Effects of blood pressure lowering in patients with acute ischemic stroke and carotid artery stenosis

Precisely what exactly are they trying to say in this research? So ask your doctor to translate. Should blood pressure be lowered? Should candesartan be given? An appalling writeup. What is the protocol?
How does this compare to these articles? Has your doctor read a single one of these articles?

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Other research here:

1. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset

2. Early Intensive Blood-Pressure Lowering Improves Recovery in Patients With Acute Intracerebral Haemorrhage

 3.  Systolic Blood Pressure During Acute Stroke Is Associated With Functional Status and Long-term Mortality in the Elderly

 4. External Counterpulsation Augments Blood Pressure and Cerebral Flow Velocities in Ischemic Stroke Patients With Cerebral Intracranial Large Artery Occlusive Disease

5.  The One Benefit Of High Blood Pressure? It May Prevent Dementia

6.  Stopping Pre-Stroke Antihypertensive Medication Advised During Acute Stroke 

7.  Mild induced hypertension improves blood flow and oxygen metabolism in transient focal cerebral ischemia

8.  Low Diastolic Pressure Linked to Brain Atrophy 

9.  New Treatment for Stroke Set to Increase Chances of Recovery - haemorrhage blood pressure lowering

 

Effects of blood pressure lowering in patients with acute ischemic stroke and carotid artery stenosis

Jusufovic M¹, Sandset EC, Bath PM, Karlson BW, Berge E; Scandinavian Candesartan Acute Stroke Trial (SCAST) Study Group.

Author information

Abstract

BACKGROUND:

The Scandinavian Candesartan Acute Stroke Trial (SCAST) showed no beneficial clinical effects of blood pressure lowering with the angiotensin receptor blocker candesartan in the acute phase of stroke. In the present analysis we wanted to see if the effects of blood pressure lowering are harmful in the subgroup of patients with carotid artery stenosis.

METHODS:

SCAST was a randomized- and placebo-controlled, double-masked trial of 2029 patients with acute stroke and high systolic blood pressure (≥140 mmHg). Of 1733 patients with ischemic stroke 993 underwent carotid artery imaging, and the degree of stenosis was categorized as no/insignificant (0-49%, n = 806), moderate (50-69%, n = 97) or severe (≥70%, n = 90). The trial's two co-primary effect variables were the composite end-point of vascular death, stroke or myocardial infarction, and functional outcome at six-months, according to the modified Rankin Scale.

RESULTS:

Among patients with moderate or severe carotid artery stenosis the vascular end-point occurred in 9 of 87 patients (10·3%) treated with candesartan and in 17 of 100 controls (17·0%), and there was no evidence of a different risk in patients with severe stenosis (adjusted hazard ratio 0·74, 95% confidence interval 0·28-1·96, P = 0·54). For functional outcome there was also no clear difference, although in patients with severe stenosis the risk of a poor outcome was somewhat higher than in any of the other groups (adjusted odds ratio 2·24, 95% confidence interval 0·71-7·09, P = 0·16). Progressive stroke also occurred more often in patients with carotid artery stenosis treated with candesartan (10 of 87 patients (11·5%) vs. 4 of 100 patients (4·0%)), with a trend towards an increased risk with increasing severity of stenosis (P-value for linear trend = 0·04).

CONCLUSIONS:

There is no clear evidence that the effect of candesartan is qualitatively different in patients with carotid artery stenosis, but there are signals that patients with severe stenosis are at particularly high risk of stroke progression and poor functional outcome.