Abstract
Cardiac troponin is a specific and sensitive biomarker to identify and quantify myocardial injury. Myocardial injury is frequently detected after acute ischemic stroke and strongly associated with unfavorable outcomes. Concomitant acute coronary syndrome is only one of several possible differential diagnoses that may cause elevation of cardiac troponin after stroke. As a result, there are uncertainties regarding the correct interpretation and optimal management of stroke patients with myocardial injury in clinical practice. Elevation of cardiac troponin may occur as part of a ‘Stroke-Heart Syndrome’. The term ‘Stroke-Heart Syndrome’ subsumes a clinical spectrum of cardiac complications after stroke including cardiac injury, dysfunction, and arrhythmia which may relate to disturbances of autonomic function and the brain–heart axis. In this review, we provide an up-to-date overview about prognostic implications, mechanisms, and management of elevated cardiac troponin levels in patients with acute ischemic stroke.
Highlights
Current guidelines on the early management of stroke recommend measuring cardiac troponin in all patients with suspected stroke [1]
Since the clinical presentation of an acute coronary syndrome (ACS) may be atypical after stroke and because treatment of suspected ACS may entail a relevant bleeding risk, there remains a clinical dilemma for stroke physicians
We provide an up-to-date overview about frequency, prognostic utility, potential mechanisms, and management of elevated cardiac troponin (cTn) levels in patients with acute ischemic stroke
Summary
Current guidelines on the early management of stroke recommend measuring cardiac troponin (cTn) in all patients with suspected stroke [1]. Previous studies indicate that in 85–95% of all stroke patients, and in approximately two thirds of stroke patients with elevated cTn upon hospital admission, serial measurements show no relevant temporal change in cTn levels [14, 25] This suggests that the majority of stroke patients have chronic rather than acute myocardial injury. The diagnosis of TGA was associated with a higher risk of hs-cTn elevation than diagnosis of transient ischemic attack (TIA), migraine with aura or acute vestibular syndrome [46] These correlations indicate that mechanisms similar to those described for the ‘Stroke-Heart syndrome’ are involved in the occurrence of myocardial injury after acute neurological conditions. Interdisciplinary collaborations of stroke neurologists and cardiologists are needed to guide reasonable management of stroke patients with elevated cTn
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