Is elevated blood pressure associated with increase of plasma c-reactive protein levels in acute ischemic stroke?

ABSTRACT

Elevated blood pressure [BP] levels have been associated with an increased risk of stroke and of cardiovascular disease. It is now well established that vascular inflammation is an independent risk factor for the development of atherosclerosis. Furthermore, low grade of inflammation, assessed by C-reactive protein [CRP], significantly predict the risk of future ischemic stroke. Thus, the mechanism underlying the link between elevated blood pressure and an increased risk of stroke may be inflammation. The aim of this work was to study the association between blood pressure and baseline concentrations of c-reactive protein levels in acute ischemic stroke among ischemic stroke patients. The original inclusion criteria were a diagnosis of first-ever ischemic stroke within 24 hours before enrollment. Sixty four patients [37 men, 27 women, mean age 63.7 +/- 11.63 yr] with all forms of ischemic infarctions diagnosed clinically and radiologically by CT and/or MRI were considered for inclusion in the study between February 2004 and October 2005. We excluded patients with diseases that might substantially affect their levels of CRP and who had a cardioembolic etiology. Complete data on systolic BP [SBP], diastolic BP [DBP], mean arterial pressure [MAP], pulse pressure [PP] values, plasma levels of CRP, cigarette smoking, total cholesterol levels, neuroradiological findings, neurological deficit severity assessed by the Canadian Neurological Stroke Scale [CNSS] and antihypertensive drugs were collected at the entry. We studied the association between BP and baseline concentrations of CRP within 24 hours after stroke onset. There was a significantly higher levels of CRP levels in patients with arterial hypertension than in patients without arterial hypertension at the entry. Patients without a history of arterial hypertension had a significantly higher levels of CRP at the entry than patients with a documented history. Those with a high CRP levels had a significant higher mean SBP, DBP, MAP and PP. Additionally, stroke patients with a high CRP level were significantly older, smokers, had a significantly higher total cholesterol levels with a more severe neurological deficit. CRP levels were significantly lower in patients receiving angiotensin converting enzyme-inhibitors. There was a significant correlation between CRP levels and SBP, DBP, MAP, PP values, total cholesterol levels, but negative with neurological deficit severity assessed by the CNSS. An increase in SBP, DBP, MAP, or PP was significantly associated with an increase in the odds of having an elevated CRP level[>1.5 mg/dL], independent of other associated study factors. Our results suggested that elevated levels of systolic or diastolic blood pressure in the acute phase after an ischemic stroke are associated with elevated CRP levels. These findings support a possible role of acute hypertension after stroke as an inflammatory stimulus contributing to ischemic brain inflammation