Differences in Endothelial Glycocalyx, Arterial Stiffness, and Left Atrial Function Among Ischemic Stroke Types

We investigated potential differences in arterial stiffness, thickness of endothelial glycocalyx, deformation of left atrium and ventricle among various ischemic stroke subtypes and controls.We included 194 ischemic stroke patients (<i>n</i> = 47 lacunar stroke, <i>n</i> = 50 large artery atherosclerotic stroke [LAA], <i>n</i> = 49 cardioembolic stroke, <i>n</i> = 48 with embolic stroke of undetermined source [ESUS]) and 50 matched controls. We measured: (1) perfused boundary region (PBR4-25) of the sublingual microvessels, (marker of endothelial glycocalyx integrity), (2) pulse wave velocity (PWV) and central systolic blood pressure (cSBP), (3) left ventricular global longitudinal strain, left atrial (LA) reservoir, conduction and contraction strain, (4) myocardial work indices, by pressure-myocardial loops, and (5) PWV/GLS ratio, to assess ventriculoarterial interaction.Compared with controls, stroke patients displayed affected LA strains, LVGLS, Wasted Work, PBR4-25, cSBP, PWV, and PWV/GLS (<i>p</i> < 0.05). We observed differences in LA strain, PWV, PWV/GLS, and PBR4-25 between different ischemic stroke subtypes (<i>p</i> < 0.05). Participants with lacunar strokes had the most impaired PBR4-25, participants with cardioembolic stroke and ESUS had the most impaired LA strain, and LAA had the most affected PWV and PWV/GLS (<i>p</i> < 0.05). PBR4-25 value of 2.29 μm could discriminate lacunar strokes (AUC: 0.81, 95% CI: 0.74-0.89; <i>p</i> < 0.001), PWV cut-off of 13 m/second could discriminate LAA (AUC: 0.80, 95% CI: 0.72-0.89; <i>p</i> < 0.001) and LA reservoir strain cut-off of 25% could discriminate ESUS/Cardioembolic strokes (AUC: 0.78, 95% CI: 0.71-0.85; <i>p</i> < 0.001).Lacunar strokes exert excessive shedding of endothelial glycocalyx, LAA show aggravated aortic stiffness, while ESUS/Cardioembolic strokes demonstrate worse LA performance. These differences in the underlying pathophysiological mechanisms among stroke subtypes may guide individualized secondary prevention strategies.