Anticoagulation in Patients With Stroke With Infective Endocarditis Is Safe
A 33-year-old man with a prosthetic mitral valve presents with an occipital infarct, fever, and leukocytosis. Work-up confirms the diagnosis of infective endocarditis due to Staphylococcus aureus. Cardiovascular surgeons recommend anticoagulation and urgent valve replacement.
(1) Is it safe to continue anticoagulants prior to or during the surgical procedure?
(2) Are other tests needed to determine benefit versus risk?
(3) When is the optimal timing to perform cardiac surgery?
The use of anticoagulation in stroke patients with infective endocarditis.
Anticoagulation is a controversial issue in Staphylococcus aureus infective endocarditis (IE) because these patients are believed to be particularly susceptible to hemorrhagic transformation of embolic lesions. However, the evidence supporting the deleterious effect of anticoagulation is at best incomplete and the adverse effect of such treatment has been questioned by most recent research. An increasing number of patients with IE receive anticoagulant treatment because of mechanical prosthetic valves, atrial fibrillation, pulmonary embolism, and factor V Leiden mutation as well as other hypercoagulability disorders. These patients carry an increased risk of thromboembolism and the decision to terminate anticoagulant treatment should therefore balance the risks and benefits of such treatment.
Cerebrovascular complications (CVCs) in IE are most often the consequence of septic embolization from vegetations located at the heart valves and occur in approximately 25% of the patients with S. aureus IE. CVCs cover a wide clinical spectrum, 1 of the most feared being cerebral hemorrhage, which is almost always associated with a poor outcome. Cerebral hemorrhage is mainly caused by hemorrhagic transformation of an ischemic stroke, whereas acute pyogenic arteritis or rupture of mycotic aneurysms is rare. In a series of studies conducted in the period 1975 to 1997, cerebral hemorrhage has been reported in 13% to 17% of the patients with S. aureus IE, which is 1 of the key arguments against anticoagulation in this group of patients.1 Thus, in a number of these studies, cerebral hemorrhage has been linked to uncontrolled infection and anticoagulation, whereas other studies have failed to find such an association. For example, in a study by Wilson et al evaluating the impact of anticoagulation in patients with prosthetic valve endocarditis, the authors showed that the incidence of CVC and death was higher if anticoagulation was discontinued supporting the use of anticoagulation in this group of patients.2 Unfortunately, these studies share a common set of limitations because they all have been conducted in an era before the introduction of the Duke criteria with poor or no access to high-quality neuroimaging (CT or MRI) and echocardiography. It is generally accepted that the clinical presentation of IE may be suggestive but mostly is unspecific and that the diagnosis of IE primarily depends on blood cultures positive for micro-organisms that commonly cause IE and echocardiographic findings. Accordingly, studies including patients only based on the clinical evidence of IE may be inclined to include the sickest patients with IE, thus overestimating the incidence of CVC and cerebral hemorrhage. A most recent study by the current author showed that although stroke was a common complication in patients with S. aureus IE, the incidence of cerebral hemorrhage was low (3%), and there was no association between this feared complication and anticoagulation.3 Contrary anticoagulation was associated with a reduction in vegetation size and CVC on admission in patients with native valve S. aureus IE.3 Because a vegetation by all means is a coagulum that forms on the damaged heart valve and consists of damaged tissue, bacteria, fibrin, and platelets, a protective effect of anticoagulation seems theoretically plausible. This finding has later been verified in the overall IE population by the same authors supporting a protective effect of anticoagulation on embolic events.4 It is important to stress, however, that the protective effect of anticoagulation on embolism is not supported by strong clinical evidence and such treatment is at present not recommended as standard treatment in all patients with IE. Importantly, the potential harmful effect of anticoagulation is clearly overestimated and no clinical evidence justifies the discontinuation of this treatment when indicated. However, in some cases, like in the present case, a switch from warfarin to heparin is recommended due to the likelihood of urgent surgery or if treatment with rifampicin is initiated making treatment with warfarin difficult to handle.
CVC in S. aureus IE is associated with a poor prognosis and concerns of neurological deterioration exist when cardiac surgery is indicated. Although cardiac surgery is associated with considerable risks, surgery is not contraindicated by ischemic stroke and can be preformed without delay in selected cases if indicated. In cases of suspected CVC, the threshold for diagnostic evaluation with CT or MRI should be low to rule out cerebral hemorrhage because this would justify the discontinuation of anticoagulation and may postpone planed cardiac surgery by at least 1 month. In general, repeated echocardiography and neuroimaging play an important role in the management of patients with IE and should be performed on low clinical suspicion.
Anticoagulation is a double-edge sword and the risk of bleeding complications should be included in the assessment of patients with IE receiving such treatment. It is important to emphasize, however, that no substantial evidence supports the widespread reluctance against anticoagulation in S. aureus IE and that discontinuation of anticoagulation without weighty reasons could be a mistake.
The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. This article is Part 1 in a 3-part series. Parts 2 and 3 appear on pages 1797 and 1799, respectively.
- Received January 18, 2011.
- Accepted April 1, 2011.
- © 2011 American Heart Association, Inc.
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