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Published on: April 25, 2014
Acute right insular ischaemic lesions and poststroke left ventricular dysfunction
Klemens Winder1,2, Carolina Villegas Millar1, Gabriela Siedler1
1Neurology, University Hospital Erlangen, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Erlangen, Germany.
Insights
Acute ischemic stroke can cause myocardial injury. This study found that damage to specific right-brain areas, particularly the insula, is linked to impaired left ventricular ejection fraction (LVEF) after stroke.
Area of Science:
- Neuroscience
- Cardiology
- Medical Imaging
Background:
- Myocardial injury is common in acute ischemic stroke, even without prior heart disease.
- The brain-heart axis plays a crucial role in cardiovascular regulation.
- Understanding stroke-related cardiac dysfunction is vital for patient outcomes.
Purpose of the Study:
- To investigate the association between left ventricular ejection fraction (LVEF) and the location of ischemic stroke lesions.
- To identify specific brain regions involved in stroke-induced cardiac impairment.
Main Methods:
- Retrospective analysis of 231 acute ischemic stroke patients without pre-existing heart disease.
- Echocardiography to assess LVEF; categorization of impaired LVEF.
- Multivariate voxelwise lesion analysis to correlate LVEF with lesion sites.
Main Results:
- 40 patients (17.3%) had impaired LVEF post-stroke.
- Impaired LVEF was associated with larger infarct volumes, troponin elevation, and atrial fibrillation.
- Decreased LVEF correlated with lesions in the right insula, amygdala, and operculum.
Conclusions:
- The right hemispheric central autonomic network, particularly the insular cortex, is implicated in the brain-heart axis.
- Acute ischemic stroke in these brain regions can directly impair cardiac function.
- These findings support the concept of a distinct stroke-heart syndrome.
Introduction:
Myocardial injury related to acute ischaemic stroke is common even without primary cardiac disease. We intended to determine associations between values of left ventricular ejection fraction (LVEF) and ischaemic stroke lesion sites.
Methods:
Of a local database, patients with acute first-ever ischaemic stroke confirmed by brain imaging but without pre-existing heart disease were included. The cardiac morphology and LVEF were obtained from transthoracic or transesophageal echocardiography, and impaired LVEF was categorised as mild (35%-50%), moderate (34%-25%) and severe (<25%). Patient age, stroke severity, ischaemic lesion volume, prevalence of troponin I increase (>0.1 ng/mL), atrial fibrillation and cardiac wall motion abnormalities were assessed and compared between patients with and without impaired LVEF after stroke (significance: p<0.05). A multivariate voxelwise lesion analysis correlated LVEF after stroke with sites of ischaemic lesions.
Results:
Of 1209 patients who had a stroke, 231 (mean age 66.3±14.0 years) met the inclusion criteria; 40 patients (17.3%) had an impaired LVEF after stroke. Patients with impaired LVEF had higher infarct volumes (53.8 mL vs 30.0 mL, p=0.042), a higher prevalence of troponin increase (17.5% vs 4.2%, p=0.006), cardiac wall motion abnormalities (42.5% vs 5.2%, p<0.001) and atrial fibrillation (60.0% vs 26.2%, p<0.001) than patients with LVEF of >50%. The multivariate voxelwise lesion analysis yielded associations between decreased LVEF and damaged voxels in the insula, amygdala and operculum of the right hemisphere.
Conclusion:
Our imaging analysis unveils a prominent role of the right hemispheric central autonomic network, especially of the insular cortex, in the brain-heart axis. Our results support preliminary evidence that acute ischaemic stroke in distinct brain regions of the central autonomic network may directly impair cardiac function and thus further supports the concept of a distinct stroke-heart syndrome.
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