(Stroke. 2004;35:1786.)
© 2004 American Heart Association, Inc.
Letters to the Editor |
Blood Pressure in Acute Stroke and Its Prognostic Value
Department of Neurology, University of Athens, Eginition Hospital, Athens, Greece
Acute Stroke Unit Department of Clinical Therapeutics, University of Athens, Alexandra Hospital, Athens, Greece
To the Editor:
We read with interest the recent paper by Castillo and colleagues evaluating the prognostic relevance of admission blood pressure (BP) values and describing a U-shaped effect in patients with acute ischemic stroke, as well as Boysen’s editorial comment on this issue.1,2 The study’s conclusion was that both high and low admission BP values are associated with poor prognosis regarding early neurological deterioration, infarct volume, and mortality at 3 months. After adjustment for the use of antihypertensive drugs and BP drop >20mm Hg, the authors found that the latter was the most important prognostic factor for poor outcome.
Before accepting these important conclusions, we think that some comments are needed. We have also evaluated the prognostic value of admission BP values in an unselected collective of acute stroke patients. Our findings demonstrated that early and late mortality in patients with ischemic stroke as well as in patients with intracerebral hemorrhage followed a U-shaped pattern in relation to systolic and diastolic BP at admission.3 Low admission BP values were associated with heart failure and coronary artery disease, whereas high BP values were associated with history of hypertension and lacunar stroke. Death due to cardiovascular disease was significantly more frequent among patients with admission BP values beneath the U-point of 130 mm Hg, whereas death due to brain edema was significantly more frequent above this U-point.3 We also demonstrated by means of 24-hour BP monitoring that persisting elevated systolic 24-hour BP values during the acute phase of stroke are associated with subsequent brain edema formation in patients not receiving antihypertensive medication during the BP monitoring.4 Investigating the relationship of 24-hour BP to baseline characteristics in stroke subtypes of different etiopathogenic mechanisms, we found that high and low 24-hour BP values correlated with brain edema and heart failure, respectively, in patients with cardioembolic stroke; whereas low BP values correlated with coronary artery disease in lacunar patients.5
The study of Castillo and colleagues differs from our own work in several aspects that deserve attention. Castillo et al suggest that both low and high admission BP values are associated with a higher mortality. However, with the exception of atrial fibrillation, no other data concerning concomitant diseases are given. In addition, details about the exact causes of death in deceased patients would be useful. Such data would be interesting and, if in accordance with ours,3,5 they would then support Boysen’s thesis that the U-shape relationship may reflect cardiac failure being more important in stroke patients with low systolic BP.2 Another issue, which probably needs further discussion, is whether not only ischemic but also edematous tissue was included in the hypodense zone, which was used for infarct volume calculation. Should that be the case, it would be in accordance with our results.3,4 Moreover, the International Stroke Trial (IST) described an independent association between death resulting from presumed cerebral edema and high systolic BP.6 We therefore support Boysen’s assumption that the U-shape relationship may reflect an adverse effect on brain edema in those with very high BP values.2 Additionally, the finding that a BP drop >20 mm Hg within the first day is the most important prognostic factor of poor outcome should be faced with caution. Christensen et al have reported that an early spontaneous BP decline is associated with good outcome.7 Furthermore, elevated weighted mean arterial blood pressure values were associated with poor outcome in the GAIN Trial.8 Finally, according to our data, the lower incidence of brain edema observed in hyperacute stroke patients who sustained a spontaneous BP decline could be attributed to an earlier normalization of poststroke hypertension.4 The fact that in Castillo’s study the physicians of the emergency department treated 22% of all patients with antihypertensive agents without following specific guidelines for BP management raises the question whether that was really indicated in all these cases. It is obvious that the described BP drop is not spontaneous and at least in part drug-induced. It also remains unclear if some or all of the patients who received antihypertensive medication in the stroke unit were already premedicated in the emergency department. This might have caused an excessive BP decline leading to hypoperfusion and clinical deterioration, especially in cases of lacunar stroke.
In conclusion, we agree that high and low BP correlates with poor prognosis and that it is unlikely that there will be one treatment for all stroke patients.1,2 Prospective randomized clinical trials with sufficient size and power to include representative patient groups of different age, concomitant diseases, severity, and etiology are required to clarify the issue of optimal BP management in the acute stroke setting.
References
- Castillo J, Leira R, Garcia MM, Serena J, Blanco M, Dávalos A. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. 2004; 35: 520–526.
[Abstract/Free Full Text] - Boysen G. Editorial comment–persisting dilemma: to treat or not to treat blood pressure in acute ischemic stroke. Stroke. 2004; 35: 526–527.
[Free Full Text] - Vemmos KN, Tsivgoulis G, Spengos K, Zakopoulos N, Synetos A, Kotsis V, Vassilopoulos D, Mavrikakis M. Association between 24-h blood pressure monitoring variables and brain oedema in patients with hyperacute stroke. J Hypertens. 2003; 21: 2167–2173.[CrossRef][Medline] [Order article via Infotrieve]
- Vemmos KN, Tsivgoulis G, Spengos K, Zakopoulos N, Synetos A, Manios E, Konstantopoulou P, Mavrikakis M. U-shaped relationship between mortality and admission blood pressure in patients with acute stroke. J Intern Med. 2004; 255: 257–265.[CrossRef][Medline] [Order article via Infotrieve]
- Vemmos KN, Spengos K, Tsivgoulis G, Zakopoulos N, Manios E, Kotsis V, Daffertshofer M, Vassilopoulos D. Factors influencing acute blood pressure values in stroke subtypes. J Hum Hypertens. 2004; 18: 253–259.[CrossRef][Medline] [Order article via Infotrieve]
- Leonardi-Bee J, Bath PM, Phillips SJ, Sandercock PA; IST Collaborative Group. Blood pressure and clinical outcomes in the International Stroke Trial. Stroke. 2002; 33: 1315–1320.
[Abstract/Free Full Text] - Christensen H, Meden P, Overgaard K, Boysen G. The course of blood pressure in acute stroke is related to the severity of the neurological deficits. Acta Neurol Scand. 2002; 106: 142–147.[CrossRef][Medline] [Order article via Infotrieve]
- Aslanyan S, Fazekas F, Weir CJ, Horner S, Lees KR; GAIN International Steering Committee and Investigators. Effect of blood pressure during the acute period of ischemic stroke on stroke outcome. A tertiary analysis of the GAIN international trial. Stroke. 2003; 34: 2420–2425.
[Abstract/Free Full Text]
Response
Department of Neurology, Hospital Clínico Universitario, Santiago de Compostela, Spain
Department of Neurology, Hospital Universitari Doctor Josep Trueta, Girona, Spain
We appreciate the interest of Tsivgoulis et al in our article on the association of high and low systolic and diastolic blood pressure (BP), as well as a relevant drop in BP, with poor prognosis in patients with ischemic stroke.1 We think that their letter raises some interesting points that may help clarify the issue of optimal BP management in the acute stroke setting. Although we did an observational study without the aim of investigating the etiopathogenic mechanisms linked to stroke prognosis, a further exploratory analysis of our data allows us to give some light to the several mechanisms that have been proposed to explain the association between both high and low BP and outcome.
According to the findings reported by Tsivgoulis et al2 and to the Boysen’s editorial comment,3 our data support the notion that the U-shape mortality pattern reflects cardiovascular diseases being more frequent in stroke patients with low systolic BP. In the 9 patients with cardiac causes of death (acute myocardial infarction, n=5; heart failure, n=4) median [range] admission systolic BP (126 [108–162] versus 166 [130–218] mm Hg, P<0.001) and diastolic BP (67 [55–81] versus 83 [70–120] mm Hg, P<0.001) were lower than in those with stroke- or infection-related death (n=16 and n=11, respectively).
As Tsivgoulis et al mention, part of the hypodensity volume on CT may reflect brain edema instead of definitive necrosis. Although we did not evaluate the potential mass effect of the ultimate infarct volume, systolic BP (217 [190–234] versus 168 [144–181] mm Hg, P<0.001) and diastolic BP (117 [108–132] versus 86 [75–102] mm Hg, P<0.0001) were higher in the 98 patients with early hypodensity on CT. Systolic BP was also significantly higher in the 12 patients who died because of brain edema compared with those with other causes of mortality (226 [184–240] versus 140 [122–175] mm Hg, P<0.001). Therefore, high systolic BP above the U-point of 180 mm Hg could have adverse effects on brain edema, and consequently increase early neurological deterioration and mortality.
A further point of interest is that high BP may also produce basal lamina disturbances, promoting hemorrhagic transformation (HT) of the cerebral infarct.4,5 In our study, HT was seen in 27% of patients with systolic BP >180 mm Hg, whereas it was present in 7% of patients with systolic BP below these values (P<0.001). HT was associated with neurological worsening and poor outcome, although the poor prognosis could be attributed to the HT itself in only 8 patients with parenchymal hemorrhage.
As we recognize in our study, the wrong use of antihypertensive drugs in many instances could lead to hypoperfusion and clinical deterioration. The administration of these agents in the emergency unit was associated with a greater reduction in BP in comparison with that observed when therapy was given by neurologists in the stroke unit (Table). Accordingly, early neurological deterioration was more frequent in patients who received the treatment in the emergency unit than in those treated in the stroke unit. This effect was of more particular importance in patients with cardioembolic stroke than in those with lacunar stroke. This finding is consistent with the idea that a drop in BP might have a less detrimental effect in lacunar infarctions or in large territorial ischemia where a penumbral area is more likely, a hypothesis that has been suggested to explain the different outcome in patients with lacunar and territorial infarctions in the IMAGES Trial.6
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References
- Castillo J, Leira R, Garcia MM, Serena J, Blanco M, Dávalos A. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. 2004; 35: 520–526.
[Abstract/Free Full Text] - Vemmos KN, Tsivgoulis G, Spengos K, Zakopoulos N, Synetos A, Kotsis V, Vasilopoulos D, Mavrikakis M. Association between 24-h blood pressure monitoring variables and brain edema in patients with hyperacute stroke. J Hypertens. 2003; 21: 2167–2173.[CrossRef][Medline] [Order article via Infotrieve]
- Boysen G. Editorial comment–persisting dilemma: to treat or not to treat blood pressure in acute ischemic stroke. Stroke. 2004; 35: 526–527.
[Free Full Text] - Bath FJ, Bath PMW. What is correct management of blood pressure in acute stroke? The Blood Pressure in Acute Stroke Collaboration. Cerebrovasc Dis. 1997; 7: 205–213.
- Dávalos A, Castillo J, Leira R, Serena J, Aneiros A, Castellanos M. Metalloproteinase-9 (MMP-9), early CT signs of cerebral ischemia and high blood pressure in acute stroke. Cerebrovasc Dis. 2001; 11 (suppl 4): 118.[CrossRef]
- Intravenous Magnesium Efficacy in Stroke (IMAGES) Study Investigators. Magnesium for acute stroke (Intravenous Magnesium Efficacy in Stroke Trial): randomised controlled trial. Lancet. 2004; 363: 439–445.[CrossRef][Medline] [Order article via Infotrieve]
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