Diagnostic Yield of TEE in Patients with Cryptogenic Stroke and TIA with Normal TTE: A Systematic Review and Meta-Analysis.

Shamik Shah,Gary S Gronseth,Yunxia Wang,Urvish Patel,Preeti Malik

doi:10.3390/neurolint13040063

Abstract

Introduction: The role of transesophageal echocardiography (TEE) in cryptogenic stroke and transient ischemic attack (TIA) with normal transthoracic echocardiography (TTE) remains controversial in the absence of definite guidelines. We aimed to perform a systematic review and meta-analysis to estimate an additional diagnostic yield and clinical impact of TEE in patients with cryptogenic stroke and TIA with normal TTE. Methods: We performed a systematic review of cohort studies on PubMed using the keywords ‘cryptogenic stroke’, cryptogenic TIA’, ‘TEE’, and ‘TTE’ with matching MeSH terms. We included studies with patients who had cryptogenic stroke or TIA and had normal TTE findings, where the study intended to obtain TEE on all patients and reported all TEE abnormalities. The studies containing patients with atrial fibrillation were excluded. All studies were evaluated for internal and external validity. Inverse variance random effects models were used to calculate the effect size, the number needed to diagnose, and the 95% confidence interval. Results: We included 15 studies with 2054 patients and found LA/LAA/aortic thrombus, valvular vegetation, PFO-ASA, valvular abnormalities, and complex aortic plaques on TEE. Of these, 37.5% (29.7%–45.1%) of patients had additional cardiac findings on TEE. Management of 13.6% (8.1%–19.1%) of patients had changed after TEE evaluation. Based on current guidelines, it should change management in 4.1% (2.1%–6.2%) of patients and could potentially change management in 30.4% (21.9%–38.9%) of patients. Sensitivity analysis was also performed with only class II studies to increase internal validity, which showed additional cardiac findings in 38.4% (28.5%–48.3%), changed management in 20.2% (8.7%–31.8%), should change management in 4.7% (1.5%–7.9%), and could potentially change management in 30.4% (17.8%–43.0%) of patients. Conclusions: The diagnostic yield of TEE to find any additional cardiac findings in patients with cryptogenic stroke or TIA is not only high, but it can also change management for certain cardiac abnormalities. TTE in cryptogenic stroke or TIA may mitigate future risks by tailoring the management of these patients.

Highlights

Review of the PubMed database identified 524 potentially relevant articles, 492 duplicated articles, and irrelevant articles were excluded during the first round of review of titles only
Our systematic review and meta-analysis results show that the diagnostic yield of transesophageal echocardiography (TEE) to find additional cardiac findings in patients with cryptogenic stroke or transient ischemic attack (TIA) is approximately 38%, TEE could change management in 30.4% of patients, TEE has changed management in approximately 20% of these patients, and transthoracic echocardiography (TTE) should change management in approximately 4.7% of patients
We found that TEE has changed management in approximately 20% of patients with cryptogenic stroke (CS)/TIA and should change management in 4.7% of the patients as per guidelines

Summary

Introduction

Of the 690,000 ischemic strokes that occur in the United States every year, approximately 30% are of unknown cause, or cryptogenic even after a thorough diagnostic work-up. Possible mechanisms underlying cryptogenic stroke (CS) include but are not limited to occult paroxysmal atrial fibrillation (AF) and other atrial cardiopathies, paradoxical embolism through a patent foramen ovale (PFO), or sub-stenotic atherosclerosis [1]. Even though the majority of the potential mechanisms in the CS are attributed to embolic phenomena which are fundamentally associated with the cardiac origin, there is still no consensus on a thorough cardiac work-up of stroke patients to identify the stroke mechanism and improve secondary prevention strategies [1,2]. Transient ischemic attacks (TIAs) are most commonly caused by the embolic or thrombotic consequences of atherothrombotic disease, which is similar to the underlying pathological mechanism for cardiovascular disease [3]

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