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Cardiac Wall Motion Abnormality After Bleeding from Vertebral Artery Aneurysms

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Journal Clin Auton Res
Date 2014 Oct 3
PMID 25273609
Citations 2
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Abstract

Objective: Lesions in the medulla oblongata may be causally associated with cardiac wall motion abnormality (WMA). Although subarachnoid hemorrhage (SAH) patients occasionally develop WMA, the relationship between aneurysmal locations and the frequency of WMA has rarely been investigated. The objective of this study was to evaluate whether the frequency of WMA was higher after the rupture of vertebral artery (VA) aneurysms than that of non-VA aneurysms.

Methods: We performed a retrospective chart analysis of 244 SAH patients who underwent transthoracic echocardiography and plasma catecholamine measurements. The frequencies of WMA and electrocardiographic (ECG) abnormalities were compared among patients classified by the location of aneurysms. Multivariate regression analysis was conducted to identify variables correlated with WMA. Furthermore, the relationship between plasma catecholamine levels and aneurysmal locations was evaluated.

Results: The frequency of WMA was significantly higher in patients with VA aneurysms than in those with non-VA aneurysms (45 vs. 22 %, p = 0.01). However, there was no significant difference in the frequency of ECG abnormalities. Multivariate regression analysis showed that VA aneurysms (OR, 3.317; 95 % CI, 1.129-9.745), poor-grade SAH (OR, 2.733; 95 % CI, 1.320-5.658) and concomitant hydrocephalus (OR, 3.658; 95 % CI, 1.690-7.917) correlated with WMA. There were no significant intergroup differences in plasma catecholamine levels.

Conclusion: VA aneurysms are close to several medullary nuclei that integrate autonomic inputs. A transient deformation and ischemia of the medulla oblongata caused by the mechanical stress related to the rupture of a VA aneurysm and/or a concomitant hydrocephalus may be responsible for the disproportionately high frequency of WMA.

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Plasma Catecholamine Profile of Subarachnoid Hemorrhage Patients with Neurogenic Cardiomyopathy.

Moussouttas M, Mearns E, Walters A, Decaro M Cerebrovasc Dis Extra. 2015; 5(2):57-67.

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