LAUSR

To the Editor: We read with great interest the recently published article by Broersen et al.1 This study demonstrated the significant association between hs-cTnT (high-sensitivity cardiac troponin T) in patients with mild-to-moderate first-ever ischemic stroke without dementia and high prevalence of cognitive impairment at baseline and during 3-year follow-up. Recently, there has been much interest in the association of elevated cTnT, a specific biomarker for myocardial injury, with cognitive impairment. The ARIC study (Atherosclerosis Risk in Communities) found that people in communities with elevated hs-cTnT at baseline had lower cognitive scores at baseline and increased risk of dementia hospitalization during follow-up.2 Coronary heart disease was also associated with accelerated cognitive decline.3 These studies show that subclinical myocardial injury may be associated with cognitive decline. For patients with mild-to-moderate first-ever ischemic stroke without dementia, similar results were found. These patients with elevated hs-cTnT at admission baseline had lower cognitive function scores and more significant cognitive impairment during follow-up. Authors proposed 3 possible underlying mechanisms for this result. First, heart disease may cause ischemic stroke. Second, stroke-heart syndrome impaired autonomic cardiac function with myocardial damage after stroke. Finally, common vascular risk factors may lead to damage of both organs simultaneously as small vessel disease. Although authors perfectly explained why patients with first-ever ischemic stroke have increased hs-cTnT, they did not explain why elevated hs-cTnT was associated with worse cognitive function at baseline and during follow-up. Unlike that in community populations, cognitive decline in patients with ischemic stroke may be influenced by more factors. For example, cardiogenic infarction may be larger and more acute and may cause severer cognitive deficiency. Patients with heart diseases may continuously shed small thrombus, which can result in brain damage and cognitive impairment. Heart failure and usage of beta-blockers may reduce the cardiac output, which can decrease the cerebral blood flow and cause white matter lesions.4 Another possible mechanism for elevated hs-cTnT in stroke patients with cognitive decline may be related to the shared risk factors. Elevated hs-cTnT levels in patients with stroke were associated with impaired cognitive function at baseline (RR, 1.66 [95% CI, 1.26– 2.17]). After adjusting for major vascular risk factors, the association became insignificant (RR, 1.20 [95% CI, 0.89–1.62]). Common vascular risk factors, such as age, sex, obesity, smoking, alcohol consumption, cysteinemia, hypertension, hyperlipidemia, and diabetes mellitus have been associated with cognitive impairments.