Stroke in right dorsal anterior insular cortex Is related to myocardial injury

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Cardiac troponin is the most sensitive and specific biomarker for myocardial necrosis and is widely used in diagnostic algorithms in patients presenting with non‐ST‐segment elevation acute coronary syndrome (ACS).1 Serial measurements of troponin can augment diagnostic accuracy by distinguishing acute (dynamic) from chronic (stable) troponin elevations.2 Current guidelines for the management of patients with acute ischemic stroke (AIS) recommend troponin assessment during the acute phase.4 Troponin levels above the 99th percentile of a normal reference population are present in up to 60% of these patients when measured with high‐sensitivity assays.5 Elevated troponin is associated with poor functional outcome,5 and high delta troponin levels (ie, increases or decreases in repeated measurements) are related to increased in‐hospital mortality.6
The underlying pathophysiological mechanisms of troponin elevation in AIS remain unclear to date, resulting in considerable diagnostic and therapeutic uncertainty for clinicians.9 As shown recently in the prospective Troponin Elevation in Acute Ischemic Stroke study (TRELAS; NCT01263964), evidence of acute coronary lesions on angiography is significantly less frequent in AIS patients than in those with ACS, despite similar baseline levels of troponin.11 Interestingly, nearly half of patients with AIS and relevant troponin elevation had no evidence of coronary artery disease (CAD) at all. Therefore, additional stroke‐related factors contributing to the phenomenon of myocardial injury accompanying AIS have to be considered.
The insular cortex (IC) is suggested to play a crucial role within a cerebral network regulating autonomic balance and cardiac function.12 Yet, evidence has been inconclusive regarding the impact of insular lesions on stroke‐associated myocardial injury, as reflected by elevated troponin levels.6 As a methodological constraint, all of these studies dichotomized patients either according to the presence or absence of insular damage, or with respect to elevated versus normal troponin levels. Consequently, these approaches were not able to account for the functional subdivisions of IC, which, presumably, have differential impact on the control of autonomic function,20 or they neglected the detailed physiological information of the patients’ continuous troponin levels.23 What is more, except for one study, the temporal dynamics of troponin evaluation, which enhance diagnostic precision, were not considered.6
In 2003, a novel method to characterize the relationship of lesion location and accompanying behavioral measures was introduced, which resolves the aforementioned shortcomings23: This so‐called voxel‐based lesion symptom mapping (VLSM) neither requires anatomical nor clinical grouping of patients. Instead, it makes use of continuous clinical variables of interest in a voxel‐by‐voxel fashion similar to that established in functional magnetic resonance imaging (MRI). Thus, it allows for a more fine‐grained three‐dimensional analysis. Over the past years, VLSM has been increasingly used to elucidate the effect of vascular damage on behavioral performance (eg, in aphasia or neglect).24 More recently, VLSM has been successfully applied to demonstrate the relationship of stroke lesions with clinical parameters or symptoms such as hyperglycemia and cardiac arrhythmias.26
Here, we aimed to examine the impact of stroke location within the anterior circulation (including the insular cortex) on troponin levels and their relative temporal changes by using VLSM in patients with AIS.

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