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Correspondence to:

ARTICLES:
S. Laowattana, S. L. Zeger, J.A.C. Lima, S. N. Goodman, I. S. Wittstein, and S. M. Oppenheimer
Left insular stroke is associated with adverse cardiac outcome
Neurology 2006; 66: 477-483 [Abstract] [Full text] [PDF]
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Correspondence published:

[Read Correspondence] Left insular stroke is associated with adverse cardiac outcome
Sascha Meyer, Matthias Strittmatter, Dept. Neurology, Merzig, Germany   (5 June 2006)
[Read Correspondence] Reply from the authors
Stephen Oppenheimer, Somchai Laowattana   (5 June 2006)

Left insular stroke is associated with adverse cardiac outcome 5 June 2006
 Next Correspondence Top
Sascha Meyer,
University Hospital of Saarland, Department of Neuropediatrics and Neurology
Kirrbergerstr., Building 9, 66421 Homburg/Saar, Germany,
Matthias Strittmatter, Dept. Neurology, Merzig, Germany

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Re: Left insular stroke is associated with adverse cardiac outcome

sascha.meyer{at}uniklinikum-saarland.de Sascha Meyer, et al.

We read with interest the article by Laowattana et al. [1] They found that left insular stroke - as opposed to right insular stroke - was associated with an increased risk of adverse cardiac outcomes or cardiac wall motion impairment. This conflicts with other clinical studies that demonstrated substantive cardio-vascular dysfunction including sudden death mainly after right insular stroke. [2]

In our study, cardiovascular (heart rate and blood pressure) and autonomic function (plasma norepinephrine and epinephrine concentration) was assessed sequentially at six defined timepoints within the first five days after insular stroke. [3] We could demonstrate a sustained up-regulation of cardio-autonomic function in right insular stroke patients. This might be of prognostic significance since PET studies have shown a reduced hemodynamic reserve in hypertensive patients which renders the penumbra vulnerable even to a small reduction in blood pressure. [4] Reports of possible adverse effects of sympathovagal shifts as a progenitor of cardiac arrhythmogenesis [2] may be offset by an increase in penumbra viability. However, involvement of the insular cortex, the occurrence of a pathologic nighttime blood pressure increase, and an initially increased serum norepinephrine concentration appear to be independent predictors of poor long-term outcome in thromboembolic stroke [5].

Instead of considering only either cardiac or neurological sequelae like Laowattana et al, future clinical trials should relate both neurological and cardiac outcome to cardio-autonomic dysfunction in the acute phase after stroke.

References

1. Laowattana S, Zeger SL, Lima JAC, Goodman SN, Wittstein IS, Oppenheimer SM. Left insular stroke is associated with adverse cardiac outcome. Neurology 2006; 66:477-483

2. Tokgozoglu SL, Batur MK, Topcuoglu MA, Saribas O, Kes S, Oto A. Effects of stroke localization on cardiac autonomic balance and sudden death. Stroke 1999; 30:1307–1312.

3. Meyer S, Strittmatter M, Fischer C, Georg, T, Schmitz B. Lateralization in autononic dysfunction in ischemic stroke involving the insular cortex. Neuroreport 2004; 15:357-362

4. Fujii K, Sadoshima S, Okada Y, et al. Cerebral blood flow and metabolism in normotensive and hypertensive patients with transient neurologic deficits. Stroke 1990; 21:283–290

5. Sander D, Winbeck K, Klingelhofer J, Etgen T, Conrad B. Prognostic relevance of pathological sympathetic activation after acute thromboembolic stroke. Neurology 2001;11:833–838

Disclosure: The authors report no conflicts of interest.

Reply from the authors 5 June 2006
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Stephen Oppenheimer,
New Jersey Neurosciences Inst
101 Wendover Road Baltimore, MD,
Somchai Laowattana

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Re: Reply from the authors

soppenh{at}hotmail.com Stephen Oppenheimer, et al.

We thank Drs. Meyer and Strittmatter for their interest in our paper. [1] They cite two articles evaluating autonomic lateralization, insular stroke, and sudden death. [2,3] These differ from ours in the timing of recruitment and in follow up. For example, their study is confined to 5 days of follow up and ours extends over one year. This complicates direct comparison. Additionally, their study examines laboratory and not clinical outcome (as in our study).

Meyer and Strittmatter mention a report to show an association between location and sudden death 5/23 patients with right insular stroke and 2/25 with left insular stroke suffered this outcome. Statistical analysis was not performed but we compute p = 0.42 (Fisher’s exact test). [2] This would actually indicate no difference in sudden death between left vs. right insular stroke. To the best of our knowledge, there has been only one previous evaluation of stroke lateralization and sudden death including sufficient numbers for statistical analysis. This indicates an association with left and not right hemispheric stroke. [6]

Finally, the association of long term clinical outcome with acute laboratory measures is complicated. Any such assessments can be potentially confounded by intervening medication changes and medical events which should therefore be accommodated in such predictive assessments.

Reference

6. Algra A, Gates P, Fox A, Hachinski V, Barnett HJM. Side of brain infarction and long-term risk of sudden death in patients with symptomatic carotid disease. Stroke 2003;34:2871-2875.

Disclosure: The authors report no conflicts of interest.


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