Arterial hypertension is the most prevalent non-communicable disease worldwide, and has long been recognized as a major risk factor for cardiovascular and cerebrovascular diseases. High blood pressure has deleterious consequences on the main target organs (heart, kidney, brain), and several studies have shown that brain damage is more frequent than heart and kidney involvement. Silent lesions can subsequently lead to cognitive decline, dementia or stroke.

Nevertheless, screening for subclinical brain deterioration is rarely performed because it requires imaging techniques whose scarcity and high cost rule out routine use by primary care physicians. The challenge is thus early detection of asymptomatic brain lesions with cost-effective techniques to test thousands of patients in the community. In this review we present an update on the status of biomarkers explored as alternatives for early detection of brain damage in arterial hypertension, potentially useful to identify patients needing referrals for brain MRI: ambulatory blood pressure monitoring, quantitative retinal microvascular assessment, quantitative electroencephalography, carotid ultrasonography, neurocognitive studies and blood-based biomarkers. We place special emphasis on blood-based biomarkers, for which our group reported the first preliminary evidence of an association between serum neuron-specific enolase and severity of white matter lesions in patients with essential hypertension. This review consequently explores the potential for blood-based biomarkers to provide a faster, cheaper and more accessible early-detection solution, particularly beneficial in resource-limited settings such as Cuba’s.

KEYWORDS Arterial hypertension,small vessel disease, brain damage, biomarkers, white matter diseases, leukoaraiosis, lacunar infarct, S100 calcium binding protein beta subunit, S100B protein, S100 calcium binding protein G, neuron specific enolase, NMDA receptors, receptors, N-methyl-D-aspartate, mass screening, Cuba

Introduction Many studies to date on the link between blood lipid levels and cerebrovascular disease have been hampered by conceptual and methodological limitations, especially failure to separate different types of stroke.

Objective Determine the relationship between serum lipid levels and the occurrence of different types of stroke.

Methods Two case and control studies were undertaken. The first consisted of three groups: subjects with cerebral infarction (CI), subjects with cerebral hemorrhage (CH) and a control group of healthy individuals with no history of cerebrovascular disease. The second study included three groups: those with atheromatous CI, those with CI of other etiology, and the healthy control group. The influence of variables such as age, sex, and presence of risk factors was also assessed.

Results CI patients were found to have higher total cholesterol levels (p<0.01), low-density lipoprotein (LDL) cholesterol (p<0.01), and triglycerides (p<0.01) than those in the control group. CH patients had lower total cholesterol levels (p<0.05), and higher triglycerides levels (p<0.05) than the control group. The second study revealed a link between blood lipid levels and CI only in cases of atheromatous stroke. This association was prevalent in women, and was independent of other risk factors.

Conclusions The type of stroke (ischemic or hemorrhagic) and the etiopathogenic subtype of CI must be considered when studying association between blood lipids and occurrence of stroke. Elevated levels of total cholesterol, LDL and triglycerides are associated with occurrence of atheromatous CI, while low total cholesterol levels and high triglycerides levels are associated with the CH occurrence.

Keywords cholesterol, HDL, LDL, triglycerides, cerebral hemorrhage, cerebral infarction, atherosclerosis, vascular diseases, cerebrovascular disorders, stroke, cerebrovascular accident, CVA, ischemia, hyperlipidemias

The following erratum has been corrected in all versions of this article.

Page 28, full paragraph 8, second sentence should read: “Serum was stored at -20ºC for no longer than 20 days.”