Stroke–heart syndrome: clinical presentation and underlying mechanisms

Scheitz, Jan F.; Nolte, Christian H.; Doehner, Wolfram; Hachinski, Vladimir; Endres, Matthias

doi:10.1016/s1474-4422(18)30336-3

Cited by 195 publications

(228 citation statements)

References 95 publications

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“…Stroke‐heart syndrome, in particular, ischemic stroke‐related cardiac alteration, may well be related to mechanisms of the brain‐heart connection (ie, the brain‐heart axis), which is the cortical modulation of the cardiovascular system . As a piece of rigorous evidence, damage to the insular cortex has been associated with myocardial injury, arrhythmia, and neuroendocrine disturbance .…”

Section: Discussionmentioning

confidence: 99%

“…Stroke-heart syndrome, in particular, ischemic stroke-related cardiac alteration, may well be related to mechanisms of the brain-heart connection (ie, the brain-heart axis), which is the cortical modulation of the cardiovascular system. 2,23,24 As a piece of rigorous evidence, damage to the insular cortex has been associated with myocardial injury, arrhythmia, and neuroendocrine disturbance. 11,23,25 Despite being a potent candidate for diagnosing acute CAD, the diagnostic specificity of hs-cTnT may be affected by many other disorders, such as respiratory or renal failure, ischemic or hemorrhagic stroke, and septic shock.…”

Section: Discussionmentioning

confidence: 99%

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Elevation of high‐sensitivity cardiac troponin T at admission is associated with increased 3‐month mortality in acute ischemic stroke patients treated with thrombolysis

Sui

Liu

Luo

et al. 2019

Clinical Cardiology

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Background Elevated levels of cardiac troponin T (cTnT) have been associated with unfavorable outcomes in cardiac patients. However, no studies, to date, have discussed the prognostic value of high‐sensitivity cTnT (hs‐cTnT) in thrombolyzed patients with acute ischemic stroke (AIS). Hypothesis We hypothesized that elevated levels of hs‐cTnT would be associated with poorer clinical outcomes in AIS patients treated with intravenous tissue‐type plasminogen activator (IV tPA). Methods From January 2017 to February 2018, a total of 241 AIS patients treated with IV tPA within 4.5 hours of onset were recruited. On admission, patients were stratified into either normal or elevated hs‐cTnT groups according to a cutoff value of 14 ng/L. Multivariable logistic regression analyses were conducted to identify determinants of hs‐cTnT elevation and to detect whether elevated hs‐cTnT was associated with disability and/or mortality. Results In multivariable regression analysis, older age (P < .001) and stroke etiology (P = .024) were significantly associated with elevated hs‐cTnT levels. After adjusting for demographic and clinical characteristics, hs‐cTnT elevation was still significantly associated with 14‐day major disability (modified Rankin Scale (mRS) 3‐5, model 1, P = .019, odds ratio [OR] 2.677; model 2, P = .015, OR 2.834), 14‐day composite unfavorable outcome (mRS 3‐6, model 1, P = .005, OR 3.525; model 2, P = .003, OR 3.976), 30‐day mortality (P = .049, OR 4.545) and 90‐day mortality (P = .049, OR 3.835). Conclusions Elevation of hs‐cTnT at admission is associated with an increased risk of 90‐day mortality in AIS patients treated with IV tPA.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Elevation of high‐sensitivity cardiac troponin T at admission is associated with increased 3‐month mortality in acute ischemic stroke patients treated with thrombolysis

Sui

Liu

Luo

et al. 2019

Clinical Cardiology

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“…ACS may even be clinically silent in AIS patients. Guidelines recommend to measure troponin (cTn) in AIS patients, but diagnostic and therapeutic consequences remain vague [9,11].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, nearly half of these AIS patients with relevant troponin elevation did not show any CAD at all. In those patients, stress induced neurocardiogenic dysregulation may contribute to cardiac injury following stroke ("stroke-heart syndrome", for details see Scheitz JF et al Lancet Neurology 2018) [9]. In support of this notion of stroke-induced cardiac injury, ischemic lesions in the right anterior dorsal insula representing the central autonomic network were significantly associated with dynamic troponin elevation as evidenced by voxel-based lesion symptom mapping [10].…”

Section: Introductionmentioning

confidence: 97%

PRediction of acute coronary syndrome in acute ischemic StrokE (PRAISE) – protocol of a prospective, multicenter trial with central reading and predefined endpoints

et al. 2020

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Background: Current guidelines recommend measurement of troponin in acute ischemic stroke (AIS) patients. In AIS patients, troponin elevation is associated with increased mortality and worse outcome. However, uncertainty remains regarding the underlying pathophysiology of troponin elevation after stroke, particularly regarding diagnostic and therapeutic consequences. Troponin elevation may be caused by coronary artery disease (CAD) and more precisely acute coronary syndrome (ACS). Both have a high prevalence in stroke patients and contribute to poor outcome. Therefore, better diagnostic algorithms are needed to identify those AIS patients likely to have ACS or other manifestations of CAD. Methods/design: The primary goal of the "PRediction of Acute coronary syndrome in acute Ischemic StrokE" (PRAISE) study is to develop a diagnostic algorithm for prediction of ACS in AIS patients. The primary hypothesis will test whether dynamic high-sensitivity troponin levels determined by repeat measurements (i.e., "rise or fall-pattern") indicate presence of ACS when compared to stable (chronic) troponin elevation. PRAISE is a prospective, multicenter, observational trial with central reading and predefined endpoints guided by a steering committee. Clinical symptoms, troponin levels as well as findings on electrocardiogram, echocardiogram, and coronary angiogram will be recorded and assessed by central academic core laboratories. Diagnosis of ACS will be made by an endpoint adjudication committee. Severe adverse events will be evaluated by a critical event committee. Safety will be judged by a data and safety monitoring board. Follow-up will be conducted at three and twelve months and will record new vascular events (i.e., stroke and myocardial infarction) as well as death, functional and cognitive status. According to sample size calculation, 251 patients have to be included.

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“…It is increasingly recognized that hs-cTn elevation may occur in the absence of ischaemic myocardial disease in patients with acute central nervous system disease [2,4]. There are reasonable arguments that this phenomenon represents a neurocardiogenic injury attributable to catecholamine-or stress-mediated disturbance of autonomic cardiac control [2,4]. Myocardial injury has been linked to ischaemic lesions within the right insular cortex and to demyelinating lesions in the medulla oblongata, both crucial regions of cardiac autonomic control [18,19].…”

Section: Discussionmentioning

confidence: 99%

Myocardial injury in transient global amnesia: a case‐control study

Erdur¹,

Siegerink

Ganeshan³

et al. 2019

Euro J of Neurology

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Background and purpose Elevation of cardiac troponin (cTn), a sensitive biomarker of myocardial injury, is frequently observed in severe acute neurological disorders. Case reports suggest that cardiac dysfunction may also occur in patients with transient global amnesia (TGA). Until now, no study has systematically assessed this phenomenon. Methods We performed a case‐control study using data of consecutive patients presenting with TGA from 2010 to 2015. Multiple logistic regression analysis accounting for age, sex and cardiovascular risk factors was performed to compare the likelihood of myocardial injury [defined as elevation of cTn > 99th percentile (≥14 ng/L); highly sensitive cardiac troponin T assay] in TGA with three reference groups: migraine with aura, vestibular neuritis and transient ischaemic attack (TIA). Results Cardiac troponin elevation occurred in 28 (25%) of 113 patients with TGA. Patients with TGA with cTn elevation were significantly older, more likely to be female and had higher blood pressure on admission compared with those without. The likelihood of myocardial injury following TGA was at least more than twofold higher compared with all three reference groups [adjusted odds ratio, 5.5; 95% confidence interval (CI), 1.2–26.4, compared with migraine with aura; adjusted odds ratio, 2.2; 95% CI, 1.2–4.4, compared with vestibular neuritis; adjusted odds ratio, 2.3; 95% CI, 1.3–4.2, compared with TIA]. Conclusions One out of four patients with TGA had evidence of myocardial injury as assessed by highly sensitive cTn assays. The likelihood of myocardial injury associated with TGA was even higher than in TIA patients with a more pronounced cardiovascular risk profile. Our findings suggest the presence of a TGA‐related disturbance of brain–heart interaction that deserves further investigation.

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Stroke–heart syndrome: clinical presentation and underlying mechanisms

Cited by 195 publications

References 95 publications

Elevation of high‐sensitivity cardiac troponin T at admission is associated with increased 3‐month mortality in acute ischemic stroke patients treated with thrombolysis

Elevation of high‐sensitivity cardiac troponin T at admission is associated with increased 3‐month mortality in acute ischemic stroke patients treated with thrombolysis

PRediction of acute coronary syndrome in acute ischemic StrokE (PRAISE) – protocol of a prospective, multicenter trial with central reading and predefined endpoints

Myocardial injury in transient global amnesia: a case‐control study

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