Insular Cortex Lesions, Cardiac Troponin, and Detection of Previously Unknown Atrial Fibrillation in Acute Ischemic Stroke

Scheitz, Jan F.; Erdur, Hebun; Hæusler, Karl Georg; Audebert, Heinrich J.; Roser, Mattias; Laufs, Ulrich; Endres, Matthias; Nolte, Christian H.

doi:10.1161/strokeaha.115.008681

Cited by 89 publications

(60 citation statements)

References 45 publications

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“…Recently, cardiac troponins have been known to be associated with incident AF in the general population,26 and are associated with delayed diagnosis of AF after stroke 27. However, it is still unclear whether the pathomechanism of troponin elevation in AF is due to AF itself (eg, accompanying tachycardia with a fast ventricular response) or due to pre‐existing heart failure with or without LAE 28.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke

Ahn

Kim

Shin

et al. 2016

JAHA

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BackgroundTroponin elevation with electrocardiography changes is not uncommon in patients with acute ischemic stroke; however, it is still unclear whether the mechanism of these changes is due to cardiac problems or neurally mediated myocytic damage. Thus, we investigated cardiac and neurological predictors of troponin elevation in those patients.Methods and ResultsWe retrospectively analyzed medical data of the prospectively registered ischemic stroke patients on stroke registry who were admitted and underwent a serum cardiac troponin I and 12‐lead electrocardiography within 24 hours of symptom onset. However, patients with well‐known troponin‐elevating comorbidities were excluded from the analysis. Among 1404 ischemic stroke patients, 121 (8.7%) had elevated troponin, which was defined as more than 0.04 mg/mL. Multivariable analysis identified electrocardiography abnormalities such as QTc‐prolongation (odds ratio [OR]: 1.52, 95% CI: 1.02–2.28), left ventricular hypertrophy (OR: 2.14, 95% CI 1.43–3.19), Q‐wave (OR: 2.53, 95% CI: 1.48–4.32), and ST elevation (OR: 2.74, 95% CI: 1.12–6.72) as cardiac variables associated with troponin elevation, and higher National Institutes of Health Stroke Scale score (OR: 1.04, 95% CI: 1.01–1.07) and insular cortical lesions (OR: 2.78, 95% CI: 1.85–4.19) as neurological variables associated with troponin elevation. Incidence of troponin elevation as well as QTc‐prolongation was increased further in combination with cardiac and neurological factors.ConclusionsCertain cardiac and neurological conditions in acute ischemic stroke may contribute to troponin elevation. The proposed concept of cardiac vulnerability to cerebrogenic stress can be a practical interpretation of troponin elevation and electrocardiography abnormalities in stroke patients.

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Section: Discussionmentioning

confidence: 99%

Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke

Ahn

Kim

Shin

et al. 2016

JAHA

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“…In stroke patients, insular cortex lesions have been frequently associated with cardiac arrhythmia, abnormal arterial pressure variations during daytime and nighttime (nondipper profile), myocardial or respiratory impairment during sleep, associated with high levels of catecholamine, troponin T and brain natriuretic peptide (BNP) [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Cortical lateralization and cardiac autonomic control. Insights from insular stroke and epilepsy

Constantinescu¹,

Detante²,

Matei³

et al. 2017

Arch Clin Cases

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Autonomic nervous system dysfunction is a common complication of stroke. Human studies and experimental data showed a hemispheric lateralization of autonomic activity concerning the forebrain and particularly the insular cortex. Insular cortex involvement is associated with more pronounced autonomic imbalance leading to life threatening arrhythmias and sudden death. We present two case reports of insular infarction in young patients without any cardiac comorbidity, illustrating a specific lateralized function of insula and its influence on the sympatho-vagal balance that implied differentiated therapeutic management after stroke. The right insular stroke was associated to sympathetic activation and left insular stroke was associated to parasympathetic predominance. The same lateralization of autonomic function with opposite effects on sympatho-vagal balance was also reported in two insular epilepsy cases, illustrating the fact that, beyond the controlling network, the cortical modulation of the autonomic nervous system is asymmetric. Identifying high risk patients prone to develop neurogenic cardiac complications, by better understanding of dysautonomia pathophysiology and consequent implementation of prophylactic and therapeutic interventions may significantly reduce mortality rate in stroke and epilepsy.

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“…Additional predictors of paroxysmal AF in patients with cryptogenic stroke may include the NIH Stroke Scale score, 25 radiologic evidence of new cortical or cerebellar infarcts, 26 and cardiac biomarkers such as B-type natriuretic peptide, 27,28 highly sensitive cardiac troponin T, 29 and others. 30 However, in the CRYSTAL AF trial, we did not observe any correlation between infarction pattern and AF detection 31 and biomarker data were not collected.…”

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confidence: 99%

Predictors for atrial fibrillation detection after cryptogenic stroke

et al. 2016

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Objective: We assessed predictors of atrial fibrillation (AF) in cryptogenic stroke (CS) or transient ischemic attack (TIA) patients who received an insertable cardiac monitor (ICM). Methods:We studied patients with CS/TIA who were randomized to ICM within the CRYSTAL AF study. We assessed whether age, sex, race, body mass index, type and severity of index ischemic event, CHADS 2 score, PR interval, and presence of diabetes, hypertension, congestive heart failure, or patent foramen ovale and premature atrial contractions predicted AF development within the initial 12 and 36 months of follow-up using Cox proportional hazards models.Results: Among 221 patients randomized to ICM (age 61.6 6 11.4 years, 64% male), AF episodes were detected in 29 patients within 12 months and 42 patients at 36 months. Significant univariate predictors of AF at 12 months included age (hazard ratio [ Conclusion:Increasing age and a prolonged PR interval at enrollment were independently associated with an increased AF incidence in CS patients. However, they offered only moderate predictive ability in determining which CS patients had AF detected by the ICM. The CRYSTAL AF trial showed that the rate of atrial fibrillation (AF) detection among patients with cryptogenic stroke (CS) or transient ischemic attack (TIA) was 30% within 3 years after insertion of an insertable cardiac monitor (ICM). 1Numerous genetic, clinical, electrocardiographic, and echocardiographic features have been proposed as risk markers for developing AF.2-12 Within the Framingham Heart Study, a risk score for development of AF within 10 years was created, which included age, sex, body mass index, systolic blood pressure, treatment for hypertension, PR interval, clinically significant cardiac murmur, and heart failure.13 Echocardiographic measures did not improve risk prediction substantially.AF episodes are frequently asymptomatic and intermittent. Most CS/TIA patients monitored by ICM for AF detection have already undergone short-term Holter monitoring or telemetry in addition to cardiac and vascular imaging before device insertion.

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Insular Cortex Lesions, Cardiac Troponin, and Detection of Previously Unknown Atrial Fibrillation in Acute Ischemic Stroke

Cited by 89 publications

References 45 publications

Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke

Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke

Cortical lateralization and cardiac autonomic control. Insights from insular stroke and epilepsy

Predictors for atrial fibrillation detection after cryptogenic stroke

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