High blood pressure in acute ischemic stroke and underlying disorders.
BACKGROUND
The Acute Candesartan Cilexetil Therapy in Stroke Survivors (ACCESS) study indicated that early treatment with an angiotensin type 1 receptor blocker in acute stroke patients who had relatively high blood pressure improved cardiovascular morbidity and mortality in the chronic stage. To better interpret the findings of this study, we determined whether stroke patients with high acute blood pressure had specific underlying conditions.


METHODS
We divided 712 consecutive patients who were hospitalized within 48 h after the onset of brain infarction into two groups: 77 patients with high acute blood pressure that met the criteria of the ACCESS study and the 635 remaining patients. Underlying risk factors and comorbidities, stroke characteristics, as well as mortality, vascular events, and disability at 3 weeks were compared between the two groups.


RESULTS
Patients with high acute blood pressure more frequently had diabetes mellitus (p < 0.01), intracranial arterial stenosis (p < 0.02), higher levels of hemoglobin A1c (p < 0.005), higher creatinine levels (p < 0.005), and tended to more frequently have ischemic heart disease (p < 0.09) and infarcts <1.5 cm in diameter (p < 0.09) than the other patients. On multivariate analysis, high levels of hemoglobin A1c, high creatinine levels, and intracranial arterial stenosis were independently predictive of high acute blood pressure. At 3 weeks after the stroke onset, patients with high acute blood pressure were more dependent in their daily living activities (p < 0.02) and more frequently developed vascular events or death (p < 0.005) than the other patients.


CONCLUSIONS
Poorly controlled diabetes mellitus and advanced renal damage appeared to correlate with acute hypertension after stroke. Since intracranial arterial stenosis also seemed to contribute to high acute blood pressure, one should be careful not to induce cerebral hypoperfusion by the early use of antihypertensives.
Toyoda
Kazunori
K
Department of Cerebrovascular Disease, Cerebrovascular Center and Clinical Research Institute, National Kyushu Medical Center, Fukuoka, Japan. toyoda@hsp.ncvc.go.jp
Okada
Yasushi
Y
Jinnouchi
Juro
J
Gotoh
Seiji
S
Yokoyama
Yoko
Y
Fujimoto
Shigeru
S
Ibayashi
Setsuro
S
D000368:Aged; D001794:Blood Pressure; D002536:Cerebral Arteries / Q000473:pathology; D003251:Constriction, Pathologic; D003404:Creatinine / Q000097:blood; D048909:Diabetes Complications / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D020765:Intracranial Arterial Diseases / Q000150:complications / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications; D012307:Risk Factors; D020521:Stroke / Q000097:blood / Q000150:complications / Q000503:physiopathology*
D003404:Creatinine; D006442:Glycated Hemoglobin