Letter Regarding Article by Banki et al, “Acute Neurocardiogenic Injury After Subarachnoid Hemorrhage”
To the Editor:
In their stimulating article, Banki et al1 showed that the left ventricular dysfunction found in a third of the patients studied with subarachnoid hemorrhage (SAH) is associated with an abnormal sympathetic innervation and a release of cardiac enzymes despite a normal myocardial perfusion.
Interestingly, the neurocardiogenic injury after SAH shares some features in common with stress cardiomyopathy (SC).2 Both have high levels of plasma catecholamine associated with regional wall motion abnormalities and sympathetic regional denervation.1,3 For these striking similarities, the authors should provide more information about (a) the amount of the increase in catecholamine concentration (is this similar to that of SC?) and (b) whether the wall motion abnormalities localized in the apical region, and whether these recover in a period of a few months, as in SC? Last but not least, women more often than men are affected by SAH4 and represent the vast majority of SC.2 I wonder if the abnormalities found are instead due to a form of SC triggered by and not belonging specifically to the SAH picture. Women indeed represent 78% of this study population, and, in the settings of SAH, female gender is known to be more susceptible than male to QT prolongation and hypokalemia, all indirect signs of an important sympathetic activation.5
Banki NM, Kopelnik A, Dae MW, Miss J, Tung P, Lawton MT, Drew BJ, Foster E, Smith W, Parmley WW, Zaroff JG. Acute neurocardiogenic injury after subarachnoid hemorrhage. Circulation. 2005; 112: 3314–3319.
Epidemiology of aneurysmal subarachnoid hemorrhage in Australia and New Zealand: incidence and case fatality from the Australasian Cooperative Research on Subarachnoid Hemorrhage Study (ACROSS). Stroke. 2000; 31: 1843–1850.
Fukui S, Otani N, Katoh H, Tsuzuki N, Ishihara S, Ohnuki A, Miyazawa T, Nawashiro H, Shima K. Female gender as a risk factor for hypokalemia and QT prolongation after subarachnoid hemorrhage. Neurology. 2002; 59: 134–136.