Author + information
- Swaminatha V. Gurudevan, MD⁎,
- Hetan Shah, MD†,
- Kirsten Tolstrup, MD⁎,
- Robert Siegel, MD⁎ and
- Subramaniam C. Krishnan, MD‡,⁎ ()
- ↵⁎Address for correspondence:
Dr. Subramaniam C. Krishnan, Arrhythmia Services, University of California Irvine Medical Center, 101 The City Drive, Orange, California 92868
cardioembolic strokes are responsible for more than 20% of all ischemic strokes. The examination of atrial sources of cardioembolic strokes has focused almost exclusively on the left atrial appendage (LAA) and the pathophysiology of thrombus formation at this site is well understood. However, especially in rheumatic heart disease, thrombi can occur in the left atrium (LA) outside the appendage a significant proportion of the time with poor understanding of the underlying mechanism. We present 3 patients in whom a thrombus was seen adherent to the septal LA. The probable underlying pathophysiology and the relationship to a recently described novel atrial structure, the left atrial septal pouch (LASP) (Fig. 1) that has the potential to be a site of stasis with thromboembolic complications, is discussed (1).
Seen in one-third of individuals, in addition to the appendage, LASP represents another LA structure that is a potential location for stasis and thromboembolism. We have presented 3 clinical examples, with a thrombus attached to the septal LA. Two patients (Figs. 2 and 3)⇓ had clear echocardiographic evidence of a LASP. The patient in Figure 4 had a thrombus with the site of attachment at the junction of the septum primum and septum secundum, where the LASP would normally be present. Due to its anatomical features, the LASP serves as a site of stasis and thrombus formation. The classic Virchow triad necessary for thrombogenesis consists of: 1) circulatory stasis; 2) endothelial injury; and 3) hypercoagulability. Of these, circulatory stasis is considered the most common trigger. In the setting of nonvalvular atrial fibrillation, stasis is felt to occur largely in the LAA and an LA thrombus is present in the LA appendage 90% of the time. However, in the presence of rheumatic mitral stenosis, an LA thrombus occurs in the appendage only one-half of the time. In the remaining, it occurs elsewhere in the LA, and LASP may comprise auxiliary site of thrombus formation especially mitral stenosis (even in sinus rhythm) or with elevated left ventricular filling pressures in heart failure. In the patient presented in Figure 2, while intrapouch stasis cannot be excluded, a thrombus occurred likely due to a combination of a hypercoagulable state and endothelial injury due to inflammation in the region of the LASP. Transesophageal echocardiography in this patient did not reveal spontaneous echo contrast (SEC) in the LA. With normal filling pressures and in the absence of mitral stenosis, right pulmonary venous blood would be expected to flow briskly through the LA (Fig. 5). In the example presented in Figure 3, dense SEC was seen due to a combination of absent atrial contractions from atrial fibrillation and likely high filling pressure evidenced by poor systolic function and elevated B-type natriuretic peptide levels. In the patient presented in Figure 4, the SEC is a consequence of high filling pressure from diastolic dysfunction. We show the complexity of thrombus formation in the LA, the cardiac chamber that is the most frequent source of cardioembolic strokes.
Dr. Krishnan is the owner of intellectual property related to closure of PFOs and to closure of the left atrial septal pouch and has commercialized intellectual property on transseptal puncture technology to St. Jude Medical. All other authors have reported that they have no relationships to disclose.
- American College of Cardiology Foundation
- Krishnan S.C.,
- Salazar M.
- Fyrenius A.,
- Wigstrom L.,
- Ebbers T.,
- Karlsson M.,
- Engwall J.,
- Bolger A.F.