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Anticoagulation for patients with prosthetic heart valves during non-cardiac surgery

An article from the e-journal of the ESC Council for Cardiology Practice

Non-cardiac surgery poses major hazards to patients with prosthetic heart valves. This article provides guidelines for anticoagulant management tailored to thromboembolic risk, duration of lowered anticoagulation and risk of haemorrhage.
Non-cardiac surgery in patients with prosthetic heart valves poses risks of infective endocarditis, bleeding and acute/subacute valve thrombosis or systemic thromboembolism associated with interrupted anticoagulation. Management is complicated by the absence of randomised trials examining peri-operative anticoagulant management.

Valvular Heart Diseases


Thromboembolic risk for patients with prosthetic valves without anticoagulation is 8-22% per annum (0.02-0.06% per day). Anticoagulant withdrawal to allow a surgical procedure with sub-therapeutic international normalised ratio (INR) for 4-6 days therefore entails a theoretical thromboembolic risk of 0.08-0.36%. However, valve thrombosis is often inapparent for 1-2 months making it difficult to identify the inciting event. In limited clinical studies the incidence of thromboembolism was 0-2% in patients with aortic valve replacements and 11-20% in those with mitral valve replacements.

Overall thromboembolic risk is governed by a number of clinical characteristics (Table). The chosen peri-operative anticoagulant regime should be tailored according to thromboembolic risk, the duration of lowered anticoagulation and the procedural risk of haemorrhage. Seamless oral anticoagulation is preferred and this is safe for most minor procedures, including cardiac catheterisation, dental and ophthalmic surgery. With careful technique many major procedures can also be performed safely whilst oral anticoagulation is continued. When this approach is inappropriate, current guidelines recommend withdrawal of oral anticoagulation 72 hours (or more for agents with long half lives) before surgery to lower the INR to <1.5 and maintained anticoagulation with unfractionated heparin. Heparin should be started when the INR is <2.5 in high risk patients and <2.0 in those at lower risk. The activated partial thromboplastin time is maintained at twice the control value. Heparin should be discontinued six hours before surgery and resumed six hours after, when surgically feasible, until the INR is >2.5 in high risk patients and >2.0 in those at lower risk. Oral anticoagulation is resumed on the day of the procedure although this may be delayed in exceptional circumstances, eg. following neurosurgery.

The evidence to support the safety of low molecular weight heparins (LMWH) in this situation is scanty and despite its widespread promulgation this approach is NOT recommended. In the only published prospective study, the LMWH enoxaparin was used to replace oral anticoagulation using a strict protocol in 82 consecutive patients with mechanical heart valves, either to allow a surgical procedure or because of bleeding complications. There were 8 minor and 1 major bleeding events during treatment with enoxaparin and no thromboembolic complications at mean 3-month follow-up. Randomised clinical trials examining the role of LMWH in patients with prosthetic heart valves are long overdue but for the time being their routine use cannot be recommended. Similarly, the oral thrombin inhibitor, ximelagatran, has shown promise in reducing thromboembolism in patients with ‘lone’ atrial fibrillation but there are no data with prosthetic valves or native valve disease.
Hospital admission or delayed discharge to give heparin may be unnecessary in low risk patients and domiciliary heparin and oral anticoagulation can provide cost-effective management. The determination of which patients require prolonged regimes of overlapping heparin and oral anticoagulants may be difficult. Clinical judgement is required but these regimes are strongly recommended for those at highest risk. With strict adherence to these guidelines, the incidence of thromboembolic and haemorrhagic complications is low.

Type of risk

Low risk

High risk

Clinical factors: Atrial fibrillation  

+

Clinical factors: Previous thromboembolism  

+

Clinical factors: Hypercoagulable condition  

+

Clinical factors: Left ventricular dysfunction  

+

Clinical factors: >3 thromboembolic risk factors*  

+

Prosthesis design: Ball valve  

+

Prosthesis design: Tilting disc

+

 
Prosthesis design: Bileaflet

+

 
Prosthesis position: Mitral  

+

Prosthesis position: Aortic

+

 
Procedure: Dental, ophthalmic

+

 
Procedure: Skin

+

 
Procedure: Gastrointestinal  

+

Pathology: Malignancy  

+

Pathology: Infection  

+

Thromboembolic risk assessment for non-cardiac surgical procedures.* Risk factors for thromboembolism: hypertension, atrial fibrillation, diabetes mellitus, previous thromboembolism, hypercoagulable condition, left ventricular impairment, left atrial enlargement, mitral stenosis, documented left atrial/left ventricular thrombus.

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.

References


1. Bonow RO, Carobello B, DeLeon AC, et al. ACC/AHA guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol 1998;32:1486-1582
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9870202&dopt=Abstract.

2. Gohlke-Barwolf C. Anticoagulation in valvar heart disease: new aspects and management during non-cardiac surgery. Heart 2000;84:567-572
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11040023&dopt=Abstract

Ferreira I, Dos L, Tornos P, et al. Experience with enoxaparin in patients with mechanical heart valves who must withhold acenocumarol. Heart 2003;89:527-530
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12695457&dopt=Abstract

 

Notes to editor


Dr B. Prendergast
Manchester, United Kingdom
Nucleus Member of the ESC Working Group on Valvular Heart Disease

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.