American Heart Journal
Volume 148, Issue 5 , Page e1, November 2004

Left atrial thrombi, transient ischemic attacks, and atrial fibrillation

  • Claudia Stöllberger, MD

      Affiliations

    • 2nd Medical Department, Krankenanstalt Rudolfstiftung,Wien, Austria
  • ,
  • Josef Finsterer, MD

      Affiliations

    • Neurological Department, Krankenanstalt Rudolfstiftung, Wien, Austria.

Article Outline

 

To the Editor:

Stoddard et al investigated the relationship between left atrial/appendage (LA) thrombi detected by transesophageal echocardiography (TEE) and transient ischemic attack (TIA) in atrial fibrillation (AF) patients.1 In the face of LA thrombi, detected in 18% of patients, clinical risk factors for thromboembolism were not predictive of TIA.

The findings contradict the current opinion that in AF, TEE is not mandatory to assess embolic risk. Previous studies showed that clinical risk factors, but not LA-thrombi, were predictors for embolism.2, 3 To find the reasons for these contradictory findings, several issues should be discussed.

The patients' characteristics and inclusion criteria differ. How many were included as inpatients or outpatients? What were the indications for TEE? Stoddard included 21 patients with mitral stenosis, which was an exclusion criterion in other studies.2, 3 Would the results change if patients with mitral stenosis were excluded? How long was the interval between event and inclusion in the 32% of patients with prior stroke/TIA? This is an important consideration because it is known that the short-term recurrence is high.4

The follow-up investigations differ. How many patients in the study by Stoddard et al were only contacted by telephone and how many were seen (and at what intervals) by a physician? Were there differences between the patients with and without LA thrombi? In clinical practice, it is not always possible to achieve a well controlled oral anticoagulation. Therefore, it would be interesting to know how many patients were on therapeutic anticoagulation when TIA/embolic events occurred.

The end points differ. Other studies did not regard TIA as an end point because it was diagnosed on the basis of clinical history alone and its diagnosis was therefor considered problematic. Other causes, like seizure, migraine, vestibular impairment, anxiety, or global cerebral ischemia from hypotension, may be impossible to distinguish from focal cerebral ischemia.4 How would the results have changed if only strokes and peripheric embolic events had been evaluated as end points?

The etiology of TIA might not be due to embolism. Because the etiology of TIA and ischemic stroke may differ,5 it would be interesting to know whether all patients who had TIA were seen by a neurologist and how long the time interval was between TIA and neurological investigation. Was the neurologist blinded to the TEE findings? Which were the results of cerebral computed tomography, magnetic resonance imaging, carotid duplex-sonography, electroencephalography, and 24-hour-Holter monitoring?

Answers to these questions may contribute to the clarification concerning whether TEE is necessary to assess embolic risk in AF.

Back to Article Outline

References 

  1. Stoddard M, Singh P, Dawn B, et al.  Left atrial thrombus predicts transient ischemic attack in patients with atrial fibrillation. Am Heart J. 2003;145:676–682
  2. Stollberger C, Chnupa P, Kronik G, et al.  Transesophageal echocardiography to assess embolic risk in patients with atrial fibrillation. Ann Intern Med. 1998;128:630–638
  3. The Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography . Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. Ann Intern Med. 1998;128:639–647
  4. Johnston SC. Transient ischemic attack. N Engl J Med. 2002;347:1687–1692
  5. Anderson DC, Kappelle LJ, Eliasziw M, et al.  Occurrence of hemispheric and retinal ischemia in atrial fibrillation compared with carotid stenosis. Stroke. 2002;33:1963–1967

PII: S0002-8703(04)00268-6

doi:10.1016/j.ahj.2004.03.053

American Heart Journal
Volume 148, Issue 5 , Page e1, November 2004