ABSTRACT
Before the statin era, any attempt to reduce total blood cholesterol levels, either by a diet approach or by a fibric acid agent-based lipid-lowering therapy, failed to significantly reduce the incidence of stroke (1). Indeed, although blood cholesterol has been closely associated with carotid atherosclerosis, which causes atherothrombotic strokes, paradoxically, the link between serum cholesterol level and all strokes has never been fully established (2). Consequently, reducing cholesterol levels after a stroke was not often considered a valuable objective by most clinicians.
