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Cerebral involvement in hypertensive cardiovascular disease

A. Coca*

Hypertension Unit, Hospital Clinic (IDIBAPS), University of Barcelona, Barcelona, Spain

* Antonio Coca, MD, PhD, Professor of Medicine, Hospital Clinic, Villarroel 170, 08036 Barcelona, Spain.

Abstract

Stroke and dementia in hypertension are the culmination of a complex and largely silent pathogenesis that involves atherosclerosis, vascular remodelling, white matter lesions (WMLs), lacunae and microaneurysms. WMLs in apparently asymptomatic hypertensive persons are associated with incipient cognitive impairment and cardiac hypertrophy. Longitudinal studies have established a link between WMLs and future stoke, and between cognitive decline and hypertension. A small, sustained lowering of systolic/diastolic blood pressure reduces the relative risk of stroke by about 35–40%. A favourable prognosis appears to be not simply a matter of blood pressure control. Angiotensin II receptor blockers are more effective than beta-blockers in reducing the risk for stroke, dementia and left ventricular hypertrophy in hypertensive persons, despite similar reductions in blood pressure. The mechanisms of cognitive decline in hypertension are unclear, but it is known that vascular remodelling and endothelial dysfunction in small arteries are better corrected by blockade of the renin-angiotensin-aldosterone system (RAAS) than by beta-blockade. The role of RAAS blockade in cerebrovascular disease and its prevention will be further investigated in The ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) Trial Programme.

Key Words: Angiotensin receptor blockers • Cognitive impairment • Dementia • Hypertension • Stroke • White matter lesions

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