ABSTRACT
Stroke is the third most frequent cause of death after cancer and heart disease in developed countries and one of the most common reasons for developing cognitive impairment and vascular dementia (VD).1 The pathogenesis of stroke and its consequences are not fully understood, and there are different factors and biological mechanisms that may play a role in stroke development (Figure 18.1).2 It is known that high blood pressure (BP) is a major risk factor for ischemic and hemorrhagic stroke in men and women3 and for small vessel disease predisposing to lacunar infarction, white matter lesions (WMLs), and cerebral microbleeds,4-6 which are frequently silent.3,4,7
A continuous relationship between BP and stroke occurrence has been well established.8,9 On the other hand, evidence from hypertension treatment trials has shown that relatively small reductions in BP (5-6 mmHg in diastolic BP [DBP], 10-12 mmHg in systolic BP [SBP] over 3-5 years) reduce the risk of stroke by more than one-third.10 The primary prevention of stroke through antihypertensive therapy and BP control is well established. Likewise, higher BP levels after stroke increase the risk of recurrent stroke,11 and recent trials indicate that BP reduction with combined antihypertensive therapy is beneficial in reducing stroke recurrence.12
