Letter by Arsava and Topcuoglu Regarding Article, “Ischemic Brain Injury Following Intracerebral Hemorrhage—A Critical Review”
To the Editor:
We read with great interest the recent review by Prabhakaran and Naidech,1 in which they nicely summarize the recent literature regarding concomitant acute ischemic lesions in patients with intracerebral hemorrhage (ICH). In their review, they emphasize the role of significant blood pressure reductions, among many other potential factors, in the cause of these lesions.1 The basis for this hypothesis stems from observations reported in 3 of the 6 publications revised by the authors, which have shown a significant association between acute ischemic lesions on diffusion-weighted imaging and blood pressure lowering. Although the induction of ischemia by sudden decrements in blood pressure is a valid assumption, we believe that there might be an alternative explanation for this observation.
Acute and sudden elevations in systemic blood pressure cause obliterative spasm and necrosis in terminal segments of cerebral arteries, leading to microinfarctions in their territories.2 In our publication analyzing the predictors of acute ischemic lesions in the setting of ICH, we found a significant relationship between acute ischemic lesions on diffusion-weighted imaging and admission mean arterial blood pressure.3 Due to the retrospective nature of the study, we were not able to analyze the effect of blood pressure fluctuations over 24 hours in our entire cohort. Nonetheless, the pattern of ischemic lesions in our patients did not resemble patterns observed in patients suffering from hemodynamic compromise. Furthermore, considering that elevations in intracranial pressure are more significant in the perihematomal regions, one would expect to observe ischemic lesions near the hemorrhage where blood pressure reductions should theoretically have the greatest impact on cerebral blood flow. However, such a predilection was evident neither in our study, nor in other patient cohorts.4 Therefore, apart from the impact of blood pressure reductions, we believe that extent of initial blood pressure elevation might play a role in the development of ischemic lesions in patients with ICH. Such an elevation, in the appropriate setting such as an already established underlying microangiopathy, might be responsible both for the incident ICH and ischemic lesions that accompany the hemorrhage.
A controlled and gradual reduction in blood pressure is the standard of care in acute management of patients with ICH. As nicely shown in figure 3 of the review,1 patients with higher admission blood pressures are also the one’s with the most significant drops in blood pressure during the initial hours. Therefore, unless magnetic resonance imaging is performed at the hyperacute stage, it is not entirely possible to tease out which of these blood pressure–related parameters, the higher admission blood pressures or the greater blood pressure reductions in these patients, are related to the development of ischemic lesions in patients with ICH. Future prospective studies, with large number of patients and magnetic resonance imaging obtained at several time points, especially before and after blood pressure control, might help us better understand the underlying pathophysiology of these lesions.
Ethem Murat Arsava, MD
Mehmet Akif Topcuoglu, MD
Department of Neurology, Faculty of Medicine, Hacettepe University, Ankara, Turkey
Stroke welcomes Letters to the Editor and will publish them, if suitable, as space permits. Letters must reference a Stroke published-ahead-of-print article or an article printed within the past 3 weeks. The maximum length is 750 words including no more than 5 references and 3 authors. Please submit letters typed double-spaced. Letters may be shortened or edited. Include a completed copyright transfer agreement form (available online at http://stroke.ahajournals.org and http://submit-stroke.ahajournals.org).
- © 2012 American Heart Association, Inc.
- Prabhakaran S,
- Naidech AM
- Murat Arsava E,
- Kayim-Yildiz O,
- Oguz KK,
- Akpinar E,
- Topcuoglu MA