Letter to the Editor 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.
Letter by Gioia et al Regarding Article, “Blood Pressure–Lowering Treatment With Candesartan in Patients With Acute Hemorrhagic Stroke” To the Editor: We read with interest the post hoc analysis of the Scandinavian Candesartan Acute Stroke Trial (SCAST) trial by Jusufovic et al,1 suggesting that there is no evidence that blood pressure (BP) lowering with candesartan is beneficial and possibly harmful. We suggest that the authors’ conclusions may be overstated and counter to observations from other recent trials. It is surprising that the primary limitation of this secondary analysis was not acknowledged. The primary predictors of early mortality in intracerebral hemorrhage (hematoma volume, presence of intraventricular hemorrhage, level of consciousness at admission, and infratentorial intracerebral hemorrhage location) were not known or accounted for in this study.2 Although the mean Scandinavian Stroke Score was similar in both groups at admission, baseline hematoma volumes may have differed. Imbalances in any of the above-mentioned predictors of mortality may account for the higher modified Rankin Scale scores seen in patients randomized to the candesartan treatment arm. The authors suggest the BP-lowering properties of candesartan as the most likely mechanism of worse outcome in the treatment group. The mean decrease in BP in the candesartan-treated patients, relative to placebo, was modest (−5/−2 mm Hg), however. Throughout the 7-day treatment period, differences between groups were significant only on day 6, making it unlikely in our opinion that BP decreases were related to outcomes. Alternative explanations are suggested by the authors, including unwanted properties of angiotensin II receptor blockade, but the possibility remains that this is simply a type I error. The authors hypothesize that BP reduction may reduce cerebral perfusion and increase brain injury even further after the first few hours from intracerebral hemorrhage onset. There is no evidence to support this statement and in fact we have reported precisely the opposite in the The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT).3 The primary objective of this randomized trial was to assess the effect of BP reduction on perihematoma cerebral blood flow, measured with computed tomography perfusion, in acute intracerebral hemorrhage patients. Despite a highly significant decrease in systolic BP in the
Letter by Gioia et al Regarding Article, “Blood Pressure–Lowering Treatment With Candesartan in Patients With Acute Hemorrhagic Stroke” To the Editor: We read with interest the post hoc analysis of the Scandinavian Candesartan Acute Stroke Trial (SCAST) trial by Jusufovic et al,1 suggesting that there is no evidence that blood pressure (BP) lowering with candesartan is beneficial and possibly harmful. We suggest that the authors’ conclusions may be overstated and counter to observations from other recent trials. It is surprising that the primary limitation of this secondary analysis was not acknowledged. The primary predictors of early mortality in intracerebral hemorrhage (hematoma volume, presence of intraventricular hemorrhage, level of consciousness at admission, and infratentorial intracerebral hemorrhage location) were not known or accounted for in this study.2 Although the mean Scandinavian Stroke Score was similar in both groups at admission, baseline hematoma volumes may have differed. Imbalances in any of the above-mentioned predictors of mortality may account for the higher modified Rankin Scale scores seen in patients randomized to the candesartan treatment arm. The authors suggest the BP-lowering properties of candesartan as the most likely mechanism of worse outcome in the treatment group. The mean decrease in BP in the candesartan-treated patients, relative to placebo, was modest (−5/−2 mm Hg), however. Throughout the 7-day treatment period, differences between groups were significant only on day 6, making it unlikely in our opinion that BP decreases were related to outcomes. Alternative explanations are suggested by the authors, including unwanted properties of angiotensin II receptor blockade, but the possibility remains that this is simply a type I error. The authors hypothesize that BP reduction may reduce cerebral perfusion and increase brain injury even further after the first few hours from intracerebral hemorrhage onset. There is no evidence to support this statement and in fact we have reported precisely the opposite in the The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT).3 The primary objective of this randomized trial was to assess the effect of BP reduction on perihematoma cerebral blood flow, measured with computed tomography perfusion, in acute intracerebral hemorrhage patients. Despite a highly significant decrease in systolic BP in the
