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In a recent article in this journal, Strandberg et al reported 441 patients who were investigated by transoesophageal echocardiography (TOE) after ischaemic stroke or transient ischaemic attacks.1 The authors looked for cardiac sources of embolism. They found that in patients who were in sinus rhythm and without any cardiac disease, 8% have been given anticoagulation drugs on the basis of TOE data.
Although we agree with their conclusions that TOE should be used in patients with stroke we have, however, concerns about the following points:
No definition is given of what is meant by “anticoagulation drugs.” Did the authors mean only oral anticoagulation with acenocoumarol or phenprocoumon, or did they also mean other antithrombotic drugs like heparin, acetylsalicylic acid, or clopidogrel?
What contraindications to anticoagulant drugs did they consider?
How long after the stroke or transient ischaemic attack was anticoagulant treatment started?
The decision about anticoagulation was based on “clinical assessment.” They report that “if a minor risk factor for a cardiac source of embolism was detected, anticoagulation treatment was started after clinical consideration of the probability of cardiac embolism and treatment hazards” but the decision criteria for “assessment” and “considerations” are not reported, and thus these decisions are not reproducible. Did the number of risk factors2 influence the decision for anticoagulation?
It would be especially interesting to know which patients in whom TOE had detected major and minor risk factors2 did not receive anticoagulation drugs. Did the type of risk factor or the TOE findings influence the decision about anticoagulation?
The detailed TOE findings of the 8% of patients in sinus rhythm in whom TOE prompted anticoagulant treatment are not given, thus making the impact of TOE in therapeutic decisions difficult to determine. We suspect that a patent foramen ovale was a frequent finding in this group of patients and are interested in the authors’ diagnostic and therapeutic approach in these patients with suspected paradoxical embolism. Our special interest in stroke patients with patent foramen ovale results not only from own experience3 but also from the recently published large prospective study in stroke patients with patent foramen ovale.4 This has not shown any differences in the recurrence rate of stroke in patients with patent foramen ovale between those treated with warfarin and those treated with acetylsalicylic acid.
In routine clinical practice, echocardiography is not only relevant to decisions about anticoagulant treatment in stroke patients, but also to other forms of medical treatment—such as ACE inhibitors or β blocking agents in left ventricular dysfunction accompanying dilated cardiomyopathy or left ventricular aneurysm, or antibiotic treatment in infective endocarditis. Furthermore, echocardiographic findings may prompt cardiac surgery, for example in patients with left atrial myxoma, aortic aneurysm, mitral or aortic valve stenosis, or infective endocarditis. Thus some of the major and minor risk factors for cardiogenic brain embolism2 are disorders which might require treatment other than by anticoagulant drugs. The authors do not indicate how often such therapeutic decisions, “beyond” anticoagulation, were prompted by echocardiographic findings.
In conclusion, we agree that TOE is a useful tool in stroke patients to clarify diagnostic and therapeutic issues. The important question, however, as to which stroke patients should undergo TOE remains unresolved.
We would like to thank Drs Stöllberger and Finsterer for their interest and noteworthy opinions concerning our paper.
By “anticoagulation drug,” we meant only oral anticoagulation with warfarin. The contraindications to this treatment were allergy to warfarin, a bleeding tendency, hepatic or renal insufficiency, serious hypertension, endocarditis, alcohol abuse, pregnancy, and dementia.
The decision to start or continue anticoagulation after a stroke with a clear cardiac source of embolism is a difficult one and must be made after careful thought. When a major risk factor for a cardiac source of embolism was detected using transoesophageal echocardiography (TOE) and none of the contraindications mentioned above was present, the patient was given anticoagulant drugs. In cases with a minor risk factor for a cardiac source of embolism the decision to start anticoagulant treatment was based on the number and type of risk factors. In the study population, anticoagulant treatment was usually started within one to three days from the event, after haemorrhagic transformation had been excluded by brain imaging.
When patients who were in sinus rhythm and had no history of cardiac disease were evaluated as an independent group, anticoagulant treatment appeared to be based on TOE data in 22 of 286 patients (8%). In this group, 12 thrombi were found on TOE: three in the left atrial appendage, seven in the aortic arch, and two in the descending aorta. One patient was treated mainly for left ventricular wall motion abnormality. Nine patients were receiving anticoagulant drugs on the basis of a patent foramen ovale, and in all these cases right to left shunting was seen, at least during a Valsalva manoeuvre. A patent foramen ovale was quite a common finding in our study group (67/441), but only 12 patients were receiving anticoagulant drugs on that basis.
In our study we concentrated only on the decision to start anticoagulant treatment. We agree with Drs Stöllberger and Finsterer that both transthoracic echocardiography (TTE) and TOE give useful information with respect to medical treatment or cardiac surgery. TTE and TOE are useful tools in patients with stroke or transient ischaemic attack if the patients are candidates for active treatment.
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