mitral valve – In a series of 326 patients undergoing bioprosthetic mitral valve replacement (approximately 80 percent receiving VKA), the rate of thromboembolic events was 1.5 percent during the first 10 days (equivalent to 55 percent per year), during 11 to 90 days it was 10 percent per year, and after 90 days it was 2.4 percent per year [3]. In a later series that included 216 patients with a bioprosthetic mitral valve replacement for mitral regurgitation (41 percent taking warfarin for >3 months), the rate of ischemic stroke was 4.6 percent during the first 30 days (equivalent to 60 percent per year), 1.5 percent per year during days 31 to 180, and 0.9 percent per year after the first 180 days [5].

Tricuspid and pulmonic valves – Limited data are available on the risk of thromboembolism in patients with tricuspid or pulmonic bioprosthetic valves, and interpretation is difficult since many patients with these valves also have prosthetic mitral and/or aortic valves and other comorbidities. A systematic review identified eight thromboembolic events in 470 patients with bioprosthetic tricuspid valves (1.7 percent) versus 42 events in 464 patients with mechanical tricuspid valves (9.1 percent) in nine studies, but the period of follow-up ranged up to 20 years or more [8].

The effects of antithrombotic therapy on thromboembolic risk are discussed below. (See 'Intermediate- and long-term antithrombotic therapy' below.)

Bioprosthetic valve thrombosis — Symptomatic or hemodynamically significant bioprosthetic valve thrombosis (BPVT) is uncommon, while subclinical BPVT is commonly identified in research imaging studies and is of uncertain clinical significance.

Diagnosis and management of BPVT is discussed separately. (See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Clinical manifestations and diagnosis" and "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

Symptomatic bioprosthetic valve thrombosis — Observational studies have suggested incidence rates of symptomatic or hemodynamically significant BPVT of 0.3 percent within the first 30 days after valve implantation [9] and a long-term risk of <0.05 percent per year [9,10]. However, some retrospective data suggest that symptomatic BPVT is frequently missed, and the incidence rate may be as high 2 percent within the first two years [10,11].

Clinical manifestations include exertional dyspnea and increased transvalvular gradients, as discussed separately. (See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Clinical manifestations and diagnosis", section on 'Clinical manifestations' and "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

The time of presentation of obstructive BPVT ranges from days to greater than five years after surgical implantation, as illustrated by the following observations:

A retrospective pathology study conducted at the Mayo Clinic, with 397 bioprosthetic valves explanted due to dysfunction, found that 46 cases (11.6 percent) were caused by BPVT [11]. The majority (65 percent) of cases of BPVT were identified more than 12 months after implantation; 15 percent of cases occurred more than five years after implantation. BPVT was identified on explanted aortic, mitral, pulmonic, and tricuspid valves.

A partially overlapping study conducted at the Mayo Clinic identified 32 cases of clinically diagnosed BPVT [12]. The peak incidence of BPVT occurred at 13 to 24 months after implantation.

Subclinical bioprosthetic valve thrombosis — Subclinical BPVT is a relatively common finding in research imaging studies (using four-dimensional computed tomography [CT] or echocardiography), but the clinical significance of asymptomatic BPVT has not been determined [10-17]. Subclinical valve thrombosis appears to be dynamic, progressing and regressing over the course of months [18].

Incidence – Imaging studies have identified high incidences of subclinical BPVT manifested as hypoattenuated leaflet thickening (HALT) and reduced leaflet motion [15]. An imaging substudy of the Evolut Low Risk trial found similar rates of HALT with transcatheter and surgical valves at one month (17.3 versus 16.5 percent) and one year (30.9 and 28.4 percent) [17]. Other studies have identified higher rates of evidence of BPVT with transcatheter than with surgically implanted bioprosthetic aortic valves, but it is unclear whether these differences were caused by differences in prosthetic valves, antithrombotic therapy, or other clinical characteristics [16,19,20].

Effect of anticoagulation – Anticoagulation appears to reduce the frequency of subclinical BPVT. Higher rates of subclinical BPVT have been observed among patients receiving dual antiplatelet therapy (eg, 15 percent) than among patients receiving anticoagulants (eg, 4 percent with a VKA, 3 percent with a direct oral anticoagulant [DOAC]) [16]. Resolution of subclinical leaflet thrombosis has been observed in some patients treated with anticoagulants (VKA or DOAC) [16,21], but regression has also been observed in some patients not treated with anticoagulant therapy [17,18].

Clinical significance – The clinical significance of subclinical BPVT is unclear, although associations with elevated bioprosthetic valve gradients and risk of TIAs, recurrent BPVT, and early valve degeneration have been observed [16,20,21]. In a study of subclinical BPVT, aortic valve gradients of greater than 20 mmHg and increases in aortic valve gradients of more than 10 mmHg were more frequent among 88 patients with subclinical BPVT than among 632 patients with normal leaflet motion (14 versus 1 percent) [16]. Subclinical thrombosis was associated with significantly increased rates of TIAs (4.18 versus 0.6 per 100 person-years) and strokes or TIAs (7.85 versus 2.36 per 100 person-years) but not a significantly increased rate of stroke (4.12 versus 1.92 per 100 person-years). Similarly, in the PARTNER 3 cardiac CT substudy, the pooled thromboembolic endpoint of stroke, TIA, and thromboembolic events was more frequently seen in patients with HALT (8.6 versus 1.6 percent at 30 days) [20].

Further investigation is required to determine contributing factors, clinical significance, and appropriate management of subclinical BPVT for surgical and transcatheter valves. (See "Transcatheter aortic valve implantation: Complications", section on 'Valve thrombosis' and "Transcatheter aortic valve implantation: Antithrombotic therapy" and "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Clinical manifestations and diagnosis" and "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

Approach for surgical bioprosthetic valves — The optimum approach to antithrombotic therapy for surgical bioprosthetic valves is uncertain, as limited evidence is available to guide management [1,2]. The goal of antithrombotic therapy after surgical bioprosthetic valve replacement is to reduce the risk of thromboembolism and valve thrombosis while minimizing the risk of bleeding complications from antithrombotic therapy. Further information about the approach summarized here (algorithm 1) is provided below. (See 'Phases of antithrombotic therapy' below.)

Early bridging For patients with a newly implanted bioprosthetic valve who will be treated with a VKA (see 'Intermediate- and long-term antithrombotic therapy' below), early bridging anticoagulation (with unfractionated heparin [UFH] or low molecular weight heparin [LMWH]) is initiated as soon as the risk of postoperative bleeding is considered acceptable (generally within 12 to 24 hours after surgery).

Bridging anticoagulation is continued while the VKA is started until the international normalized ratio (INR) is at therapeutic levels for two consecutive days. (See 'Early bridging after bioprosthetic valve replacement' below.)

For patients with a newly implanted bioprosthetic valve who will be treated with a DOAC, bridging anticoagulation is not indicated.

Intermediate-term antithrombotic therapy – Antithrombotic therapy is administered during the first three to six months after valve implantation to reduce the risk of thrombotic complications (algorithm 1). (See 'Intermediate- and long-term antithrombotic therapy' below.)

For patients without a concurrent indication for anticoagulation – If there is no concurrent indication for anticoagulation (such as AF), management is based on the estimated bleeding risk. Indicators of elevated bleeding risk include previous major bleed, active peptic ulcer disease, uncontrolled hypertension, bleeding disorder, platelet count <50,000/microL, and barriers to anticoagulation monitoring and management. (See 'Without a concurrent indication for anticoagulation' below and "Risks and prevention of bleeding with oral anticoagulants", section on 'Risk factors for bleeding'.)

-With low bleeding risk – For patients with a surgical bioprosthetic valve with estimated low risk of bleeding, we suggest anticoagulation for the first three to six months after valve implantation. In this setting, we suggest a VKA (target INR 2.5) rather than a DOAC. The target described here follows the convention in the 2020 American College of Cardiology/American Heart Association (ACC/AHA) valve guidelines of specifying INR targets rather than ranges [1]. The acceptable range extends to 0.5 INR units on each side of the target. The use of targets was deemed preferable to avoid a patient's INRs consistently targeted near the upper or lower limit of the range.

After the period of anticoagulation, we suggest long-term low-dose aspirin therapy as described below.

-With elevated bleeding risk – For patients with a surgical bioprosthetic valve, no concurrent indication for anticoagulation, and elevated bleeding risk, we suggest aspirin 75 to 100 mg per day. A decision on whether to proceed with aspirin therapy is based upon an individualized assessment of estimated risks and benefits.

For patients with concurrent indication for anticoagulation – For patients with a bioprosthetic valve with a concurrent indication for anticoagulation (eg, AF), the selection of anticoagulant (VKA or DOAC) and duration of therapy (if indicated beyond the first three to six months) is based upon the indication for anticoagulation and other clinical factors. (See 'With a concurrent indication for anticoagulation' below.)

If anticoagulation for the concurrent indication is no longer required within the first three to six months after surgical bioprosthetic valve implantation, then anticoagulation for the bioprosthetic valve is continued to complete three to six months total if the bleeding risk is low. If the period of anticoagulation for the concurrent indication is finite, routine long-term aspirin therapy for the bioprosthesis is initiated after anticoagulation is stopped.

Long-term aspirin for all patients For patients receiving intermediate-term (three to six months) or long-term anticoagulation, aspirin 75 to 100 mg per day is started after the period of anticoagulation is completed. For patients not receiving intermediate-term (or long-term) anticoagulation, aspirin is generally started within 24 hours after surgery. (See 'Intermediate- and long-term antithrombotic therapy' below.)

The approach described above is similar to that described in the 2020 ACC/AHA valve guidelines and the 2021 ESC valve guidelines [1,2].

Phases of antithrombotic therapy — The following sections provide further information about the approach to antithrombotic therapy summarized above (algorithm 1). (See 'Approach for surgical bioprosthetic valves' above.)

Early bridging after bioprosthetic valve replacement — Early therapeutic heparin bridging after surgical bioprosthetic valve implantation is indicated only for patients who will be treated with a VKA postoperatively. Heparin bridging is generally not indicated for patients who will be treated with a DOAC (given the rapid onset of action of DOAC) or those who will receive no anticoagulant. (See 'Approach for surgical bioprosthetic valves' above.)

Choice of heparin for bridging — When early bridging is indicated, either subcutaneous LMWH or intravenous (IV) UFH is used. Subcutaneous LMWH is more convenient to use and may result in a more predictable degree of anticoagulation. A potential concern with LMWH is that, if severe bleeding occurs, the effect of LMWH cannot be reversed as easily as that of UFH. Reversal of LMWH and UFH is discussed separately. (See "Heparin and LMW heparin: Dosing and adverse effects" and "Reversal of anticoagulation in intracranial hemorrhage", section on 'LMW heparin'.)

How to bridge

For patients who have an indication for early therapeutic heparin bridging, one of the following agents is started 12 to 24 hours after valve surgery [2], unless there is a contraindication (eg, active bleeding):

IV UFH (eg, 18 units/kg/hour; no bolus) adjusted to achieve an activated partial thromboplastin time (aPTT) that is 2 times control

OR

Subcutaneous therapeutic weight-adjusted, twice daily LMWH (eg, enoxaparin 1 mg/kg every 12 hours)

VKA is generally started 12 to 24 hours after the procedure unless there is a contraindication. IV UFH or subcutaneous LMWH should be discontinued once the INR has been in the therapeutic range for two consecutive days. Since LMWH therapy is likely inferior to VKA in preventing bioprosthetic valve thrombotic complications (given differences in efficacy seen in pregnant women with mechanical valves), VKA should be started as soon as is prudent, in consultation with the surgeon.

A rationale for early bridging for patients starting VKA for newly implanted bioprosthetic valves is to reduce the high rate of thromboembolism seen during the first 10 days after implantation, although direct evidence to support this approach is lacking. Indirect evidence comes from the use of bridging anticoagulation early after mechanical valve replacement. (See 'Risk of thrombotic complications with a surgical bioprosthetic valve' above and "Antithrombotic therapy for mechanical heart valves", section on 'Early heparin bridging'.)

Use of LMWH or UFH for early bridging after surgical bioprosthetic valve implantation should be distinguished from long-term use, particularly during pregnancy in patients with primarily mechanical valves, which is discussed separately. (See "Management of antithrombotic therapy for a prosthetic heart valve during pregnancy".)

Intermediate- and long-term antithrombotic therapy — A rationale for intermediate-term (three to six months) anticoagulation following surgical bioprosthetic valve implantation is to reduce the high early rate of thromboembolism. However, limited data are available concerning the efficacy and safety of antithrombotic therapy (antiplatelet therapy and/or anticoagulation) after bioprosthetic valve replacement (see 'Thromboembolism' above). A potential contributor to the high early rate of thromboembolism is the high incidence of AF (up to 50 percent during the first three months after valve surgery). (See "Atrial fibrillation and flutter after cardiac surgery".)

Without a concurrent indication for anticoagulation — For patients with surgical bioprosthetic valves without a concurrent indication for anticoagulation, VKA is the preferred agent for intermediate-term anticoagulation in those with low bleeding risk since data are lacking on use of DOACs in this setting. The VKA is generally started 12 to 24 hours after the procedure unless there is a contraindication, such as active bleeding.

Studies of the effects of intermediate- and long-term VKA therapy in patients in sinus rhythm with bioprosthetic valves have yielded mixed results. (See 'Intermediate- and long-term antithrombotic therapy' above.)

Many of the studies of antithrombotic therapy for bioprosthetic valves have focused on patients with bioprosthetic aortic valves. Meta-analyses of observational studies have generally found similar rates of thromboembolic events and mortality and higher rates of bleeding with intermediate- or long-term anticoagulation versus antiplatelet therapy in patients with surgical bioprosthetic valves [22-24]. A meta-analysis of 13 observational studies with a total of 6431 patients treated with warfarin and 18,210 patients treated with aspirin or no antithrombotic therapy after surgical bioprosthetic aortic valve implantation identified no benefit from the VKA [22]. The duration of anticoagulation was three months in most of the included studies. Rates of the composite primary outcome at three months (venous thromboembolism, stroke, or TIA) were similar with and without VKA (odds ratio [OR] 1.01, 95% CI 0.56-1.84). Use of a VKA was associated with a trend toward increased bleeding at three months (OR 1.26, 95% CI 0.97-1.64) and an increased risk of bleeding during the overall study period (OR 1.38, 95% CI 1.07-1.78).

Two observational studies in patients with surgical bioprosthetic aortic valves suggested an association between anticoagulation and reduced risk of stroke as well as increased risk of bleeding:

In a series of 943 patients undergoing surgical bioprosthetic valve implantation in the pooled cohort of PARTNER2 randomized trials and nonrandomized registries, a lower incidence of stroke or TIA after discharge to one year was identified in patients discharged with anticoagulation (agents not reported) compared with those not anticoagulated (1.7 versus 5.5 percent) [25]. This difference in risk of stroke or TIA remained significant after adjustment for baseline characteristics (hazard ratio [HR] 0.17, 95% CI 0.05-0.60). The rate of major bleeding was similar with and without anticoagulation (6.6 versus 5.9 percent).

In a series of 9539 patients in Sweden who underwent surgical bioprosthetic aortic valve implantation with a mean follow-up of 3.13 years, warfarin use was associated with a similar mortality rate (adjusted HR 0.94, 95% CI 0.78-1.13), lower incidences of ischemic stroke (HR 0.49, 95% CI 0.35-0.70), lower rate of any thromboembolism (HR 0.75, 95% CI 0.60-0.94), and higher rates of hemorrhagic stroke (HR 1.94, 95% CI 1.07-3.51) and major bleeding (HR 1.67, 95% CI 1.30-2.15) compared with single antiplatelet therapy [26].

With a concurrent indication for anticoagulation — For patients with a concurrent indication for anticoagulation, the choice of anticoagulant is based upon the indication for anticoagulation and other clinical factors. For example, a DOAC is generally preferred for patients with AF with risk factors favoring anticoagulation, as discussed separately. Oral anticoagulation is generally started 12 to 24 hours after the procedure unless there is a contraindication, such as active bleeding. (See "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Choice of anticoagulant'.)

This approach is supported by the results of the RIVER trial, in which 1005 patients with a bioprosthetic mitral valve and AF were randomly assigned to treatment with rivaroxaban (20 mg once daily) or dose-adjusted warfarin (target INR 2 to 3) [27]. The incidence of stroke was lower in the rivaroxaban group (0.6 versus 2.4 percent; HR 0.25, 95% CI 0.07-0.88). Mortality from cardiovascular causes or thromboembolic events occurred at similar rates in the two groups (3.4 and 5.1 percent; HR 0.65, 95% CI 0.35-1.20). Major bleeding also occurred at similar rates in the two groups (1.4 and 2.6 percent; HR 0.54, 95% CI 0.21-1.35).

SURGICAL VALVE REPAIR

Risk of thrombotic complications following surgical valve repair — Surgical valve repair procedures include diverse procedures on different valves (eg, aortic versus mitral) treating a variety of valve pathologies (eg, myxomatous degeneration, rheumatic disease, endocarditis, and congenital valve disease), and thromboembolic risk varies among different clinical settings. The goal of antithrombotic therapy following surgical valve repair is to reduce the risk of thromboembolism and valve thrombosis, but limited data are available on the risk of these complications.

The magnitude of thromboembolic risk is illustrated by a study that included 897 patients who underwent surgical mitral valve repair (41 percent treated with a vitamin K antagonist [VKA] postoperatively); the risk of ischemic stroke was 1.5 percent during the first 30 days (equivalent to 18.3 percent per year), 2.1 percent per year during days 31 to 180, and 0.9 percent per year after 180 days [5].

Approach for surgical valve repair — The following recommendations apply to patients who have undergone surgical valve repair:

Mitral and tricuspid – For patients who have undergone surgical mitral or tricuspid valve repair with prosthetic material (eg, annuloplasty ring), we suggest anticoagulation for the first three months. Following the period of anticoagulation, we suggest aspirin therapy 75 to 100 mg per day. For patients without prosthetic material, we suggest aspirin therapy alone. Aspirin therapy alone is also a reasonable alternative for patients with repairs involving prosthetic material, and some clinicians prefer this approach.

When anticoagulation is chosen, we suggest a VKA with a goal international normalized ratio (INR) of 2.5 rather than a direct oral anticoagulant (DOAC). Evidence on DOAC use in this setting is lacking. When VKA is initiated in the early postoperative period, early heparin bridging is administered (using intravenous unfractionated heparin or subcutaneous low molecular weight heparin) with the same protocol described for patients treated with VKA after bioprosthetic valve implantation. (See 'Early bridging after bioprosthetic valve replacement' above.)

Aortic – For patients who have undergone surgical aortic valve repair, we suggest aspirin 75 to 100 mg per day.

Efficacy — Limited evidence is available to guide antithrombotic therapy following surgical valve repair. Studies of patients who have undergone surgical valve repair indicate a significant risk of thromboembolism [28,29]. Annuloplasty ring-associated thrombus and thromboembolism have been reported, even in patients receiving short-term anticoagulation [30]. However, the optimum regimen to reduce the risk of thrombotic complications of valve repair has not been established.

Observational studies of patients with surgical mitral valve repair have not established a significant benefit from routine postoperative VKA therapy compared with aspirin therapy [28,29], but the findings are inconclusive given study limitations. Evidence is lacking on DOAC use after surgical valve repair.

In a study of 469 patients without prior AF who underwent mitral valve repair, 325 were treated with a VKA and 144 were treated initially with aspirin; however, 32 percent of patients in the aspirin group were switched to VKA therapy because of new onset AF [28]. At three months, the two groups had similar thromboembolic rates (1.6 versus 2.6 percent; adjusted hazard ratio [HR] 0.82, 95% CI 0.16-4.2) and rates of major bleeding (9.1 versus 6.8 percent; adjusted HR 1.89, 95% CI 0.90-3.9).

A retrospective multicenter study of 1882 patients at 19 centers who underwent mitral valve repair with ring implantation included 1517 treated with VKA and 365 treated with antiplatelet drugs who were followed for six months [29]. Patients with prior AF were excluded, and the incidence of new AF was not reported. In propensity-matched cohorts (858 treated with VKA and 286 treated with antiplatelet agents), rates of embolic complications were similar (1.6 and 2.1 percent). Major bleeding events were more frequent in the VKA group (3.9 versus 0.7 percent) and the mortality rate was higher in the VKA group (2.7 versus 0.3 percent). However, the reported rates of mortality and embolic complications are of uncertain significance given the likely effects of unaccounted-for comorbidities and risk factors including postoperative AF.

Observational studies have reported low risk of embolism with aspirin therapy following aortic valve repair [31,32].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Prosthetic valves (The Basics)")

Beyond the Basics topic (see "Patient education: Warfarin (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Thrombotic complications of bioprosthetic valves – Complications caused by thrombus on a bioprosthetic valve include:

Thromboembolism – The risk varies depending upon time after implantation (highest immediately after implantation), valve position (higher risk with mitral versus aortic valves), and risk factors such as atrial fibrillation (AF). AF occurs in up to 50 percent of patients during the first three months after valve surgery. (See 'Thromboembolism' above.)

Valve thrombosis – Symptomatic bioprosthetic valve thrombosis (BPVT) is uncommon and a cause of valve obstruction, while subclinical BPVT is commonly identified in research imaging studies and is of uncertain clinical significance. (See 'Bioprosthetic valve thrombosis' above and "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

Goal of antithrombotic therapy – The goal of antithrombotic therapy following surgical bioprosthetic valve replacement or surgical valve repair is to reduce the risk of thromboembolism and valve thrombosis. Evidence to guide management is limited. (See 'Approach for surgical bioprosthetic valves' above and 'Approach for surgical valve repair' above and "Atrial fibrillation and flutter after cardiac surgery".)

Antithrombotic therapy for a surgical bioprosthetic valve (algorithm 1) (see 'Approach for surgical bioprosthetic valves' above):

With no concurrent indication for anticoagulation (see 'Without a concurrent indication for anticoagulation' above):

-With low bleeding risk – For patients with a surgical bioprosthetic valve with no concurrent indication for anticoagulation and low bleeding risk, we suggest anticoagulation for three to six months after implantation (Grade 2C). We suggest a vitamin K antagonist (VKA) with a goal international normalized ratio (INR) of 2.5 rather than a direct oral anticoagulant (DOAC) (Grade 2C). Evidence on DOAC use in this setting is lacking. After the period of anticoagulation, we suggest aspirin 75 to 100 mg per day (Grade 2C).

-With elevated bleeding risk – For patients with a surgical bioprosthetic valve with no concurrent indication for anticoagulation and elevated bleeding risk, we suggest aspirin 75 to 100 mg per day (Grade 2C). The decision on whether or not to proceed with aspirin therapy is based upon an individualized assessment of estimated benefits and risks. (See "Nonselective NSAIDs: Overview of adverse effects".)

With a concurrent indication for anticoagulation – For patients with a surgical bioprosthetic valve who have a concurrent indication for anticoagulation (such as AF), the choice of anticoagulant and duration of therapy is based upon the concurrent indication and clinical factors (including risk of bleeding). As an example, a DOAC is generally preferred for patients with AF who require anticoagulation. (See 'With a concurrent indication for anticoagulation' above and "Atrial fibrillation in adults: Use of oral anticoagulants", section on 'Approach to anticoagulation' and "Transcatheter aortic valve implantation: Antithrombotic therapy", section on 'Introduction'.)

Early heparin bridging after bioprosthetic valve replacement – Early therapeutic heparin bridging is indicated for patients who will be treated with VKA postoperatively (for three to six months). Bridging is not indicated for patients who will receive a DOAC or no anticoagulant. (See 'Early bridging after bioprosthetic valve replacement' above.)

For surgical valve repair (see 'Approach for surgical valve repair' above)

Mitral and tricuspid – For patients who have undergone surgical mitral or tricuspid valve repair with prosthetic material (eg, annuloplasty ring), we suggest anticoagulation for three months (Grade 2C). Following the period of anticoagulation, we suggest aspirin 75 to 100 mg daily (Grade 2C). For patients without prosthetic material, we suggest aspirin alone (Grade 2C). Aspirin alone is also a reasonable alternative for patients with surgical mitral or tricuspid valve repair involving prosthetic material, and some clinicians prefer this approach.

When anticoagulation is chosen, we suggest a VKA with a goal INR of 2.5 rather than a DOAC (Grade 2C). Evidence on DOAC use in this setting is lacking.

Aortic – For patients who have undergone surgical aortic valve repair, we suggest aspirin 75 to 100 mg daily (Grade 2C).

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Gerard P Aurigemma, MD, who contributed to prior versions of this topic review.

The UpToDate editorial staff acknowledges William Gaasch, MD (deceased), who contributed to an earlier version of this topic review.

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Topic 132746 Version 6.0

References

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