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Response by Jordan et al to Letter Regarding Article, "Left Atrial Volume Index Is Associated With Cardioembolic Stroke and Atrial Fibrillation Detection After Embolic Stroke of Undetermined Source".

In Response: We thank Ho et al for their letter in response to our article “Left Atrial Volume Index Is Associated With Cardioembolic Stroke and Atrial Fibrillation Detection After Embolic Stroke of Undetermined Source.” The authors highlight an important discussion on the relationship between left atrial enlargement and left ventricular diastolic dysfunction (LVDD), and the implications this relationship has on our understanding of thromboembolic risk. As Ho et al point out, multiple studies have demonstrated a clear association between increased left atrial volume index (LAVI) and diastolic dysfunction. In fact, the association seems to be graded and one study expressed this relationship with the following equation—(Indexed LA volume =8.67 [diastolic function grade] + 21.30 [P=0.001, r=0.78]). Furthermore, both LAVI and LVDD have be shown to be associated with increased thromboembolic risk and cardiovascular outcomes, particularly with respect to development of atrial fibrillation and ischemic stroke risk. Therefore, it is likely these 2 entities play a complex role in the pathogenesis of thromboembolic risk. While the role of left atrial dysfunction in thromboembolic risk has been more extensively studied, the role of LVDD has been a poorly studied area. Increasing awareness to the role of LVDD in thromboembolism should greatly improve our understanding of cardioembolic stroke risk and inform secondary prevention strategies. LVDD has long been implicated as a driver of left atrial dysfunction and dilatation. One study of 1589 ischemic stroke patients demonstrated an independent association between atrial fibrillation and grade II LVDD (odds ratio, 4.37; CI, 2.99–6.41; P≤0.001), grade III LVDD (odds ratio, 5.6; CI, 3.42–9.17; P<0.001), and left atrial enlargement (odds ratio, 5.19; CI, 3.67– 7.35; P<0.001). To our knowledge, no study at present has independently associated both LAVI and LVDD with cardioembolic stroke. The importance and value of LVDD as an independent cardiac biomarker, however, would only be demonstrated if the association between LVDD and thromboembolic risk is shown to be independent of other markers of atrial cardiopathy such as N-terminal B-type natriuretic peptide, left atrial enlargement, and increased p-wave terminal force in lead V1 on ECG. These have been shown to be independent predictors of stroke risk. We did not include LVDD as a parameter in our multivariate analysis comparing the association of LAVI and stroke subtype (CE and ESUS). We look forward to the evolving discourse on LVDD and LAVI with regarding to thromboembolic risk and hope these biomarkers prove useful in our understanding of appropriate strategies for mitigating recurrent stroke risk in patients with cryptogenic stroke and ESUS.