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Stroke. 2006;37:944-945
doi: 10.1161/01.STR.0000210147.60258.53
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(Stroke. 2006;37:944.)
© 2006 American Heart Association, Inc.


Letters to the Editor

Hyperglycemia and Hyperinsulinemia in Circulatory Disorder After Subarachnoid Hemorrhage

Kazushi Tsuda, MD, FAHA

Division of Cardiology, Department of Medicine, Wakayama Medical University, Wakayama, Japan


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

We read with great interest the recent article by Dr Frontera and colleagues1 dealing with the relationship between hyperglycemia and complications after subarachnoid hemorrhage (SAH). The results of their study demonstrated that hyperglycemia (the average peak daily glucose level >105 mg/dL) after SAH was associated with serious hospital complications, such as congestive heart failure, increased intensive care unit length of stay, and an increased risk of death or severe disability. The authors proposed that strict normoglycemic management in patients with SAH might be important.

Numerous studies have shown that hyperglycemia may actively participate in the regulation of cellular functions. Barbagallo et al2 showed that hyperglycemia elevated cytosolic free calcium (Ca) both in myocardial and vascular smooth muscle cells, suggesting that glucose-related excess intracellular Ca might be a fundamental lesion in diabetes that contribute to the elevated blood pressure and cardiac mass in this disease. On the other hand, it is well recognized that hyperglycemia may be associated with hyperinsulinemia. Evidence indicates that hyperinsulinemia might actively participate in the regulation of circulatory disorders. Sela et al3 demonstrated that polymorphonuclear leukocytes (PMN) in essential hypertension showed increased level of intracellular Ca content correlating positively with the individulal’s blood pressure and plasma insulin. They proposed that, because PMN priming may lead to oxidative stress and inflammation, intracellular Ca and insulin are involved in the pathogenesis of hypertension-induced vascular injury. In a study we presented earlier, a relationship between membrane fluidity (a reciprocal value of membrane microviscosity) of erythrocytes and insulin . . . [Full Text of this Article]

Jennifer Frontera, MD Stephan Mayer, MD

Division of Stroke and Neuro-Critical Care, Columbia University College of Physicians and Surgeons, New York, NY